The Practice of Clinical Echocardiography

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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The Practice of Clinical Echocardiography III

Second Edition Catherine M. Otto MD Professor of Medicine Acting Director, Division of Cardiology Director, Training Programs in Cardiovascular Disease Associate Director, Echocardiography Laboratory University of Washington Seattle, Washington

W.B. SAUNDERS COMPANY An Imprint of Elsevier Science Philadelphia•London•New York•St. Louis•Sydney•Toronto

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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W.B. SAUNDERS COMPANY An Imprint of Elsevier Science The Curtis Center Independence Square West Philadelphia, Pennsylvania 19106 Library of Congress Cataloging-in-Publication Data The practice of clinical echocardiography / [edited by] Catherine M. Otto.—2nd ed. p. cm. Includes bibliographical references and index. ISBN 0-7216-9204-4 1. Echocardiography. I. Otto, Catherine M. [DNLM: 1. Echocardiography. WG 141.5.E2 P8942 2002] RC683.5.U5 C57 2002 616.1'207543-dc21 2001049709 Acquisitions Editor: Richard Zorab Production Editor: Robin E. Davis Production Manager: Mary Stermel Illustration Specialist: Rita Martello Book Designers: Catherine Bradish and Lynn Foulk THE PRACTICE OF CLINICAL ECHOCARDIOGRAPHY, Second Edition ISBN 0-7216-9204-4

Copyright © 2002, 1997 by W.B. Saunders Company. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1

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Contributors

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Gerard P. Aurigemma MD Professor of Medicine and Radiology, University of Massachusetts Medical School; Director, Noninvasive Cardiology, University of Massachusetts Medical Center, Worcester, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas J. Benedetti MD Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Ann F. Bolger MD Associate Clinical Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco General Hospital, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of

Echocardiography Hans G. Bosch MSc Senior Staff Member, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Ian G. Burwash MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Benjamin F. Byrd III MD Associate Professor of Medicine, Division of Cardiology, Vanderbilt University School of Medicine; Director, Echocardiography Laboratory, Vanderbilt University Medical Center, Nashville, Tennessee Maintaining Quality in the Echocardiography Laboratory Kwan-Leung Chan MD Professor of Medicine, University of Ottawa; Active Attending Staff, University of Ottawa Heart Institute, Ottawa, Ontario, Canada Indications, Procedure, Image Planes, and Doppler Flows Edmond W. Chen MD Fellow, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic

Embolic Event John S. Child MD Professor, University of California, Los Angeles, School of Medicine; Co-Chief, Division of Cardiology, Director, Ahmanson/UCLA Adult Congenital Heart Disease Center, UCLA Medical Center, Los Angeles, California Echocardiographic Evaluation of the Adult with Postoperative Congenital Heart Disease Joseph A. Diamond MD Assistant Professor of Medicine, Mount Sinai School of Medicine; Assistant Attending, The Mount Sinai Medical Center, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Pamela S. Douglas MD Tuchman Professor of Medicine; Head, Cardiovascular Medicine Section, University of Wisconsin Medical School, Madison, Wisconsin Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Thomas R. Easterling MD Associate Professor of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy Peter J. Fitzgerald MD, PhD Associate Professor of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical

Applications Kirsten E. Fleischman MD, MPH Assistant Professor in Residence, University of California, San Francisco, School of Medicine; Attending Physician, University of California, San Francisco, Medical Center, San Francisco, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome Elyse Foster MD Professor of Clinical Medicine, University of California, San Francisco, School of Medicine; Director, Adult Echocardiography Laboratory, Moffitt-Long Hospital, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myicardial Infarction, Detection of Complications, and Prognostic Implications

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William H. Gaasch MD Professor of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts; Director, Cardiovascular Research, Lahey Clinic, Burlington, Massachusetts Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Edward F. Gibbons MD Assistant Clinical Professor of Medicine, University of Washington School of Medicine; Director of Echocardiography, Director of Inpatient Cardiology Services, Virginia Mason Medical Center, Seattle, Washington

Education and Training of Physicians and Sonographers John S. Gottdiener MD Professor of Medicine, State University of New York at Stony Brook, School of Medicine; Director, Noninvasive Cardiac Imaging, St. Francis Hospital, Roslyn, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Brian P. Griffin MD Director, Cardiovascular Disease Training Program, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning and Intraoperative Evaluation of Mitral Valve Repair Sheila K. Heinle MD Clinical Assistant Professor of Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas Quantitation of Valvular Regurgitation: Beyond Color Flow Mapping Mary Etta E. King MD Associate Professor of Pediatrics, Harvard Medical School; Director, Pediatric Echocardiography, Massachusetts General Hospital, Boston, Massachusetts Echocardiographic Evaluation of the Adult with Unoperated Congenital Heart Disease Tim Kinnaird MB Fellow in Cardiovascular Medicine, London Chest Hospital, London, United Kingdom Pericardial Disease

Katsuhiro Kitamura MD Research Fellow in Medicine, Stanford University Medical Center, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Allan L. Klein MD Professor of Medicine, Ohio State University College of Medicine; Director, Cardiovascular Imaging Research, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Carol Kraft RDCS Lead Cardiac Sonographer, Virginia Mason Medical Center, Seattle, Washington Education and Training of Physicians and Sonographers Carolyn K. Landolfo MD Assistant Professor of Medicine, Duke University School of Medicine; Director, Adult Echocardiography, Duke University Medical Center, Durham, North Carolina The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation Jannet F. Lewis MD Professor of Medicine, George Washington University Medical Center; Director of Echocardiography, George Washington University Hospital, Washington, D.C. Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient David T. Linker MD

Associate Professor of Medicine, Division of Cardiology; Adjunct Associate Professor of Bioengineering; University of Washington School of Medicine, Seattle, Washington Principles of Intravascular Ultrasound Warren J. Manning MD Associate Professor of Medicine and Radiology, Harvard Medical School; Section Chief, Non-invasive Cardiac Imaging, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Pamela A. Marcovitz MD Director, Clinical Cardiology Fellowship Program; Director, Echocardiographic Research, William Beaumont Hospital, Royal Oak, Michigan Exercise Echocardiography: Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Roy W. Martin PhD Research Professor, Department of Anesthesiology and Center for Bioengineering, Applied Physics Laboratory, University of Washington School of Medicine, Seattle, Washington Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Thomas H. Marwick MD, PhD Professor of Medicine, Head of Section, University of Queensland Department of Medicine; Director of Echocardiography, Princess Alexandra Hospital, Brisbane, Queensland, Australia Stress Echocardiography with Nonexercise Techniques: Principles, Protocals, Interpretation, and Clinical Applications David J. Meier MD

Cardiology Fellow, University of Michigan Health System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention of Chronic Mitral and Aortic Regurgitation

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Bradley I. Munt MD Clinical Instructor, The University of British Columbia Department of Medicine; Cardiologist, Providence Healthcare and St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Danielle Noll MD Department of Cardiology, Echocardiography, Medizinische Klinik, Klinikum Innentadt, Munich, Germany Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Catherine M. Otto MD Professor of Medicine; Acting Director, Division of Cardiology; Director, Training Programs in Cardiovascular Disease; Associate Director, Echocardiography Laboratory, University of Washington School of Medicine, Seattle, Washington Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making; The Role of Echocardiography in the Diagnosis and Management of Heart Disease in Pregnancy; Echocardiographic Findings in Acute and Chronic Pulmonary Disease Donald C. Oxorn MD

Associate Professor of Anesthesiology, Adjunct Associate Professor of Medicine, University of Washington School of Medicine, Seattle, Washington Monitoring Ventricular Function in the Operating Room: Impact on Clinical Outcome Abraham C. Parail MD Fellow in Cardiology, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Robert A. Phillips MD, PhD Associate Professor of Medicine, Mount Sinai School of Medicine; Director, Department of Medicine, Lenox Hill Hospital, New York, New York Hypertension: Impact of Echocardiographic Data on the Mechanism of Hypertension, Treatment Options, Prognosis, and Assessment of Therapy Thomas R. Porter MD Associate Professor, University of Nebraska College of Medicine, Diagnostic Cardiac Ultrasound and Noninvasive Diagnostics, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Harry Rakowski MD Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Rita F. Redberg MD

Associate Professor of Medicine, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiographic Evaluation of the Patient with a Systemic Embolic Event Johan H. C. Reiber PhD Professor of Medical Imaging, Director, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands Two-Dimensional Echocardiographi Digital Image Processing and Approaches to Endocardial Edge Detection Cheryl L. Reid MD Associate Professor of Medicine, University of California, Irvine College of Medicine; Director, Non-invasive Cardiology, University of California, Irvine, Medical Center, Orange, California Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy: Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Carlos A. Roldan MD Associate Professor of Medicine, University of New Mexico School of Medicine; Staff Cardiologist, Director, Echocardiography Laboratory, Veterans Affairs Medical Center; Staff Cardiologist, University of New Mexico Health Sciences Center, Albuquerque, New Mexico Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Elizabeth W. Ryan MD

Research Fellow in Cardiology, Division of Cardiology, University of California, San Francisco, School of Medicine, San Francisco, California Aortic Dissection and Trauma: Value and Limitations of Echocardiography Kiran B. Sagar MD Professor of Cardiology and Medicine, University of Wisconsin Medical School, Milwaukee, Wisconsin Aging Changes Seen on Echocardiography Nelson B. Schiller MD Professor of Medicine, Radiology, and Anesthesia, University of California, San Francisco, School of Medicine; Director of Echocardiography, San Francisco Veterans Affairs Medical Center; Attending Physician, Cardiology, Echocardiography, and Adult Congenital Heart Disease, Moffitt-Long Hospital, San Francisco, California Clinical Decision Making in Endocarditis Ingela Schnittger MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Douglas S. Segar MD Clinical Associate Professor of Medicine, Indiana University School of Medicine, Indiana Heart Institute, Indianapolis, Indiana The Digital Echocardiography Laboratory

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David M. Shavelle MD

Interventional Cardiology Fellow, Good Samaritan Hospital, Los Angeles, California Aortic Stenosis: Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making Florence H. Sheehan MD Research Professor of Medicine, Division of Cardiology, University of Washington School of Medicine, Seattle, Washington Quantitative Evaluation of Regional Left Ventricular Systolic Function; Three-Dimensional Echocardiography: Approaches and Applications Bruce K. Shively MD Associate Professor of Cardiology, Oregon Health and Science University; Co-Director, Echocardiography Laboratory, Oregon Health and Science University Hospital, Portland, Oregon Echocardiographic Findings in Systemic Diseases Characterized by Immune-Mediated Injury Mikel D. Smith MD Professor of Internal Medicine/Cardiology, University of Kentucky College of Medicine; Director, Adult Echocardiography Laboratory, Gill Cardiovascular Institute, Albert B. Chandler Medical Center, Lexington, Kentucky Left Ventricular Diastolic Function: Clinical Utility of Doppler Echocardiography A. Rebecca Snider MD Consultant, Pediatric Cardiology, Monmouth Junction, New Jersey General Echocardiographic Approach to the Adult with Suspected Congenital Heart Disease Mark R. Starling MD Professor of Internal Medicine,

Director of Cardiology Training Program, Associate Chief of Cardiology, University of Michigan Medical School; Chief, Cardiology Section, VA Ann Arbor Healthcare System, Ann Arbor, Michigan The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation William J. Stewart MD Associate Professor of Medicine, Department of Cardiology, Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Marcus F. Stoddard MD Professor of Medicine, University of Louisville School of Medicine; Director, Noninvasive Cardiology, University of Louisville Hospital, Louisville, Kentucky Echocardiography in the Evaluation of Cardiac Disease Due to Endocinopathies, Renal Disease, Obesity, and Nutritional Deficiencies Maran Thamilarasan MD Assistant Staff Cardiologist, The Cleveland Clinic Foundation, Cleveland, Ohio Restrictive Cardiomyopathy: Diagnosis and Prognostic Implications Christopher R. Thompson MD, CM Clinical Associate Professor of Medicine (Cardiology), Director, Echocardiography Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada Pericardial Disease Aneesh V. Tolat MD

Clinical Fellow in Medicine, Harvard Medical School; Clinical Fellow in Cardiovascular Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts The Role of Echocardiography in Atrial Fibrillation and Flutter Brandon R. Travis PhD School of Chemical Engineering, Georgia Institute of Technology, Atlanta, Georgia Fluid Dynamics of Prosthetic Valves Zian H. Tseng MD Cardiology Fellow, University of California, San Francisco, School of Medicine, San Francisco, California Echocardiography in the Coronary Care Unit: Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Hannah A. Valantine MD Professor of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California The Role of Echocardiography in the Evaluation of Patients After Heart Transplantation Samuel Wang MD Assistant Professor of Clinical Internal Medicine, University of California, Davis, School of Medicine; Attending Physician, University of California, Davis, Medical Center, Sacramento, California The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room: Diagnosis, Triage, Treatment Decisions, Outcome E. Douglas Wigle MD Professor of Medicine, University of Toronto; Staff Cardiologist,

Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Selwyn P. Wong MD Cardiologist, Middlemore Hospital, Auckland, New Zealand Echocardiographic Findings in Acute and Chronic Pulmonary Disease Anna Woo MD Assistant Professor of Medicine, Division of Cardiology, University of Toronto; Staff Cardiologist, Toronto General Hospital, Toronto, Ontario, Canada Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy

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Feng Xie MD Research Assistant Professor, Cardiology, University of Nebraska Medical Center, Omaha, Nebraska Myocardial Contrast Echocardiography: Methods, Analysis, and Applications Paul G. Yock MD Professor of Medicine, Stanford University School of Medicine, Stanford, California Intravascular Ultrasound: Histologic Correlation and Clinical Applications Ajit P. Yoganathan PhD Regents Professor of Biomedical Engineering, The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia

Fluid Dynamics of Prosthetic Valves Miguel Zabalgoitia MD Professor of Medicine; Director, Echocardiography Laboratory, University of Texas Health Science Center, San Antonio, Texas Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction William A. Zoghbi MD Professor of Medicine, Director of Echocardiography Research, Baylor College of Medicine; Associate Director, Echocardiography Laboratory, The Methodist Hospital, Houston, Texas Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Preface Echocardiography increasingly has become a key component in the routine evaluation of patients with suspected or known cardiovascular disease. As this technique has evolved and matured, the role of the echocardiographer has shifted from simply providing a description of images to providing an integrated assessment of echocardiographic data in conjunction with the other clinical data from each patient. In effect, echocardiography has become a specialized type of cardiology consultation. The information now requested by the referring physician includes not only the qualitative and quantitative interpretation of the echocardiographic images and Doppler flow data but also a discussion of how this information might affect clinical decision making. Specific examples include decisions regarding medical or surgical therapy (e.g., treatment of endocarditis, surgery for aortic dissection), optimal timing of intervention in patients with chronic cardiac diseases (e.g., valvular regurgitation, mitral stenosis), prognostic implications (e.g., heart disease in pregnancy, heart failure patients), and the possible need for and frequency of periodic diagnostic evaluation (e.g., congenital heart disease, the postoperative patient). This book reflects our role as clinicians with specialized expertise in echocardiography and is of value to cardiology fellows pursuing advanced training in echocardiography, cardiologists in clinical practice, researchers using echocardiographic techniques, and other individuals using echocardiographic approaches in the clinical setting (including anesthesiologists, radiologists, emergency medicine physicians, and obstetricians), as well as to cardiac sonographers, cardiovascular technologists, and nursing professionals.

Each chapter provides an advanced level of discussion, written by an expert in the field, building upon the basic material in the Textbook of Clinical Echocardiography (C. M. Otto, 2nd Edition, WB Saunders, Philadelphia, 2000). The emphasis is on optimal data acquisition, results of recent studies, quantitative approaches to data analysis, potential technical limitations, and areas of active research, in addition to a detailed discussion of the impact of echocardiographic data on patient management. Tables, line drawings, echocardiographic images, and Doppler tracings are used to summarize and illustrate key points. In this Second Edition, the text has been revised to reflect recent advances, illustrations and tables have been updated, and new references have been added to each chapter. The book is organized into sections based on major diagnostic categories. In this new edition, an introductory section on transesophageal echocardiography has been added. Chapters include basic principles of transesophageal imaging, monitoring of ventricular function in the operating room, and a discussion of echocardiographic evaluation of aortic dissection and trauma. Other detailed information on the role of transesophageal echocardiography is integrated into subsequent chapters, which are organized by disease categories. The next section focuses on the left ventricle, with chapters spanning the spectrum from emerging new techniques (e.g., myocardial contrast echocardiography, automated edge detection, tissue characterization, three-dimensional echocardiography) to critical appraisals of quantitative techniques (e.g., left ventricular geometry and systolic function, evaluation of regional function, and assessment of diastolic function). The section on ischemic heart disease includes chapters on the role of echocardiography in the emergency room and coronary care unit, stress echocardiography (exercise and nonexercise), and the basic principles, instrumentation, and clinical applications of intravascular ultrasound in patients with coronary artery disease. The critical role that echocardiography now plays in management of patients with valvular heart disease is evident in a section of chapters on technical aspects of echocardiographic evaluation, optimal timing of surgery and periodic evaluation of patients with valvular regurgitation, management of patients undergoing balloon mitral commissurotomy, clinical decision making in patients with endocarditis, evaluation of disease severity, progression in valvular aortic stenosis, and evaluation of prosthetic valves. The following clinically oriented sections bring together data from both the

echocardiographic and general cardiology literature to discuss the role of echocardiography in patients with cardiomyopathies (heart failure, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and the posttransplant patient) and pericardial disease, pregnant patients with cardiac disease, and a wide range of other vascular and systemic diseases that lead to cardiac dysfunction (hypertension, aortic dissection, pulmonary disease, systemic immune-mediated diseases, renal disease, aging, systemic embolic events, and cardiac arrhythmias). In recognition of the increasing number of adult patients presenting with congenital heart disease, either as a new diagnosis or following prior surgical procedures, three chapters are devoted to this topic. In addition, a new section has been added on the echocardiography laboratory to address issues that increasingly affect our clinical practice, including education and training of echocardiographers, quality improvement in the echocardiography laboratory, and the transition to a digital laboratory. It is hoped that this book will provide the needed background to support and supplement clinical experience and expertise. Of course, competency in the acquisition and interpretation of echocardiographic and Doppler data depends on appropriate clinical education and training as detailed in accreditation requirements for both physicians and technologists, and as recommended by professional societies including the American Society of Echocardiography, the American College of Cardiology, and the American Heart Association. I strongly support these educational requirements and training recommendations; XII

readers of this book are urged to review the relevant documents. In addition, there continue to be advances both in the the technical aspects of image and flow data acquisition and in our understanding of the clinical implications of specific echocardiographic findings. This book represents our knowledge base at one point in time; readers should consult the current literature for the most up-to-date information. Although an extensive list of carefully selected references is provided with each chapter, the echocardiographic literature is so robust that it is impractical to include all relevant references; the reader can use an online medical literature search if an all-inclusive listing is desired. Catherine M. Otto MD

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Acknowledgments

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Sincere thanks are due to the many individuals who made this book possible. Primary recognition goes to the chapter contributors who provided scholarly, thoughtful, and insightful discussions and who integrated the clinical and echocardiographic information into a format that benefits our readers. The support staff at each of our institutions deserves our appreciation for manuscript preparation and providing effective communication, with special thanks to Sharon Kemp and Bev Bubela. The many research subjects who contributed to the data on which our current understanding is based certainly are worthy of our appreciation. The cardiac sonographers at the University of Washington Medical Center (Rachel Elizalde, RDCS; Michelle C. Fujioka, RDMS; Carolyn J. Gardner, RDCS; Caryn D'Jang, RDCS; Scott Simicich, RDCS; David Stolte, RDCS; Rebecca G. Schwaegler, RDMS; Erin Trent, RDCS; and Todd R. Zwink, RDMS) merit acknowledgment. In addition, gratitude is due to Richard Zorab and the production team at W.B. Saunders. Finally, I thank my family for their constant encouragement and support.

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NOTICE Medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this publication. THE PUBLISHER

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Section 1 - Transesophageal Echocardiography

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Chapter 1 - Indications, Procedure, Image Planes, and Doppler Flows Ian G. Burwash MD Kwan-Leung Chan MD

Transesophageal echocardiography (TEE) has become a valuable diagnostic imaging modality for the dynamic assessment of cardiac anatomy and function. Since the initial description of esophageal echocardiography in 1976,[1] the potential role and utility of TEE in the evaluation of diseases of the heart and great vessels have expanded to involve all aspects of cardiac disease. The close proximity of the esophagus to the heart and great vessels provided the echocardiographer with an easily accessible window with the potential for excellent visualization of cardiac structures, avoiding the intervening lung and chest wall tissues that limit transthoracic imaging. The potential of TEE to provide a valuable imaging tool became widely recognized in the 1980s with advancements in TEE probe technology, including the availability of single-plane phased array transducers and the addition of color flow and continuous wave Doppler imaging technology. TEE does not supplant transthoracic echocardiography

(TTE), however; it is a complementary imaging modality with its own strengths and weaknesses. The 2

introduction of biplane TEE transducers in the late 1980s and multiplane transducers in the 1990s has resulted in a further expansion of potential diagnostic applications. Perhaps the best evidence of TEE's diagnostic utility and value in patient management is the widespread use of this technology. TEE is found in the inpatient and outpatient ambulatory setting, in the operating room, in the intensive care unit, and in the emergency department. Currently, TEE accounts for approximately 5% to 10% of all echocardiography studies performed. The indications and utility of TEE will likely expand in the future with new technologic advancements such as three-dimensional echocardiography.

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Performance of Transesophageal Echocardiography Transesophageal echocardiography is a semi-invasive procedure that should be performed only by a properly trained physician who understands the indications for and potential complications of the procedure. Both technical and cognitive skills are required for the competent performance and interpretation of TEE studies (Table 1-1) , and guidelines on training have been published.[2] The physician should be assisted by an experienced sonographer whose tasks are to ensure that optimal images are obtained by adjusting the controls of the echocardiographic system and to ensure safety by monitoring the responses of the patient during the procedure. Although family members or friends are usually not allowed in the room when the procedure is being performed, there are situations in which their presence can be helpful. The presence of a parent can have a calming effect when one is dealing with an apprehensive teenager. A friend or a relative who speaks the same language can relieve much of the anxiety when dealing with an anxious patient who is not fluent in English. Transesophageal echocardiography should be performed in a spacious room that can comfortably accommodate a stretcher. The room should be equipped with an oxygen outlet and suction facilities. A pulse oximeter should be available, to be used mainly in cyanotic patients and patients with severe lung disease. The TEE probe should be carefully examined prior to each use. In addition to visual inspection, it is important to palpate the probe, particularly the flexion portion, to ensure that there is no unusual wear and tear of the probe.[3] Stretching of the steering cables may result in increased flexibility and mobility of the probe tip with buckling of the probe tip within the esophagus.[4] This phenomenon is associated with a poor TEE image and resistance to probe withdrawal. The probe should be advanced into the stomach and straightened by retroflexion of the extreme antiflexed probe tip. We have also detected perforation of the TEE probe sheath by a ruptured steering cable and recommend inspection of the casing for any protruding wires prior to probe insertion.[3] The flexion controls

need to be tested on a regular basis. Anterior flexion should exceed 90 degrees, and right and left flexion should approach 90 degrees. TABLE 1-1 -- Cognitive and Technical Skills Required for the Performance of Transesophageal Echocardiography (TEE) Cognitive Skills Knowledge of appropriate indications, contraindications, and risks of TEE Understanding of differential diagnostic considerations in each clinical case Knowledge of physical principles of echocardiographic image formation and blood flow velocity measurement Familiarity with the operation of the ultrasonographic instrument, including the function of all controls affecting the quality of the data displayed Knowledge of normal cardiovascular anatomy, as visualized tomographically Knowledge of alterations in cardiovascular anatomy resulting from acquired and congenital heart diseases Knowledge of normal cardiovascular hemodynamics and fluid dynamics Knowledge of alterations in cardiovascular hemodynamics and blood flow resulting from acquired and congenital heart diseases Understanding of component techniques for general echocardiography and TEE, including when to use these methods to investigate specific clinical questions Ability to distinguish adequate from inadequate echocardiographic data and to distinguish an adequate from an inadequate TEE examination Knowledge of other cardiovascular diagnostic methods for correlation with TEE findings Ability to communicate examination results to patient, other health care professionals, and medical record Technical Skills Proficiency in performing a complete standard echocardiographic examination, using all echocardiographic modalities relevant to the case Proficiency in safely passing the TEE transducer into the esophagus and

stomach and in adjusting probe position to obtain the necessary tomographic images and Doppler data Proficiency in correctly operating the ultrasonographic instrument, including all controls affecting the quality of the data displayed Proficiency in recognizing abnormalities of cardiac structure and function as detected from the transesophageal and transgastric windows, in distinguishing normal from abnormal findings, and in recognizing artifacts Proficiency in performing qualitative and quantitative analysis of the echocardiographic data From Pearlman AS, Gardin JM, Martin RP, et al: J Am Soc Echocardiogr 1992;5:187–194. Preparation of Patient Patients should be contacted at least 12 hours before the procedure and instructed to fast for at least 4 hours before the procedure. They are informed that they should be accompanied, because they will not be able to drive or return to work for several hours owing to the lingering effect of sedation. On the day of the study, the procedure is explained in greater detail, and informed consent is obtained. Patients are told to expect mild abdominal discomfort and gagging following the insertion of the probe and are reassured that these responses are transient. A 20-gauge intravenous cannula is then inserted for administration of medications and contrast agents, if necessary. Lidocaine hydrochloride spray is routinely used for topical anesthesia, which should cover the posterior pharynx and the tongue. We usually use diazepam 2 to 10 mg intravenously 3

for sedation.[5] Midazolam at 0.05 mg/kg, with a total dose between 1 and 5 mg, can also be used. Sedation is used in about 85% of our patients and should be more sparingly used in elderly patients, because they tend to be more stoic and the effect of sedation is more likely prolonged. On the other hand, sedation is essential in young anxious patients and when the study is expected to be protracted. We aim for light sedation so that at the end of the procedure the patients are awake and can leave with an escort. Heavy sedation is needed in situations in which blunting the hemodynamic responses to the procedure is desirable. One obvious example is a patient undergoing TEE for suspected aortic

dissection.[6] It has not been our practice to use anticholinergic agents such as glycopyrrolate to decrease salivation. In the rare circumstances in which there is excessive salivation, it is usually adequate to simply instruct the patient to let the saliva dribble onto the towel placed under the chin, or the saliva can be removed by intermittent suction. Bacteremia is not a significant risk in TEE, and we do not use antibiotic prophylaxis to prevent endocarditis even in patients with prosthetic heart valves.[7] [8] Esophageal Intubation We perform the TEE study with the patient in the left decubitus position. The physician, the sonographer, and the echocardiographic system are all positioned on the left-hand side of the patient.[5] Artificial teeth or dentures are routinely removed. The flexion controls should be unlocked to allow for maximum flexibility of the probe when it is being inserted. The patient's head should be in a flexed position. The tip of the probe is kept relatively straight and gently advanced to the back of the throat. It should be maintained in a central position, because deviation to either side increases the likelihood that it may become lodged in the piriform fossa. The operator can facilitate this process by inserting one or two fingers into the patient's oropharynx to direct the path of the probe. Gentle pressure is exerted and the patient is instructed to swallow. The swallowing mechanism helps guide the probe into the esophagus. In older patients, cervical spondylosis with prominent protrusion into the posterior pharynx can create difficulty with passage of the probe.[5] Manually depressing the back of the tongue provides more room, allowing the TEE probe to assume a less acute angle and facilitating the intubation of the esophagus. If significant resistance is encountered when the probe is advanced, it is prudent to withdraw the probe and then initiate a new attempt. Esophageal intubation is more difficult with the multiplane probe than with the smaller monoplane and biplane probes.[9] [10] The latter can be used, if available, when esophageal intubation cannot be achieved with a multiplane probe. In experienced hands, the rate of failure of esophageal intubation should be less than 2%.[5] [9] [11]

A bite guard should always be used, except in edentulous patients. Our practice is to put it between the patient's teeth after the TEE probe has been successfully passed into the esophagus. Patients with a very sensitive pharynx may close their mouths involuntarily during esophageal intubation. In these patients, it is safer to insert the bite guard before the insertion of

the TEE probe. The patient should be instructed to keep the guard between the teeth throughout the procedure, and regular checks should be made to ensure that it is in the proper position to prevent damage to the probe or injury to the patient. Even when the probe is inserted without difficulties, it is not uncommon for the patient to develop nausea with or without mild retrosternal or abdominal discomfort. We find it useful to pause for 10 to 15 seconds to allow these symptoms to subside before proceeding with echocardiographic imaging. Our practice is to start with images acquired from the esophagus before advancing the probe into the stomach for the gastric views. The gastroesophageal sphincter is usually reached when the probe is advanced 40 cm from the teeth. Gentle pressure is all that is required to advance the probe through the gastroesophageal sphincter. The patient may again experience nausea and mild discomfort, and it may be advisable to pause momentarily for these symptoms to subside. Imaging of the proximal descending thoracic aorta and aortic arch is generally reserved for the end of the study, because the probe needs to be positioned in the upper esophagus and the patient is generally more aware of the probe at this position and tends to have more discomfort and gagging. Inadvertent passage of the probe into the trachea can occur, particularly in deeply sedated patients. The development of stridor and incessant cough should alert the operator of this possibility. Furthermore, it would be difficult to advance the probe beyond 30 cm from the teeth and the image quality is usually poor.[5] In patients on mechanical ventilation, esophageal intubation is more difficult. We usually introduce the probe with the patient lying supine, because the airway is protected and aspiration is unlikely. The probe is positioned behind the endotracheal tube and gently advanced. It is helpful to have the patient's mandible pulled forward when the probe is being advanced. If there is undue resistance at about 25 to 30 cm from the teeth, slight deflation of the cuff of the endotracheal tube can be considered to ease the passage of the probe. We do not usually remove the gastric tube, which can be used as a guide to help in the proper positioning and passage of the TEE probe. In a minority of intubated patients, successful esophageal intubation may be achieved only with direct laryngoscopy. Image Format There is no general agreement on how the imaging planes should be

displayed. Our preference is to orient the images such that the right-sided structures are on the left side of the screen and the left-sided on the right. The apex of the imaging plane with the electronic artifact is at the top of the screen. Thus, in the longitudinal views, superior structures are to the right of the screen and the inferior to the left.[12]

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TABLE 1-2 -- Standard Imaging Planes with Multiplane Transesophageal Echocardiography (TEE) at the University of Ottawa Heart Institute

Imaging View Basal

Fourchamber

Standard Imaging Plane Aortic valve

Angle of Imaging Array (degrees) 0–60

Atrial septum

90–120

Pulmonary bifurcation

0–30

Left ventricle

0–180

Mitral valve

0–180

Left ventricular outflow tract

120–160

Transgastric Left ventricle Mitral valve

0–150 0–150

Main Cardiac Structures Aortic valve, coronary arteries, left atrial appendage, pulmonary veins Fossa ovalis, superior vena cava, inferior vena cava Pulmonic valve, main and right pulmonary arteries, proximal left pulmonary artery Left ventricle (regional and global function), right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles, chords Aortic valve, ascending aorta, left and right ventricular outflow tracts, pulmonic valve, main pulmonary artery Left ventricle, right ventricle, tricuspid valve Anterior and posterior mitral leaflets, papillary muscles,

Aortic

Coronary sinus Descending thoracic aorta Aortic arch

0

chords Coronary sinus, tricuspid valve

0

Entire descending thoracic aorta

90

Aortic arch, arch vessels, left pulmonary artery

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Standard Imaging Planes Advances in TEE transducer technology have culminated in the development of the multiplane probe capable of two-dimensional and color flow imaging in multiple planes. The imaging plane can be steered electronically from 0 to 180 degrees by means of a pressure-sensitive switch, providing views unattainable by monoplane and biplane probes. The following discussion focuses only on standard imaging views routinely performed at the University of Ottawa Heart Institute using multiplane TEE (Table 1-2) . These views are considered "standard" because they have important clinical relevance and can be obtained in most patients with specific imaging planes. Four basic maneuvers are used to obtain specific tomographic views with TEE.[13] The first relates to the positioning of the probe by advancement or withdrawal of the probe. Although this is a simple maneuver, it is the most crucial, and the imaging views can be conveniently categorized according to the location of the TEE probe within the esophagus or stomach (Fig. 11) . The second maneuver involves rotation of the probe from side to side. This is particularly useful when using longitudinal imaging planes, which provide a better demonstration of the continuity between vertically aligned structures such as the superior vena cava and the arch vessels.[12] [13] Steering the imaging plane using the pressure-sensitive switch is the third maneuver to obtain different tomographic views. The ability to image cardiac structures from 0 to 180 degrees not only enhances understanding of cardiac anatomy but also provides a ready means for three-dimensional reconstruction. [14] [15] The fourth maneuver involves manipulation of the anterior-posterior and right-left flexion control knobs. The availability of a steerable imaging plane has drastically reduced the need to use the flexion knobs, but there are situations in which these knobs play a crucial role in obtaining proper tomographic views.[10] [13] The versatility of multiplane TEE provides an almost infinite number of

imaging planes. In our experience, it is useful to categorize them into four groups: basal, four-chamber, transgastric, and aortic views (see Fig. 1-1) . Table 1-2 summarizes the standard imaging planes and the cardiac structures evaluated in these four groups of views. Basal Views The basal group of views is obtained with the TEE probe located in the midesophagus. The base of the heart, Figure 1-1 Diagram showing the transesophageal echocardiography transducer locations for the four standard imaging views: basal (A), fourchamber (B), transgastric (C), and aortic (D).

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particularly the aortic valve, is well seen. The relationship of the two great arteries can be very well defined and followed cephalad to at least the level of the pulmonary bifurcation. Beyond this level, the interposing trachea make imaging impossible. Three tomographic planes are found to be particularly useful and are routinely performed at our laboratory. Aortic Valve

A short-axis view of the aortic valve can be obtained with the probe at about 30 to 35 cm from the teeth. The left coronary cusp often appears to have nodular thickening if the aortic valve is cut obliquely, which is often the case at 0 degrees.[12] Steering the imaging plane to 30 to 60 degrees should eliminate this artifact by providing an optimal short-axis view of the aortic valve (Fig. 1-2) . [13] A slight pull-back of the transducer should allow visualization of both the left and right coronary arteries. The left coronary artery can be followed to its bifurcation into the left anterior descending and circumflex arteries (Fig. 1-3) . The right coronary artery is more difficult to display, and usually only the proximal 2 to 3 cm is seen (Fig. 14) . Other structures well seen in this view are the left atrial appendage and the left pulmonary veins. The partition between these structures can be quite bulbous and should not be confused with an abnormal intracardiac mass (see Fig. 1-4) .[16] Rotating the probe to the right should reveal the right pulmonary veins.

We like the horizontal plane in imaging the four pulmonary veins. The left and right pulmonary veins are imaged separately. It is difficult to image the upper and lower pulmonary veins, left or right, in the same view because the veins are not located in the same plane with the lower pulmonary veins posterior and inferior to the upper pulmonary veins.[17] When one pulmonary vein is identified, a slight translational movement of the probe should bring out the other, because the orifices of the upper and Figure 1-2 The aortic valve was imaged with the imaging plane at about 60 degrees, showing the three cusps in systole. LA, left atrium; RA, right atrium; RV, right ventricle.

Figure 1-3 The left coronary artery (arrows) was imaged at 0 degrees. Ao, aorta; LA, left atrium.

lower pulmonary veins are in close proximity. The lower pulmonary veins run horizontal to the imaging plane, whereas the upper veins are more anterior and at an obtuse angle, making them more suitable for Doppler assessment. The right and left atrial appendages wrap around the great arteries anteriorly. The left atrial appendage is more prominent and can consist of multiple lobes.[18] A comprehensive interrogation using multiple imaging planes should be performed to exclude left atrial appendage thrombus in the appropriate clinical setting. The right atrial appendage is smaller and triangular in shape (Fig. 1-5) . The endocardial surfaces of both appendages are corrugated and should not be confused with small thrombi.[16] A long-axis view of the aorta can be achieved with the imaging plane at about 120 degrees. A more rightward imaging plane, such as 150 degrees, may be Figure 1-4 The proximal right coronary artery (small arrows) and the bulbous partition between the left atrial appendage and the left upper pulmonary vein (large arrow) are demonstrated. Ao, aorta; LA, left atrium.

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Figure 1-5 The atrial septum was preferentially imaged using the longitudinal plane to demonstrate its relation with the superior vena cava (SVC). LA, left atrium; RA, right atrium; RAA, right atrial appendage.

needed if the ascending aorta is dilated and tortuous. This view allows the visualization of a longer length of the ascending aorta and thus significantly reduces the blind spot caused by the interposing trachea. Atrial Septum

We prefer to image the atrial septum using the longitudinal plane at 90 to 120 degrees. The fossa ovalis, which is the thinnest part of the atrial septum, and the continuity of the superior vena cava with the right atrium are very well demonstrated in this view (see Fig. 1-5) . This view is particularly valuable in demonstrating the sinus venosus atrial septal defect, which is usually located just inferior to the entrance of the superior vena cava.[19] [20] The foramen ovale, if present, is located at the superior aspect of the fossa ovalis and is readily seen in this view. It is important to advance the probe to the level of the inferior vena cava so as not to neglect the inferior aspect of the atrial septum.[21] Careful sweep of the atrial septum with left-right rotation is needed to visualize the entire atrial septum. Continuous rotation from right to left will sequentially demonstrate the left ventricular outflow tract and the right ventricular outflow tract. Rotating the probe to the right shows the right upper pulmonary vein and provides parallel alignment for Doppler assessment. Pulmonary Bifurcation

The pulmonary bifurcation view is achieved by withdrawal of the probe with the imaging plane at 0 degrees. The pulmonic valve and main pulmonary artery are best seen slightly superior to the aortic valve (Fig. 16) . The pulmonic valve is thinner than the aortic valve and is usually difficult to image in a true cross section. Further slight withdrawal allows imaging the pulmonary bifurcation. The entire length of the right pulmonary artery but only the very proximal portion of the left pulmonary artery can be seen. The right pulmonary artery can usually be followed to its first bifurcation by rotation of the probe rightward, but this maneuver is better performed with the longitudinal plane at 90 degrees. Gradual rotation from left to right provides good visualization in cross section of the entire right pulmonary artery and its first bifurcation. This is an important view in

the detection of proximal pulmonary emboli.[22] [23] Four-Chamber Views Four-chamber views are obtained with the transducer within the middle to lower esophagus. It is difficult to image the left ventricle in its true long axis. Excessive anterior flexion should be avoided to prevent foreshortening of the ventricles. Indeed, to optimize visualization of the left ventricle, it is advisable to withdraw the probe slightly and at the same time attempt gentle retroflexion while maintaining adequate contact between the imaging surface and the esophagus. In the setting of a dilated and unfolded aorta, rotating the imaging plane to about 20 to 30 degrees may be necessary to obtain the four-chamber view without the aorta obscuring the tricuspid valve and part of the right ventricle. Left Ventricle

The inferior septum and anterolateral wall are usually seen in the fourchamber view (Fig. 1-7) . The left ventricular apex is difficult to visualize, particularly in patients with a dilated left ventricle. In addition to retroflexion, rightward flexion can often be helpful to minimize foreshortening of the left ventricle. Far-field imaging can be improved by decreasing the transmission frequency. A continuous sweep from 0 to 180 degrees should be performed to examine the different left ventricular segments Figure 1-6 The bifurcation of the main pulmonary artery (MPA) into the right (RPA) and left (LPA) pulmonary arteries was imaged using the transverse plane. Ao, aorta.

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Figure 1-7 The four-chamber view showing the left ventricle (LV) and mitral valve. LA, left atrium; RA, right atrium; RV, right ventricle.

so as to have a comprehensive assessment of left ventricular global and regional function (Fig. 1-8) .

Mitral Valve

The mitral valve is well seen using the four-chamber view, but the depth of the imaging plane should be reduced to enhance the resolution of the image ( see Fig. 1-7 and Fig. 1-8 ). To identify the individual scallops of the anterior and posterior mitral leaflets, a careful sweep from 0 to 180 degrees should be made. The technique of visualizing specific scallops of the mitral leaflets have been published,[24] but patient-to-patient variation should be kept in mind. The presence of a good long-axis view of the aortic valve and proximal ascending aorta, usually at Figure 1-8 The left ventricle and mitral valve can be comprehensively assessed by a continuous sweep of the imaging plane, which was about 100 degrees in this example. LA, left atrium; LV, left ventricle.

120 degrees, is a good indication that the middle scallops of both the anterior and the posterior mitral leaflets are imaged and provides the internal reference for the analysis of the other imaging planes. Both papillary muscles can be imaged but usually not in the same plane. The subvalvular chords are seldom completely imaged because they are frequently obscured by the mitral leaflets. The morphologic information obtained from this view should be corroborated by the short-axis view of the mitral valve obtained from the transgastric view, which also allows a better assessment of the subvalvular structures, including the papillary muscles and chords. Four-chamber views are ideal for the assessment of mitral regurgitation in relation to the number of regurgitant jets, the direction of the regurgitant jets, and the severity of regurgitation. [25] [26] Left Ventricular Outflow Tract

We like to image the left ventricular outflow tract at 120 to 160 degrees, because the outflow tract has a horizontal alignment in this plane that may allow optimal imaging even in the setting of a prosthetic aortic valve (Fig. 1-9) . The opening and closing of the aortic valve as well as the presence or absence of aortic regurgitation can be well visualized. The proximal ascending aorta is present in this view. A slight withdrawal of the probe will allow more of the ascending aorta to be visualized (Fig. 1-10) . A slight rotation to the left will show the right ventricular outflow tract with the thin pulmonic valve. Both the motion of the pulmonic valve and the presence or absence of pulmonic regurgitation can be adequately assessed

using this view. Transgastric Views There is slight resistance during the passage of the TEE probe through the gastroesophageal junction, and the Figure 1-9 The left ventricular outflow tract was well seen with the imaging plane at about 120 degrees. Ao, aorta; LA, left atrium; LV, left ventricle; RVOT, right ventricular outflow tract.

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Figure 1-10 Slight withdrawal of the probe relative to the probe position used to acquire the image shown in Figure 1-9 showed the right pulmonary artery (RPA) in short axis and more of the ascending aorta (Ao). LA, left atrium.

appearance of the liver is a clear indication that the probe is in the stomach. Anterior flexion, often with leftward rotation and flexion, is required to achieve good contact between the imaging surface and the gastric wall. Extreme anterior flexion with further advancement of the probe can sometimes produce images similar to the five-chamber views obtained from the subxiphoid surface approach. Left Ventricle

Multiple cross sections of the left ventricle can usually be obtained using the transgastric approach ( Fig. 1-11 and Fig. 1-12 ). These are the views commonly used in the intraoperative assessment of left ventricular function.[24] Optimization of the short-axis views of the left ventricle Figure 1-11 Transgastric short-axis view of the left ventricle (LV) at the papillary muscle level.

Figure 1-12 Transgastric long-axis view of the left ventricle (LV) with

visualization of the apex.

can be achieved with leftward rotation accompanied by leftward flexion. To visualize the left ventricular apex, gentle advancement of the probe is required together with slight retroflexion. In our experience, the short-axis view of the left ventricular apex can be obtained in about 60% of cases. Another way to visualize the left ventricular apex is to use the longitudinal plane at about 90 degrees (see Fig. 1-12) . Careful lateral rotation can be used to obtain comprehensive regional assessment of the left ventricle. Leftward rotation of this imaging plane can yield a good alignment with the left ventricular outflow tract and aortic valve to allow accurate measurement of the transaortic pressure gradients in the setting of aortic stenosis (Fig. 1-13) . [27] The right ventricle can be seen with rightward rotation of the probe. Both short- and long-axis views of the tricuspid valve are achievable, although Figure 1-13 Transgastric transesophageal echocardiography approach to assess the severity of aortic stenosis using continuous wave Doppler echocardiography.

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the tricuspid valve and its papillary muscles are better assessed with the long-axis plane. Mitral Valve

The mitral valve can be best assessed using the horizontal imaging plane with the transducer brought up to near the gastroesophageal junction (Fig. 1-14) . Anterior flexion and leftward flexion are usually required to optimize this view. Adjusting the imaging plane to about 20 degrees will help to bring out the lateral commissure. This view provides unambiguous assessment of the individual scallops of both the anterior and posterior mitral leaflets and thus should be attempted in all patients with myxomatous mitral valve degeneration. In our experience, this view is achievable in about 70% of patients. Both the papillary muscle and chords can be demonstrated, and the continuity between these structures and the mitral leaflets is best seen in the long-axis plane. Coronary Sinus

The coronary sinus comes into view when the probe is withdrawn to be near the gastroesophageal junction and the flexion knobs are in relatively neutral positions (Fig. 1-15) . This view can also be achieved by retroflexion with the probe in the lower esophagus. The coronary sinus is seen as a vascular structure located posterior to the left ventricle at the atrioventricular groove draining into the right atrium. The tricuspid valve can be visualized to the right and anterior. A dilated coronary sinus should raise the possibility of the presence of a persistent left superior vena cava, which is the most common cause. Leftward rotation while following the coronary sinus may sometimes demonstrate this anomalous vein. In the esophageal views, the left superior vena cava is usually sandwiched between the left atrial appendage and the left upper pulmonary vein.[28] Figure 1-14 The mitral valve was demonstrated in the short axis showing the anterior (arrows) and posterior (arrowheads) mitral leaflets.

Figure 1-15 The coronary sinus (CS) was demonstrated with the probe at the gastroesophageal junction. LV, left ventricle; RV, right ventricle.

Aortic Views The thoracic aorta is well assessed by TEE because of its close proximity to the esophagus. Descending Thoracic Aorta

The best way to assess the descending thoracic aorta is to use the horizontal imaging plane with the transducer rotated leftward and posterior, followed by slow withdrawal from the level of the diaphragm to the aortic arch (Fig. 1-16) .[16] Because of the relationship between the Figure 1-16 The descending aorta was imaged in the short axis to allow good visualization of entire circumference.

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Figure 1-17 The aortic arch (AA) was imaged using the longitudinal plane, showing the origin of the left subclavian artery (LSA).

esophagus and the aorta, slight rotational adjustment is required to visualize the entire circumference of the aortic wall as the probe is slowly withdrawn.[29] If the aorta is dilated or tortuous, proper short-axis views of the descending aorta will require adjustment of the imaging plane by 0 to 90 degrees. Aortic Arch

The longitudinal imaging plane at 90 degrees is preferred in imaging the aortic arch because it allows visualization of the entire circumference of the aorta (Fig. 1-17) .[29] Anterior rotation of the longitudinal plane should visualize the entire aortic arch, but the proximal aortic arch may not be visualized when the aortic arch is unfolded. The transducer will need to be withdrawn slightly to image the arch vessels, which course superiorly. In one third of patients, all three arch vessels can be imaged, but in the other two thirds of patients, only the two distal arch vessels can be imaged. It is rare not to be able to image at least one arch vessel. As a rule, the brachiocephalic artery, which is anterior and more rightward, is the most difficult to image because of the interposing trachea. The transverse plane in a more superior location may sometimes show the three arch vessels in their short axis. Advancing the probe by 1 to 2 cm so that the imaging plane is just inferior to the aortic arch can frequently image the proximal left pulmonary artery. It is sometimes possible to follow it to the first bifurcation. This view should be sought in the assessment of patients suspected of having pulmonary embolism.

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Doppler Examination Transesophageal echocardiography can be used to assess the flow patterns across the four cardiac valves, but it does not provide additional information to TTE. Furthermore, good alignment with the transvalvular flows may not be feasible because of the anatomic confines of the esophagus. On the other hand, intracardiac flows such as pulmonary vein flow and left atrial appendage flow are best evaluated by TEE and provide important insight into intracardiac hemodynamics. Pulmonary Vein Flow The pulmonary veins are imaged from the midesophagus level. Pulmonary vein flow can be assessed by placing the pulsed Doppler = sample=20 volume 0.5 to 1.0 cm into the pulmonary veins. The anterior to posterior = direction of the left and right upper pulmonary veins allows the Doppler = ultrasound beam to be aligned parallel to blood flow. This often cannot = be=20 achieved when interrogating the left and right lower pulmonary = veins. The normal pulmonary venous flow pattern can be = divided=20 into three phases: (1) antegrade systolic flow, (2) antegrade diastolic = flow,=20 and (3) retrograde atrial contraction flow reversal (F= ig.=20 1-18) . Two phases of antegrade systolic flow can usually be = appreciated on=20 transesophageal study. Systolic flow is dependent on apical displacement = of the=20 annulus, which is predominantly determined by left ventricular function, = atrial=20 relaxation, and atrial compliance.[3= 0]=20 [3= 1]=20 Left atrial pressure also affects antegrade systolic flow, with = increases in=20 left atrial pressure reducing systolic flow.[3= 0]=20 [3= 1]=20 Mitral regurgitation increases left atrial pressure during systole and = may=20 result in systolic flow reversal in one or all pulmonary=20 veins.[3= 0]=20 [3= 1] =20 Diastolic antegrade flow occurs as the mitral valve opens and left = atrial=20 pressure falls. The diastolic flow profile is dependent on left atrial = pressure,=20 left ventricular relaxation, and ventricular compliance. = [3= 0] =20 [3= 1]=20 Atrial contraction flow reversal is dependent on atrial contractility, = atrial=20 systolic pressure, and left ventricular compliance. The normal pulmonary = venous=20 flow pattern is dependent on heart rate and age.[3= 1]=20 [3= 2]=20 Higher systolic pulmonary venous flow velocities, higher atrial reversal = velocities, and smaller diastolic flow velocities=20

Figure = 1-18 Normal pulmonary venous flow showing two antegrade = flows in=20 ventricular systole and diastole, with a diminutive retrograde flow = caused by=20 atrial contraction. .

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patients younger than 50 years of=20 age.[3= 1]=20 [3= 2]=20 Left Atrial Appendage Flow The left atrial appendage can be imaged from = the=20 midesophagus

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aortic valve short-axis view (30 to 60 degrees) or the = midesophagus=20 two-chamber view (80 to 100 degrees). Left atrial appendage flow should = be=20 recorded by positioning the color flow sector over the left atrial = appendage and=20 placing the pulsed-Doppler sample volume at the site of maximal flow = velocity.=20 This usually occurs in the proximal or middle third of the left atrial=20 appendage. Velocity recordings from the distal third of the left atrial=20 appendage frequently incorporate wall motion artefacts and are usually=20 unsatisfactory. Low-velocity flow may be present, and wall filters = should be set=20 low. The pattern of left atrial appendage flow is = dependent on=20 cardiac rhythm.[3= 3]=20 In patients with sinus rhythm, four left atrial appendage flow waves = have been=20 described (F= ig.=20 1-19) : (1) a large positive wave after the electrocardiographic = P-wave,=20 which represents left atrial appendage contraction and emptying; (2) a = large=20 negative early systolic wave immediately following the QRS complex = representing=20 left atrial appendage filling; (3) alternating positive and negative = waves of=20 decreasing velocity throughout the remainder of systole representing = passive=20 flow in and out of the appendage; and (4) a low-velocity positive = emptying wave=20 in early diastole coinciding with rapid left ventricular filling. In = addition, a=20 low-velocity middiastolic negative filling wave representing appendage = filling=20 from the pulmonary veins may follow the early diastolic atrial appendage = emptying wave. The normal velocities are as follows: left atrial = appendage=20 contraction, 60 =B1 14; left atrial appendage filling, 52 =B1 13; and = early=20 diastolic filling, 20 =B1 11 cm per second.[3= 3]=20 [3= 4] =20 In patients with atrial fibrillation, a regular = atrial=20 contraction wave is absent. However, the left atrial appendage continues = to=20 contract, resulting in irregular oscillating positive and negative = emptying and=20 filling waves with variable velocities. The velocities are usually = larger during=20 ventricular diastole when the mitral valve is open, and=20

Figure = 1-19 Normal left atrial appendage flow pattern in sinus = rhythm,=20 showing prominent atrial emptying and filling = velocities.

smaller during systole when the mitral valve is closed. = Of note,=20 mean left atrial appendage velocities tend to be lower with higher heart = rates=20 because of the smaller proportion of time spent during diastole.

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The = early=20 diastolic appendage emptying wave, which coincides with early rapid left = ventricular filling, may still be visualized in atrial fibrillation. In = patients=20 with atrial flutter, the velocity waves are more regular and tend to be = of=20 greater velocity because of the slower atrial contraction rate.=20 Factors other than cardiac rhythm that may = affect left=20 atrial appendage velocities have recently been reviewed and include age, = heart=20 rate, left atrial contractility, left atrial pressure, left ventricular = systolic=20 and diastolic function, mitral stenosis, and mitral=20 regurgitation.[3= 3]=20 The potential clinical utility of assessing = left atrial=20 appendage velocities relates to the association of left atrial appendage = velocities with left atrial spontaneous echo contrast and left atrial = appendage=20 thrombus.[3= 3]=20 [3= 5]=20 [3= 6]=20 Atrial fibrillation patients with a left atrial appendage contraction = velocity=20 of less than 20 cm per second are more likely to have left atrial = appendage=20 thrombus and have a greater risk of ischemic stroke compared with = patients with=20 left atrial appendage velocities of 20 cm per second or=20 greater.[3= 5]=20 [3= 6]=20 Lower left atrial appendage velocity has also been observed in stroke = patients=20 with normal sinus rhythm.[3= 7]=20 Other potential utilities may relate to an ability of left atrial = appendage=20 velocities to predict the success of maintaining sinus rhythm following=20 cardioversion of atrial fibrillation.[3= 3]=20 [3= 8]=20 Coronary Artery Flow The assessment of coronary artery flow may be = limited by=20 motion of the heart during the cardiac cycle and difficulties aligning = the=20 Doppler ultrasound beam parallel to coronary blood flow. Coronary artery = blood=20 flow and coronary artery blood flow reserve are best measured in the = distal left=20 main coronary artery or proximal left anterior descending artery using = the=20 midesophagus aortic valve short-axis view, in which the pulsed-Doppler=20 ultrasound beam can be aligned parallel to coronary blood flow. The = ultrasound=20 beam can only rarely be aligned parallel to flow in the left circumflex = artery,=20 and the right coronary artery cannot be imaged in up to half of all = patients.=20 The normal Doppler flow signal is characterized by a large diastolic = component=20 and small systolic component moving away from the transducer. In = general, normal=20 diastolic velocities are 60 cm per second or less, and diastolic = velocities=20 greater 100 cm per second

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suggest significant obstruction in the=20 artery.[3= 9]=20 [4= 0]=20 [4= 1]=20 Additionally, coronary artery flow reserve can be assessed by measuring = peak or=20 mean diastolic coronary flow velocities at rest and then following = dipyridamole=20 or adenosine infusion. [4= 0]=20 [4= 2]=20 Transaortic and Transpulmonary Flow Transaortic flow can be assessed by imaging the = left=20 ventricular outflow tract and aortic valve in the transgastric long-axis = view=20 (100 to 135 degrees) or deep transgastric long-axis view (0 degrees), in = which=20 the probe is=20 12

advanced deep into the stomach = adjacent=20 to the left ventricular apex and anteflexed until the imaging plane is = directed=20 superiorly to the base of the heart. In these views, the pulsed-Doppler = or=20 continuous wave Doppler beam can be aligned parallel to blood flow to = measure=20 transaortic velocity. Stroke volume can be derived with the additional=20 measurement of either the midesophagus left ventricular outflow tract = diameter=20 or the short-axis aortic valve orifice area at valve leaflet=20 level.[4= 3]=20 [4= 4]=20 In patients with aortic stenosis or other forms of left ventricular = outflow=20 tract obstruction, the transvalvular pressure gradients can be derived = using the=20 simplified Bernoulli equation and continuous wave Doppler signals = obtained from=20 the transgastric longaxis or deep transgastric long-axis view.=20 [2= 7]=20 Transpulmonary flow has been measured by = combining either=20 pulsed Doppler or continuous wave Doppler velocity measurements of = pulmonary=20 artery flow obtained from mid-esophagus short- axis images of the main = pulmonary=20 artery and measurements of the main pulmonary artery=20 diameter.[4= 5]=20 [4= 6]=20 Transmitral and Transtricuspid Flow In the midesophageal four-chamber view or = long-axis view,=20 the pulsed Doppler ultrasound beam can be aligned parallel to = transmitral flow=20 to accurately measure transmitral filling velocities. The pulsed Doppler = sample=20 volume should be kept small (3 to 5 mm) and positioned at the mitral = valve=20 leaflet tips for the evaluation of diastolic function and filling=20 pressures.[3= 0]=20 In contrast, transmitral stroke volume is measured by placing the sample = volume=20 at the mitral

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valve annulus, so that velocity and annular dimensions are = measured at the same location.[4= 7]=20 [4= 8]=20 Transtricuspid filling can be assessed by = pulsed Doppler=20 measurements obtained in the midesophageal four-chamber view. However, = it is=20 frequently not possible to align the Doppler ultrasound beam parallel to = blood=20 flow. The transtricuspid filling pattern is similar to the transmitral = filling=20 pattern, although lower velocities are present.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Indications for Transesophageal Echocardiography The potential utility of TEE in the assessment and management of patients with suspected and overt cardiac disease is wide-ranging and encompasses the spectrum of cardiac problems encountered in clinical cardiology. TEE can be performed on patients in the ambulatory setting, intensive care unit, coronary care unit, or operating room. In general, TTE should be employed as the initial diagnostic investigation, as this technique is noninvasive and will entail no risk to the patient. Patient factors such as obesity, emphysema, or chest deformities frequently limit ultrasound penetration, resulting in nondiagnostic TTE studies. Surgical bandages may limit the number of available acoustic windows, and mechanical ventilation and surgical devices, such as traction and intra-aortic balloon pumps, may limit the ability to properly position the patient. Subcutaneous emphysema may result in the complete TABLE 1-3 -- Common Indications for Transesophageal Echocardiography Nondiagnostic transthoracic echocardiogram Assessment of native valve disease Assessment of prosthetic valves Assessment of infective endocarditis Assessment of a suspected cardioembolic event Assessment of cardiac tumors Assessment of atrial septal abnormalities Assessment of aortic dissection, intramural hematomas, and aortic rupture Evaluation of congenital heart disease Detection of anatomic coronary artery disease Stress echocardiography

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Evaluation of pericardial disease Evaluation of critically ill patients Intraoperative monitoring Monitoring during interventional procedures inability of TTE to visualize cardiac structures. TEE should be considered in these patients to obtain the necessary diagnostic information. Despite an adequate TTE study, TEE may be indicated to assess cardiac structures not usually seen by TTE, such as the superior vena cava, pulmonary veins, and the descending thoracic aorta, or to provide improved anatomic details such as the detection of flail mitral valve leaflet scallops and valvular vegetations, which are not consistently detected by TTE. Finally, TEE has important applications in the operating room, which are discussed in Chapter 2 and Chapter 19 . The common clinical indications for TEE are given in Table 1-3 . Native Valve Disease The presence, etiology, and severity of native valve disease can usually be determined by TTE. TEE should be reserved for the clinical situation in which TTE findings are inconclusive or a more precise characterization of the valve lesion will alter the patient management plan. Excellent visualization of the mitral valve anatomy is possible by TEE because of the close proximity of the mitral valve to the TEE transducer and the ability to image with high-frequency transducers. The mitral annulus, leaflets, chordal structures, and papillary muscles can all be visualized and evaluated. The use of a multiplane transducer allows a comprehensive, detailed examination of the valve to determine the location and mechanism of mitral regurgitation (see Chapter 19) . Ruptured chordae tendineae can be visualized, and precise anatomic localization of prolapsing or flail leaflet scallops is possible to predict the potential for successful mitral valve repair.[25] [49] [50] Abnormalities of the papillary muscles, such as a partial or complete rupture, are better visualized by TEE than TTE.[51] The severity of mitral valve regurgitation can be quantified using the methods employed for TTE,[52] but color Doppler velocity regurgitant jet areas tend to be larger in size on TEE than TTE because higher transducer frequencies are used and because of the close proximity of the transducer to

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the regurgitant jet.[53] Pulmonary vein flow can be assessed in nearly all patients and provides 13

a valuable measure of mitral regurgitation severity.[54] [55] Regurgitant vena contracta width, regurgitant volumes, and regurgitant orifice areas using the proximal flow convergence zone can be obtained by TEE.[56] [57] In mitral stenosis, TTE is usually satisfactory in assessing the valve morphology and severity of stenosis (see Chapter 20) . TEE appears equivalent to TTE in assessing valve mobility and leaflet thickening, but subvalvular disease and calcification may be underestimated owing to the shadowing effect of thickening and calcification of the mitral leaflets and annulus in the esophageal views.[58] Transvalvular pressure gradients can be measured by aligning the continuous wave Doppler beam parallel to left ventricular inflow through the mitral valve in the midesophageal views.[59] Effective orifice areas can be derived by the pressure half-time method,[59] the proximal flow convergence method, or orifice planimetry.[60] Orifice planimetry requires a tomographic cut of the distal or most narrow mitral orifice, however, which is technically more difficult to obtain by TEE and frequently not possible. The potential suitability of a patient for percutaneous balloon mitral valvuloplasty usually incorporates a detailed TEE assessment of the left atrial chamber and appendage to identify thrombus, in addition to an evaluation of the mitral valve morphology score and mitral regurgitation severity.[61] Transthoracic echocardiography can adequately visualize most aortic valve abnormalities, and only rarely is TEE required for assessment. However, subvalvular abnormalities such as subaortic membranes frequently require TEE for definitive diagnosis. [62] The assessment of aortic regurgitation severity only rarely necessitates a TEE evaluation (see Chapter 17) . Standard Doppler methods used for TTE may be employed using TEE.[63] One of the best measures, the ratio of color jet area to left ventricular outflow tract area, can be obtained from esophageal short-axis images of the outflow tract immediately inferior to the aortic valve. Jet height to outflow tract height can be obtained from esophageal long-axis images. Holodiastolic flow reversal in the descending aorta is always present with severe aortic regurgitation and can be detected by biplane or multiplane TEE using pulsed Doppler.[64] Aortic regurgitation severity may also be quantified by TEE using proximal flow convergence methods and vena

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contracta width.[65] [66] The severity of aortic stenosis is best quantified using transvalvular pressure gradients or valve areas derived by TTE (see Chapter 22) . Continuous wave Doppler interrogation of the aortic valve is possible by TEE using the transgastric long-axis view (100 to 135 degrees) or deep transgastric long-axis view (0 degrees) in which the probe is advanced deep into the stomach adjacent to the left ventricular apex and anteflexed until the imaging plane is directed superiorly to the base of the heart (see Fig. 113) . Good correlations between TTE and TEE gradients have been reported, despite the limited TEE windows.[27] Anatomic orifice area can be derived by planimetry of the maximum systolic aortic valve orifice visualized from esophageal short-axis images. Proper transducer position should be confirmed by rotating to the longitudinal plane and verifying that the leaflet tips are being imaged. Aortic valve areas derived by orifice planimetry correlate well with valve areas derived by TTE using the continuity equation and Gorlin equation valve areas.[27] , [67] [68] Valve calcification may affect the accuracy of TEEmeasured orifice areas.[69] Importantly, orifice planimetry is often more feasible and accurate using multiplane than biplane TEE.[68] Prosthetic Valves Transesophageal echocardiography is an extremely valuable technique in the assessment of prosthetic valve function, because TTE visualization of the prosthetic valve components and function is often limited by the echogenicity of the prosthetic components (see Chapter 24 and Chapter 25) . Reverberation artifacts, attenuation artifact, and acoustic shadowing obscure visualization of the prosthetic components and limit the visualization of structures beyond the prosthesis. Thickening and calcification of the leaflets, or the presence of a torn or flail bioprosthetic leaflet, are better appreciated on TEE. The structure and motion of the occluding device of a mechanical prosthesis may also be better evaluated. TEE provides increased sensitivity for detecting abnormalities of bioprosthetic and mechanical prostheses when compared to TTE.[70] [71] Small abnormalities of prosthetic valves such as leaflet thickening, flail leaflets, vegetations, thrombi, and filamentous strands can be missed on TTE but appreciated on TEE.[70] [71] [72] [73] [74] [75] [76] [77] TEE can be used to distinguish pannus from thrombus formation[78] and to guide thrombolytic therapy use in patients with the latter condition.[79] TEE is especially valuable in assessing mitral prostheses, as the transducer's posterior

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position provides excellent visualization of vegetations and thrombi, which usually locate on the left atrial aspect of the prosthesis.[70] [73] However, the ventricular aspect of a mitral prosthesis may not be adequately seen, and so TTE should complement the TEE assessment. [80] Transesophageal echocardiography can differentiate between normal variant and pathologic prosthetic valve regurgitation.[71] [72] [73] [74] [75] [81] Prosthetic mitral regurgitation is frequently better evaluated by TEE than TTE,[71] [72] [74] because TEE provides excellent visualization of the left atrial cavity without any intervening prosthetic material. TEE should be performed in patients in whom significant mitral regurgitation is not seen on TTE but is a clinical concern. Importantly, TEE allows characterization of mitral regurgitation jets as paravalvular or transvalvular in origin, which may modify the surgical procedure.[72] [74] [82] Multiplane TEE appears to better delineate paraprosthetic mitral regurgitation as compared with biplane TEE.[82] The incremental benefit of TEE in the assessment of regurgitation severity is less clear for aortic prostheses because the aortic regurgitation jet is usually well seen on TTE, and TEE visualization of prosthetic aortic regurgitation may be compromised by partial obstruction of the aortic regurgitation jet by either a mitral or aortic prosthesis in the esophageal views.[75] All bioprostheses and mechanical prostheses are inherently stenotic. The degree of stenosis is dependent on the prosthesis type and size and the presence of an associated pathologic condition such as leaflet calcification, pannus formation, or valve thrombosis.[83] In general, TTE is sufficient to assess the severity of prosthetic aortic or mitral 14

stenosis, but only TEE has sufficient resolution to distinguish these pathologic conditions.[78] In patients with inadequate TTE findings, TEE can quantify prosthetic mitral stenosis by measuring diastolic pressure gradients, pressure half-time, and effective orifice area using the proximal flow convergence method, as described for native mitral stenosis.[60] [84] Prosthetic aortic stenosis can be assessed by measuring transvalvular pressure gradients, as described for native aortic stenosis. [27] Importantly, flow through certain mechanical aortic prostheses results in localized pressure gradients and significant pressure recovery, which may lead to a discrepancy between Doppler and catheterization pressure gradients and an apparent "overestimation" of Doppler gradients.[85]

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Infective Endocarditis The presence of a vegetation is a hallmark finding of infective endocarditis, and its identification in the clinical setting of suspected endocarditis confirms the diagnosis[86] (see Chapter 21) In native valve endocarditis, the sensitivity of TTE for the detection of vegetations was 28% to 63%, and the sensitivity of TEE was 86% to 98%. [87] [88] [89] [90] [91] The specificity of the TTE and TEE findings for a vegetation appears similar and exceeds 90% when strict echocardiographic criteria are used for diagnosis.[87] [88] [90] Smaller vegetations are more likely to be detected by TEE than TTE.[88] Isolated case reports have suggested that pulmonic valve vegetations may also be better seen by TEE.[92] TEE does not appear to have an increased sensitivity compared with TTE, however, in the detection of tricuspid valve vegetations.[93] Prosthetic valve endocarditis is more difficult to diagnose using either TTE or TEE. The reported sensitivity of TTE for detecting vegetations was 0 to 43%, and the sensitivity of TEE was superior at 33% to 86%.[70] [89] [94] , [95] Thus, TEE should be performed in patients with suspected prosthetic valve endocarditis if the TTE procedure does not identify a vegetation. Although TEE has an improved sensitivity for detecting vegetations compared with TTE, the impact of TEE on diagnosis appears to be greatest in patients with suspected endocarditis with an intermediate clinical probability of endocarditis, especially patients with prosthetic valves.[96] Importantly, the absence of a vegetation on TEE makes the diagnosis of endocarditis unlikely (<10%), and alternative diagnoses should be considered.[95] [97] However, false-negative TEE studies have been reported, and patients with a high index of suspicion of endocarditis, prosthetic valves, or a persistent bacteremia may benefit from follow-up TEE if the initial study was negative.[95] [97] The complications of infective endocarditis, including abscess formation, leaflet diverticula, leaflet perforation, fistula tracts, mycotic aneurysms, and pseudoaneurysm formation, are better detected by TEE than TTE.[89] [98] [99] [100] [101] In a large series of patients with infective endocarditis, only 28% of surgically or autopsy confirmed abscess cavities were identified by TTE, as opposed to an 87% detection rate by TEE.[98] The specificity of both techniques in the detection of abscess formation exceeded 90%. Thus, patients with a suspected abscess based on clinical grounds or persistent bacteremia should undergo TEE.

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The role or potential utility of TEE in uncomplicated confirmed endocarditis is controversial. TEE may provide the clinician with prognostic information. Larger, mobile vegetations on TEE are associated with systemic embolization.[91] Additionally, complications including embolism, abscess formation, need for valve replacement, and death may be more likely to occur in patients with a vegetation that fails to decrease in size with therapy.[102] At this time, we do not perform routine follow-up TEE for cases of uncomplicated confirmed endocarditis. Suspected Cardioembolic Event The potential for a cardioembolic event should be considered in patients suffering cerebral ischemia or a peripheral arterial embolus. The Cerebral Embolism Task Force has suggested that cardiac emboli account for 15% of cerebral ischemic events.[103] Several cardiac abnormalities have a strong association with cardioembolic events and are considered a major risk source (see Chapter 37) . These abnormalities include atrial fibrillation, left atrial or left ventricular thrombi, vegetations, intracardiac tumor, mitral stenosis, mechanical valves, recent myocardial infarction, dilated cardiomyopathy, and intra-aortic debris.[104] Minor risk sources with weaker associations include cardiac abnormalities such as atrial septal aneurysms, patent foramen ovale, spontaneous echo contrast, mitral annular calcification, and mitral valve prolapse.[104] Many of these conditions can be diagnosed by clinical assessment, but echocardiography is frequently required for the diagnosis of many of the anatomic abnormalities. Approximately 7% of patients with a suspected cardioembolic event will have left atrial thrombus in the absence of atrial fibrillation and mitral stenosis. [105] The thrombus is frequently located in the left atrial appendage, a region poorly visualized on TTE. The sensitivity of TTE in detecting left atrial thrombus has been reported to be only 0 to 53%, whereas TEE has a sensitivity of 93% to 100% and a specificity exceeding 95%.[106] [107] In contrast, left ventricular thrombi may be better appreciated by TTE than TEE because of the close proximity of the left ventricular apex to the TTE transducer and the far field position and frequent apical foreshortening of the left ventricular apex on TEE.[108] However, TEE assessment may be beneficial if the TTE findings are inconclusive. [109] Left atrial spontaneous echo contrast is rarely appreciated on TTE, but well seen on TEE because of the close proximity of the left atrium to the TEE transducer and use of higher frequency transducers.[110] TEE may better detect small myxomas and aid in the diagnosis and management by better characterizing the

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attachment site.[111] [112] Similarly, TEE is superior in the detection of patent foramen ovale and atrial septal aneurysms.[113] [114] The size of the patent foramen ovale is associated with the cardioembolic risk and can better be appreciated by TEE.[115] A comprehensive characterization of aortic arch atheroma is rarely possible by TTE alone and requires TEE assessment.[35] [116] [117]

The indication for performing a TEE in patients with a suspected cardioembolic event is controversial. Although TEE has a better sensitivity than TTE for detecting potential 15

cardioembolic abnormalities, the yield for identifying a major risk source is limited. An analysis of pooled data from more than 30 cross-sectional studies suggested an overall detection rate for intracardiac masses of 4% for TTE and 11% for TEE.[104] However, the yield was greater in patients with evidence of cardiac disease. TTE and TEE identified an intracardiac mass in 13% and 19% of patients with cardiac disease and only 0.7% and 1.6% in patients without cardiac disease, respectively. In addition, the information obtained by TEE, which may include the identification of minor risk sources, may not significantly alter patient management.[104] [118] Many management decisions will be predetermined by the clinical setting (e.g., the patient with atrial fibrillation requires anticoagulation), and the management of patients with minor-risk cardiac abnormalities is frequently controversial. Thus, TEE should only be performed if the results have a reasonable chance of altering patient management or therapy. In this regard, TEE may have the greatest impact on patient management in the clinical setting of patients younger than 55 years of age with unexplained cerebral ischemia, in patients having recurrent events, or in patients with suspected endocarditis. Atrial Septal Abnormalities Transesophageal echocardiography provides excellent visualization of the atrial septum because of the atrial septum's close proximity to the transducer and perpendicular orientation to the ultrasound beam. Abnormalities of the atrial septum, including atrial septal defects, atrial septal aneurysms, and patent foramen ovale, are identified more frequently by TEE than by TTE.[19] [113] [114] , [119] [120] Sinus venosus defects and associated anomalous pulmonary venous drainage are frequently not

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identified on transthoracic imaging but can be easily detected on TEE study. [19] [20] TEE can be used to assess the severity of left-to-right shunting across the defect, determine the potential for percutaneous closure by accurate localization and characterization of the defect, and be used to assist in proper device placement during percutaneous closure.[121] [122] TEE can also detect thrombus formation within an atrial septal aneurysm and paradoxic emboli across an atrial septal defect.[115] [120] Cardiac Tumors For detecting intracardiac tumors, TEE appears superior to TTE, computed tomography, angiography, and magnetic resonance imaging.[112] [123] The sensitivity of TTE and TEE for the detection of atrial myxomas has been reported to be 95% and 100%, respectively.[123] Nonmyxomatous intracardiac tumors are identified by TTE and TEE in 91% and 100% of patients, respectively.[123] Pericardial or paracardial tumors are detected in only 67% by TTE and 97% by TEE.[123] TEE appears especially valuable in the detection of tumors located at the base of the heart, adjacent to the great vessels, or adjacent to the right heart.[112] [123] In addition, TEE is superior to TTE in characterizing features of a cardiac tumor that may assist in the diagnosis and management, such as the involvement of multiple chambers, the site of tumor attachment, the presence of multiple tumors, infiltration of adjacent structures, tumor calcification, or cyst formation.[112] [123] TEE has been used to guide percutaneous biopsy of intracardiac tumors.[124] However, the size and extent of paracardial involvement is not well assessed by TTE or TEE. In this setting, tomographic imaging with a wider field of view (magnetic resonance imaging or computed tomography) is needed. Aortic Dissection, Intramural Hematoma, and Rupture Aortic dissection can be detected by TEE with a high degree of accuracy and is the diagnostic investigation of choice for suspected aortic dissection in many institutions (see Chapter 3) . [125] The ascending aorta, aortic arch, and descending thoracic aorta can be visualized with excellent resolution owing to the close proximity of the aorta to the transducer and the use of high-frequency transducers. Importantly, a small segment of the superior ascending aorta cannot be visualized using TEE owing to the interposition of the air-filled trachea and bronchus. The sensitivity of monoplane and biplane TEE for the diagnosis of aortic dissection has been reported to be 97% to 100%, with a specificity that has ranged from 77% to 100%.[125] [126] [127] [128] The specificity was found to be greater than 95%, except in one

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study.[126] Multiplane TEE has been associated with similar sensitivities and specificities of 98% to 100% and 94% to 95%, respectively.[129] [130] The sensitivity and specificity of TEE compares favorably with those of other technologies, including aortography, computed tomography, and magnetic resonance imaging.[126] [127] [128] In addition to diagnosis, TEE can determine the extent of the dissection, differentiate the true and false lumens, identify thrombus within the false lumen, identify the site of the intimal tear, and assess for aortic valve involvement. [125] , [126] Involvement of the arch vessels and coronary arteries can also be determined.[125] Additionally, TEE can detect findings of aortic rupture, such as a pericardial effusion, pleural effusion, or mediastinal hematoma, which may significantly alter surgical therapy.[125] Aortic complications after repair may also be detected.[131] Associated aortic abnormalities, such as intramural hematoma and penetrating aortic ulcers, may have a similar presentation to aortic dissection and can be diagnosed using TEE.[128] [129] [132] TEE appears to have a high sensitivity and specificity for the detection of intramural hematoma, [129] but the diagnostic accuracy in the detection of penetrating aortic ulcers is unclear. In the largest series of 12 patients, penetrating aortic ulcers were identified by TEE in 83% of patients.[132] Transesophageal echocardiography has been used in the setting of chest trauma for the diagnosis of traumatic aortic rupture. The reported sensitivity and specificity for the detection of traumatic aortic rupture has ranged from 63% to 100% and 84% to 100%, respectively.[117] [133] However, TEE cannot consistently visualize the superior ascending aorta and aortic arch branch vessels, a frequent site of traumatic injury.[134] Thus, the role of TEE in the diagnostic evaluation of chest trauma patients remains undefined. Congenital Heart Disease

16

Transesophageal echocardiography commonly adds information to the preoperative, intraoperative, and postoperative assessment and management of patients with congenital heart disease[135] [136] (see Chapter 39 , Chapter 40 , Chapter 41 ). TEE can better appreciate abnormalities of the atrial septum and pulmonary veins, and it can be used to guide percutaneous

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closure of atrial septal defects.[19] [20] [119] , [121] [122] [124] In patients with atrioventricular canal defects, the atrioventricular valves and site of chordal insertion can be visualized to determine the potential for surgical valvuloplasty. [137] TEE provides good visualization of an atrial baffle and can detect stenoses or leaks.[138] Complications of a Fontan procedure, such as obstruction or thrombosis, can be evaluated.[139] TEE can characterize right and left ventricular outflow tract obstructions.[62] [135] [137] Abnormalities of the aorta, including aortic coarctation and patent ductus arteriosus, are also better appreciated by TEE than by TTE.[140] [141] Coronary Artery Disease Transesophageal echocardiography can be employed for the diagnosis of coronary artery disease by (1) visualization of coronary stenoses in the proximal vessels or (2) detection of stress-induced regional wall motion abnormalities. The left main coronary artery can be visualized in more than 85% of patients.[39] [142] [143] [144] [145] The proximal left anterior descending artery and proximal left circumflex artery can also be visualized in most patients.[142] [143] [144] The proximal right coronary artery is more difficult to visualize but may still be seen in 50% of patients or more.[142] [144] Several studies have examined the accuracy of TEE in identifying coronary stenoses in the proximal segments of the coronary arteries using two-dimensional and color flow imaging. In patients with visualized vessels, the sensitivity of TEE in identifying significant left main coronary stenoses has been reported to be 91% to 100%, with specificities greater than 90%.[39] [142] [143] [144] [145] The sensitivity for detecting significant proximal left anterior descending artery disease, left circumflex artery disease, and right coronary artery disease has been reported to be 78% to 100%, 50% to 89%, and 82% to 100%, respectively.[142] [143] [144] The sensitivity for detecting coronary artery stenoses significantly decreases, however, if patients with nonvisualized segments are included in the analysis.[144] One author has reported employing TEE and the continuity equation to quantify the severity of stenoses in the left anterior descending artery.[41] In addition, coronary artery flow reserve can be measured using TEE, and differences in flow reserve can be detected in patients with left anterior descending artery stenoses.[40] [42] TEE should not replace coronary angiography in the diagnosis of proximal coronary artery stenoses, but it may be useful in assessing angiographically questionable stenoses involving the left main ostium or the left anterior descending artery in centers in which

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intravascular ultrasonography is not available.[146] Stress echocardiography with TEE imaging has been used to evaluate patients with suspected or confirmed coronary artery disease.[147] [148] TEE provides high-quality images with excellent endocardial resolution. Stress techniques employed to induce ischemia have included transesophageal atrial pacing and pharmacologic methods using either dobutamine or dipyridamole.[147] [148] These techniques have been shown to be highly accurate in the detection of coronary artery disease and to provide information useful in risk stratification, and they may be useful in the assessment of myocardial viability in patients with left ventricular dysfunction.[147] [148] TEE is an invasive procedure with potential risks, however, and stress echocardiography with TEE imaging should be reserved for patients who have poor TTE images. Additional applications of TEE in the assessment of coronary artery disease include the detection of anomalous coronary arteries and the detection and mapping of coronary artery fistulas.[149] Pericardial Disease Pericardial effusions and cardiac tamponade are usually easily diagnosed on TTE and do not require TEE (see Chapter 29) . However, the detection of cardiac tamponade after cardiac surgery can be difficult to diagnose by TTE. Local compression of the right atrium by extracardiac thrombus may not be apparent on TTE because of the posterior position of the thrombus and poor TTE images related to suboptimal patient position, surgical bandages, and drainage tubes. TEE circumvents these problems and can better detect extracardiac compression.[150] Constrictive pericarditis and restrictive physiologic diseases can usually be differentiated on TTE using respiratory monitoring. In patients with nondiagnostic TTE, however, TEE with respiratory monitoring may be useful in differentiating these diseases. [151] Pericardial thickening can be measured by TEE and correlates with computed tomography. [152] In one study, TEE was shown to be superior to TTE in assessing pericardial thickening, intrapericardial metastases, intrapericardial thrombus, and pericardial cysts.[150] Intensive Care Unit The TTE images obtained in the intensive care unit are frequently inadequate because of poor acoustic penetration, limited windows from surgical bandages and drains, mechanical ventilation, and an inability to

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properly position patients. In this setting, TEE can provide essential information that alters patient management. TEE has been shown to be valuable in the assessment of the patient with unexplained hypotension, pulmonary edema, and hypoxia.[153] [154] TEE provides information on myocardial function, valve function, and volume status, which is critical in evaluating the patient with unexplained hypotension or unexplained pulmonary edema. TEE can detect right-to-left intracardiac shunting through a patent foramen ovale, which may occur in ventilated patients requiring high levels of pressure support and right ventricular infarction. [155] [156] The presence of massive or proximal pulmonary emboli can be diagnosed by TEE.[22] [23] Potential complications of myocardial infarction, including left ventricular 17

dysfunction, papillary muscle rupture, and myocardial rupture, may be detected. Intraoperative Monitoring Intraoperative TEE can provide detailed information on cardiac anatomy and function not obtainable by other monitoring technologies and can obtain this information without disrupting the surgical procedure.[157] [158] TEE can evaluate global and segmental left ventricular function, detect intraoperative myocardial ischemia, and monitor hemodynamics, including cardiac output, left ventricular filling pressures, and volume status. The cause of hemodynamic disturbances can be determined and intraoperative complications identified. Importantly, the adequacy of valve repairs or replacements and surgical reconstructions for congenital and acquired diseases can be evaluated prior to leaving the operating room. In 1996, the American Society of Anesthesiologists published recommendations for performing TEE based on the strength of supporting evidence and expert opinion that TEE improved clinical outcome.[157] The complete list of potential indications for TEE in the intraoperative period is extensive and is discussed in more detail in Chapter 2 and Chapter 19 . Monitoring During Interventional Procedures Transesophageal echocardiography is a valuable adjunct to percutaneous mitral valvuloplasty. TEE can guide catheter placement during trans-septal puncture, assist in proper balloon placement, evaluate the valvuloplasty result, identify complications, and shorten procedure and fluoroscopy

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times.[121] [159] It has been used to assist in right ventricular biopsies and biopsies of intracardiac masses.[124] [160] TEE may assist in trans-septal puncture and proper catheter position for radiofrequency ablation.[161] TEE has been used to guide catheter position for percutaneous closure of atrial septal defects, patent ductus arteriosus, ventricular septal defects, and coronary artery fistulas.[122] [162] [163] [164] TEE has also been found to be useful in the pediatric population during creation or enlargement of an interatrial communication or balloon dilation of obstructive left heart lesions. [165] Electrical cardioversion of atrial fibrillation without prolonged anticoagulation has been proposed as a safe procedure if TEE excludes left atrial thrombus.[166] However, this management scheme is controversial and requires further investigation (see Chapter 38) .[167]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Contraindications to Transesophageal Echocardiography Patients undergoing TEE should be kept on NPO (nothing by mouth) status for 4 to 6 hours prior to the procedure because of the potential for vomiting and aspiration. However, urgent procedures can likely be performed earlier with minimal risk of vomiting and aspiration if there has been only clear fluid intake up to 2 hours prior to the procedure.[168] TEE should not be performed in the uncooperative patient. Patients who are uncooperative should either have the study deferred or be sedated and paralyzed, if necessary. Patients with a tenuous cardiorespiratory status should be intubated and ventilated to avoid decompensation during the procedure. To avoid esophageal rupture, TEE should not be attempted in a patient with esophageal obstruction caused by a stricture or mass. The presence of an esophageal diverticulum should also be considered a relative contraindication because of the possibility of the probe entering and perforating the diverticulum. TEE is contraindicated in the patient with a perforated viscus or active gastrointestinal bleed. Esophageal varices are not a contraindication to TEE. However, the potential additive information should be weighed against the small risk of major bleeding. Severe cervical arthritis or dislocation of the atlantoaxial joint, in which flexion of the neck is severely limited or impossible, should be considered a relative contraindication to TEE. TEE can be performed safely in patients receiving anticoagulation therapy.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Complications of Transesophageal Echocardiography Transesophageal echocardiography is a relatively safe procedure with a low complication rate. Procedural complications have been observed in 0.47% to 2.80% of patients with successful esophageal intubation, however (Table 1-4) .[5] [9] [11] [169] The vast majority of complications are minor. Major complications, defined in one study as death, laryngospasm, sustained ventricular tachycardia, or congestive heart failure, occur in approximately 0.3% of patients.[169] In the Multicenter European Survey of 10,419 examinations, the TEE examination had to be interrupted prior to completion in 0.88% of studies.[11] Patient TABLE 1-4 -- Procedural Complications with Transesophageal Echocardiography Major Complications Death Esophageal rupture Laryngospasm or bronchospasm Congestive heart failure or pulmonary edema Sustained ventricular tachycardia Minor Complications Excessive retching or vomiting Sore throat Hoarseness Minor pharyngeal bleeding Blood-tinged sputum Nonsustained or sustained supraventricular tachycardia Atrial fibrillation

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Nonsustained ventricular tachycardia Bradycardia or heart block Transient hypotension Transient hypertension Angina Transient hypoxia Parotid swelling Tracheal intubation

18

intolerance of the probe, including excessive retching or vomiting, was the most common complication, resulting in premature termination of the procedure.[11] In the largest series, deaths have been reported in 0 to 0.03% of patients.[5] [9] [11] , [169] Cardiac complications reported include nonsustained and sustained supraventricular tachycardias or atrial fibrillation, nonsustained and sustained ventricular tachycardia, bradycardia, transient hypotension or hypertension, angina pectoris, congestive heart failure, and pulmonary edema. Pulmonary complications have included transient hypoxia and laryngospasm. Bleeding complications have included minor pharyngeal bleeding or blood-tinged sputum, MalloryWeiss tear, and severe hematemesis in a patient with a malignant tumor invading the esophagus. A minor sore throat may be present for 24 hours after the procedure. Adverse reactions may occur as a result of intravenous sedation, topical anesthesia, or drying agents such glycopyrrolate. Intravenous sedation may result in respiratory depression and hypoxia, hypotension, or paradoxical reactions. Topical anesthesia with benzocaine or lidocaine may result in acute toxic methemoglobinemia, a rare condition in which hemoglobin is oxidized by the topical anesthesia agent and is unable to carry oxygen to the tissues.[170] The partial pressure of oxygen in the blood is normal, but oxyhemoglobin levels are decreased. Patients usually develop cyanosis and dyspnea. On pulse oximetry, oxygen saturation often appears only mildly reduced because this technique cannot distinguish methemoglobin and reduced hemoglobin. The diagnosis can be confirmed with an arterial blood gas sample with measurement of methemoglobinemia. Methylene blue (1

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Transesophageal echocardiography is a very powerful tool that provides a unique acoustic window to assess cardiac structure and function. In our view, a comprehensive study should include the standard views discussed in this chapter. When dealing with specific clinical problems, additional views should be used to obtain the necessary diagnostic information. In critically ill patients, we believe that the initial views should be those that are most pertinent to the clinical question. Adequate diagnostic information would then have been obtained even if the study needs to be terminated prematurely. Finally, we need to be mindful that TEE is a semi-invasive procedure and is not free of risks. Clear and convincing indications should be present before a TEE study is performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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and biplane versus multiplane transesophageal imaging: A review of 2947 consecutive studies. Can J Cardiol 1997;13:81–84. 10. Yvorchuk K, Sochowski R, Chan K: A prospective comparison of the multiplane

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21. Fagan S, Veinot JP, Chan KL: Residual sinus venosus atrial septal defect following

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30. Nishimura RA, Tajik AJ: Evaluation of diastolic filling of left ventricle in health

and disease: Doppler echocardiography is the clinician's Rosetta stone. J Am Coll Cardiol 1997;30:8–18. 31. Klein AL, Tajik AJ: Doppler assessment of pulmonary venous flow in healthy

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velocity patterns in normal subjects. J Am Soc Echocardiogr 1996;9:274–280. 35. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography: Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med 1998;128:639–647. 36. Goldman ME, Pearce LA, Hart RG, et al: Pathophysiologic correlates of

thromboembolism in nonvalvular atrial fibrillation: I. Reduced flow velocity in the left atrial appendage (The Stroke Prevention in Atrial Fibrillation [SPAFF-III] study). J Am Soc Echocardiogr 1999;12:1080–1087. 37. Kamalesh M, Copeland TB, Sawada S: Severely reduced left atrial appendage function: A cause of embolic stroke in patients in sinus rhythm? J Am Soc Echocardiogr 1998;11:902–904. 38. Verhorst PM, Kamp O, Welling RC, et al: Transesophageal echocardiographic

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with left main coronary artery stenosis by transesophageal Doppler color flow echocardiography. J Am Coll Cardiol 1991;17:87–93. 40. Kozakova M, Palombo C, Pratali L, et al: Assessment of coronary reserve by

transoesophageal Doppler echocardiography: Direct comparison between different modalities of dipyridamole and adenosine administration. Eur Heart J 1997;18:514– 523.

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41. Isaaz K, da Costa A, de Pasquale JP, et al: Use of the continuity equation for

transesophageal Doppler assessment of severity of proximal left coronary artery stenosis: A quantitative coronary angiography validation study. J Am Coll Cardiol 1998;32:42–48. 42. Redberg RF, Sobol Y, Chou TM, et al: Adenosine-induced coronary vasodilation during transesophageal Doppler echocardiography: Rapid and safe measurement of coronary flow reserve ratio can predict significant left anterior descending coronary stenosis. Circulation 1995;92:190–196. 43. Feinberg MS, Hopkins WE, Davila-Roman VG, et al: Multiplane transesophageal

echocardiographic Doppler imaging accurately determines cardiac output measurement in critically ill patients. Chest 1995;107:679–673. 44. Katz WE, Gasior TA, Quinlan JJ, et al: Transgastric continuous-wave Doppler to

determine cardiac output. Am J Cardiol 1993;71:853–857. 45. Gorscan J III, Diana P, Ball BA, et al: Intraoperative determination of cardiac

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output by transesophageal pulsed Doppler echocardiography. Anesthesiology 1991;74:9–14. 47. Hozumi T, Shakudo M, Applegate R, et al: Accuracy of cardiac output estimation

with biplane transesophageal echocardiography. J Am Soc Echocardiogr 1993;6:62– 68. 48. Pu M, Griffin BP, Vandervoort PM, et al: Intraoperative validation of mitral inflow

determination by transesophageal echocardiography: Comparison of single-plane, biplane and thermodilution techniques. J Am Coll Cardiol 1995;26:1047–1053. 49. Foster GP, Iselbacher EM, Rose GA, et al: Accurate localization of mitral

regurgitation defects using multiplane transesophageal echocardiography. Ann Thorac Surg 1998;65:1025–1031. 50. Grewal KS, Malkowski MJ, Kramer CM, et al: Multiplane transesophageal

echocardiographic identification of the involved scallop in patients with flail mitral valve leaflet: Intraoperative correlation. J Am Soc Echocardiogr 1998;11:966–971. 51. Moursi MH, Bhatnagar SK, Vilacosta I, et al: Transesophageal echocardiographic

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evaluation of mitral regurgitation: The twenty-four signs of severe mitral regurgitation. Cardiol Clin 1993;11:399–408. 53. Smith MD, Harrison MR, Pinton R, et al: Regurgitant jet size by transesophageal

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patterns in detecting mitral regurgitation and left ventricular abnormalities. Can J Cardiol 1999;15:665–670. 56. Grayburn PA, Fehske W, Omran H, et al: Multiplane transesophageal

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score by transthoracic and transesophageal echocardiography. Am J Cardiol 1991;68:1106–1107. 59. Stoddard MF, Prince CR, Tuman WL, et al: Angle of incidence does not affect accuracy of mitral stenosis area calculation by pressure half-time: Application to Doppler transesophageal echocardiography. Am Heart J 1994;127:1562–1572. 60. Degertekin M, Basaran Y, Gencbay M, et al: Validation of flow convergence

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the assessment of percutaneous mitral commissurotomy. Eur Heart J 1991;12(suppl B):61–65. 62. Essop MR, Skudicky D, Sareli P: Diagnostic value of transesophageal versus

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by transesophageal echocardiography: Correlation with angiographic determination. Echocardiography 1993;10:269–278. 64. Sutton DC, Kluger R, Ahmed SU, et al: Flow reversal in the descending aorta: A

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65. Sato Y, Kawazoe K, Nasu M, et al: Clinical usefulness of the proximal isovelocity

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orifice area determined by transesophageal echocardiography in patients with eccentric aortic regurgitation. J Heart Valve Dis 1997;6:580–586. 67. Hoffmann R, Flachskampf FA, Hanrath P: Planimetry of orifice area in aortic stenosis using multiplane transesophageal echocardiography. J Am Coll Cardiol 1993;22:529–534. 68. Kim KS, Maxted W, Nanda NC, et al: Comparison of multiplane and biplane

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echocardiography in determining aortic valve area in aortic stenosis. Am J Cardiol 1996;77:882–885. 70. Daniel WG, Mugge A, Grote J, et al: Comparison of transthoracic and

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71. Alton ME, Pasierski TJ, Orsinelli DA, et al: Comparison of transthoracic and

transesophageal echocardiography in evaluation of 47 Starr-Edwards prosthetic valves. J Am Coll Cardiol 1992;20:1503–1511. 72. Daniel LB, Grigg LE, Weisel RD, et al: Comparison of transthoracic and

transesophageal assessment of prosthetic valve dysfunction. Echocardiography 1990;7:83–95.

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73. Khandheria BK, Seward JB, Oh JK, et al: Value and limitations of transesophageal

echocardiography in the assessment of mitral valve prosthesis. Circulation 1991;83:1956–1968. 74. Chaudhry FA, Herrera C, DeFrino PF, et al: Pathologic and angiographic

correlations of transesophageal echocardiography in the prosthetic heart valve dysfunction. Am Heart J 1991;122:1057–1064. 75. Karalis DG, Chandrasekaran K, Ross JJ Jr, et al: Single-plane transesophageal

echocardiography for assessing function of mechanical or bioprosthetic valves in the aortic valve position. Am J Cardiol 1992;69:1310–1315. 76. Gueret P, Vignon P, Fournier P, et al: Transesophageal echocardiography for the

diagnosis and management of nonobstructive thrombosis of mechanical mitral prosthesis. Circulation 1995;91:103–110. 77. Orsinelli DA, Pearson AC: Detection of prosthetic valve strands by

transesophageal echocardiography: Clinical significance in patients with suspected cardiac source of embolism. J Am Coll Cardiol 1995;26:1713–1718. 78. Barbetseas J, Nagueh SF, Pitsavos C, et al: Differentiating thrombus from pannus

formation in obstructed mechanical prosthetic valves: An evaluation of clinical, transthoracic and transesophageal echocardiographic parameters. J Am Coll Cardiol 1998;32:1410–1417. 79. Ozkan M, Kaymaz C, Kirma C, et al: Intravenous thrombolytic treatment of

mechanical prosthetic valve thrombosis: A study using serial transesophageal echocardiography. J Am Coll Cardiol 2000;35:1881–1889. 80. Tenenbaum A, Fisman EZ, Vered Z, et al: Failure of transesophageal

echocardiography to visualize a large mitral prosthesis vegetation detected solely by transthoracic echocardiography. J Am Soc Echocardiogr 1995;8:944–946. 81. Flachskampf FA, O'Shea JP, Griffin BP, et al: Patterns of transvalvular

regurgitation in normal mechanical prosthetic valves. J Am Coll Cardiol 1991;18:1493–1498. 82. Flachskampf FA, Hoffmann R, Franke A, et al: Does multiplane transesophageal

echocardiography improve the assessment of prosthetic valve regurgitation? J Am Soc Echocardiogr 1995;8:70–78. 83. Reisner SA, Meltzer RS: Normal values of prosthetic valve Doppler

echocardiographic parameters: A review. J Am Soc Echocardiogr 1998;11:201–210.

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84. Gorscan J III, Kenny WM, Diana P, et al: Transesophageal continuous-wave

Doppler to evaluate mitral prosthetic stenosis. Am Heart J 1991;121:911–914. 85. Baumgartner H, Khan S, DeRobertis M, et al: Effect of prosthetic aortic design on

the Doppler-catheter gradient correlation: An in vitro study of normal St. Jude, Medtronic-Hall, Starr-Edwards, and Hancock valves. J Am Coll Cardiol 1992;19:324– 332. 86. Durak DT, Lukes AS, Bright DK: New criteria for diagnosis of infective

endocarditis: Utilization of specific echocardiographic findings. Am J Med 1994;96:200–209. 87. Birmingham GD, Rahko PS, Ballantyne FE: Improved detection of infective

endocarditis with transesophageal echocardiography. Am Heart J 1992;123:774–781. 88. Erbel R, Rohmann S, Drexler M, et al: Improved diagnostic value of

echocardiography in patients with infective endocarditis by transesophageal approach: A prospective study. Eur Heart J 1988;9:43–53. 89. Taams MA, Gussenhoven EJ, Bos E, et al: Enhanced morphologic diagnosis in

infective endocarditis by transoesphageal echocardiography. Br Heart J 1990;63:109– 113. 90. Shively BK, Gurule FT, Roldan CA, et al: Diagnostic value of transesophageal

compared with transthoracic echocardiography in infective endocarditis. J Am Coll Cardiol 1991;18:391–397. 91. Mügge A, Daniel WG, Frank G, et al: Echocardiography in infective endocarditis:

Reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol 1989;14:631–638. 92. Shapiro SM, Young E, Ginzton LE, et al: Pulmonic valve endocarditis as an underdiagnosed disease: Role of transesophageal echocardiography. J Am Soc Echocardiogr 1992;5:48–51. 93. San Roman JA, Vilacosta I, Zamorano JL, et al: Transesophageal

echocardiography in right-sided endocarditis. J Am Coll Cardiol 1993;21:1226–1230. 94. Zabalgoitia M, Herrera CJ, Chaudhry FA, et al: Improvement in the diagnosis of

bioprosthetic valve dysfunction by transesophageal echocardiography. J Heart Valve Dis 1993;2:595–603. 95. Lowry RW, Zoghbi WA, Baker WB, et al: Clinical impact of transesophageal

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echocardiography in the diagnosis and management of infective endocarditis. Am J Cardiol 1994;73:1089–1091. 96. Lindner JR, Case RA, Dent JM, et al: Diagnostic value of echocardiography in

suspected endocarditis: An evaluation based on the pretest probability of disease. Circulation 1996;93:730–736. 97. Sochowski RA, Chan K-L: Implication of negative results on a monoplane

transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol 1994;21:216–221. 98. Daniel WG, Mugge A, Martin RP, et al: Improvement in the diagnosis of abscesses

associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:795–800. 99. Massey WM, Samdarshi TE, Nanda NC, et al: Serial documentation of changes in

a mitral valve vegetation progressing to abscess rupture and fistula formation by transesophageal echocardiography. Am Heart J 1992;124:241–248. 100. Castro SD, Cartoni D, d'Amati G, et al: Diagnostic accuracy of transthoracic and

multiplane transesophageal echocardiography for valvular perforation in acute infective endocarditis: Correlation with anatomic findings. Clin Infect Dis 2000;30:825–826. 101. Vilacosta I, San Roman JA, Sarria C, et al: Clinical, anatomic, and

echocardiographic characteristics of aneurysms of the mitral valve. Am J Cardiol 1999;84:110–113. 102. Rohmann S, Erhel R, Darius H, et al: Effect of antibiotic treatment on vegetation

size and complication rate in infective endocarditis. Clin Cardiol 1997;20:132–140. 103. Cerebral Embolism Task Force: Cardiogenic brain embolism: The second report

of the Cerebral Embolism Task Force. Arch Neurol 1989;46:727–743. 104. Kapral MK, Silver FL, with the Canadian Task Force on Preventive Health Care:

Preventive health care, 1999 update: 2. Echocardiography for the detection of a cardiac source of embolus in patients with stroke. Can Med Assoc J 1999;161:989– 996. 105. Dressler FA, Labovitz AJ: Systemic arterial emboli and cardiac masses:

Assessment with transesophageal echocardiography. Cardiol Clin 1993;11:447–460. 106. Hwang JJ, Chen JJ, Lin SC, et al: Diagnostic accuracy of transesophageal

echocardiography for detecting left atrial thrombi in patients with rheumatic heart

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disease having undergone mitral valve operations. Am J Cardiol 1993;72:677–681. 107. Manning WJ, Weintraub RM, Wakomonski CA, et al: Accuracy of

transesophageal echocardiography for identifying left atrial thrombi. A prospective intraoperative study. Ann Intern Med 1995;123:817–822. 21

108. Mugge A, Daniel WG, Haverich A, et al: Diagnosis of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 109. Chen C, Koschyk D, Hamm C, et al: Usefulness of transesophageal

echocardiography in identifying small left ventricular apical thrombus. J Am Coll Cardiol 1993;21:208–215. 110. Black IW, Hopkins AP, Lee LCL, et al: Left atrial spontaneous echo contrast: A

clinical transesophageal echocardiographic analysis. J Am Coll Cardiol 1991;18:398– 404. 111. Rittoo D, Cotter L: Detection of a small left atrial myxoma: Value and limitations

of four imaging modalities. J Am Soc Echocardiogr 1997;10:874–876. 112. Mügge A, Daniel WG, Haverich A, et al: Diagnoses of noninfective cardiac mass

lesions by two-dimensional echocardiography: Comparison of the transthoracic and transesophageal approaches. Circulation 1991;83:70–78. 113. Siostrzonek P, Zangeneh M, Gössinger H, et al: Comparison of transesophageal

and transthoracic contrast echocardiography for detection of a patent foramen ovale. Am J Cardiol 1991;68:1247–1249. 114. Pearson AC, Nagelhout D, Castello R, et al: Atrial septal aneurysm and stroke: A

transesophageal echocardiographic study. J Am Coll Cardiol 1991;18:1223–1229. 115. Hausmann D, Mügge A, Daniel WG: Identification of patent foramen ovale

permitting paradoxical embolism. J Am Coll Cardiol 1995;26:1030–1038. 116. Tunick PA, Kronzon I: Atheromas of the thoracic aorta: Clinical and therapeutic

update. J Am Coll Cardiol 2000;35:545–554. 117. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

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diseases of the thoracic aorta: Part II—atherosclerotic and traumatic diseases of the aorta. Chest 2000;117:233–243. 118. Rauh G, Fischereder M, Spengel FA: Transesophageal echocardiography in

patients with focal cerebral ischemia of unknown cause. Stroke 1996;27:691–694. 119. Mehta RH, Helmcke F, Nanda NC, et al: Transesophageal Doppler color flow

mapping assessment of atrial septal defect. J Am Coll Cardiol 1990;16;1010–1016. 120. Mugge A, Daniel WG, Angermann C, et al: Atrial septal aneurysm in adult

patients: A multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;91:2785–2792. 121. Rittoo D, Sutherland GR, Shaw TR: Quantification of left-to-right shunting and

defect size after balloon mitral commissurotomy using biplane transesophageal echocardiography, color flow Doppler mapping, and the principle of proximal flow convergence. Circulation 1993;87:1591–1603. 122. Ewert P, Berger F, Daehnert I, et al: Transcatheter closure of atrial septal defects

without fluoroscopy: Feasibility of a new method. Circulation 2000;101:847–849. 123. Engberding R, Daniel WG, Erbel R, et al: Diagnosis of heart tumours by

transoesophageal echocardiography: A multicentre study in 154 patients. Eur Heart J 1993;14:1223–1228. 124. Beaver TA, Robb JF, Teufel EJ, et al: Right ventricular outflow tract obstruction

in an older woman: Facilitated diagnosis with transesophageal echocardiographyguided biopsy. J Am Soc Echocardiogr 2000;13:622–625. 125. Cigarrao JE, Isselbacher EM, DeSanctis RW, et al: Diagnostic imaging in the

evaluation of suspected aortic dissection: Old standards and new directions. N Engl J Med 1993:328:35–43. 126. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic

dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9. 127. Bansal RC, Chandrasekaran K, Ayala K, et al: Frequency and explanation of false

negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393–1401. 128. Willens HJ, Kessler KM: Transesophageal echocardiography in the diagnosis of

diseases of the thoracic aorta: Part I—aortic dissection, aortic intramural hematoma, and penetrating atherosclerotic ulcer of the aorta. Chest 2000;116:1772–1779.

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129. Keren A, Kim CB, Hu BS, et al: Accuracy of biplane and multiplane

transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol 1996;28:627–636. 130. Sommer T, Fehske W, Holzkuecht N, et al: Aortic dissection: A comparative

study of diagnosis with spiral CT, multiplanar transesophageal echocardiography and MR imaging. Radiology 1996;199:347–352. 131. Masani ND, Banning AP, Jones RA, et al: Follow-up of chronic thoracic aortic

dissection: Comparison of transesophageal echocardiography and magnetic resonance imaging. Am Heart J 1996;131:1156–1163. 132. Vilacosta I, San Roman JA, Aragoncillo P, et al: Penetrating atherosclerotic aortic

ulcer: Documentation by transesophageal echocardiography. J Am Coll Cardiol 1998;32:83–89. 133. Smith MD, Cassidy JM, Souther S, et al: Transesophageal echocardiography in

the diagnosis of traumatic rupture of the aorta. N Engl J Med 1995;332:356–362. 134. Ahrar K, Smith DC, Bansal RC, et al: Angiography in blunt thoracic aortic injury.

J Trauma 1997;42:665–669. 135. Ritter SB: Transesophageal real-time echocardiography in infants and children

with congenital heart disease. J Am Coll Cardiol 1991;18:569–580. 136. Weintraub R, Shiota T, Elkadi T, et al: Transesophageal echocardiography in

infants and children with congenital heart disease. Circulation 1992;86:711–722. 137. Sreeram N, Stumper OF, Kaulitz R, et al: Comparative value of transthoracic and

transesophageal echocardiography in the assessment of congenital abnormalities of the atrioventricular junction. J Am Coll Cardiol 1990;16:1205–1214. 138. Kaulitz R, Stümper OFW, Geuskens R, et al: Comparative values of the

precordial and transesophageal approaches in the echocardiographic evaluation of atrial baffle function after an atrial correction procedure. Am J Coll Cardiol 1990;16:686–694. 139. Stümper O, Sutherland GR, Geuskens R, et al: Transesophageal echocardiography

in evaluation and management after a Fontan procedure. J Am Coll Cardiol 1991;17:1152–1160. 140. Engvall J, Sjoqvist L, Nylander E, et al: Biplane transoesophageal

echocardiography, transthoracic Doppler, and magnetic resonance imaging in the

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assessment of coarctation of the aorta. Eur Heart J 1995;10:1399–1409. 141. Andrade A, Vargas-Barron J, Rijlaarsdam M, et al: Utility of transesophageal

echocardiography in the examination of adult patients with patent ductus arteriosus. Am Heart J 1995;130:543–546. 142. Tardif JC, Vannon MA, Taylor K, et al: Delineation of extended lengths of coronary arteries by multiplane transesophageal echocardiography. J Am Coll Cardiol 1994;24:909–919. 143. Reichert SL, Visser CA, Koolen JJ, et al: Transesophageal examination of the left

coronary artery with a 7.5 MHz annular array two-dimensional color flow Doppler transducer. J Am Soc Echocardiogr 1990;3:118–124. 144. Samdarshi TE, Nanda NC, Gatewood RP Jr, et al: Usefulness and limitations of

transesophageal echocardiography in the assessment of proximal coronary artery stenosis. J Am Coll Cardiol 1992;19:572–580. 145. Yoshida K, Yoshikawa J, Hozumi T, et al: Detection of left main coronary artery

stenosis by transesophageal color Doppler and two-dimensional echocardiography. Circulation 1990;81:1271–1276. 146. Firstenberg MS, Greenberg NL, Lin SS, et al: Transesophageal echocardiography

assessment of severe ostial left main coronary stenosis. J Am Soc Echocardiogr 2000;13:696–698. 147. Panza JA: Transesophageal echocardiography with stress for the evaluation of

patients with coronary artery disease. Cardiol Clin 1999;17:501–520. 148. Madu EC: Transesophageal dobutamine stress echocardiography in the evaluation

of myocardial ischemia in morbidly obese subjects. Chest 2000;117;657–661. 149. Lin FC, Chang HJ, Chern MS, et al: Multiplane transesophageal

echocardiography in the diagnosis of congenital coronary artery fistula. Am Heart J 1995;130:1236–1242. 150. Hutchison SJ, Smalling RG, Albornoz M, et al: Comparison of transthoracic and

transesophageal echocardiography in clinically overt or suspected pericardial heart disease. Am J Cardiol 1994;74:962–965. 151. Klein AL, Cohen GI, Pietrolungo JF, et al: Differentiation of constrictive

pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol 1993;22:1935–1943.

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152. Ling LH, Oh JK, Tei C, et al: Pericardial thickness measured with

transesophageal echocardiography: Feasibility and potential clinical usefulness. J Am Coll Cardiol 1997;29:1317–1323. 153. Heidenreich PA, Stainback RF, Redberg RF, et al: Transesophageal

echocardiography predicts mortality in critically ill patients with unexplained hypotension. J Am Coll Cardiol 1995;26:152–158. 154. Vignon P, Mentec H, Terre S, et al: Diagnostic accuracy and therapeutic impact of

transthoracic and transesophageal echocardiography in mechanically ventilated patients in the ICU. Chest 1994;106;1829–1834. 155. Dewan NA, Gayasaddin M, Angelillo VA, et al: Persistent hypoxemia due to

patent foramen ovale in a patient with adult respiratory distress syndrome. Chest 1986;89:611. 156. Bansal RC, Marsa RJ, Holland D, et al: Severe hypoxemia due to shunting

through a patent foramen ovale: A correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;15:499–504. 157. American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography: Practice guidelines for perioperative transesophageal echocardiography. Anesthesiology 1996;84:986–1006. 158. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767–773. 159. Park SH, Kim MA, Hyon MS: The advantages of on-line transesophageal

echocardiography guide during percutaneous balloon mitral valvuloplasty. J Am Soc Echocardiogr 2000;13:26–34. 160. Pytlewski G, Georgeson S, Burke J, et al: Endomyocardial biopsy under

transesophageal echocardiographic guidance can be safely performed in the critically ill cardiac transplant recipient. Am J Cardiol 1994;73:1019–1020. 161. Kantoch MJ, Frost GF, Robertson MA: Use of transesophageal echocardiography

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in radiofrequency catheter ablation in children and adolescents. Can J Cardiol 1998;14:519–523. 162. Tumbarello R, Sanna A, Cardu G, et al: Usefulness of transesophageal

echocardiography in the pediatric catheterization laboratory. Am J Cardiol 1993;71:1321–1325. 163. van der Velde ME, Sanders SP, Keane JF, et al: Transesophageal

echocardiographic guidance of transcatheter ventricular septal defect closure. J Am Coll Cardiol 1994;23:1660–1665. 164. McElhinney DB, Burch GH, Kung GC, et al: Echocardiographic guidance for

transcatheter coil embolization of congenital coronary arterial fistulas in children. Pediatr Cardiol 2000;21:253–258. 165. Cheung YF, Leung MP, Lee J, et al: An evolving role of transesophageal

echocardiography for the monitoring of interventional catheterization in children. Clin Cardiol 1999;22:804–810. 166. Manning WJ, Silverman DI, Gordon SP, et al: Cardioversion from atrial

fibrillation without prolonged anticoagulation with use of transesophageal echocardiography to exclude the presence of atrial thrombi. N Engl J Med 1993;328:750–755. 167. Moreyra E, Finkelhor RS, Cebul RD: Limitations of transesophageal

echocardiography in the risk assessment of patients before nonanticoagulated cardioversion from atrial fibrillation and flutter: An analysis of pooled trials. Am Heart J 1995:129:71–75. 168. Greenfield SM, Webster GJ, Brar AS, et al: Assessment of residual gastric

volume and thirst in patients who drink before gastroscopy. Gut 1996;39:360–362. 169. Khandheria BK, Seward JB, Tajik AJ: Concise review for primary-care

physicians: Transesophageal echocardiography. Mayo Clin Proc 1994;69:856–863. 170. Grauer SE, Giraud GD: Toxic methemoglobinemia after topical anesthesia for

transesophageal echocardiography. J Am Soc Echocardiogr 1996;9:874–876.

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23

Chapter 2 - Monitoring Ventricular Function in the Operating Room Impact on Clinical Outcome Donald C. Oxorn MD

Since being introduced into anesthetic practice in the late 1980s, transesophageal echocardiography (TEE) for intraoperative monitoring during cardiac surgery has gained wide acceptance. In 1995, Poterack[1] reported a national survey of anesthesia residency program directors in which 91% reported its use. TEE is relatively noninvasive, can be used in the vast majority of patients, and does not interfere physically with most surgical procedures. In some centers, TEE is used routinely for all cases involving cardiopulmonary bypass, whereas it is used more selectively at others. The usefulness of TEE during noncardiac surgery has been less thoroughly investigated, although if one extrapolates from the experience with hemodynamically unstable intensive care unit patients,[2] its utility in the differential diagnosis of intraoperative hemodynamic instability would appear intuitive. In this chapter, after I offer a general approach to and a personal philosophy on intraoperative TEE, the focus will be on the assessment of cardiac

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function in the setting of both cardiac and noncardiac surgery. In addition, the impact intraoperative TEE has had on the quality of perioperative care is discussed. Intraoperative assessment of valvular function, chamber size, masses, and great vessels are covered in other sections of the book.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

An Approach to Intraoperative Transesophageal Echocardiography Intraoperative TEE has become inextricably linked with cardiac anesthesiology. Over the past decade, guidelines for physician training in TEE have been directed primarily at cardiologists[3] [4] [5] and have stressed a background in transthoracic echocardiography, the acquisition of both cognitive and technical skills, and an ongoing program of maintenance of competence (see Chapter 42) . What is the standard that anesthesiologists should hold themselves up to? No written standard exists, although there are several distinct levels of expertise. Some individuals have taken advanced training that has included the performance and interpretation of surface studies under the tutelage of cardiologists and sonographers; others have studied TEE in the operating room during cardiac anesthesiology fellowships or "on the job"; and many have taught themselves by observation in the operating room, attendance at educational symposia, and the study of text and videotape. The educational program for intraoperative TEE at the Cleveland Clinic is a joint effort between cardiac anesthesiologists and cardiologists and is designed to train individuals to the highest level.[6] There are now two examinations of special competence under the auspices of the National Board of Echocardiography. The curriculum for the intraoperative examination focuses primarily on TEE, whereas the curriculum for the examination in general echocardiography emphasizes a broad knowledge of most aspects of echocardiography, both transthoracic and transesophageal. I believe that anesthesiologists who wish to practice intraoperative TEE should adhere to several tenets. Firstly, although attendance at lectures and reviewing written matter is important, didactic material should not

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replace direct interaction with knowledgeable colleagues. My personal experience suggests that beginning with transthoracic echocardiography is an invaluable first step. Secondly, it must be recognized that there will be different comfort levels among practitioners, and consultation with more skilled colleagues, be they anesthesiologists or cardiologists, should be encouraged. Even if intraoperative TEE is used solely as a monitor of ventricular function, it behooves the practitioner to perform a complete examination and to recognize that unexpected pathologic lesions, when present, may necessitate consultation. And lastly, all practitioners who are involved with TEE would serve themselves and their institutions by striving to pass one of the examinations of special competence. A working group of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists developed guidelines for performing a comprehensive intraoperative TEE examination.[7] Their recommendations are summarized in Figure 2-1 (Figure Not Available) . It is the committee's contention that if the practitioner performs a careful and systematized examination every time the probe is inserted, the chance of missing important findings is minimized, and the potential for teaching is enhanced. Figure 2-1 (Figure Not Available) Twenty cross-sectional views composing the recommended comprehensive transesophageal echocardiography examination. The icon adjacent to each view indicates the approximate multiplane angle. ME, midesophageal; LAX, long axis; TG, transgastric; SAX, short axis; AV, aortic valve; RV, right ventricle; asc, ascending; desc, descending; UE, upper esophageal. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870.)

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Intraoperative Ventricular Function Left Ventricular Filling In the operating room, rapidity is needed in the assessment of preload during periods of hemodynamic instability. Since the introduction of the pulmonary artery catheter in the 1970s, measurement of pulmonary capillary wedge pressure as a surrogate of left ventricular end diastolic volume has been the intraoperative practice standard; however, it is recognized that especially in situations of decreased ventricular compliance, the pulmonary capillary wedge pressure is an inaccurate estimate of preload.[8] TEE has the potential to refine this measurement by allowing Doppler estimation of left atrial pressure, two-dimensional measurement of left ventricular cross-sectional area, and calculation of left ventricular volume. Left Atrial Pressure

Left atrial pressure can be estimated with Doppler TEE by several methods. If mitral regurgitation is present, 25

measurement of the peak velocity of the regurgitant jet and application of the modified Bernoulli equation allows calculation of the left ventriculoatrial pressure gradient; subtraction of this number from the peak systolic blood pressure yields left atrial pressure[9] (Fig. 2-2) . Certain mitral inflow and pulmonary venous variables also correlate with left atrial pressure; Kuecherer et al[10] found that in patients undergoing cardiovascular surgery, changes in the systolic fraction of the pulmonary venous tracing correlated inversely and strongly with pulmonary capillary wedge pressure, and they theorized that this related to decreased atrial compliance. Nomura et al[11] found that in patients with ejection fractions

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less than 35%, the deceleration time of the early velocity of mitral inflow correlated with pulmonary capillary wedge pressure, and that a deceleration time greater than 150 msec was strongly predictive of a pulmonary capillary wedge pressure of less than 10 mm Hg. There are a number of caveats related to the intraoperative estimation of left atrial pressure with TEE. Patients with a rhythm other than sinus or with valvular regurgitation were excluded in most studies; these are the very patients in whom preload estimates are often crucial. In suitable patients, correlations but not absolute values of left atrial pressure are usually yielded. Use of the mitral regurgitation jet to calculate left atrial pressure dictates that mitral regurgitation must be present. And finally, an estimate of left atrial pressure, whether obtained by Doppler echocardiography or by pulmonary artery catheter, may still yield inaccurate estimates of preload in patients with decreased ventricular compliance. End-Diastolic Area and End-Systolic Area

A number of authors have examined the intraoperative relationship between end-diastolic and end-systolic area Figure 2-2 Measuring the peak velocity (V) of the mitral regurgitation (MR) jet and applying the modified Bernoulli equation yields a pressure gradient (PG) between the left atrium and ventricle of 56 mm Hg. Subtracting this value from the systolic arterial pressure of 86 mm Hg gives a left atrial pressure (LAP) of 30 mm Hg. BP, blood pressure.

measured at the transgastric midpapillary level and cardiac volume status. Cheung et al[12] performed an elegant study examining the effect of graded hypovolemia produced by autologous blood collection on hemodynamic and TEE-derived indices of left ventricular preload in patients undergoing coronary artery bypass surgery. Patients with valvular insufficiency, rhythms other than sinus, and overt congestive heart failure were excluded. Patients were stratified on the basis of resting left ventricular function. Enddiastolic area, end-systolic area, pulmonary capillary wedge pressure, and measures of end-diastolic and end-systolic wall stress decreased linearly as blood volume was reduced from 0 to 15% in all patients; however, in patients with impaired left ventricular function, only the TEE-derived indices maintained linearity (Fig. 2-3) (Figure Not Available) . Other studies have also demonstrated that single plane areas, although not

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predictive of absolute left ventricular volumes,[13] [14] can generally be used to monitor for a trend toward increased or decreased volume.[15] [16] [17] It must also be remembered that the presence of a small end-diastolic area or end-systolic area does not always reflect decreased intravascular volume. Small left ventricular volumes can be seen with restrictions to filling, as in pericardial disease, or decreased right heart function, as in right ventricular infarction or large pulmonary embolus[18] (Fig. 2-4) . Patients presenting for cardiac surgery often have preexisting impairment of diastolic function. De Hert et al[19] obtained transmitral flow signals with TEE and high-fidelity recordings of left ventricular pressure in patients anesthetized for coronary bypass. A subset of patients was identified in whom leg elevation resulted in a decreased dP/dt; those same patients developed a restrictive pattern on mitral inflow. Diastolic function is worsened to a variable degree following cardiopulmonary bypass.[20] This explains the frequent inadequacy of left ventricular filling despite seemingly adequate filling pressures.

26

The presence of end-systolic obliteration of the left ventricular cavity, although usually associated with hypovolemia (Fig. 2-5) , may also be associated with increased inotropy, or redistribution of blood out of the thoracic cavity.[21] Left Ventricular Volumes

In an in vitro study using silicone rubber models of the left ventricle, the calculation of left ventricular volumes using multiplane TEE and the disk summation method[22] was found to be highly accurate.[23] However, problems related to the moving heart, exclusion of akinetic segments of the left ventricle, and difficulty in getting a true long-axis view of the left ventricle have led to disappointing Figure 2-3 (Figure Not Available) End-diastolic area (EDA) and end-systolic area (ESA) in response to graded hypovolemia yielded estimated blood volume (EBV) deficits of 0 to 15%. Patients had either normal left ventricular (LV) function or reduced LV function. Control patients were not subjected to hypovolemia. (From Cheung AT, Savino JS, Weiss SJ, et al: Anesthesiology 1994;81:376–387.)

Figure 2-4 Transgastric image of a transesophageal echocardiography

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scan obtained in a patient who had suffered massive fat embolism. Increased pulmonary vascular resistance and subsequent right ventricular (RV) dilation led to impaired left ventricular (LV) filling.

results when used in the perioperative setting.[14] [24] Technologic advances such as three-dimensional TEE,[25] harmonic imaging,[26] and automated border detection may lead to improved intraoperative accuracy. In summary, the assessment of preload with intraoperative TEE is in most cases a semiquantitative estimate based on visual inspection of enddiastolic and end-systolic areas and on temporal comparison with the use of videotape or stored cine loops. Confounding conditions such as right ventricular failure or the administration of inotropic agents must be considered. Global Systolic Function Cardiac Output

Ventricular filling, contractility, wall stress, and heart rate all influence cardiac output. Thus, cardiac output is the measurement most often used in anesthetic and critical care practice as a guide to therapeutic manipulations of cardiac function. Despite its limitations,[27] [28] thermodilution cardiac output measurement has been considered the "gold standard" since being popularized in the early 1970s. Doppler transesophageal echocardiography has the potential to be used in the intraoperative setting for the continuous measurement of cardiac output. These methods utilize the concept that the cross-sectional area of a conduit within the cardiovascular system multiplied by the Doppler-derived timevelocity integral yields the stroke volume through that conduit. When the result is multiplied by heart rate, the product is cardiac output. Several important assumptions are inherent to this approach. Valid area formulas must be applicable to the anatomic site being analyzed. The velocity profile across the valve must be flat and devoid of skew.[29] [30] Whichever anatomic area is chosen, the ability to consistently obtain the image and to interrogate parallel to flow is mandatory. Pulmonary Artery.

With the probe at 0 degrees and retroflexed, the main pulmonary artery and pulmonic valve can be imaged at the base of the heart (Fig. 2-6) . This

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Figure 2-5 Transesophageal echocardiogram from a hypovolemic patient. During systole, the posteromedial and anterolateral papillary muscles touch. LV, left ventricle; RV, right ventricle.

Figure 2-6 Imaging at the base of the heart of the main pulmonary artery (PA) and its branches. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; PV, pulmonary valve; Vmax, maximum velocity.

28

site has been examined with pulsed wave Doppler,[30] [31] [32] and in a study by Gorcsan et al,[33] using both pulsed wave and continuous wave methodologies, pulmonary artery diameter was measured just distal to the pulmonic valve. Interobserver variability was low in all studies, and correlation with thermodilution was strong in all but the study by Muhiudeen et al,[31] in which patients with inaccurate thermodilution measurements may have been included. The major limitation with using the pulmonary artery is the inability to obtain an adequate two-dimensional image for diameter measurement in up to 25% of patients. Right Ventricular Outflow Tract.

With the probe turned rightward and flexed, the right ventricular outflow tract is imaged from the stomach between 0 and 120 degrees (Fig. 2-7) . Imaging frequency must usually be reduced to ensure optimal penetration. Maslow et al[34] found excellent correlation between cardiac output calculated with pulsed wave Doppler and thermodilution. Patients with pulmonary hypertension, significant tricuspid regurgitation, and non-sinus rhythms were excluded. Again, in a significant percentage (16%) of patients, the two-dimensional image was not suitable. Left Ventricular Outflow Tract.

With the probe in the stomach, turned leftward, in the flexed position, and at low imaging frequency, the aortic valve and left ventricular outflow tract

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can usually be imaged between 0 and 140 degrees (Fig. 2-8) (Figure Not Available) . Imaging from the stomach allows parallel pulsed Doppler interrogation of the left ventricular outflow tract, and its diameter, obtained from either the stomach or the midesophageal 120-degree view, allows calculation of the cross-sectional area and cardiac output (Fig. 2-9) . Strong correlation with thermodilution and low interobserver variability have been described.[35] [36] To avoid contamination of the Doppler signal by the region of flow acceleration adjacent to the aortic Figure 2-7 Pulsed wave (PW) Doppler measurement from the right ventricular outflow tract (RVOT) (color plate). RV, right ventricle.

valve orifice, the sample volume must be placed precisely in the left ventricular outflow tract. Aortic Valve.

Using the transgastric view described for left ventricular outflow tract, several investigators have studied the combination of continuous wave Doppler positioned through the left ventricular outflow tract and aortic valve and cross-sectional area of the aortic valve using the triangle method (Fig. 2-10) .[37] [38] In brief, the triangular shape of the aortic valve orifice at mid-systole is assumed to represent the time averaged value for the aortic valve area. Strong correlation with thermodilution and low interobserver variability were again obtained (Fig. 2-11) . As continuous wave Doppler is used, it is important to confirm that the maximal peak velocity is occurring at the aortic valve. The triangle method is limited to patients with unrestricted aortic valve opening. Mitral Valve.

Using the mitral valve for calculation of cardiac output has the advantages of consistent imaging and parallel Doppler alignment. However, the saddle shape of the mitral annulus makes the area measurement unpredictable, and the cross-sectional velocity skew[29] is of concern when using pulsed wave Doppler. Practical Considerations.

For intraoperative transesophageal Doppler calculation of cardiac output, the left ventricular outflow tract method is the most reproducible. Adjustments in the degree of probe flexion and imaging angle should be

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made to ensure that the aortic valve and ascending aorta are clearly visualized and that the Doppler intercept angle is small (see Fig. 2-9) . Several measurements should be made and averaged, this being especially important when dealing with rhythms other than sinus. In practical terms, Doppler measurement of cardiac output is used when a pulmonary artery catheter is not in place, or when conditions such as severe tricuspid regurgitation render thermodilution inaccurate. There is a need for 29

Figure 2-8 (Figure Not Available) Transesophageal echocardiography imaging from the stomach allows parallel alignment with the ascending aorta. (From Perrino AC Jr., Harris SN, Luther MA: Anesthesiology 1998;89:350–357.) Figure 2-9 Transgastric imaging of the left ventricular outflow tract (LVOT). The ascending aorta is well visualized, and the Doppler intercept angle is small. Pulsed Doppler velocity time integral (VTI) and diameter measurement are used to calculate stroke volume. MnGRAD, mean gradient; PGRAD, peak gradient; Vmax, maximum velocity.

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Figure 2-10 The triangle method of aortic valve area measurement. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796–805.)

further validation of this approach in patients with a spectrum of cardiovascular diseases. Ejection Fraction and Stroke Volume

Although it is somewhat load dependent and therefore not a pure index of "left ventricular function,"[39] ejection fraction is often assumed to reflect ventricular contractility. During intraoperative TEE, the fractional area of change measured at the transgastric midpapillary level is often used interchangeably with ejection fraction, although gauging volume in a potentially asymmetric Figure 2-11 Regression analysis: thermodilution cardiac output (TCO)

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and Doppler cardiac output (DCO) using the aortic valve triangle method. (From Darmon PL, Hillel Z, Mogtader A, et al: Anesthesiology 1994;80:796– 805.)

chamber based on a measure of area has obvious limitations.[40] [41] A number of studies report the relationship between TEE-derived fractional area of change and radionuclide-derived ejection fraction. Clements et al[42] examined the relationship in 12 patients having abdominal aortic aneurysm surgery. There was excellent correlation in patients with both normal and abnormal left ventricular function. In patients with ventricular dyssynergy, fractional area of change led to a slight overestimate of ejection fraction. Urbanowicz et al[13] found strong correlation in 10 patients following coronary artery bypass grafting. In a series of 15 patients following coronary artery bypass grafting, Ryan et al[14] measured TEE ejection fraction using volumes calculated from the modified Simpson's and arealength methods[43] in addition to TEE-derived fractional area of change and radionuclide-derived ejection fraction. Unlike previous studies, variability was calculated and found to be small and not significantly different between the three measurement techniques. Not surprisingly, the TEE volumetric results were more representative of radionuclide ejection fraction than fractional area of change. Smith et al[24] also found that ejection fraction based on TEE volumetric methods were comparable to those obtained with angiography. In an attempt to develop online methods of intraoperative functional assessment, the technique of automated border detection has been used (see Chapter 7) . Automated border detection is based on the principle of acoustic quantification of ultrasonic back scatter signals to detect the bloodtissue interface and thereby define the endocardial edge.[44] Measurements correlate closely to those obtained by manual tracing of the endocardial border. [45] [46] [47] Gorcsan et al[17] examined stroke area, defined as the difference between end-systolic area and end-diastolic area measured at the midpapillary level, and compared the results to stroke volume measured in the ascending aorta by an electromagnetic flow probe in nine patients undergoing coronary artery bypass. Preoperative left ventricular function was largely preserved. Measurements were made before and after cardiopulmonary bypass. There was a strong correlation between the measurements at all periods of the study. Katz et al[48] compared stroke volume as measured by thermodilution to stroke volume obtained with automated border detection determination of end-systolic and end-diastolic areas and volumetric formulas (Fig. 2-12) ; these latter measurements were

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made at the two-chamber and four-chamber midesophageal views. There was a close correlation between stroke volumes obtained by the two methods, but whereas the two-chamber view led to an average underestimate of 0.4 L, the four-chamber view led to an average underestimate of 1.9 L. In a similar study, Greim et al[49] used the twochamber view alone. Directional changes in stroke volume between thermodilution and automated border detection again correlated closely; however, the automated border detection technique significantly underestimated stroke volume. Ejection fraction has been estimated using automated border detection derived measurements of fractional area of change at the midpapillary level and compared to radionuclide-derived ejection fraction.[45] [46] [47] Although the directionality of change was significantly 31

Figure 2-12 An example of transesophageal echocardiography automated border detection from the four-chamber view with ventricular volume estimated on line by the area length method. (From Katz WE, Gasior TA, Reddy SC, et al: Am Heart J 1994;128:389–396.)

correlated, fractional area of change derived by automated border detection consistently overestimated radionuclide-derived ejection fraction. It would appear that fractional area of change more closely estimates ejection fraction in patients with normal ventricular function. The use of TEE-derived volumetric data to estimate ejection fraction is more accurate, but the cumbersome calculations involved do not lend themselves to rapid intraoperative derivation. The use of automated border detection algorithms and programmed volume calculations may prove superior but are largely untested in clinical practice. At present, the intraoperative assessment of ejection fraction is impractical, and stroke volume measurement is best accomplished with either Doppler or thermodilution methodology. Contractility

The end-systolic pressure-volume relationship and resultant end-systolic elastance defines contractility in a load-independent fashion[50] and would therefore be of potential use in the estimation of intraoperative left ventricle contractility and in the quantification of changes resulting from manipulations such as cardiopulmonary bypass.

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A number of surrogates of this relationship have been described to facilitate the practical acquisition of this information in an operating room setting. The substitution of femoral arterial pressure for left ventricular end-systolic pressure,[51] end-systolic area for end-systolic volume,[20] [52] [53] and endsystolic wall stress for end-systolic pressure[53] have been made. Although these substituted measurements are not construed as replacements for traditional measures of pressure and volume, their directional change suggests that in cardiac surgical patients undergoing cardiopulmonary bypass, they may be used as an alternative way of assessing loadindependent left ventricular function. The changes in contractility as a result of cardiopulmonary bypass[20] [54] and the administration of anesthetic agents[52] appear better assessed with estimates of end-systolic elastance than with more traditional indices of ventricular performance such as fractional area of change. Figure 2-13 illustrates the decrease in elastance (Ees) and increased chamber stiffness (Kc) that occur following cardiopulmonary bypass, and the mitigating effect of volume loading prior to bypass termination. At present, the methods for data analysis are prohibitively complex.[55] [56] Right Ventricular Function

In the setting of cardiopulmonary bypass, the evaluation of right ventricular function is important. Right ventricular dysfunction often occurs secondary to the inadequate delivery of cardioplegia[57] and to the embolization of intracardiac air down the right coronary artery following separation from cardiopulmonary bypass. The triangular shape of the right ventricle makes its global function hard to quantitate with TEE, and the abnormal septal motion often seen following cardiopulmonary bypass[58] compounds this difficulty. Rafferty et al[59] measured planimetered areas and major and minor axes in both long-axis and short-axis images of the right ventricle with TEE, before and after cardiopulmonary bypass. Unfortunately, the echo measurements, obtained offline, were not compared in a meaningful way to results obtained by thermodilution. Semiquantitative analysis of right ventricular function with TEE has also been attempted with the analysis of hepatic venous flow.[60] Many factors other than right ventricular systolic function, however, affect hepatic venous flow. In patients with diverse causes of right ventricular dysfunction, Vignon et al[61] demonstrated the ability to 32

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Figure 2-13 Effect of cardiopulmonary bypass (CPB) on elastance (Ees) and chamber stiffness (Kc) of the left ventricle. Times of measurement were before the start of CPB (baseline); immediately after separation from CPB (time 0); and 5 minutes (time 5), 10 minutes (time 10), and 15 minutes (time 15) later. In protocol 1, preload was optimized just before the start of the separation procedure from CPB. In protocol 2, preload was optimized 10 minutes before the anticipated separation time. Data are shown as mean ± SEM. In protocol 1, ventricular function after separation from CPB was impaired, with a decrease in Ees and an increase in Kc, and a progressive improvement of ventricular function within the first 10 minutes after separation from CPB. These findings were not seen in protocol 2, in which ventricular function remained unchanged and comparable to baseline values. *Difference between both groups is statistically significant at P < 0.01. (From De Hert SG, Rodrigus IE, Haenen LR, et al: Anesthesiology 1996;85:1063–1075.)

quantitate right ventricular function with color kinesis and surface echocardiography. This method of examining right ventricular function has not been evaluated in an intraoperative setting with TEE. At the present time, TEE assessment of intraoperative right ventricular function is best accomplished by visual inspection and semiquantitative assessment in both the transgastric and the four-chamber views. Excellent transgastric views of all three leaflets of the tricuspid valve and the entire free wall of the right ventricle are best obtained by scanning at approximately 40 degrees (Fig. 2-14) . Regional Wall Motion The suggestion of a link between perioperative myocardial ischemia and cardiac morbidity[62] [63] has led to an intensive search for accurate methods of its intraoperative detection (Fig. 2-15) (Figure Not Available) . Visual inspection of ST segment changes has been the foundation upon which the newer technologies of automated ST analysis and TEE detection of regional wall motion abnormalities have been added. There are several points on which to judge the merits of TEE: Applicability, accuracy, reproducibility, cost, expertise required for interpretation, and prognostic importance. Segmental analysis is most frequently undertaken using the 16-segment model first proposed by Schiller et al[64] and later modified for TEE by Shanewise et al[7] (Fig. 2-16) (Figure Not Available) . Excellent inter- and intraobserver variability has been documented when six segments at the midpapillary level were analyzed offline by an anesthesiologist trained in

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TEE and an echocardiographer.[65] The recognition that coronary occlusion leads to the immediate development of regional wall motion abnormalities[66] and their frequent regression following revascularization[67] has prompted investigators to examine the usefulness of intraoperative TEE as a monitor of ischemia. The paucity of contraindications to TEE means that it can be used in most patients undergoing general anesthesia. The midpapillary view is generally easy to obtain and demonstrates areas of myocardium subtended by the three major coronary arteries. Interpretation is rarely confounded by rhythm disturbances, as is the case for automated ST analysis. TEE cannot be used, however, in patients receiving regional anesthesia, and, because the probe is not inserted until after anesthetic induction, it cannot detect changes during this vulnerable period. Assessment of the accuracy of TEE in the detection of myocardial ischemia has been limited somewhat by the lack of a reliable reference standard. Smith et al[68] found that in patients at high risk of myocardial ischemia who were analyzed offline, wall motion changes could be detected Figure 2-14 Transgastric image of the right ventricular (RV) free wall, septum, and the leaflets of the tricuspid valve.

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Figure 2-15 (Figure Not Available) Causes of ischemic changes on intraoperative monitors (color plate). (From Fleisher LA: Anesthesiology 2000;92:1183–1188.)

more quickly and commonly than ST segment changes. Conflicting studies[69] [70] regarding the prognostic importance of regional wall motion abnormalities were subsequently published. In a study by London et al,[69] 156 patients undergoing noncardiac surgery who were at high risk for coronary artery disease were studied. Specific clinical, electrocardiographic, or hemodynamic events prompted analysis of stored images. The number of new wall motion abnormalities detected was low, and discordance with electrocardiographic findings was significant (Table 2-1) . The number of postoperative cardiac complications was low. In the

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study by Leung et al,[70] patients undergoing coronary artery bypass were examined with electrocardiography and TEE. Although prebypass ischemia was rare, postbypass ischemia was more common and postoperative cardiovascular complications were associated more closely with TEE findings than with electrocardiography alone. It is now accepted that regional wall motion abnormalities, although often the result of myocardial ischemia, may be due to hypovolemia, tethering of nonischemic myocardium, and myocardial stunning after cardiopulmonary bypass.[71] [72] Offline analysis has been employed in most of the large-scale studies involving comparison of TEE with other methods of ischemia detection, but extrapolation to the accuracy of real-time TEE analysis should not be assumed. Regional wall motion abnormalities that subtend the anatomic distribution of coronary TABLE 2-1 -- Comparison of Transesophageal Echocardiography (TEE) and Intraoperative Electrocardiography (ECG) Monitoring for Myocardial Ischemia * TEE + TEE ECG + 8 (1 MI) 11 ECG 24 (2 MI, 1 UA) MI, myocardial infarction; UA, unstable angina. From London MJ, Tuban JF, Wong MG, et al: Anesthesiology 1990;73 (4):644. * P < 0.05.

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Figure 2-16 (Figure Not Available) A 16-segment model of the left ventricle. A, Fourchamber views show the three septal and three lateral segments. B, Two-chamber views show the three anterior and three inferior segments. C, Long-axis views show the two anteroseptal and two posterior segments. D, Middle short-axis views show all six segments at the midpapillary level. E, Basal short-axis views show all six segments at the basal level. (From Shanewise JS, Cheung AT, Aronson S, et al: Anesth Analg 1999;89:870–884.)

artery flow are more often a result of ischemia than those that do not.

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Comunale et al[73] also documented the poor concordance between the TEE and electrocardiography and attributed this finding to the lack of standard definitions of significant regional wall motion abnormalities and ischemic ST changes, the exclusion of longitudinal TEE views, and the use of different models of segment nomenclature. The role of intraoperative monitoring of myocardial ischemia with TEE remains unclear. Intraoperative TEE monitoring is better suited to patients undergoing cardiac as opposed to noncardiac surgery and to those patients in whom more traditional methods of ischemia are deemed inadequate. The ability to monitor additional tomographic planes,[74] [75] the use of cine loops for comparison, and the advent of new technologies such as automated border detection and Doppler tissue imaging should improve accuracy. Regional wall motion abnormalities precede electrocardiographic changes, [76] and, once ischemia is diagnosed, TEE can be used to directly monitor the effects of intervention. Personnel with expertise in the online assessment of wall motion abnormalities are needed, however. Lastly, studies examining the outcomes of patients monitored for myocardial ischemia with TEE are needed. Intraoperative Assessment of Coronary Reserve Dobutamine stress echocardiography is a well-established technique for diagnosing coronary artery disease and predicting the improvement of dysfunctional myocardium postoperatively (see Chapter 14) .[77] [78] The ability to predict the reversibility of left ventricular dysfunction with the use of intraoperative low-dose dobutamine TEE was examined by Aronson et al[79] in the setting of coronary artery bypass grafting. The odds ratios for early and late improvement in myocardial function were 20.7 and 34.6 times higher if preoperative low-dose dobutamine produced improved function than if it did not. The instances when this intraoperative strategy might supplant the normal preoperative assessment of myocardial viability by transthoracic dobutamine stress echocardiography[78] or low-dose dobutamine technetium-99m sestamibi scintigraphy[80] have yet to be determined.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Use of Transesophageal Echocardiography to Monitor Intraoperative Cardiac Function in Specific Clinical Entities The use of TEE has improved our ability to intelligently manage postcardiopulmonary bypass instability. It has allowed us to understand the intraoperative changes that occur during some of the newer techniques in coronary revascularization and can guide us in placement of numerous intracardiac and intravascular devices. Its use in monitoring cardiac function during noncardiac surgery is most advantageous in the diagnosis of sudden and unexplained hemodynamic instability. Separation from Cardiopulmonary Bypass At the time of separation of the patient from cardiopulmonary bypass, the use of TEE may guide the anesthesiologist in the use of pharmacologic and nonpharmacologic therapies and can maximize the likelihood of a smooth transition. Intracardiac Air

Left-sided intracardiac air is ubiquitous following procedures in which leftsided chambers have been open to atmosphere and is identified by its characteristic "firefly" appearance. Air is often seen entering the left atrium from the pulmonary veins or enmeshed in the mitral subvalvular apparatus (Fig. 2-17) . Echocardiographic inspection is carried out in the fourchamber and transgastric long-axis views. Careful evacuation by the surgeon is important and involves suctioning on the aortic root vent or needle aspiration of the left ventricular apex to evacuate trapped pockets. As well as guiding evacuation, TEE is 35

Figure 2-17 Four-chamber midesophageal view. As the patient is being

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separated from cardiopulmonary bypass (CPB), a pocket of air enmeshed in the left ventricular subvalvular apparatus is noted (asterisk), with numerous bubbles emanating from it. LA, left atrium; LV, left ventricle.

useful in diagnosing the consequences of embolization through the right coronary ostium, which results in ventricular dysfunction in a right coronary distribution. Cardiac Output

There are a number of potential causes of low cardiac output immediately following cardiopulmonary bypass: perioperative infarction, coronary air emboli, metabolic abnormalities, hypovolemia, left ventricular outflow tract obstruction, and inadequate myocardial protection. It seems intuitive that the yield of TEE when it is used during hemodynamic instability during and after cardiac surgery would be high. Two published series[81] [82] have demonstrated the myriad diagnoses that have been made TABLE 2-2 -- Relevant Intraoperative Transesophageal Echocardiograph Findings Categorized by Indication Indication, n

Finding Severe left ventricular dysfunction ± regional wall motion abnormality Aortic dissection ± aortic regurgitation Significant mitral regurgitation Intracardiac/great vessel shunt Hyperdynamic left ventricular function

HEMODYNAMIC SURGICAL INSTABILITY PLANNING TRAUMA HYPOXEMIA 15 2

1

13

4

2

1

1

2

TOTA NO. O PATIE

2 1

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Severe right 2 1 ventricular dysfunction Extracardiac clot 2 Significant aortic 2 regurgitation Significant 1 tricuspid regurgitation Pericardial 1 tamponade No relevant 5 1 4 3 findings From Brandt RR, Oh JK, Abel MD, et al: J Am Soc Echocardiogr 1998;1 (10):972. and the ability to intervene on many (Table 2-2) . No attempt was made to compare TEE with other diagnostic modalities, although the speed with which information is made available appears hard to supersede. The use of myocardial contrast echocardiography has improved our understanding of the distribution of cardioplegia delivered by both anterograde and retrograde routes. The ability to predict the adequacy of delivery based on knowledge of coronary anatomy and the presence of angiographically demonstrated collateral flow is marginal at best.[83] It is also clear that retrograde cardioplegia does not reliably perfuse the right ventricular free wall,[57] [84] and, in some centers, this observation has led to a strategy of early cardioplegia administration down a vein graft to the right coronary artery.[85] In the future, the use of myocardial contrast echocardiography may help to 36

Figure 2-18 A, Transesophageal echocardiography to investigate hypoxia revealed an expanding ascending aortic aneurysm with main pulmonary artery (PA) compression. B, Normal image for comparison. LA, left atrium; SVC, superior vena cava.

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differentiate postbypass stunning, which would be treated with cardiopulmonary support, from graft obstruction, which would be treated with surgical correction.[86] [87] Off-Pump Coronary Bypass Surgery The off-pump bypass surgical approach to coronary revascularization involves bypassing coronary arteries without cardiopulmonary bypass, otherwise known as the "beating heart" operation. TEE can detect regional wall motion abnormalities during intermittent coronary occlusion and cardiac lifting, which, if persistent, may necessitate the institution of cardiopulmonary bypass. The use of color kinesis to better define regional wall motion abnormalities intraoperatively has been described [88] but is limited somewhat by cardiac translocation during surgical manipulation. Cardiac Function in Noncardiac Surgery The use of TEE to monitor cardiac function in noncardiac surgery has been described largely in anecdotal form. In most of the case reports, unexplained hypotension prompted the use of TEE, and subsequent diagnoses have included massive pulmonary embolism,[89] [90] intracardiac tumor extension,[91] retroperitoneal hemorrhage,[92] cardiac tamponade,[93] main pulmonary artery obstruction by an expanding aortic aneurysm[94] (Fig. 2-18) , traumatic cardiac injury,[95] [96] [97] ventilator-induced systemic air embolism,[98] [99] and a case of venous air embolism during pelvic surgery, which resulted in pulseless electrical activity until open cardiac aspiration was undertaken (Fig. 2-19) . Positioning of Intravascular Devices Intraoperative TEE can be used to guide the positioning of a number of intravascular devices: Central Venous Pressure Air Aspiration Catheters.

These are often used during sitting craniotomies to aspirate air that has gained access to the venous circulation. Correct positioning is at the right atrial-superior vena caval junction, and imaging is best in the midesophagus with rightward rotation and a transducer angle of approximately 90 degrees (Fig. 2-20) . Intra-aortic Balloon Pump.

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The benefits of intra-aortic balloon pump have been demonstrated with TEE and include improved left ventricular function and decreased wall stress. [100] [101] The balloon pump is best imaged in the descending aorta in a vertical plane. Correct positioning is at the inferior border of the transverse aortic arch.[102] Once the tip of the balloon is visualized at a transducer angle of approximately 90 degrees, the probe marking at the teeth is noted. The probe is slowly withdrawn until the left subclavian artery orifice is seen; the marking is again noted. The distance between the balloon and the subclavian orifice should be approximately 5 cm (Fig. 2-21) . Left Ventricular Assist Device.

As the left ventricular assist device withdraws blood from the left ventricle, left atrial pressure falls below right atrial pressure. It is important Figure 2-19 During pelvic surgery, massive amounts of air are seen entering the right atrium (RA) via the inferior vena cava (IVC).

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Figure 2-20 A catheter inserted from the arm is positioned at the junction of the right atrium (RA) and superior vena cava (SVC) to evacuate any air that gains access to the venous circulation during sitting craniotomy. LA, left atrium.

to determine whether a patent foramen ovale is present, as right-to-left shunting will invariably occur. The orifice of the ventricular apical cannula should be imaged in the four-chamber view, and the lack of obstruction by adjacent walls should be ascertained[103] (Fig. 2-22) . Right Ventricular Assist Device.

In positioning the right atrial drainage cannula, it is preferable to avoid impingement on the tricuspid valve (Fig. 2-23) . Minimally Invasive Cardiac Surgery.

Port access surgery

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Figure 2-21 Intra-aortic balloon pump (IABP) positioned in the descending thoracic aorta. The left subclavian artery is visualized and not encroached upon.

involves the performance of a variety of surgical procedures through small thoracic ports or very limited incisions. Cannulation for the purposes of cardiopulmonary bypass and cardioplegic arrest is achieved percutaneously. TEE is used to position the various endovascular catheters and to monitor their position during surgery[104] [105] (Fig. 2-24) (Figure Not Available) . Some surgeons prefer an upper sternotomy incision. Cannulation is then achieved directly, except for the retrograde cardioplegia cannula, 38

Figure 2-22 The drainage component of the left ventricular assist device (LVAD) is seen to freely enter the apical region of the left ventricle (LV). LA, left atrium.

which is inserted through blind right atrial puncture and maneuvered into the coronary sinus under TEE guidance[106] (Fig. 2-25) . Left Ventricular Vent.

A left ventricular vent is placed through the right upper pulmonary vein into the left atrium and advanced through the mitral valve into the left ventricle to drain excess ventricular volume on bypass (Fig. 2-26) . Transplant Surgery Transesophageal echocardiography can be used to assess the function of the donor heart prior to procurement and after separation from cardiopulmonary bypass, when Figure 2-23 (color plate.) The drainage component of the right ventricular assist device (RVAD) enters the right atrium (RA) through the appendage (left, arrow). The tip is seen in the right atrium and free of the tricuspid valve on TEE (right). PA, pulmonary artery. Figure 2-24 (Figure Not Available) The various endovascular cardiopulmonary

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bypass catheters for post-access surgery are depicted. (From Siegel LC, St. Goar FG, Stevens JH, et al.: Circulation 1997;96:562–568.)

the effects of the ischemic time may become evident. During lung transplantation, the use of TEE has been described in the evaluation of vascular anastomoses,[107] and a recent case report documented a diagnosis of post-transplant pulmonary venous obstruction.[108] Laparoscopic Surgery As laparoscopic surgery has grown in its application, so has the realization that the associated pneumoperitoneum 39

Figure 2-25 During minimally invasive cardiac surgery, the coronary sinus catheter is seen entering the right atrium (RA) and passing into the coronary sinus. LA, left atrium.

leads to increased left ventricular wall stress[109] and decreased fractional area of change.[110] Following release of the pneumoperitoneum, higher than baseline fractional area of change has been described.[110] These hemodynamic alterations have been attributed to the physical effect of increased intra-abdominal pressure and to the associated neurohumoral changes. TEE has also been used to monitor for intraoperative gas embolization.[111]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Transesophageal Echocardiography as a Monitor of Intraoperative Ventricular Function: Impact on Perioperative Complications and Cost-Effectiveness Medical technology assessment has become an important step in the introduction and clinical use of increasingly sophisticated and costly methods of monitoring and diagnosis.[112] In anesthetic and critical care practice, no technology has engendered more controversy than the use of pulmonary artery catheterization, which has become an established monitor of cardiovascular function, despite the lack of significant outcome and costeffectiveness data.[113] [114] The use of TEE to monitor intraoperative ventricular function varies significantly between institutions[1] [115] and relates in part to the experience of the operator, the type of surgical procedure, and the cardiopulmonary reserve of the patient. For TEE to be deemed an effective mode of intraoperative monitoring, it must be shown to provide at least the same if not more information than currently accepted monitoring techniques, have a reasonable cost profile, involve acceptable risk, and alter outcome in a positive way. Kato et al[116] demonstrates the ability to diagnose and effectively manage intraoperative ischemia under TEE guidance, but, as is the case with many subsequent studies, their study falls short in not evaluating the effects of intraoperative TEE monitoring on patient outcome. Several studies have addressed the impact of intraoperative TEE monitoring of ventricular function during coronary bypass surgery. Bergquist et al[117] studied the concordance between real-time intraoperative TEE interpretation by five cardiac anesthesiologists and offline analysis by two blinded investigators in the assessment of left ventricular filling, ejection fraction area, and regional wall motion. Results obtained by the two methods were within 10% of each other 75% of the time with respect to ejection fraction and filling. The accuracy of regional assessment

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Figure 2-26 A left ventricular (LV) vent is seen passing into the left atrium (LA) via a right-sided pulmonary vein. MV, mitral valve.

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TABLE 2-3 -- Surgical Management Alterations During Coronary Artery Bypass Grafting Based on Transesophageal Echocardiographic Findings

Before CPB, n 2 NA NA 0 8

Before CPB After CPB After Total No. Separation, Separation, CC, of n n n Patients NA NA NA 2 NA 3 1 4 NA NA 2 2 0 0 1 1 2 3 1 12

Alteration Rush to CPB Return to CPB Reopen LVAD/ECMO Additional redo grafts IABP 4 3 2 0 9 CC, chest closure; CPB, cardiopulmonary bypass; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; NA, not applicable. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997;64(2):368. was variable: more accurate for normal than for abnormal wall motion and better in anesthesiologists with more advanced echocardiographic training. In the second part of the study,[118] TEE was found to be the most important factor in guiding hemodynamic interventions in 17% of cases examined. What is lacking is a clear demonstration that the TEE assessments were correct and that the same interventions would not have been undertaken if guided by more traditional monitors. Cost and outcome were not examined. Savage et al,[87] at the Cleveland Clinic, examined the use of intraoperative

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TEE monitoring in a group of high-risk patients undergoing coronary artery bypass grafting. As well as documenting numerous management changes related to TEE-derived information (Table 2-3) , they documented lower short-term morbidity and mortality rates as compared with a historical group of patients with similar severity scores[119] who were not monitored with TEE (Table 2-4) . An individual not part of the anesthetic or surgical team read the TEE scan; it is uncertain whether someone involved in direct patient management would have as readily garnered the information. In studies from Australia,[120] Europe,[121] Canada,[122] and India,[123] the realtime accrual of information with TEE was demonstrated to be of value in the management of hemodynamic perturbations and the planning of the surgical procedure in coronary bypass grafting as well as other cardiac surgical procedures Table 2-5 , Table 2-6 , and Table 2-7 ). No assessment of the effect of intraoperative TEE TABLE 2-4 -- Patient Outcomes with and without Intraoperative Transesophageal Echocardiography (TEE) Management without TEE 478 64.8 5.9 18 (3.8) 14 (3.5)

Variable Management with TEE Patients, n 82 Age, y 68.4 Severity score 6.1 Hospital deaths, n (%) 1 (1.2) Myocardial Infarction, n 1 (1.2) (%) Cardiac morbidity, n (%) 1 (1.2) 7 (1.5) ICU CNS morbidity, n (%) 3 (3.6) 18 (3.8) Hospital CNS morbidity, n 1 (1.2) 16 (3.3) (%) CNS, central nervous system; ICU, intensive care unit. From Savage RM, Lytle BW, Aronson S, et al: Ann Thorac Surg 1997; 64(2):368.

monitoring on patient outcome was made. These studies are summarized in Table 2-8 . The impact of monitoring of ventricular function during noncardiac surgery

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has not been studied as closely. In a retrospective review by Suriani et al, [124] the use of TEE was associated with some alterations in anesthetic and surgical management in a majority of cases. However, the indications for TEE were subjective, and neither the cost-effectiveness nor the effect on outcome was studied.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Has the burden of proof been met with respect to intraoperative TEE as a monitor of ventricular function? If one adopts the premise that rigorously designed, randomized, controlled clinical trials are society's benchmark,[125] TABLE 2-5 -- Impact of Routine Transesophageal Echocardiographic (TEE) Findings on Medical and Surgical Management: Coronary Artery Bypass Grafting After Cardiopulmonary Bypass (N = 120) Clinical Problem/TEE Finding (no. of patients) Consequence (no. of patients) Acute SWMA (8), acute Graft revision (3), papaverine (1), SWMA and medical therapy (5) moderate/severe mitral regurgitation (1) IABP not in optimal position (2) IABP not in descending aorta ST depression (II and V5)/no SWMA (3) Pulmonary

Impact E (3) * †

IABP advanced

I (6) V (2) ‡

IABP reinserted

V (1)

De-cannulation-good outcome

I (3)

Medical therapy for ischemia, not protamine reaction

I (1)

hypertension 3 minutes post protamine/

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widespread SWMA, moderate to severe mitral regurgitation E, essential; I, informative; IABP, intra-aortic balloon pump; SWMA, segmental wall motion abnormality; V, valuable. From Sutton DC, Kluger R: Anaesth Intensive Care 1998;26(3):287. * One patient also classified as valuable for IABP not in descending aorta. † One patient also classified as informative for ST depression without SWMA. ‡ Two patients also classified as informative in problems separating from CPB.

41

TABLE 2-6 -- Influence of Intraoperative Transesophageal Echocardiogra as the Driving Force on Interventions Compared with Other Monito Monitor Intervention, n (%) TEE ELECTROCARDIOGRAPHY Fluid bolus 275 0 (28) Anti-ischemic 207 114 (31) therapy (56) Vasopressor 56 3 (1) or inotrope (16) therapy Change in 4 0 anesthetic (2) depth Vasodilator 6 9 (6) therapy (4) Antiarrythmic 0 55 (89) therapy

ARTERIAL CATHETER 129 (13)

PULMONARY ARTERY OTH CATHETER 73 (7)

11 (3)

31 (8)

183 (51)

27 (7)

164 (78)

2 (1)

96 (68)

13 (9)

0

0

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Surgical 9 17 (33) 12 (23) 0 intervention (17) Miscellaneous 3 2 (6) 27 (75) 3 (8) (8) Total 560 200 (9) 622 (28) 149 (7) (25) From Kolev N, Brase R, Swanefelder J, et al: Anaesthesia 1998;53(8):76 *Indicates that the interventions were not based on information from the four monitors studied. More than half of these interventions were transfusion of blood for low hematocrit.

TABLE 2-7 -- Summary of Surgical Modifications Related to the Intraoperative Use of Transesophageal Echocardiography Modification Number Return on bypass for revision of coronary artery bypass graft 4 Modification of planned surgery: Valvular replacement cancelled 5 Valvular replacement or repair 11 Pleural drainage 3 Detection of air emboli before aortic unclamping 2 Surgical exploration for hemodynamic instability 7 Femoral artery bypass for aortic dissection 2 Others: Ventricular aneurysm resection 1 Aortoplasty 1 Cancellation of aortic dissection (diagnostic error) 1 Left ventricular assist device 1 Total 38 From Couture P, Denault AY, McKenty S, et al: Can J Anaesth 2000;47 (1):20.

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TABLE 2-8 -- Summary of Studies Examining the Alterations in Therapy During Cardiac Surgery with the Use of Intraoperative Transesophageal Echocardiography Altered Therapy, Study Population Surgery n/% 98/17% of all Bergquist n = 75, 584 C[118] Interventions revasc interventions et al Savage et n = 82 "High CSurgical change: [87] al risk" revasc 27/33% of patients Hemodynamic change: 42/51% of patients Sutton & n = 120 C16/13% of all patients Kluger revasc

Outcome Reported No Compared to historical controls

No

[120]

C-all 560/25% of all No Kolev et n = 224, [121] 2232 NC interventions al interventions Couture n = 851 C-all 125/15% of all No [122] et al patients Mishra et n = 5016 C-all 1146/23% of all No [123] al patients C-all, coronary and non-coronary cardiac surgery; C-revasc, coronary revascularizations; NC, noncardiac surgery.

42

then the jury is still out. The cost-effectiveness data that have been generated by studies of the use of TEE in congenital cardiac surgery,[126] preparation for elective cardioversion,[127] and determination of antibiotic treatment duration in endocarditis[128] have not yet demonstrated the benefits of monitoring of ventricular function in cardiac or noncardiac surgery. The data collected for studies are often reviewed offline, whereas clinical utility comes from online interpretation. Outcome data are scarce and sometimes conflicting. The "division of labor" in the operating room is also important, as too much attention to TEE may distract the anesthesiologist from other

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monitoring tasks.[129] Transesophageal echocardiography is an expensive undertaking and is not practically carried into the postoperative phase of patient management. Case studies and observational data cannot be dismissed, however. [130] [131] TEE has a unique ability to facilitate the rapid diagnosis of circulatory instability, and a number of observational studies show that information gained during intraoperative TEE frequently guides subsequent therapeutic maneuvers. In response, most fellowships in cardiac anesthesiology have incorporated instruction in the monitoring of ventricular function with intraoperative TEE. It must be emphasized that appropriate physician training and quality assurance[132] are crucial to the correct interpretation of data. Further technologic advancements such as color kinesis, automated border detection, and the use of loop storage for comparison should improve accuracy. Studies examining cost-effectiveness and outcome are needed.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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References 1. Poterack KA: Who uses transesophageal echocardiography in the operating room?

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9. Gorcsan JD, Snow FR, Paulsen W, et al: Noninvasive estimation of left atrial

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transmitral flow velocity patterns. Anesthesiology 2000;93:374. 20. De Hert SG, Rodrigus IE, Haenen LR, et al.: Recovery of systolic and diastolic left

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31. Muhiudeen IA, Kuecherer HF, Lee E, et al: Intraoperative estimation of cardiac

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Comparison of short axis imaging and simultaneous radionuclide angiography. Br J Anaesth 1990;64:331. 43. Wyatt HL, Haendchen RV, Meerbaum S, et al: Assessment of quantitative methods

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54. Gorcsan J 3rd, Gasior TA, Mandarino WA, et al: Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressurearea relations. Circulation 1994;89:180. 55. Deneault LG, Kancel MJ, Denault A, et al: A system for the on-line acquisition,

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wall motion abnormalities with transesophageal echocardiography. Can J Anaesth

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1999;46:827. 66. Tennant R, Wiggers CJ: The effect of coronary occlusion on myocardiol

contraction. Am J Physiol 1935;112:351. 67. Koh TW, Pepper JR, Gibson DG: Early changes in left ventricular anterior wall

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74. Koide Y, Keehn L, Nomura T, et al: Relationship of regional wall motion

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wall-motion abnormalities by transesophageal echocardiography: The incremental value of additional cross sections in the transverse and longitudinal planes. Anesth Analg 1996;83:1141. 76. Hauser AM, Gangadharan V, Ramos RG, et al: Sequence of mechanical,

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dobutamine technetium-99m sestamibi scintigraphy with low-dose dobutamine echocardiography for predicting functional recovery after revascularization. Am J Cardiol 2000;86:153. 81. Chan KL: Transesophageal echocardiography for assessing cause of hypotension

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antegrade and retrograde cardioplegia: A contrast echo study. Ann Thorac Surg 1999;68:955.

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86. Aronson S, Savage R, Toledano A, et al: Identifying the cause of left ventricular

systolic dysfunction after coronary artery bypass surgery: The role of myocardial contrast echocardiography. J Cardiothorac Vasc Anesth 1998;12:512. 87. Savage RM, Lytle BW, Aronson S, et al: Intraoperative echocardiography is

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intraoperative pulmonary embolism. Anesth Analg 1995;81:188. 91. Plowman AN, Bolsin SN, Patrick AJ: Unusual cause of intraoperative hypotension

diagnosed with transoesophageal echocardiography in a patient with renal cell carcinoma. Anaesth Intensive Care 1999;27:63. 92. Yamaura K, Okamoto H, Maekawa T, et al: Detection of retroperitoneal

hemorrhage by transesophageal echocardiography during cardiac surgery. Can J Anaesth 1999;46:169. 93. Hsin ST, Luk HN, Lin SM, et al: Detection of iatrogenic cardiac tamponade by

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with a left ventricular assist device in a patient with multiple trauma. J Thorac Cardiovasc Surg 1999;118:189. 96. Weiss RL, Brier JA, O'Connor W, et al: The usefulness of transesophageal

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critical care. Can J Surg 1999;42:171.

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98. Ibrahim AE, Stanwood PL, Freund PR: Pneumothorax and systemic air embolism

during positive-pressure ventilation. Anesthesiology 1999;90:1479. 99. Ho AM, Ling E: Systemic air embolism after lung trauma. Anesthesiology

1999;90:564. 100. Cheung AT, Savino JS, Weiss SJ: Beat-to-beat augmentation of left ventricular

function by intraaortic counterpulsation. Anesthesiology 1996;84:545. 101. Reichert CL, Koolen JJ, Visser CA: Transesophageal echocardiographic

evaluation of left ventricular function during intraaortic balloon pump counterpulsation. J Am Soc Echocardiogr 1993;6:490. 102. Shanewise JS, Sadel SM: Intraoperative transesophageal echocardiography to

assist the insertion and positioning of the intraaortic balloon pump. Anesth Analg 1994;79:577. 103. Scalia GM, McCarthy PM, Savage RM, et al: Clinical utility of echocardiography

in the management of implantable ventricular assist devices. J Am Soc Echocardiogr 2000;13:754. 104. Siegel LC, St. Goar FG, Stevens JH, et al: Monitoring considerations for port-

access cardiac surgery. Circulation 1997;96:562. 105. Coddens J, Deloof T, Hendrickx J, et al: Transesophageal echocardiography for

port-access surgery. J Cardiothorac Vasc Anesth 1999;13:614. 106. Secknus MA, Asher CR, Scalia GM, et al: Intraoperative transesophageal

echocardiography in minimally invasive cardiac valve surgery. J Am Soc Echocardiogr 1999;12:231. 107. Michel-Cherqui M, Brusset A, Liu N, et al: Intraoperative transesophageal

echocardiographic assessment of vascular anastomoses in lung transplantation. A report on 18 cases. Chest 1997;111:1229. 108. Huang YC, Cheng YJ, Lin YH, et al: Graft failure caused by pulmonary venous

obstruction diagnosed by intraoperative transesophageal echocardiography during lung transplantation. Anesth Analg 2000;91:558. 109. Branche PE, Duperret SL, Sagnard PE, et al: Left ventricular loading

modifications induced by pneumoperitoneum: A time course echocardiographic study. Anesth Analg 1998;86:482.

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110. Harris SN, Ballantyne GH, Luther MA, et al: Alterations of cardiovascular

performance during laparoscopic colectomy: A combined hemodynamic and echocardiographic analysis. Anesth Analg 1996;83:482. 111. Fahy BG, Hasnain JU, Flowers JL, et al: Transesophageal echocardiographic

detection of gas embolism and cardiac valvular dysfunction during laparoscopic nephrectomy. Anesth Analg 1999;88:500. 112. Fleisher LA, Mantha S, Roizen MF: Medical technology assessment: An

overview. Anesth Analg 1998;87:1271. 113. Connors AF Jr, Speroff T, Dawson NV, et al: The effectiveness of right heart

catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889. 114. Robin ED: Death by pulmonary artery flow-directed catheter: Time for a

moratorium? Chest 1987;92:727. 115. London MJ, Shroyer AL, Grover FL, et al: Evaluating anesthesia health care

delivery for cardiac surgery: The role of process and structure variables. Med Care 1995;33(10 suppl):OS66. 116. Kato M, Nakashima Y, Levine J, et al: Does transesophageal echocardiography

improve postoperative outcome in patients undergoing coronary artery bypass surgery? J Cardiothorac Vasc Anesth 1993;7:285. 117. Bergquist BD, Leung JM, Bellows WH: Transesophageal echocardiography in

myocardial revascularization: I. Accuracy of intraoperative real-time interpretation. Anesth Analg 1996;82:1132. 118. Bergquist BD, Bellows WH, Leung JM: Transesophageal echocardiography in

myocardial revascularization: II. Influence on intraoperative decision making. Anesth Analg 1996;82:1139. 45

119. Higgins TL, Estafanous FG, Loop FD, et al: Stratification of morbidity and

mortality outcome by preoperative risk factors in coronary artery bypass patients: A clinical severity score. JAMA 1992;267:2344. 120. Sutton DC, Kluger R: Intraoperative transoesophageal echocardiography: Impact

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on adult cardiac surgery. Anaesth Intensive Care 1998;26:287. 121. Kolev N, Brase R, Swanevelder J, et al: The influence of transoesophageal

echocardiography on intra-operative decision making: A European multicentre study. European Perioperative TOE Research Group. Anaesthesia 1998;53:767. 122. Couture P, Denault AY, McKenty S, et al: Impact of routine use of intraoperative

transesophageal echocardiography during cardiac surgery. Can J Anaesth 2000;47:20. 123. Mishra M, Chauhan R, Sharma KKHP, et al: Real-time intraoperative

transesophageal echocardiography: How useful? Experience of 5,016 cases. J Cardiothorac Vasc Anesth 1998;12:625. 124. Suriani RJ, Neustein S, Shore-Lesserson L, et al: Intraoperative transesophageal

echocardiography during noncardiac surgery. J Cardiothorac Vasc Anesth 1998;12:274. 125. Pocock SJ, Elbourne DR: Randomized trials or observational tribulations?

[editorial; comment]. N Engl J Med 2000;342:1907. 126. Siwik ES, Spector ML, Patel CR, et al: Costs and cost-effectiveness of routine

transesophageal echocardiography in congenital heart surgery. Am Heart J 1999;138(4 Pt 1):771. 127. Seto TB, Taira DA, Tsevat J, et al: Cost-effectiveness of transesophageal

echocardiographic-guided cardioversion: A decision analytic model for patients admitted to the hospital with atrial fibrillation. J Am Coll Cardiol 1997;29:122. 128. Rosen AB, Fowler VG Jr, Corey GR, et al: Cost-effectiveness of transesophageal

echocardiography to determine the duration of therapy for intravascular catheterassociated Staphylococcus aureus bacteremia. Ann Intern Med 1999;130:810. 129. Weinger MB, Herndon OW, Gaba DM: The effect of electronic record keeping

and transesophageal echocardiography on task distribution, workload, and vigilance during cardiac anesthesia. Anesthesiology 1997;87:144. 130. Benson K, Hartz AJ: A comparison of observational studies and randomized,

controlled trials [see comments]. N Engl J Med 2000;342:1878. 131. Concato J, Shah N, Horwitz RI: Randomized, controlled trials, observational

studies, and the hierarchy of research designs. N Engl J Med 2000;342:1887. 132. Rafferty T, LaMantia KR, Davis E, et al: Quality assurance for intraoperative

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46

Chapter 3 - Aortic Dissection and Trauma Value and Limitations of Echocardiography Elizabeth W. Ryan MD Ann F. Bolger MD

The rate of mortality with acute aortic dissection escalates hourly, [1] reaching 50% by 48 hours. Immediate diagnosis and therapy are critical for survival. Two thousand new cases of acute dissection are reported in the United States per year[2] the true incidence, including the large numbers of patients who die from unrecognized dissection, has been estimated at more that 10,000 per year.[3] Further, 10% to 30% of acute dissections occurring in the hospital may be misdiagnosed. Prompt diagnosis is a clinical challenge because patient's presenting symptoms may be nonspecific or even misleading. Aortic dissection must be included in the differential diagnosis of chest pain in many patients at risk for dissection and also when simultaneous acute involvement of multiple organ systems does not have a ready explanation. Acute dissection of the aorta can share many of the features of acute myocardial infarction: pain (related to the dissection itself or to myocardial ischemia), electrocardiographic abnormalities consistent with ischemia (resulting from involvement of the coronary ostia in proximal dissection),[4] and elevated serum creatinine kinase levels.[5] True myocardial ischemia is a potential component of the syndrome of aortic dissection. On pathologic examination, Hirst et al[6] found

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involvement of the coronary arteries in 39 of 505 cases of acute dissection (7.7%). Confusion of acute dissection with myocardial infarction not only delays appropriate treatment but also may lead to disastrous consequences if thrombolytic agents are administered.[7] [8] Thrombolysis impedes compensatory thrombosis of the false channel and promotes uncontrollable hemorrhage in the event of aortic rupture. Given that the incidence of aortic dissection is far less than that of myocardial infarction (0.26% of 5011 patients in the Anglo-Scandinavian Study of Early Thrombolysis trial[7] ) and that ST segment elevation is a relatively rare finding in patients with aortic dissection, classic electrocardiographic changes without physical findings suggesting dissection will rarely mislead clinicians toward thrombolysis.[9] Maintenance of a high suspicion for dissection must be paired with highly reliable tests to avoid such infrequent but catastrophic misdiagnoses. The optimal diagnostic test for acute aortic dissection, therefore, must be accurate, safe, and immediately applicable in a broad range of medical environments. The limited sensitivity of echocardiography for dissection from the transthoracic approach has been greatly improved by transesophageal approaches; transesophageal examinations can be performed within minutes in the emergency department, operating room, or intensive care unit and provides high-quality images of the thoracic aorta as well as of other cardiac and vascular structures at risk. The advantages and limitations of echocardiographic techniques 47

in the management of patients with aortic dissection have been carefully investigated at many centers, and, as a result, their strengths and weaknesses relative to other imaging techniques are being better defined. Ongoing advances in transesophageal probe technology and other ultrasonographic imaging methods are proceeding rapidly, with smaller transducers, multiple and variable imaging planes, and wider ranges of frequencies being made available. These improvements are solidifying the already well-established role of echocardiography in the diagnosis and follow-up of aortic dissection.

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Pathophysiology of Aortic Dissection Anatomy and Histology The aortic wall consists of three layers: the intima, which is a single layer of vascular endothelium; the media, with concentric layers of smooth muscle cells, collagen, elastin, and extracellular matrix proteoglycans; and the peripheral adventitia, consisting of loose connective tissue that anchors the aorta in surrounding tissues. The vaso vasorum, which perfuses the aortic wall, is contained within the adventitia. Of the three layers of the aortic wall, the structure of the media dominates the wall's mechanical properties.[10] Medial smooth muscle directly influences wall stiffness by contraction. In addition, smooth muscle cells are the major source of the extracellular matrix components. These include the elastin fibers, which can be stretched to 300% of their resting length without rupturing[11] and are important contributors to the normal pulsatile behavior of the vessel. Elastin is less important to the overall strength of the aorta than collagen, however, which is both stiffer and much stronger than elastin. The components of the media vary from vessel to vessel and change with age. In the aortas of older patients, the elastin content decreases and the collagen content increases, resulting in increased vascular stiffness.[12] The mechanical properties of the vasculature are also almost always disturbed in cases of systemic hypertension.[13] Mechanical and Shear Stresses The aortic wall is subjected to mechanical stresses of several forms. Stress, which is expressed as force per unit area, may occur in radial, circumferential, or longitudinal directions.[14] The normal intima bears little of the aorta's stress load. It is exposed to shear stresses, however, which are forces applied parallel to the vessel wall as a result of the viscous effects of blood flow. The amount of these shear stresses varies with the distribution of velocity across the vessel lumen and with local vessel geometry.

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Circumferential stress predominantly affects the media. This type of stress (δ) increases with the radial pressure from the aortic lumen (P) and the aortic radius (r), and decreases with increasing wall thickness (h): δ = Pr/h The danger of aortic dilation can therefore be understood: in dilated, thinwalled aortas, the circumferential stresses may be increased many times above normal. In addition, the geometry of the dilating aorta changes progressively from the normal cylinder to an ellipsoidal or even spherical shape. This slowly increases the circumferential stress but quickly exacerbates longitudinal stress. Most atraumatic aortic tears are caused by longitudinal stress, which explains why they are generally transverse in orientation.[15] The ascending aorta experiences additional longitudinal stress owing to the motion of the aortic annulus. Finally, dilated or aneurysmal vessels demonstrate marked stiffness, in part because of loss of elastin.[16] Combined aortic dilation, wall thinning, and shape change sets the stage for intimal rupture and the initiation of dissection. Intimal or medial abnormalities of the aorta increase the resistance to both shear and circumferential stresses. Stress failures of both types may play a role in aortic dissection. Circumferential stress failure can occur when the stresses caused by intraluminal pressure are greatly magnified in the thin fibrous cap of an atheromatous lesion. If the lesion fractures and a small crack develops, the circumferential stress will cause it to extend through the wall.[10] Shear stress failure is due to inhomogeneity in the properties of the vessel wall. Even under normal conditions, mural stresses are greater on the inner than on the outer wall.[15] In the presence of atherosclerosis, incremental variations in the shear resistance between contiguous regions of diseased and normal wall occur. The progression of aortic dissection probably represents an example of shear failure, in which the interface between two such aortic segments with different stiffness leads to separation of medial and intimal layers: the two layers slide relative to one another, because the "glue" of the extracellular matrix cannot withstand the shear stress.[10] Once initiated, dissections behave like a two-ply tube. The intima and the internal elastic lamina of the media form the inner layer, and the outer layer consists of the external elastic lamina and the adventitia. A velocitydependent shear force will then further separate the two layers, creating a false lumen separated from the true lumen by the intima and internal elastic

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lamina.[15] Experimentally, it has been demonstrated that the work per unit area of tissue required to propagate a tear in the aorta is small (15.9 ± 0.9 mJ cm2 ), and independent of the depth of the tear.[17] These concepts of shear and tensile failure are the basis for understanding why different patient populations are at increased risk for aortic dissection. Medial elastic tissue degeneration resulting from hereditary defects of the arterial wall creates the substrate for dissection in patients with Marfan's syndrome, Turner's syndrome,[18] Noonan's disease, Ehlers-Danlos syndrome, and osteogenesis imperfecta.[15] [19] In these patients, as well as in other groups, dilation of the aorta is an important source of tensile failure and a precursor to dissection. Both wall abnormalities (shear failure) and increased wall stress (tensile failure) caused by dilation are important in nonhereditary risk groups. Dissection occurring in hypertensive patients is generally based on 48

high blood pressure, moderate aortic dilation, and medial muscular degeneration predisposing the internal layer to tear.[15] The contribution of shear stress in those patients is infrequent and unpredictable. Atherosclerosis In atherosclerosis, both generalized and focal manifestations can predispose to dissection. True aortic aneurysms are caused by atherosclerotic degeneration of the media and progress to involve all three layers of the vessel wall and to gradual dilation. Increasing risk accompanies diameters exceeding 10 cm, rapid expansion, or symptoms. Formation of laminar thrombus within the aneurysm does not decrease the wall stress. The 1-year survival rate in patients with thoracic aortic aneurysms is less than 60%, and the 5-year survival rate is approximately 20%. False aneurysms are created by through-and-through disruption of the media, with the adventitia alone confining the extravasation.[20] The risk of rupture is even higher in this setting. A third type of atherosclerotic aortic abnormality is penetrating aortic ulceration.[21] [22] In this case, rupture of atherosclerotic plaque causes fissuring into the media and creation of an intramural hematoma, which may progress to rupture or pseudoaneurysm formation. Trauma

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Trauma is another important cause of dissection. Dissection may occur in external, accidental trauma and be difficult to assess in the setting of major multisystem injuries. The region most prone to traumatic injury is the aortic isthmus, where relative tethering by the spinal arteries and ligamentum arteriosum resists abrupt deceleration more than the more mobile transverse arch.[23] Other vulnerable sites include the origin of the innominate artery, particularly with vertical forces from falls, and the ascending aorta above the sinus of Valsalva. [24] Traumatic injuries to the aorta may result in intimal tears, recognizable on transesophageal echocardiography (TEE) scans as mobile flaps. Thrombus may be seen protruding into the lumen; in other cases, intramural hematoma without apparent intimal discontinuity is seen. Although very minor lesions such as minimal hematomas may regress spontaneously, the prognosis of significant aortic trauma is grave. Without repair, there is a 30% rate of mortality within the first 24 hours. Within 1 week, the mortality rate is greater than 50%.[25] Prompt recognition is therefore critical to patient outcome. TEE has been shown to be safe and highly sensitive for aortic trauma after motor vehicle accidents, equivalent to angiography and more expeditiously applied.[26] TEE may also detect other signs of cardiac trauma, including wall motion abnormalities, pericardial effusion, and valvular insufficiency. When the suspicion of aortic rupture in the territory of the transverse arch remains high, computed tomography (CT) may provide better images of those territories. Other sources of trauma include the Heimlich maneuver for respiratory obstruction and cardiovascular procedures. Operative sources of tears in the aorta include cannulation sites for cardiopulmonary bypass, aortic transections for valve or aortic segment replacement, and proximal anastomotic sites for coronary bypass grafts.[27] [28] Very uncommonly, aortic catheterization for angiography may traumatize an atherosclerotic region and prompt dissection.[29] Angioplasty procedures of coronary or renal vessels can also initiate the process.[30] A history of these procedures may be important in alerting the clinician to the possibility of dissection in these patients. Pregnancy Although aortic dissection is mostly a disease of middle-aged or elderly men, women and children can also experience dissection. It has been claimed that half of all aortic dissections occurring in women younger than 40 years of age are associated with pregnancy, particularly during the third trimester or the postpartum period.[31] [32] [33] This finding has been disputed

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by Oskoui and Lindsay,[34] who reviewed their own experience and published a series of 1253 dissections in consecutive patients (868 men and 385 women), with no cases occurring in pregnancy. They concluded that most women experiencing aortic dissection in pregnancy had other risk factors such as hypertension or Marfan's syndrome, and that the apparent association could result from selective reporting and coincidental occurrence of dissection with the very common condition of pregnancy. There are also other well-recognized causes of aortic dissection (Table 31) .[35] [36] [37] [38] [39] [40] [41] [42] [43] Genetic Diseases Of the genetic causes of aortic medial disease and aortic dissection, Marfan's syndrome is the most common and best studied. Although a clinical diagnosis, Marfan's syndrome can be confirmed by linkage to the dominantly inherited gene MFS-1 on 15q21 or by determination of the specific family mutation.[44] Histologic examination of the aortic wall in patients with Marfan's syndrome reveals fragmentation of aortic components, especially the elastic fibers,[45] and abnormal accumulation of collagenous and mucoid materials in the media.[46] Fragmentation of elastinassociated microfibrils also occurs in aortic valve leaflets. [47] The disruption and loss of elastic tissue of the media is attributed to a deficiency of fibrillin, a microfibrillar protein that scaffolds the elastic lamellae in the aortic wall.[48] [49] These changes are greatest in the ascending aorta, which is subject to the greatest pulsatile expansion and therefore the highest stress in systole.[15] The alterations in aortic wall components are associated with abnormal functional properties: aortic elasticity is abnormal in patients with Marfan's syndrome, irrespective of the aortic diameter. [50] A comparative study of aortic wall dynamics between patients with Marfan's syndrome and normal control subjects confirmed that, in both groups, stiffness of the wall increases with age and aortic diameter, but at all ages the patients in the Marfan's syndrome group exhibit a stiffer aorta for a given diameter than the control subjects do.[51] Furthermore, Marfan's syndrome patients have large ascending aortic diameters, but not 49

TABLE 3-1 -- Patient Populations at Risk for Aortic Dissection Genetic disorders (medial abnormalities)

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Marfan's syndrome Turner's syndrome Noonan's disease Ehlers-Danlos syndrome Osteogenesis imperfecta Congenital disorders Aortic coarctation Unicuspid or bicuspid aortic valve Degenerative disorders Hypertension Atherosclerotic vascular disease Aortic ulcer Aortic aneurysm Non-Marfan's syndrome cystic medial necrosis Traumatic causes Deceleration injury Penetrating injury Heimlich maneuver Postprocedural causes Cardiac surgery Cannulation Cross-clamping Aortic valve replacement Angioplasty Coronary Renal Inflammatory disorders Syphilis Giant cell arteritis Other conditions

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Pregnancy Weight lifting Cocaine use Discontinuation of beta blockers Polycystic kidney disease abdominal aortic size, after correction for body surface area.[50] Dissection occurs in Marfan's syndrome patients because of this dilation in combination with wall weakness; mural stress increases dramatically with increasing radius and becomes self-perpetuating[15] (Fig. 3-1) . Echocardiographic evidence of aortic root dilation is present in 60% to 80% of patients with Marfan's syndrome.[52] [53] In one series, aortic dilation was generalized in 51% and localized in 28% of patients.[54] Localized dilation did not appear to represent an earlier stage of aortic involvement, as the patient ages in both groups were identical, as was the duration of follow-up. It could not be determined whether generalized dilation reflected more severe underlying cystic medial necrosis from different specific mutations in fibrillin. Generalized dilation, however, was associated with higher rates of expansion as well as aortic regurgitation. In Marfan's syndrome patients, aortic insufficiency has been associated with decreased survival.[43] The existence of mitral valve prolapse does not appear to be an independent predictor of outcome. The clinical course of patients with Marfan's syndrome with respect to progressive aortic dilation and dissection is variable[55] increased risk has been associated with older age,[54] [55] male gender, aortic root diameters exceeding 60 mm,[56] aortic growth rate,[54] [55] and a family history of dissection.[57] Of great concern is the observation that aortic dissection can occur in Marfan's syndrome patients even in the absence of aortic root dilation.[58] Medical management of Marfan's syndrome patients with aortic dilatation involves beta blockers and observation of aortic root diameter to determine the timing of elective surgery aimed at preventing aortic dissection. Longterm fatality rates are improved with prophylactic aortic root replacement; the 5-year survival rate approximates 97% for elective surgery versus only 51% with emergency surgery for dissection.[59] Operative mortality in experienced centers for elective surgery in Marfan's syndrome patients is low (1.3% to 1.5% 30-day mortality rate versus 11.7% for emergency surgery).[60] [61] In patients with normal aortic valve leaflets, elective aortic valve-sparing surgery may provide better clinical outcomes than aortic root

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replacement,[62] although in this retrospective review, patients undergoing aortic root replacement with aortic valve replacement had more cardiac comorbidities than the patients in whom valve-sparing surgery was possible. The size of aneurysm often determines the feasibility of valvesparing surgery; therefore, some centers recommend elective surgery when the aortic root reaches 50 mm.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Spectrum of Aortic Dissection The primary entry tear that initiates aortic dissection is usually transverse and involves more than half of the circumference of the aorta. In 65% of cases, it occurs within 3 cm of the coronary ostia. Ten percent of tears occur in the descending thoracic aorta and another 10% in the arch. Primary tears are rare in the abdominal aorta.[63] Whatever the location of the initial tear, dissections may extend caudally, proximally, or occasionally in both directions. Figure 3-1 Type A aortic dissection (arrows indicate intimal flap) in a patient with Marfan's syndrome. Prolapse of the posterior mitral valve leaflet is also noted.

Anatomic Classification

50

There are several widely used classification systems for dissection (Table 3-2) . The DeBakey classification divides dissections with involvement of the ascending aorta into type I, which extends into the transverse arch and distal aorta, type II, which is confined to the ascending aorta, and type III, which involves the descending aorta only.[64] The Stanford classification[65] was developed from a functional approach based on whether the ascending aorta is involved, regardless of the site of primary intimal tear and irrespective of the extent of distal propagation. This reflects clinical observations that the biologic behavior of the dissection, the clinical prognosis, and how the patient should be managed pivot almost exclusively on whether the ascending aorta is involved.[66] [67] [68] This system of nomenclature describes type A dissections as any with involvement of the

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ascending aorta (including DeBakey types I and II), and type B dissections as dissection limited to the descending aorta (DeBakey type III). The clinical classification schemes described do not emphasize the location of the primary entry tear or the extent of the distal propagation of the dissection. These two factors are of less prognostic value and can be technically difficult to determine.[69] [70] When identification of the entry site is possible, the culprit primary intimal tear is more easily resected. Although successful resection of the primary tear does not appear to affect early or late survival rates, it may decrease the incidence of late reoperation.[71] Some cases of aortic dissection will present with multiple "primary" tears. Two separate dissections in the same patient may be more common than previously reported. Roberts and Roberts[72] reported that 3 of 40 necropsy patients had separate proximal and distal thoracic dissections. Although all fatal events were caused by rupture of the acute proximal dissections, a separate distal dissection may still pose a risk for late complications, and therefore recognizing two separate dissections may have important implications in terms of follow-up and therapy.[73] Multiple distal "exit" tears, which decompress the false lumen, are extremely common. Time Course Dissections are also differentiated with respect to their time course. Acute dissections are detected within 14 days of the onset of initial symptoms. Chronic dissections TABLE 3-2 -- Nomenclature of Aortic Dissection Dissection Type Ascending aorta involved

Ascending aorta not involved

Classification Stanford type A DeBakey I DeBakey II University of Alabama "ascending"[56] Massachusetts General Hospital "proximal"[57] Stanford type B DeBakey III University of Alabama "descending"[56] Massachusetts General Hospital "distal"[57]

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present more than 2 weeks after onset.[68] [74] This division is arbitrary; it may primarily reflect the fact that the majority of type A dissection patients will die within 2 weeks if untreated.[75] Chronic dissections may be detected because of symptoms or may be an incidental finding. They are differentiated from aortic aneurysms by the presence of an intimal flap and false lumen. These may not be easy to recognize when the false lumen is largely thrombosed. Pronounced atherosclerotic changes may be present in the false lumen in chronic dissections, even when the true lumen walls appear normal and hyperlipidemia is absent.[76] Sequelae The concomitant sequelae of aortic dissection are many and varied. Obstruction of branch vessels may explain acute myocardial ischemia and infarction of cerebral, spinal, bowel, and renal territories. Aortic valve dehiscence with regurgitation, cardiac tamponade from retrograde extension into the pericardium, and frank aortic rupture are all highly morbid consequences.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in Aortic Dissection Time is of the essence when aortic dissection is suspected, and the entire thoracic aorta must be visualized. Transthoracic echocardiography is immediately available, and, in some cases of proximal dissection, it may visualize the ascending aortic intimal flap and false lumen, or a flap in the descending aorta may be visible from the suprasternal (Fig. 3-2) or subcostal windows. Other clues to dissection available from transthoracic approaches include pericardial effusion with or without tamponade, aortic valve insufficiency with or without leaflet dehiscence, aortic root dilation, or regional wall motion abnormalities. Given the variable occurrence of any of these abnormalities, it is not surprising that the sensitivity of transthoracic echocardiography has been limited (Table 3-3) . Transesophageal Imaging Transesophageal echocardiography has elevated ultrasonic diagnosis of dissection into the first line of clinical options (Fig. 3-3) . Multiple studies have documented specificity and sensitivity in the range of 98% and 99%, respectively. The recognized blind spot of TEE, involving the distal ascending aorta and superior aspect of the arch, is an important limitation, especially because entry tears in this region are important to clinical management. The goal of imaging the entire thoracic aorta may therefore require a combination of modalities and approaches, including transthoracic views (often from the suprasternal notch), transesophageal windows, and often direct epiaortic or epicardial views at the time of surgery. Transesophageal echocardiography has many discrete advantages in the diagnosis of acute aortic dissection, the most important of which is its documented accuracy. Erbel 51

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Figure 3-2 Suprasternal views of the transverse and descending aorta demonstrate the intimal flap (A, arrows) as well as an entry tear with systolic flow from the true lumen into the false lumen (B) (color plate).

et al,[77] reporting for the European Cooperative Study Group for Echocardiography on a series of 164 patients suspected of acute dissection, demonstrated sensitivity and specificity rates of 99% and 98%, respectively. Another large study by Nienaber et al[78] compared TEE with magnetic resonance imaging (MRI). Both TEE and MRI had perfect sensitivity; the 100% specificity of MRI exceeded the 68% specificity of TEE. The authors suggested that TEE's limited visualization of common ascending aorta pathologic lesions might have accounted for the higher rate of false-positive findings. In that study, strict criteria for diagnosing dissection were not applied (see later discussion); more stringent criteria could minimize false-positive results. Transthoracic echocardiography TABLE 3-3 -- Imaging Modalities for Aortic Dissection

Study Appelbaum et al[67] Miller[66] Daily et al

Modality TTE

Positive Negative Sensitivity, Specificity, Predictive Predictive A % % Value, % Value, % 77 93 — —

TTE TTE

59 83

83 63

— 80

— 70

Miller[66] TEE Chirillo et TEE al[1] Daily et al TEE

98 98

77 97

— 98

— 97

100

68

82

100

88

94

96

84

88

97

97

85

100

100

100

100

98

98

—

—

[65]

[65]

DeBakey Aortography et al[64] Chirillo et Aortography al[1] Daily et al MRI [65]

Miller[66]

MRI

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83

100

100

86

94

87

—

—

[83]

Erbel et al CT [94]

CT, computed tomography; MRI, magnetic resonance imaging; TE transesophageal echocardiography; TTE, transthoracic echocardiograp from the suprasternal notch provides additional views of this vulnerable area. The sequential use of TEE and CT, aortography, or MRI is clearly extremely powerful in clarifying suspicious or clinically incongruous results.[79] [80] Transesophageal echocardiography provides additional information about left and right ventricular wall motion and global function and aortic and mitral valve competence. Importantly, with acute type A dissections, TEE is able to detect and determine the severity and mechanism of aortic valve regurgitation[81] and may influence the decision to replace or repair the valve. An important advantage of TEE in cases of dissection is its rapid and safe performance in a wide range of clinical environments, including emergency departments, 52

Figure 3-3 Examining the aorta in multiple planes is essential. In this case, the short-axis view (A) suggests an abscess cavity. The long-axis view (B), however, demonstrates a longitudinal dissection flap (arrows). Ao, aorta; LA, left atrium.

intensive care units, and the operating room. TEE requires minimal patient preparation, avoids the contrast agent and x-ray exposure associated with CT and angiography, and eliminates the time delays and practical encumbrances of MRI. Choice of a "best test" must always take into account the individual center's track record with each modality, as well as access issues. Safety of Transesophageal Echocardiography The safety of transesophageal examinations depends on adequate patient

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preparation with respect to pain, anxiety, and airway protection. Careful monitoring of the electrocardiogram and blood pressure is critical to avoiding adverse affects of TEE. In a study of 54 ambulatory patients, TEE was accompanied by an increase in systolic pressure in 77% of patients. This elevation was moderate (average increase of 16 mm Hg) in most patients, but some patients had acute increases of as much as 51 mm Hg.[82] Abrupt increases of blood pressure must clearly be avoided in any patient suspected of having a dissection. Serial blood pressure monitoring, pulse oximetry, intravenous sedation, topical anesthesia, and control of blood pressure with intravenous vasodilators and beta blockers, if needed, are important to patient safety. With these precautions, the majority of patients can undergo esophageal intubation with minimal distress and good hemodynamic stability. Even so, there has been a reported case of aortic rupture occurring during TEE in a patient with an acute dissection, which might have been elicited by retching and elevated blood pressure.[83] Other commonly reported adverse events during transesophageal studies that must be anticipated and avoided are nonsustained atrial and ventricular arrhythmias, excessive vagotonia with transient atrioventricular block, and arterial hypoxemia.[84] Diagnostic Features The diagnosis of aortic dissection is most secure when very specific criteria are met. Identification of an intimal flap, seen as a mobile, linear echo within the vascular lumen, and flow in the true and false channels on either side of the flap are highly sensitive features of dissection. The motion of the intimal flap toward the false lumen during systole may be a helpful feature. A thickening of the aortic wall in excess of 15 mm has also been used as a sign of dissection, suggesting thrombosis of a false channel, which makes the intimal flap difficult to recognize.[85] Strict adherence to these criteria can avoid confusion with imaging artifacts and manifestations of other types of disease and minimize false-positive results.[86] This is particularly important because most patients suspected of having an aortic dissection have evidence of vascular disease involving the thoracic aorta. In one series of 40 patients evaluated for dissection, abnormal aortic findings (including atherosclerotic plaques, intravascular and extravascular masses, thrombi, and dilation) were found in 16 of 17 patients in whom aortic dissection and coronary artery disease were excluded as explanations for their chest pain.[87] Other underlying aortic abnormalities such as coarctation or prior surgical repair may affect clinical management, but they are also important potential sources of misdiagnosis.

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Doppler Findings Color Doppler flow imaging during TEE is an excellent descriptor of aortic flow patterns with acute dissection. Flow in the false channel is variable and complicated; the true lumen, which is often dwarfed by the false channel, is identified by forward systolic flow (Fig. 3-4) . With large proximal entry tears, flow in the nearby segments of the false lumen may have the same direction and timing as the true lumen flow and may reverse in diastole.[88] [89] With 53

Figure 3-4 A short-axis transesophageal echocardiographic view of the descending aorta shows a small anterior true lumen and a larger posterior false lumen that is partially thrombosed (left, arrow). A pulsed Doppler signal from the true lumen, oriented from a long-axis view (right), demonstrates forward systolic flow.

smaller or more distal tears, false lumen flow is less similar to true lumen flow: it may be directed in the opposite direction, and peak velocity may occur later in the cardiac cycle, representing delay of flow into the false lumen. Many areas will show extremely slow, swirling flow with spontaneous echo contrast or partial thrombosis (Fig. 3-5) . These segments tend to be remote from large entry or exit sites, where high-velocity flow keeps these changes from occurring. Finally, areas of complete thrombosis are also seen, and care must be taken to ascertain that the hematoma is entirely intravascular and not actually Figure 3-5 Transesophageal echocardiogram of the descending thoracic aorta demonstrates the true lumen anteriorly and a thrombosing false lumen posteriorly in a patient with acute aortic dissection. As the false lumen thrombosis proceeds, the only clue to dissection may be the apparent "thickening" of the aortic wall.

the result of adventitial rupture, pseudoaneurysm formation, or intramural hematoma (Fig. 3-6) . Multiple communications between the true and false lumens are often identified on careful scanning of the entire thoracic aorta. Some will represent entry sites with flow from the true toward the false channel, and others will be exit sites or have bidirectional flow (Fig. 3-7) . Exit tears,

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where flow re-enters the true lumen from the false lumen, may occur at one or multiple sites. The exact location of a given tear can be estimated from the depth of probe insertion from the incisors, an arbitrary but 54

Figure 3-6 Transesophageal view of the descending aorta at 40 cm from the incisors in a patient with a prior proximal dissection and repair. There is discontinuity of the posterior aortic wall and a large thrombus extending into the periaortic tissues. This was confirmed to be a descending thoracic aortic rupture on subsequent surgery.

convenient reference point. Recording this information at the time of the procedure and on the written report not only is helpful in the surgical correction of dissection, but also is extremely important for comparison with postoperative follow-up TEE studies, in which many of the original tears may still be detectable. Identification of the primary entry site must be deduced from location, size, and flow patterns. In some cases, the primary tear cannot clearly be assigned to any one tear, either because of multiple tears as described Figure 3-7 A short-axis transesophageal echocardiographic view of the descending aorta with a large entry tear in the intimal flap. Pulsed Doppler echocardiography demonstrates flow from true to false lumen during systole. FL, false lumen; TL, true lumen.

earlier or, in some cases, because of the TEE blind spot. Adachi et al[90] were able to identify the entry site in 50 of 57 patients with acute dissection. They were more successful in this with type B dissections (90%) than with type A (83%). As mentioned previously, identification of the primary tear is mostly important because ensuring that the surgical repair resects the primary entry site may decrease the incidence of late reoperation. Complications of Dissection An important goal of echocardiographic imaging in aortic dissection is identifying associated complications. Type A dissections may produce acute aortic insufficiency because of annular dilation or disruption of leaflet suspension. TEE can provide detailed morphologic information regarding

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the quality of the leaflet tissue and the mechanism of aortic insufficiency; these can help in the decision regarding valve resuspension versus replacement. Pericardial effusion and tamponade are manifestations of aortic rupture with dissection and are often readily identified on transthoracic views. The Doppler manifestations of pericardial tamponade may be best obtained from external apical views and may obviate preoperative TEE in the interest of moving the patient emergently to the operating room. Small effusions unassociated with tamponade physiology may not be related to rupture and can be evaluated with contrast echocardiography if time and patient stability allow (Fig. 3-8) . Other rupture syndromes can occur at different sites. Uncontained rupture into the mediastinum or pleural space causes sudden death. Some ruptures are contained by the aortic adventitia, resulting in pseudoaneurysm formation or hematoma. In these cases, TEE can detect the intimal breach as well as the extension of the hematoma into the surrounding tissues; contrast can be helpful in delineating protuberant thrombus and rupture (Fig. 3-9) . An important proviso is to image the aorta at an adequate imaging depth so that such a hematoma 55

Figure 3-8 A four-chamber transesophageal echocardiographic view during contrast injection (Optison) shows contrast in the left ventricular cavity but not in the small pericardial effusion (arrow), which was unassociated with tamponade physiology.

can be recognized. These extravasations can be missed if the imaging field is restricted to the expected aortic contours; disastrous consequences can ensue if the site of the extravasation is not corrected along with the proximal aortic repair. Intramural Hematoma A small number of aortic dissections, estimated at 3% to 5%, occur without apparent intimal disruption.[6] [91] The pathologic process in these cases is rupture of the vasa vasorum into a region of medial degeneration, or possibly rupture of atherosclerotic plaque. Patients with this form of disease tend to be older (mean age, 70 years versus 56 years for communicating dissection) and have frequently had long-term hypertension. Transesophageal images

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Figure 3-9 A transesophageal echocardiographic view of the ascending aorta suggests an intimal flap with possible lumen rupture. Contrast injection (A, Optison) does not confirm extravasation outside the aorta (B, arrow).

demonstrate a thickened aortic wall with intramural echo-free spaces, an increased distance from the TEE probe to the inner aortic wall, and focal distortion of the transverse circular configuration of the aorta. This process has been described on CT images as well, seen as circular high-intensity areas along the aortic wall. [92] In their series, Mohr-Kahaly et al[93] described this type of noncommunicating aortic dissection as a dissection membrane without intimal tear and often involving the entire descending thoracic aorta. Early prognosis in those patients was somewhat better than in those with acute "communicating" dissections; this may reflect the tendency for the noncommunicating medial space to heal with complete thrombus formation.[94] These intramural hematomas may progress to typical dissection (in 33%) or to rupture (in 27%) and therefore usually require surgical rather than medical management.[95] Coronary Artery Involvement Involvement of coronary arteries by aortic dissection is an important issue, and one that raises the question of whether preoperative coronary angiography is mandatory. Involvement of one or both coronary arteries by acute aortic dissection has been estimated to occur in 10% to 20% of cases. [96] In a series of 34 aortic dissection patients, Ballal et al[97] detected coronary involvement with TEE in six of seven surgically documented dissected coronary arteries. Of note, electrocardiographic changes were demonstrated in only two of the six patients with coronary involvement. Adequate views of the ostia and proximal vessel were obtained for 88% of left main arteries and 50% of right coronary arteries overall. Visualization of the ostia and proximal coronary arteries continues to improve as variable imaging plane TEE probes are utilized and higher frequencies become available (Fig. 3-10) . A separate but related issue is whether concomitant coronary artery disease, independent of coronary dissection, is an important consideration that should prompt routine angiography. Given the underlying vascular disease 56

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Figure 3-10 A short-axis transesophageal echocardiographic view of the aortic root demonstrates an intimal flap in proximity to the left coronary ostium. LC, left coronary.

that affects many patients with dissection, it is not surprising that coronary disease has been found in up to 43% of patients with aortic dissection. The benefits of addressing potentially important coronary stenoses must be weighed against the risk of delays and aortic manipulation during acute dissection and adjusted for the patient's baseline likelihood of coronary disease. A series of 122 patients from the Cleveland Clinic found no difference in the in-hospital mortality rate between patients who had emergency coronary arteriography before dissection repair and those who did not. Three fourths of all coronary artery bypass procedures performed in that series were done because of coronary dissection rather than obstruction owing to coronary artery disease.[98]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Surgical Considerations The planning of surgical correction of aortic dissection is heavily influenced by many of the features discussed earlier. The extent of the dissection, the location of primary tears, and concomitant valvular insufficiency and coronary disease are all critically important to the surgical team. In addition, safe cannulation sites, aortic valve repair strategies, need for coronary reimplantation with root replacement, and confirmation of adequate cardiopulmonary bypass and even intra-aortic balloon function can all be addressed with intraoperative ultrasonography (Table 3-4) . Transesophageal imaging during surgery has the advantage of being nonobtrusive (at least for the surgeon, if not for the anesthesiologist) and is commonly also used as an accurate monitor of left ventricular wall motion and volume status. Intraoperative Echocardiographic Monitoring An additional tool for completing the scan of the aorta is intraoperative imaging from the epicardium or surface of the aorta. The unlimited number of acoustic windows from this approach allows careful interrogation of the aortic root, origins of the great vessels, cardiac valves, and left ventricular wall motion. The transesophageal blind spots in the ascending aorta and transverse arch can be thoroughly inspected from the epicardium, and potential aortic cannulation sites can be evaluated from the exterior aortic surface (Fig. 3-11) . Epicardial views give much greater freedom of visualization and measurement of the aortic valve and allow precise annular sizing before cardiopulmonary bypass to expedite selection of the valvular prosthesis. The position of the coronary ostia relative to the dissection and the annulus can be defined precisely with epicardial views, which may also aid in surgical decisions regarding valve-graft conduit placement or coronary ostial reimplantation. The amount of time required for imaging in the surgical field can be limited

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to a few minutes, but this achievement requires an experienced team with a surgeon or cardiologist familiar with the epicardial techniques and TABLE 3-4 -- Operative Uses of Transesophageal Echocardiography in Aortic Dissection Site Feature Pre–Cardiopulmonary Bypass Assessment Aorta Intimal flap Entry tear * Intramural hematoma Aortic rupture Aortic pseudoaneurysm Distal extent of extension Additional tears False lumen flow patterns, including thrombus Branch vessel involvement * Coronary situs and dissection Involvement of origins of great vessels Underlying pathologic condition Atheromatous disease Coarctation Sites of previous repairs Cannulation and cross-clamp sites Aortic valve Insufficiency Suitability for repair vs. replacement Sizing for allograft replacement Mitral valve Insufficiency Suitability for repair vs. replacement Left and right ventricle Wall motion abnormalities Pericardium Effusion Post–Cardiopulmonary Bypass Assessment Aorta Confirm competency of proximal anastomosis

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Establish baseline for false lumen flow and distal tears Aortic valve Confirm competency of repaired valve Mitral valve Confirm competency Left and right ventricle Wall motion Intra-aortic balloon Confirm position in true lumen * Epicardial and/or epiaortic scanning may be important in fully defining these features.

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Figure 3-11 Intraoperative epiaortic view of the transverse aortic arch in a patient with acute proximal aortic dissection. The intima is widely dissected and highly mobile. Note the linear streaking artifact from electrocautery.

views. The combination of epicardial and transesophageal techniques ensures that a high-quality ultrasonographic image is acquired of all segments of the aorta above the diaphragm and eliminates any uncertainty regarding involvement of the ascending aorta. Post-cardiopulmonary bypass images from the epicardium can also be extremely helpful in reassessing proximal tears and interrogating suture lines between aorta and conduit. Transesophageal views at the conclusion of cardiac surgery confirm aortic valve or prosthetic valve competency and allow prompt reinstitution of support if significant aortic insufficiency demands surgical revision. Intraaortic balloon pump position can be assessed with TEE (Fig. 3-12) ; accidental placement of the balloon in the false lumen can be disastrous if not immediately recognized.[99] Finally, postoperative TEE images of the graft and native aorta create a baseline for subsequent follow-up studies. Choice of Surgical Procedure The goal of surgical correction of aortic dissection is to prevent the most common causes of death. For type A dissections, death is caused by

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intrapericardial rupture and tamponade in 80% to 90% of cases and by extrapericardial rupture in 5% to 10%. For type B dissection, rupture causes 60% to 70% of deaths. A localized and conservative operative procedure prevents most deaths and is associated with the lowest number of operative risks. This generally consists of resection of a limited segment of aorta containing the worst damage, including the primary intimal tear if possible, and reconstruction of the local pathologic lesion. If required, however, extensive aortic reconstruction for dissection has been reported with longterm survival rates of 88.5% at 1 year and 81.7% at 9 years in a small series of Marfan's syndrome patients.[100] Coexisting Aortic Insufficiency Aortic valve insufficiency complicating aortic dissection has negative effects on outcome and may dictate important issues in the surgical approach. Preservation of the native aortic valve is possible in 86% of type A dissections with excellent results.[101] If the aortic annulus is abnormal because of Marfan's syndrome or annuloaortic ectasia, aortic valve replacement is preferred because of the limited long-term durability of aortic valve reconstruction in these patients. Initiation of cardioplegia for cardiopulmonary bypass usually depends on a competent aortic valve to allow antegrade perfusion of the coronary arteries; in the presence of significant aortic insufficiency, therefore, individual ostial cannulation or coronary sinus retroperfusion may be indicated. The specific causes of aortic insufficiency are also important[81] normal-appearing leaflets with a prolapsing cusp caused by avulsion of the leaflet base may be amenable to aortic repair with resuspension. Other cases may require aortic valve replacement. The specific involvement of the adjacent aortic root is also critical and may require a variable extent of prosthetic conduit. In some cases, human aortic allografts are used, which have the advantage of supplying both natural aortic valve and root. In proximal aortic involvement, the position and involvement of the coronary ostia are important. Ostial reimplantation may be necessary; coronary bypass grafting may be unavoidable if the coronary arteries are dissected. Coronary arteries may be reattached by direct reimplantation with or without a surrounding button of aortic tissue, reattached to a piece of prosthetic conduit (the Cabrol procedure), or completely bypassed with saphenous vein or internal mammary artery grafts. Figure 3-12 The position of the intra-aortic balloon pump (bright echo,

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upper right) can be confirmed with transesophageal echocardiography. This balloon is placed correctly in the anterior true lumen.

Coexisting Mitral Regurgitation

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Mitral regurgitation is a different example of a valvular abnormality associated with aortic dissection. New insufficiency may result from wall motion abnormalities induced by coronary involvement in the dissection, or from acute left ventricular dilation induced by aortic insufficiency. In other cases, mitral regurgitation is part of the underlying disorder, as is the case with Marfan's syndrome with mitral valve prolapse. Identification of the etiologic factors in the mitral insufficiency (e.g., leaflet degeneration, ventricular dilation, papillary muscle ischemia) will influence the need for repair or prosthetic replacement. Confirmation of results on early postcardiopulmonary bypass images is important, especially when the decision is made to leave the mitral valve alone despite some insufficiency in hopes that correction of acute ischemia or dilation will remedy it. Perfusion of Distal Vascular Beds In an acute aortic dissection, organs may be perfused by either the true or the false lumen flow. Organ under-perfusion may occur if flow to the source lumen is compromised. During surgery, malperfusion may be caused by flow reversal when cardiopulmonary bypass is established by cannulation of the femoral artery, with obliteration of major communications between the two lumens from cross-clamping, or with repair of the dissection itself. Neustein et al[102] describe a case in which femoral cardiopulmonary bypass compressed the true lumen and created severe malperfusion once the dissection was repaired. Perfusion through the new ascending aortic graft allowed immediate reinstitution of forward flow.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Follow-up of Patients after Repair of Aortic Dissection Persistent Intimal Flaps Despite successful surgical repair of aortic dissection, the aorta retains many abnormalities of structure and Figure 3-13 (color plate.) Distal tears are frequently present in aortic dissection. A, During systole, flow crosses from the true lumen into the false lumen. B, During diastole, flow reverses as the false lumen decompresses. C, Tears are usually multiple; here, two discrete tears with systolic flow into the false lumen are seen at the same level of the aorta. TRUE, true lumen; FALSE, false lumen; DESC AO, descending aorta.

flow. Distal to the repair, the intimal flap and false lumen persist. The false lumen may thrombose, or it may retain flow along with entry and exit flow through multiple fenestrations (Fig. 3-13) . One study detected persistent flap and false lumen in 100% of post-repair patients by MRI.[103] Persistent flow in the false lumen can be detected with TEE in the majority of patients after surgical repair. Mohr-Kahaly et al[89] found persistence of the false lumen in 71% of their postoperative patients at a follow-up interval of 1 to 41 months, and in 82% of their medically treated patients. Dinsmore and Willerson[104] have suggested that long-term survival is poorer in patients with persistent flow in the false lumen. Thrombosis of the false channel seems to be protective, a "natural buttress against future or further extension of the dissection." TEE confirms that sites without communications develop low-velocity flow and thrombus, whereas "healing" changes are less likely to occur in regions with significant tears and persistent flow. TEE also demonstrates aggressive atherosclerotic changes and calcification of the "neointima" lining the false channel. Progression of Disease

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Patients with previous dissection may develop progressive abnormalities of both operated and nonoperated aortic segments. Twenty-five to 40% of original dissections will enlarge over time, and the rate and extent of enlargement are primary factors driving the need for reoperation.[96] In addition, dilation of noncontiguous, nonoperated aortic segments develops in 17% of patients with prior acute type A dissections. Early recognition of this progressive downstream aortic pathology allows reoperation in hopes of preventing rupture or redissection.[105] The concern regarding disease progression commits these patients to routine follow-up studies indefinitely. Pseudoaneurysm Formation Pseudoaneurysms form in 7% to 25% of patients with composite grafts, such as a Bentall procedure, secondary to hemorrhage at a suture line dehiscence. [106] Blood between 59

the graft and aortic wall can create supravalvular aortic stenosis.[107] Both of these complications can be detected and completely delineated by TEE,[108] as well as by CT, angiography, and MRI.[109] [110] Color flow Doppler will demonstrate blood flow into the echo-free space between the graft and the aortic wall. Other postoperative complications include endocarditis and the development of an aneurysm in the sinus of Valsalva.[111] Recurrent Disease Because the symptoms of acute redissection or expansion of a chronic dissection are nonspecific, the ability to reassess rapidly and compare the current findings with previous images is extremely important. Younger patients, those with Marfan's syndrome, and those with primary tears involving the transverse arch are particularly prone to progression of their disease.[112] Because TEE may not be able to reproducibly measure the true transverse diameter of an ectatic aorta, suspicion of chronic expansion usually requires additional confirmatory tests such as CT or MRI. Excellent definition of the intimal flap, false channel thrombi and flow patterns, and consistent reference landmarks for serial sizing over time make MRI a highly reliable method. When recurrent chest pain or hemodynamic instability suggests acute redissection, TEE can rapidly define the new pathologic abnormality and its extent. Changes from baseline postoperative or postdissection images can be extremely helpful in clarifying the etiologic

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Limitations of Transesophageal Echocardiography False-Negative Results The interposition of the trachea between the esophagus and the heart creates a blind spot that obscures portions of the distal ascending aorta, superior transverse arch, and origins of the great vessels. As a result, a dissection limited to these areas could be missed by transesophageal imaging alone. This is of concern because the clinical behavior and therapeutic approach to the patient depends largely on whether the proximal aorta is involved in the dissection. The occurrence of this extremely limited type of dissection must be very rare, because the incidence of false-negative studies has been minimal in large series.[76] In addition, large series have not confirmed a positive angiographic or CT result when the initial TEE result was negative. The involvement of the great vessels may not modify the surgical approach and can be assessed at operation.[113] The combination of transesophageal imaging with transthoracic imaging from suprasternal and parasternal windows yields a much more thorough assessment of the arch. CT, MRI, or angiography can also be used to assess this area when there is persistent clinical suspicion of a dissection that is not detectable by TEE. False-Positive Results The path of ultrasound through the esophageal wall and surrounding tissues may generate near-field artifacts that are often disconcertingly linear and run parallel to the aortic wall, mimicking an intimal flap. In patients with severe atherosclerotic disease, calcification in the wall can present similar artifacts and shadows. Abrupt aortic dilation can create a "shelf," which can resemble a flap as well. Determining that these do not represent true intimal flaps depends on recognizing the minimal mobility of these "structures" and the homogeneity of flow on both sides of the line. The ability to change to a second imaging plane, as is possible with biplane or multiple-plane TEE

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probes, is extremely helpful in resolving the issue of artifactual "flaps."[86] [114] Multiple-plane imaging also allows better visualization of the proximal ascending aorta, where atherosclerosis and ectasia can be misinterpreted as dissection.[77] Aneurysmal dilation of the aorta is another source of false-positive TEE studies for dissection. Flow in aneurysmal areas is often low-velocity and swirling, similar to the flow in false channels. The absence of an intimal flap is important in avoiding misdiagnosis in this situation. The possibility that the intimal flap is not seen because the false channel has thrombosed must be excluded by carefully scanning up and down the aorta from the abnormal site. An intimal layer identified proximally or distally may be followed back to the suspicious dilated segment to suggest dissection.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Alternative Approaches to the Diagnosis of Dissection Echocardiography is only one of several diagnostic tests for dissection. The choice of imaging procedure, as well as the clinical confidence in positive or negative results, needs to be gauged relative to the test's performance (see Table 3-3) . Angiography is a time-honored diagnostic method for aortic dissection that may identify the intimal flap and false lumen. In addition, it can define coronary and great vessel ostial involvement. Its sensitivity and specificity for dissection (88% and 94%, respectively) are limited by false lumen thrombosis, intramural hematomas, and equal flow in true and false lumens.[115] [116] The last case is also an important limitation for CT studies, in which differential flow may not be detectable even with dynamic CT imaging.[117] The lower sensitivity (83%) of CT reflects its poor definition of the intimal flap and entry tear. Despite CT's high specificity (90% to 100%), a negative CT result in the presence of high clinical suspicion of dissection requires a second confirmatory test. Extremely slow, swirling flow within a segment of the false channel may not be completely differentiated from thrombus by MRI.[118] MRI's excellent definition of the important components of aortic dissection have resulted in its excellent sensitivity, however, which approaches 100%.[119] The pragmatic issues of imaging acutely ill patients with needs for hemodynamic monitoring or infusion of medications or those at risk for hemodynamic collapse continue to make TEE preferable in many acute settings. As mentioned earlier, MRI may be the procedure of choice for the follow-up of patients with repaired or chronic dissections.

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In their comparison of angiography, TEE, CT, and MRI techniques for aortic dissection, Barbant et al[120] used data from several published series to compare the accuracy and predictive value of these tests in populations

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with high, intermediate, and low prevalence of disease. For populations with a high risk of dissection, positive predictive values for all tests exceeded 85%. In intermediaterisk populations (prevalence, 10%), positive predictive values were greater than 90% for CT, MRI, and TEE but less than 65% for angiography. When the disease prevalence was low (1%), as it probably is in most clinical applications of these tests, the positive predictive values were less than 50% for angiography, CT, and TEE, and remained high only for MRI (100%). In any population, the negative predictive value was greater than or equal to 85% for all tests. These results suggest that TEE and other imaging techniques may not perform as well in a low-risk ambulatory population, as suggested by published results from higher-prevalence populations.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications and Future Directions Transesophageal echocardiographic images provide excellent spatial resolution, especially with the higher frequencies that are becoming available. Combining this with the high temporal resolution of M-mode methods has allowed investigation of aortic distensibility in normal patients, in patients at risk for vascular disease, and after repair of aneurysms or dissection. These types of methods have documented decreases in elastic aortic properties after aortic surgery, which predispose patients to redissection.[121] Two-dimensional echocardiographic assessments of aortic distensibility have been shown to estimate changes in aortic mechanical properties resulting from increasing age[122] Doppler estimates of pulse wave velocity Figure 3-14 Three-dimensional constructed views of the aorta in shortaxis (left) and long-axis (right) orientations demonstrate the intimal flap separating true and false lumens.

are also being investigated as measures of aortic compliance.[123] Animal models for validation of these parameters include chronic models of accelerated atherogenesis, as well as acute aortic ischemia and decreased distensibility generated by removal of the vasa vasorum.[124] High-frequency ultrasonic integrated backscatter methods are also being applied to the aortic wall (see Chapter 9) . Recchia et al[125] detected sixfold decreases in backscatter and 15-fold decreases in anisotropy, suggesting marked disorganization of the three-dimensional aortic architecture in the aortas of Marfan's syndrome patients as compared with the aortas of normal patients. These types of functional and structural investigations may improve our recognition of aortic disease of many stages and refine our prediction of risk of dissection. Technologic advances in aortic visualization are occurring based on

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improved transducer designs with more elements, greater freedom in imaging plane, and higher frequencies. These will be the basis for expanding the role of echocardiography in caring for aortic dissection patients, who will be undergoing new types of surgery involving new developments such as stents, balloon fenestration, and aortic valve resuspension.[126] Intravascular ultrasonography has become an extremely important imaging technique within the coronary vessels ( see Chapter 15 Chapter 16 ). Expanding this technology to the larger vessels and cardiac chambers has required lower-frequency transducers.[127] The potentially powerful role of intravascular ultrasonography in combination with angiography may have an important effect on the sensitivity of that technique. Similarly, tissue characterization with ultrasonography may be useful in identifying abnormalities of vessel wall composition, architecture, and material properties and aid in the prediction of primary or secondary dissection events. New ultrasonographic contrast agents that pass from venous injections through the pulmonary bed and into 61

the left-sided circulation may potentially aid in defining entry tears and important communications between true and false lumens.[128] [129] This improved spatial information will also be greatly aided by threedimensional constructs that can be generated from tomographic echocardiographic acquisitions (Fig. 3-14) .[130]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary The grim prognosis of patients with undetected acute aortic dissection demands a rapid, highly sensitive, and efficient diagnostic approach. Transesophageal imaging has excellent sensitivity for aortic dissection, its multiple complications, and its imitators. Intraoperatively, TEE or epicardial imaging identifies surgically relevant features of aortic valve damage and ventricular function. Patients with postoperative or chronic dissection can be followed with TEE, and serious events such as expansion or redissection can be quickly defined when symptoms of recurrent pain appear. Echocardiography is already established as a mainstay in the emergent diagnosis, treatment, and follow-up of patients with acute and chronic aortic dissection, and new technologies and applications will continue to expand its role in the future.

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References 1. Chirillo F, Marchiori MC, Andriolo L, et al: Outcome of 290 patients with aortic

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10. Lee RT, Kamm RD: Vascular mechanics for the cardiologist. J Am Coll Cardiol

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38. Schor JS, Horowitz MD, Livingstone AS: Recreational weight lifting and aortic

dissection: Case report. J Vasc Surg 1993;17:774–776. 39. Chauvel C, Cohen A, Albo C, et al: Aortic dissection and cardiovascular syphilis:

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to giant cell arteritis. Eur J Cardiothorac Surg 1993;7:667–670. 43. Marsalese DL, Moodie DS, Lytle BW, et al: Cystic medial necrosis of the aorta in

patients without Marfan's syndrome: Surgical outcome and long-term follow-up. J Am Coll Cardiol 1990;16:68–73. 44. Child AH: Marfan syndrome—current medical and genetic knowledge: How to

treat and when. J Card Surg 1997;12(2 suppl):131–135. 45. McDonald GR, Schaff HV, Pyeritz RE, et al: Surgical management of patients with

Marfan syndrome and dilatation of the ascending aorta. J Thorac Cardiovasc Surg 1981;81:180–186. 46. Murdoch JL, Walker BA, Halpern BL, et al: Life expectancy and causes of death in

the Marfan syndrome. N Engl J Med 1972;286:804–808. 47. Gott VL, Laschinger JC, Cameron DE, et al: The Marfan syndrome and the

cardiovascular surgeon. Eur J Cardiothorac Surg 1996;10:149–158. 48. Pyeritz RE, McKusick VA: The Marfan syndrome diagnosis and management. N

Engl J Med 1979;300:772–777. 49. Hollister DW, Godfrey M, Sakai LY, Pyeritz RE: Immunohistologic abnormalities

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of the microfibrillar-fiber system in the Marfan syndrome. N Engl J Med 1990;323:152–159. 50. Hirata K, Triposkiadis F, Sparks E, et al: The Marfan syndrome: Abnormal aortic

elastic properties. J Am Coll Cardiol 1991;18:57–63. 51. Jeremy RW, Huang H, Hwa J, et al: Relation between age, arterial distensibility,

and aortic dilatation in the Marfan syndrome. Am J Cardiol 1994;74:369–373. 52. Come PC, Fortuin NJ, White RI, McKusick VA: Echocardiographic assessment of

cardiovascular abnormalities in the Marfan syndrome: Comparison with clinical findings and with roentgenographic estimation of aortic root size. Am J Med 1983;74:465–474. 53. Brown OR, DeMots H, Kloster FE, et al: Aortic root dilatation and mitral valve

prolapse in Marfan's syndrome: An echocardiographic study. Circulation 1975;52:651–657. 54. Roman MJ, Rosen SE, Kramer-Fox R, Devereux RB: Prognostic significance of

the pattern of aortic root dilation in the Marfan syndrome. J Am Coll Cardiol 1993;22:1470–1476. 55. Legget ME, Unger TA, O'Sullivan CK, et al: Aortic root complications in the

Marfan's syndrome: Identification of a lower risk group. Heart 1996;75:389–395. 56. Gott VL, Pyeritz RE, Magovern GJ Jr, et al: Surgical treatment of aneurysms of the

ascending aorta in the Marfan syndrome: Results of composite-graft repair in 50 patients. N Engl J Med 1986;314:1070–1074. 57. Pyeritz RE: Predictors of dissection of the ascending aorta in Marfan syndrome

[abstract]. Circulation 1991;84(suppl II):II-351. 58. Roberts WC, Honig HS: The spectrum of cardiovascular disease in the Marfan

syndrome: A clinicomorphologic study of 18 necropsy patients and comparison to 151 previously reported necropsy patients. Am Heart J 1982;104:115–135. 59. Groenink M, Lohuis TA, Tijssen JG, et al: Survival and complication free survival

in Marfan's syndrome: Implications of current guidelines. Heart 1999;82:499–504. 60. Gott VL, Greene PS, Alejo DE, et al: Replacement of the aortic root in patients

with Marfan's syndrome. N Engl J Med 1999;29;340:1307–1313. 61. Coselli JS, LeMaire SA, Buket S: Marfan syndrome: The variability and outcome

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of operative management. J Vasc Surg 1995;21:432–443. 62. Tambeur L, David TE, Unger M, et al: Results of surgery for aortic root aneurysm

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Cardiol 1994;9:191–199. 64. DeBakey ME, McCollum CH, Crawford ES, et al: Dissection and dissecting

aneurysms of the aorta: Twenty year follow-up of five hundred twenty seven patients treated surgically. Surgery 1982;92:1118–1134. 65. Daily PO, Trueblood HW, Stinson EB, et al: Management of acute aortic

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management, and long term results. In Doroghazi RM, Slater EE (eds): Aortic Dissection. New York, McGraw-Hill, 1983, pp 193–243. 67. Applebaum A, Karp RB, Kirklin JW: Ascending vs. descending aortic dissections.

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North Am 1992;2:347–378. 70. Dinsmore RE, Willerson JT: Dissecting aneurysms of the aorta: Angiographic

features affecting prognosis. Radiology 1972;105:567. 71. Miller DC: Improved follow-up for patients with chronic dissections. Semin

Thorac Cardiovasc Surg 1991;3:270–276. 72. Roberts CS, Roberts WC: Aortic dissection with the entrance tear in the

descending thoracic aorta: Analysis of 40 necropsy patients. Ann Surg 1991;213:356– 368. 73. Duch PM, Chandrasekaran K, Karalis DG, Ross JJ Jr: Improved diagnosis of

coexisting types II and III aortic dissection with multiplane transesophageal echocardiography. Am Heart J 1994;127:699–701. 74. Slater EE: Aortic dissection: Presentation and diagnosis. In Doroghazi RM, Slater

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EE (eds): Aortic Dissection. New York, McGraw-Hill, 1983, pp 61–70. 75. Wheat MW Jr: Intensive drug therapy. In Doroghazi RM, Slater EE (eds): Aortic

Dissection. New York, McGraw-Hill, 1983, pp 165–192. 76. Grossman CM, D'Agostino AN: Advanced atherosclerosis in false channels of

chronic aortic dissection. Lancet 1993;342:1428–1429. 77. Erbel R, Engberding R, Daniel W, et al: Echocardiography in diagnosis of aortic

dissection. Lancet 1989;1:457–461. 78. Nienaber CA, Spielmann RP, von Kodolitsch Y, et al: Diagnosis of thoracic aortic

dissection: Magnetic resonance imaging versus transesophageal echocardiography. Circulation 1992;85:434–447. 79. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic

dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1–9. 80. Victor MF, Mintz GS, Kotler MN, et al: Two-dimensional echocardiographic

diagnosis of aortic dissection. Am J Cardiol 1981;48:1155–1159. 81. Movsowitz HD, Levine RA, Hilgenberg AD, et al: Transesophageal

echocardiographic description of the mechanisms of aortic regurgitation in acute type A aortic dissection: Implications for aortic valve repair. J Am Coll Cardiol 2000;36:884–890. 82. Geibel A, Kasper W, Behroz A, et al: Risk of transesophageal echocardiography in

awake patients with cardiac diseases. Am J Cardiol 1988;62:337–339. 83. Silvey SV, Stroughton TL, Pearl W, et al: Rupture of the outer partition of aortic

dissection during transesophageal echocardiography. Am J Cardiol 1991;68:286–287. 84. Pearson AC, Castello R, Labovitz AJ: Safety and utility of transesophageal

echocardiography in the critically ill patient. Am Heart J 1990;119:1083–1089. 85. Iliceto S, Nanda NC, Rizzon P, et al: Color Doppler evaluation of aortic dissection.

Circulation 1987;75:748–755. 86. Appelbe AF, Walker PG, Yeoh JK, et al: Clinical significance and origin of

artifacts in transesophageal echocardiography of the thoracic aorta. J Am Coll Cardiol 1993;21:754–760. 87. Chan KL: Usefulness of transesophageal echocardiography in the diagnosis of

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conditions mimicking aortic dissection. Am Heart J 1991;122:495–504. 88. Erbel R, Mohr-Kahaly S, Rennollet H, et al: Diagnosis of aortic dissection: The

value of transesophageal echocardiography. Thorac Cardiovasc Surg 1987;35:126– 133. 89. Mohr-Kahaly S, Erbel R, Rennollet H, et al: Ambulatory follow-up of aortic dissection by transesophageal two-dimensional and color-coded Doppler echocardiography. Circulation 1989;80:24–33. 90. Adachi H, Kyo S, Takamoto S, et al: Early diagnosis and surgical intervention of

acute aortic dissection by transesophageal color flow mapping. Circulation 1990;82 (suppl 4):19–23. 91. Eichelberger JP: Aortic dissection without intimal tear: Case report and findings on

transesophageal echocardiography. J Am Soc Echocardiogr 1994;7:82–86. 63

92. Yamada T, Tada S, Harada J: Aortic dissection without intimal rupture: Diagnosis

with MR imaging and CT. Radiology 1988;168:347–352. 93. Mohr-Kahaly S, Erbel R, Kearney P, et al: Aortic intramural hemorrhage

visualized by transesophageal echocardiography: Findings and prognostic implications. J Am Coll Cardiol 1994;23:658–664. 94. Erbel R, Oelert H, Meyer J, et al: Effect of medical and surgical therapy on aortic

dissection evaluated by transesophageal echocardiography: Implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993;87:1604–1615. 95. Robbins RC, McManus RP, Mitchell RS, et al: Management of patients with

intramural hematoma of the thoracic aorta. Circulation 1993;88:II1–II10. 96. Crawford ES: The diagnosis and management of aortic dissection. JAMA

1990;264:2537–2541. 97. Ballal RS, Nanda NC, Gatewood R, et al: Usefulness of transesophageal

echocardiography in assessment of aortic dissection. Circulation 1991;84:1903–1914. 98. Penn MS, Smedira N, Lytle B, et al: Does coronary angiography before emergency

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aortic surgery affect in-hospital mortality? J Am Coll Cardiol 2000;35:889–894. 99. Nakatani S, Beppu S, Tanaka N, et al: Application of abdominal and

transesophageal echocardiography as a guide for insertion of intraaortic balloon pump in aortic dissection. Am J Cardiol 1989;64:1082–1083. 100. Niinami H, Aomi S, Tagusari O, et al: Extensive aortic reconstruction for aortic

aneurysms in Marfan syndrome. Ann Thorac Surg 1999;67:1864–1867. 101. Mazzucotelli JP, Deleuze PH, Baufreton C, et al: Preservation of the aortic valve

in acute aortic dissection: Long-term echocardiographic assessment and clinical outcome. Ann Thorac Surg 1993;55:1513–1517. 102. Neustein SM, Lansman SL, Quintana CS, et al: Transesophageal Doppler

echocardiographic monitoring for malperfusion during aortic dissection repair. Ann Thorac Surg 1993;56:358–361. 103. Laissy JP, Blanc F, Soyer P, et al: Thoracic aortic dissection: Diagnosis with

transesophageal echocardiography versus MR imaging. Radiology 1995;194:331–336.

104. Dinsmore RE, Willerson JT: Dissecting aneurysms of the aorta: Angiographic

features affecting prognosis. Radiology 1972;105:567–572. 105. Heinemann M, Laas J, Karck M, Borst HG: Thoracic aortic aneurysms after acute

type A aortic dissection: Necessity for follow-up. Ann Thorac Surg 1990;49:580–584.

106. Barbetseas J, Crawford S, Safi HJ, et al: Doppler echocardiographic evaluation of

pseudoaneurysms complicating composite grafts of the ascending aorta. Circulation 1992;85:212–222. 107. Vilacosta I, Camino A, San Roman JA, et al: Supravalvular aortic stenosis after

replacement of the ascending aorta. Am J Cardiol 1992;70:1505–1507. 108. San Roman JA, Vilacosta I, Castillo JA, et al: Role of transesophageal

echocardiography in the assessment of patients with composite aortic grafts for therapy in acute aortic dissection. Am J Cardiol 1994;73:519–521. 109. Nath PH, Zollikofer C, Castaneda-Zuniga WR, et al: Radiological evaluation of

composite aortic grafts. Radiology 1979;131:43–51. 110. Pucillo AL, Schechter AG, Moggio RA, et al: Postoperative evaluation of

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ascending aortic prosthetic conduits by magnetic resonance imaging. Chest 1990;97:106–110. 111. Simon P, Owen AN, Moidl R, et al: Sinus of Valsalva aneurysm: A late

complication after repair of ascending aortic dissection. Thorac Cardiovasc Surg 1994;42:29–31. 112. Haverich A, Miller DC, Scott WC, et al: Acute and chronic aortic dissections:

Determinant of long-term outcome for operative survivors. Circulation 1985;72(suppl 2):22–34. 113. Chan KL: Impact of transesophageal echocardiography on the treatment of

patients with aortic dissection. Chest 1992;101:406–410. 114. Adachi H, Omoto R, Kyo S, et al: Emergency surgical intervention of acute aortic

dissection with the rapid diagnosis by transesophageal echocardiography. Circulation 1991;84(suppl 3):14–19. 115. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA: Diagnostic imaging in

the evaluation of suspected aortic dissection: Old standards and new directions. N Engl J Med 1993;328:35–43. 116. Bansal RC, Chandrasekaran K, Ayala K, Smith DC: Frequency and explanation of

false negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393–1401. 117. Mugge A, Daniel WG, Laas J, et al: False-negative diagnosis of proximal aortic

dissection by computed tomography or angiography and possible explanations based on transesophageal echocardiographic findings. Am J Cardiol 1990;65:527–529. 118. Barzilai B, Waggoner AD: Diagnosis of aortic dissection with transesophageal

echocardiography. Cardiology 1991;91:73–83. 119. Laissy JP, Blanc F, Soyer P, et al: Thoracic aortic dissection: Diagnosis with

transesophageal echocardiography versus MR imaging. Radiology 1995;194:331–336.

120. Barbant SD, Eisenberg MJ, Schiller NB: The diagnostic value of imaging

techniques for aortic dissection. Am Heart J 1992;124:541–543. 121. Imawaki S, Maeta H, Shiraishi Y, et al: Decrease in aortic distensibility after an

extended aortic reconstruction for Marfan's syndrome as a cause of postoperative acute aortic dissection DeBakey type I: A report of two cases. Surg Today

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1993;23:1010–1013. 122. Lacombe F, Dart A, Dewar E, et al: Arterial elastic properties in man: A

comparison of echo-Doppler indices of aortic stiffness. Eur Heart J 1992;13:1040– 1045. 123. Lehmann ED, Hopkins KD, Gosling RG: Aortic compliance measurements using Doppler ultrasound: In vivo biochemical correlates. Ultrasound Med Biol 1993;19:683–710. 124. Stefanadis CI, Karayannacos PE, Boudoulas HK, et al: Medial necrosis and acute

alterations in aortic distensibility following removal of the vasa vasorum of canine ascending aorta. Cardiovasc Res 1993;27:951–956. 125. Recchia D, Sharkey AM, Bosner MS, et al: Sensitive detection of abnormal aortic

architecture in Marfan syndrome with high-frequency ultrasonic tissue characterization. Circulation 1995;91:1036–1043. 126. Peterson AH, Williams DM, Rodriguez JL, Francis IR: Percutaneous treatment of

a traumatic aortic dissection by balloon fenestration and stent placement. Am J Roentgenol 1995;164:1274–1276. 127. Weintraub AR, Schwartz SL, Pandian NG, et al: Evaluation of acute aortic

dissection by intravascular ultrasonography. N Engl J Med 1990;323:1566–1567. 128. McRee D, Matsuda M, Stratton J, et al: Transthoracic contrast echocardiographic

detection of ascending aortic dissection. J Am Soc Echocardiogr 1999;12:1122–1124. 129. Kimura BJ, Phan JN, Housman LB: Utility of contrast echocardiography in the

diagnosis of aortic dissection. J Am Soc Echocardiogr 1999;12:155–159. 130. Sugeng L, Cao QL, Delabays A, et al: Three-dimensional echocardiographic

evaluation of aortic disorders with rotational multiplanar imaging: Experimental and clinical studies. J Am Soc Echocardiogr 199;10:120–132.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Section 2 - The Left Ventricle 65

Chapter 4 - Quantitative Evaluation of Left Ventricular Structure, Wall Stress, and Systolic Function Gerard P. Aurigemma MD Pamela S. Douglas MD William H. Gaasch MD

The quantitation of left ventricular (LV) systolic function, size, and geometry is critical to the proper evaluation and management of patients with all types of heart disease.[1] For example, the assessment of LV function in patients with coronary artery disease provides better prognostic information than does knowledge of the number of diseased vessels (Fig. 41) . Even when only one or two vessels are diseased, a low ejection fraction (EF) is associated with a higher mortality than that seen in patients with three-vessel disease and a normal EF.[2] Large LV systolic and diastolic volumes are also associated with a poor prognosis[3] [4] thus, a patient with a reduced EF after a myocardial infarction can be categorized according to subsequent risk based on the absolute end-systolic volume (Fig. 4-2) . Furthermore, information concerning LV size and geometry has important

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therapeutic implications, in view of the salutary effects of therapy with angiotensin converting enzyme inhibitors on postinfarction remodeling and prognosis in patients with a reduced EF.[5] Similarly, in cardiomyopathy of any cause, mortality remains high in patients with an EF less than 35%,[6] [7] even with medical therapy. A depressed EF is uniformly present in patients with idiopathic dilated cardiomyopathy and is due to a combination of afterload excess and depressed contractility. In this setting, indices of LV geometry, such as the relative wall thickness or the mass/volume ratio (Fig. 4-3) , provide prognostic information that is independent of the EF.[8] Conversely, it is important to identify the significant percentage of patients with congestive heart failure symptoms who have a normal EF.[9] [10] Measurement of LV volume, mass, and function can provide data that are necessary to define the optimal time for surgery in patients with volume overload hypertrophy owing to chronic, severe mitral or aortic regurgitation. In this regard, the prognostic usefulness of ventricular enddiastolic and end-systolic volumes, the EF, the ratio of end-diastolic volume to mass, systolic stress-shortening relations, and end-systolic pressure-volume relations has been tested in a variety of clinical studies. The end-systolic volume and EF appear to provide the most useful clues to prognosis.[11] [12] [13] [14] [15] [16] [17] [18] [19] [20] Certainly, a most important determinant of postoperative survival is the level of LV systolic function (Fig. 4-4) (Figure Not Available) . In pressure overload hypertrophy owing to aortic stenosis, an assessment of systolic function is perhaps less important than in the regurgitant lesions. Although severe depression of the EF may indicate an increased surgical risk, patients with an EF as low as 20% to 25% can show substantial clinical improvement after aortic valve replacement.[21] [22] [23] In such patients, excessive systolic loads are usually responsible for the low EF; this situation is termed inadequate hypertrophy or afterload excess. Alternatively, 66

Figure 4-1 The relation between left ventricular ejection fraction (EF) and survival in patients with single-, double-, and triple-vessel coronary artery disease (CAD). The negative impact of a low EF is seen in all three groups. Survival is better in patients with three-vessel CAD and a

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normal EF than in those with one- or two-vessel disease and a low EF. (Adapted from Mock MB, Rindqvist I, Fisher LD, et al: Circulation 1982;66:562–567. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:368.) Figure 4-2 The relation between left ventricular end-systolic volume (ESV) and survival in patients with normal, near-normal, and abnormal ejection fraction (EF). Data were obtained from patients with a history of myocardial infarction. ESV is a major predictor of survival when the EF is less than 50%. (Adapted from White HD, Norris RM, Brown MA, et al: Circulation 1987;76:44–51. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:369.) Figure 4-3 The relation between left ventricular mass/volume (M/V) ratio and survival in patients with an ejection fraction (EF) higher than and less than 20%. Data were obtained from patients with dilated cardiomyopathy. Patients with a normal M/V ratio exhibit better survival than those with a low ratio; this trend is seen in EF categories. (Adapted from Feild BJ, Baxley WA, Russell RO Jr, et al: Circulation 1973;47:1022–1031. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:370.)

67

Figure 4-4 (Figure Not Available) Relation of preoperative ventricular function to postoperative survival. These and other published data (see text) indicated that preoperative ventricular function is an important determinant of postoperative survival. ESD (echo), end-systolic dimension by echocardiography; SEF (angio), systolic ejection fraction by angiography; SEF (echo), systolic ejection fraction by echocardiography. (Adapted from Hoshino PK, Gaasch WH: Arch Intern Med 1986;146:349–352. Copyright © 1986 American Medical Association. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:371.)

excessive or inappropriate hypertrophy, indicated by a high relative wall thickness, appears to identify a group of patients having a high perioperative risk[24] [25] in this situation, a normal or high EF does not seem to be beneficial. In aortic stenosis, therefore, indices of LV geometry[26] (relative wall thickness) appear to provide prognostic clues that are not reflected in the EF. It is well established that increased LV mass is a strong predictor of

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cardiovascular morbidity as well as cardiovascular and all-cause mortality, even when age, blood pressure, and other risk factors are considered[27] [28] [29] [30] [31] [32] (see Chapter 32) . Some investigators have suggested that LV geometry provides prognostic information that is incremental to the extent of LV hypertrophy.[29] [30] [31] For example, an increased ratio of LV wall thickness to cavity dimension[32] identifies patients at higher risk for cardiovascular morbidity and mortality (Table 4-1) ; whether this incremental risk is truly independent of LV mass has been called into question by other data.[33] Thus, a substantial body of clinical research has demonstrated the prognostic value of indices of LV volume, mass, geometry, and function. Most if not all of these indices are routinely available to the clinician from standard M-mode and two-dimensional (2D) and Doppler echocardiography. In this chapter the echocardiographic techniques for evaluating LV geometry, stress, and systolic function are reviewed. Principles and methods are discussed, TABLE 4-1 -- Relation Between Morbid Events and the Pattern of Left Ventricular Geometry Normal LV Mass LVH P RWT ≥ RWT < RWT ≥ RWT < 0.45 (N = 0.45 (N = 0.45 (N = 0.45 (N = 29) 40) 34) 150) 0 3 10 21 < .001

CV deaths (%) CV events 11 15 23 31 .03 (%) All deaths 1 6 10 24 < .01 (%) The prognostic value of LVH for morbid events in men (at an average of 10.2 years of follow-up) is striking. For all end points, the RWT provides incremental value for assessing risk. P-value obtained by analysis of variance. CV, cardiovascular; LVH, left ventricular hypertrophy; RWT, relative wall thickness. From Koren M, Devereux R, Casale PN, et al: Ann Intern Med 1991;114:345–352.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Definitions and Theoretical Considerations The systolic pumping of the left ventricle is a complex process that involves a coordinated contraction of subendocardial, midwall, and subepicardial muscle fibers. These fibers are arranged in a complex, helical fashion. At the equator of the ventricle, midwall fibers are oriented circumferentially; contraction of these fibers mainly contributes to a decrease in the minor axis (or dimension) of the ventricle and is responsible for generation of much of the stroke volume (Fig. 4-5) . Longitudinally oriented fibers in the subendocardium and subepicardium contribute to shortening of the long axis of the ventricle, also contributing to stroke volume. In addition to circumferential and long-axis shortening, the apex of the left ventricle rotates counterclockwise during systolic contraction, and the base rotates clockwise (as viewed from the apex).[34] [35] Such "twist," like fiber shortening, appears to be influenced by the contractile state of the myocardium. In concert with these shortening and twisting motions, wall thickening contributes to volume displacement and generation of the stroke volume.[36] Preload, afterload, contractility, and geometry influence shortening and thickening.[37] The pumping activity of the left ventricle provides oxygenated blood to the tissues of the body; therefore, the stroke volume can be used as a parameter of the pump performance of the ventricle (Table 4-2) . Because LV systolic pressure and stroke volume are inversely related, using stroke work as an index of ventricular performance can be more appropriate; a stroke work parameter credits the ventricle for the development of pressure and for shortening. When performance is assessed relative to end-diastolic fiber length or a related parameter, ventricular function can be described. Thus, a ventricular function curve can be generated by plotting stroke work against end-diastolic pressure, diameter, volume, or wall stress. Volume loading therefore produces an increment in stroke work (i.e., performance) through use of the Frank-Starling

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68

Figure 4-5 Circumferential and longitudinal fibers contribute to wall thickening and volume displacement. These functions are influenced by left ventricular preload, afterload, contractile state, and geometry. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:374.)

mechanism. By contrast, increased myocardial contractility also can produce an increment in stroke work, but in this case performance is augmented through a change in inotropic state rather than by a change in end-diastolic fiber length. In other words, contractility refers to a basic property of the myocardium that reflects the intensity of its active state. The use of the term contractility should be restricted to situations in which a change in performance or EF cannot be ascribed to a change in preload or afterload. Contractile function is a more general term used to describe changes in performance or function that could be affected by changes in inotropic state, fiber length, or loads. Thus, a change in the EF might best be classified as a change in contractile function; this term is often used interchangeably with systolic function. To fully describe the ventricle, it is necessary to define several additional terms that refer to its mechanical properties. Stress is defined as the force per unit cross-sectional area of a material. It is an engineering term used to compare loads borne by different-sized elements of a material; the total load is less important than the load per unit of material. If the same load is borne by a smaller amount of material, the stress on that material is higher. In a spherical model of the left ventricle, wall stress (σ) is directly proportional to the transmural pressure (P) and inversely proportional to the product of chamber radius (R) and wall thickness (Th): σ = PR/2Th In the left ventricle, geometry is much more complex, and several components of stress exist within the wall (Fig. 4-6) . Of these, meridional and circumferential TABLE 4-2 -- Aspects of Ventricular Function Pump performance The pumping activity of the left ventricle that results in the delivery of oxygenated blood to the tissues. Stroke volume and stroke work are

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parameters of pump performance Ventricular function Left ventricular performance assessed relative to end-diastolic fiber length (or related parameter) Myocardial contractility A basic property of the myocardium that reflects its active state, rather than loading conditions Contractile function A descriptor of ventricular performance or function that is affected by inotropic state, fiber length, or load stresses have most commonly been used in the analysis of LV mechanics. The meridional stress vector is oriented in the longitudinal or apex-to-base direction and represents the component of the load resisting long-axis shortening; circumferential stress is oriented along the equator, perpendicular to the long axis (see Fig. 4-6) and represents the component of the load resisting minor-axis shortening. Meridional stress (σm ) can be calculated as

σm = P · LVID / [4 · Th(1 + LVID/Th)] where P is pressure (mm Hg), Th is wall thickness, and LVID is cavity dimension.[38] This stress parameter does not require measurement of the long axis of the LV cavity. Circumferential stress (σc ) can be calculated as σc = P · a2 [1 + (b2 /r2 )]/(b2 − a2 ) where P is end-systolic pressure (mm Hg), a is the internal (endocardial) radius, b is the external (epicardial) radius, and r is the midwall radius.[39] Other approaches to the calculation of circumferential stress, using minorand major-axis dimensions, have been evaluated.[40] Formulas for calculation of meridional and circumferential stress using 2D echocardiographic data are as follows:[41] σm = 1.33P Am /Ac · 103 kdyn/cm2

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where At is the short-axis area subtended by the LV epicardium and right

side of the septum, Ac is the cavity (endocardial) area, and Am = At − Ac or

myocardial area, and L is the LV cavity length, obtained from the apical four-chamber view. Two-dimensional and M-mode methods yield somewhat different results, with M-mode-derived σm being higher than 2D-

derived values, even in normal subjects. In spherical ventricles, σm by any method tends to overestimate afterload.[42]

The determination of wall stress requires assessment of LV pressure. Invasively determined values may be combined with echocardiographic dimensions, but they are often not available or simultaneously obtained. Three methods have been proposed for using noninvasive recordings to ascertain LV systolic pressures; LV diastolic 69

Figure 4-6 Schematic of the left ventricle (LV) (represented as a truncated ellipsoid) illustrating the major stress vectors. Meridional stress (σm ) is the force acting along the long axis of the LV; meridional stress opposes long-axis shortening. Circumferential stress (σc ) is the force acting in the equatorial direction; circumferential stress opposes circumferential fiber shortening, and circumferentially oriented fibers are located in the midwall of the left ventricle. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:375.)

pressures (and therefore diastolic stress) cannot be reliably determined noninvasively. Although these methods assume that there is no LV outflow gradient, the first and easiest method assumes that end-systolic LV pressure can be approximated by peak arterial pressure.[38] Thus, cuff systolic blood pressure is substituted for LV end-systolic pressure. The second method involves calibration of an externally recorded pulse recording using cuff systolic and diastolic pressures, with calculation of arterial pressures at the dicrotic notch.[43] The third involves the substitution of mean arterial pressure, derived from cuff recording, for end-systolic pressure, given the

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close correlation between these two values, as shown by Rozich.[44] Because wall stress parameters incorporate appropriate size normalization, they allow comparison among the mechanical properties of different hearts. End-systolic wall stresses, calculated using end-systolic pressures (or the surrogates discussed earlier) and dimensions, are taken as indices of LV afterload, whereas end-diastolic wall stress, calculated using end-diastolic pressure and dimension, is a measure of LV preload. Preload is the force (i.e., load) acting to stretch the resting myofibril. Preload is commonly estimated as the LV end-diastolic pressure, diameter, or volume, but to be more precise, this force should be normalized for each unit cross-sectional area of muscle and expressed as end-diastolic wall stress. In this manner, LV preload is analogous to the preload on a strip of isolated cardiac muscle in a myograph. This force, which acts to stretch the myocardium, is resisted by the stiffness of the muscle. Thus, the extent to which the myocardial fiber is stretched depends on an interaction between preload and muscle stiffness. [45] Because preload influences initial fiber length, it affects LV systolic performance. This phenomenon, which operates on a beat-to-beat basis, is generally referred to as Starling's law of the heart or the Frank-Starling mechanism. The preload reserve of the ventricle depends on the baseline hemodynamic conditions and the stiffness of the myocardium. Thus, in the upright posture, normal human subjects exhibit a substantial preload reserve, whereas in the recumbent posture they may exhibit a minimal preload reserve. The difference in preload reserve is related to difference in the baseline end-diastolic volume, which is lower in the upright posture than it is when the subject is recumbent, owing to the differences in venous return. This fact should be kept in mind when interpreting exercise studies; the end-diastolic volume of the normal left ventricle generally increases during upright exercise, but it may not during recumbent exercise. Moreover, the ability to recruit the Frank-Starling mechanism may also be limited in hypertrophied ventricles that have abnormal ventricular compliance characteristics. Thus, in patients with aortic stenosis or hypertensive heart disease, there may be little or no increment in LV end-diastolic volume during exercise, and consequently the EF may not increase normally.[46] [47] [48] Such limited preload reserve occurs as a result of a steep diastolic pressure-volume relation in which large changes in filling pressure cause only small changes in volume.[49] This mechanism may even underlie marginal LV function in the basal state.[45]

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Despite a low EF, many dilated hearts (particularly those with compensated mitral or aortic regurgitation) generate a normal or high stroke volume. In this instance, although the Frank-Starling mechanism may be a contributing factor, the large stroke volume is primarily a function of the large enddiastolic volume. In other words, the presence of a large LV chamber does not necessarily indicate use of preload reserve at the fiber level. Many such hearts retain the ability to use preload reserve to augment stroke volume. By contrast, in end-stage heart failure, preload reserve may be exhausted (Fig. 4-7) . Afterload can be thought of as the force (i.e., stress) developed by the myocardium after the onset of contraction. As described by the Laplace relation, afterload (systolic wall stress) is directly related to LV systolic pressure and radius, and inversely related to wall thickness. Afterload varies with time, and thus it can be calculated at the instant of aortic valve opening, at the end of ejection, or at any instant throughout systole. Whereas LV systolic pressure and systemic vascular resistance can affect afterload, neither of these should be considered the equivalent of afterload. [50] [51] [52] Likewise, aortic input impedance influences systolic pressure and stress, but impedance is not the equivalent of afterload.[53] In aortic stenosis, the LV systolic pressure may exceed 250 mm Hg, but if there is an appropriate increase in LV wall thickness, the force borne by each unit of heart muscle might remain near normal (i.e., afterload is normal). [51] [52] , [54] On the other hand, an acute increase in systolic pressure or chamber size can result in an increased afterload.[55] By virtue of the inverse relation between load and shortening, an acute increase in afterload generally causes a decrease in shortening, and vice versa (see Fig. 4-7) . Contractility can be defined as the quality of cardiac muscle that determines performance independent of loading conditions. Contractility is easiest to study and define in isolated heart muscles when loading conditions are held constant. For example, if resting length is held constant, the addition of digitalis or norepinephrine to an isolated muscle preparation results in an increase in the 70

Figure 4-7 Left, The relation between left ventricular afterload and fiber shortening. Two coordinates of afterload are shown on a normal curve. If preload is constant, an acute increase in afterload will cause a decrease in

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shortening. During acute interventions in a clinical setting, the relation between aortic pressure and stroke volume is similar to this schematic afterload-shortening curve. A failing ventricle exhibits a depressed curve with reduced shortening; thus, the ejection fraction and stroke volume can be depressed despite a normal afterload. Middle and right, Afterload-shortening relations in moderate and severe left ventricular dysfunction. In moderate dysfunction (middle), shortening in the basal state (A) is depressed; if some preload reserve is present, mild pressor stress does not substantially reduce shortening (B); more marked pressor stress will depress shortening (C). In severe dysfunction (right), inotropic state is markedly depressed and preload reserve is exhausted; under these circumstances, any pressor stress will cause a decrease in shortening. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:377–378.)

extent and velocity of force development and shortening; such increased performance under constant loading conditions reflects an augmented inotropic state (i.e., increased contractility). In many cardiac diseases, abnormal LV pump function may be caused by disordered loading conditions, depression of contractility, or both. For this reason, it may be difficult to determine the exact cause of decreased fiber shortening. Accordingly, there has been considerable interest in the development of a sensitive index of contractility that is not affected by changes in loading conditions.[56] [57] Unfortunately, there is no completely load-independent index of basal contractile state. Thus, directional changes in contractility (during acute hemodynamic interventions) are relatively easy to demonstrate, but it is not possible to define a basal level of contractility in patients with chronic heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Mass, Volume, and Geometry Remodeling of the left ventricle in valvular heart disease, heart failure, and hypertensive heart disease is characterized by changes in LV mass and geometry. Descriptors of LV geometry include the relative wall thickness, short axis/long axis ratio, and volume/mass ratio. These descriptors are easily obtained by M-mode and 2D echocardiography. As suggested earlier, alterations in LV geometry have been used to assist risk stratification in a variety of diseases and to describe more completely remodeling changes effected by valve replacement. In patients with idiopathic dilated cardiomyopathy, for example, a poorer survival is associated with larger short-axis dimension and a greater ratio of short/long axes (i.e., a more spherical LV geometry).[58] The relative wall thickness, when used to estimate the "adequacy" of LV hypertrophy in patients with idiopathic dilated cardiomyopathy, also predicts the increase in contractility in response to dobutamine infusion[59] cardiomyopathy patients with a diminution in relative wall thickness appear to have an attenuated contractile response to dobutamine infusion. In the following section, the methods used to calculate LV mass and describe LV geometry are reviewed. M-mode Echocardiography Mass

Whereas newer and more costly tomographic methods, such as ultrafast computed tomography (CT) and magnetic resonance imaging (MRI), permit more precise quantitation, echocardiography remains the most commonly used technique for estimating LV mass and geometry. M-mode echocardiography is universally available and relatively low cost, and there is a considerable body of evidence supporting its accuracy in LV mass quantitation.[60] [61] [62] [63] Quantitation of mass (see also Chapter 32) is based on the geometric assumption that the ventricle is a prolate ellipsoid with a

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2:1 long axis/short axis ratio.[60] [61] [62] [63] [64] [65] In practical terms, LV mass estimates are most accurate in ventricles with normal shape,[64] [65] specifically, a long axis/short axis ratio that approximates 2:1. It is assumed, of course, that minor axis dimensions are measured in a region free of wall motion abnormalities. This assumption is invalidated in ischemic heart disease with focal wall motion abnormality or in right ventricular overload. Estimates of myocardial mass and volume are derived from LV minor axis dimensions obtained with the transducer in the parasternal position (Fig. 4-8) . Under 2D echocardiographic guidance, the ultrasound beam is aligned so that it is perpendicular to the interventricular septum and 71

Figure 4-8 Schematic of an M-mode echocardiogram obtained using two-dimensional echocardiographic guidance. Measurements are made coincident with the Q wave of the simultaneous electrocardiogram. LVIDd, left ventricular internal dimensions in diastole; LVIDs, left ventricular internal dimensions in systole; PWTd, posterior wall thickness in diastole; PWTs, posterior wall thickness in systole; STd, ventricular septal thickness in diastole; STs, ventricular septal thickness in systole. (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:381.)

posterior wall at a level slightly below the mitral leaflet tips; the transducer is then rotated to obtain a short-axis view. This approach maximizes the LV cavity dimension and ensures that proper beam orientation with respect to the papillary muscles is obtained. LV mass is estimated from measurements of septal and posterior wall thickness and LV cavity dimensions at enddiastole using the anatomically validated cube formula[60] [61] [62] [63] [64] [65] LV mass = 0.8{1.04(STd + LVIDd + PWTd )3 − LVIDd 3 } + 0.6 g where STd is the diastolic septal thickness, LVIDd is the diastolic LV cavity dimension, PWTd is the diastolic posterior wall thickness, and 1.04 is the

specific gravity of myocardium. The measurements are made using the American Society of Echocardiography standard technique.[60] As shown by Devereux et al,[61] LV mass estimates made with American Society of Echocardiography measurements overestimate true anatomic LV weights by 20%, necessitating a correction factor of 0.8.

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Volume

A simple estimate of LV volume may be obtained from the minor-axis dimension, derived by M-mode echocardiography as V = LVID3 The geometric assumptions are similar to those used for LV mass calculation. However, in the dilated, spherical left ventricle encountered in long-standing valvular regurgitation or dilated cardiomyopathy, the ratio of length to minor-axis dimension decreases, leading to significant overestimation of LV volumes by this simple method. Teichholz et al[66] derived a formula that attempts to correct for this problem: Vd = [7/(2.4 + LVIDd )] · LVIDd 3 LV volumes derived with this formula correlate well with single-plane angiographic estimates.[64] The Teichholz method produces the most accurate volume estimates of any of the M-mode formulas.[67] Because Mmode echocardiography provides minor-axis dimensions of the left ventricle in systole and diastole, the Teichholz method may be used to compute LV volumes at end-systole and end-diastole, and thus to derive stroke volume and cardiac output. A compelling advantage of this method is that LV volume can be determined rapidly from easily obtained M-mode measurements. Relative Wall Thickness

M-mode estimates of myocardial mass and volume are derived from LV minor-axis dimensions obtained with the transducer in the parasternal position (see Fig. 4-8) . These same measurements are used to describe LV geometry. Although the amount of LV mass is an important 72

predictor of subsequent cardiac events in hypertensive disease, the geometry and pattern of LV hypertrophy also provide insight into the pathophysiology of hypertensive hypertrophy[68] and may confer prognostic information. [29] [30] [31] The most commonly used index of the pattern of hypertrophy is the relative wall thickness (RWT),[32] [68] which is calculated as

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RWT ± 2 · PWT/LVID where PWT is the posterior wall thickness and LVID is the LV internal dimension, respectively; relative wall thickness may be measured in diastole or systole. Relative wall thickness also has been expressed as h/R, where h is wall thickness and R is cavity radius. Ford[69] and others[52] [54] have shown that in the normal or compensated ventricle, the relative wall thickness increases in direct proportion to elevations in systolic pressure (Fig. 4-9) . Assuming that there is not a substantial shape change as the ventricle enlarges (i.e., during normal growth), the relation is independent of absolute chamber size. [52] It is also assumed that the magnitude and transmural distribution of stresses are the same in normal ventricles of different size. Systolic dysfunction with dilation is usually associated with a lower relative wall thickness; in contrast, chronic pressure overload produces an increment in wall thickness with little change in the chamber radius (a high relative wall thickness).[70] In untreated hypertensive patients, LV mass and relative wall thickness determinations may be used to subdivide Figure 4-9 Relationship between relative wall thickness (RWT, equivalent to the ratio of thickness to radius) and level of systolic pressure in patients with aortic stenosis (black circles). In normal hearts (open diamonds), RWT increases in direct proportion to the level of systolic pressure. Individuals with a higher thickness-to-radius ratio than predicted by the level of pressure are considered to have inappropriate (or excessive) hypertrophy; by contrast, individuals whose thickness-to-radius ratio is less than that predicted by the level of pressure have inadequate hypertrophy. In normal hearts the relationship between peak pressure (P) and RWT, as defined by Ford,[69] is RWT = 0.0027P.

the population into four general categories (Fig. 4-10) : 1. Concentric hypertrophy (elevations in both LV mass and relative wall thickness) 2. Eccentric hypertrophy (elevation in LV mass with normal relative wall thickness) 3. Concentric remodeling (normal mass but abnormally high relative wall thickness) 4. Normal LV mass and relative wall thickness

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In a population of untreated hypertensive patients, the majority had normal LV mass and normal relative wall thickness; concentric hypertrophy was the least common abnormal pattern observed. [68] What is the clinical relevance of the mass and geometry subcategories? Patients with concentric hypertrophy have a relatively high incidence of adverse cardiovascular and noncardiovascular events compared with patients with eccentric hypertrophy.[30] [31] [32] In addition, concentric geometry, even without hypertrophy, appears to be associated with adverse consequences during follow-up (see Table 4-1) , although not all studies have confirmed that the incremental risk is independent of LV mass. [71] Thus, in hypertensive disease, as noted earlier, incremental information regarding risk for both cardiovascular and noncardiovascular events is provided by assessing geometry as well as LV mass. The relative wall thickness may provide insight into the appropriateness of hypertrophy. There is occasionally more muscle mass than would be required for the observed pressure; thus, a very high relative wall thickness, such as is encountered in hypertrophic cardiomyopathies, "hypertensive hypertrophic cardiomyopathy of the elderly,"[72] [73] [74] [75] uncommonly in hypertension, and not infrequently in aortic stenosis,[70] indicates excessive or inappropriate LV hypertrophy. In our experience, relative wall thickness values greater than 0.8 are uncommon in aortic stenosis, but when present, they appear to represent inappropriate hypertrophy. Indeed, values exceeding 0.8 predict a systolic pressure in excess of 300 mm Hg, a pressure rarely seen, even in adults with aortic stenosis[70] (see Fig. 4-9) . Extreme concentric hypertrophy, with exceedingly high values for relative wall thickness, has been described in elderly patients undergoing aortic valve replacement for aortic stenosis.[25] The interaction among shape, load, and function is complex and important, because each one may influence the others. A decompensated heart clearly demonstrates abnormalities of all three—low relative wall thickness, high afterload, and reduced function—yet it is not possible to state which abnormality is primary. Does the ventricle dilate, thereby raising afterload and reducing pump performance, or is shortening impaired first, leading to dilation, which then raises afterload? Human studies shed little light because of the lengthy time course of disease and other confounding factors; animal studies suggest that all three events may occur in concert.[76] Two-Dimensional Echocardiography Two-dimensional echocardiography permits acquisition of data with

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excellent spatial orientation, because the left 73

Figure 4-10 Left ventricular (LV) volume, mass, and geometry, stress, and systolic shortening in various cardiac disorders. Different cardiac disorders are classified with respect to LV mass, volume, relative wall thickness (RWT), and volume/mass (V/M) ratio, as well as stress and shortening. (Redrawn from Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:385.)

ventricle can be sampled in real time at multiple levels. In many laboratories, therefore, 2D echocardiography is the principal noninvasive means for quantitation of LV volume as well as for the assessment of global and regional systolic function. LV mass and volume quantitation by 2D echocardiography requires high-quality images and true long- and short-axis images of the left ventricle. A variety of geometric models is used to approximate the shape of the left ventricle and to compute LV volumes, including the prolate ellipse model, the hemiellipse model, and others that represent a combination of geometric shapes. Detailed review of the geometric principles underlying these volumes for formulas may be found elsewhere.[64] [65] [77] This chapter emphasizes the applications most suited for clinical use. Mass

Theoretically, 2D echocardiographic assessment of LV mass can improve on the limitations of M-mode methods; mean wall thickness can be backcalculated from planimetered short-axis myocardial area, which helps avoid reliance on single-dimensional determinations. One of the most practical 2D methods for mass calculation, the area-length method, approximates the left ventricle as a cylinder-hemiellipsoid; volume is calculated for both the inner and outer "shells" (the LV cavity and total myocardial area, respectively), as shown schematically in Figure 4-11 : V = 5/6 A × L where A is planimetered short-axis area obtained at the high papillary muscle level and L is the LV length obtained from the apical four-chamber view; area and length measurements are made at end-diastole. In this way, total LV and internal (LV cavity) volume are determined; myocardial

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volume is the difference between the inner and outer shells. [65] [77] [78] [79] Myocardial volume is then multiplied by the specific gravity of myocardium (1.04 g/cc) to compute myocardial mass. The model has been validated by comparing echocardiographic and anatomic LV mass in 21 patients who underwent 2D echocardiographic studies shortly before death [79] there was an excellent correlation between anatomic and echocardiographic mass (r = 0.93 and SEE = 31 g). It is important to note that phantom-generated regression equations were used to correct clinical mass measurements for each 2D echocardiographic machine. Although more complicated 2D echocardiographic methods for mass determination have been associated with greater accuracy, the cylinder-hemiellipsoid area-length method represents a relatively simple and practical approach that yields acceptable results.[64] [65] Volume

As noted earlier, a variety of geometric approaches is described for the quantitation of LV volume from 2D 74

Figure 4-11 Schematic illustrating the technique used to calculate left ventricular (LV) mass with the area-length method. Endocardial and epicardial borders are traced (and papillary muscles excluded). Mean wall thickness (t) is back-calculated from the LV cavity area (A2 ) and total area (A1 ), and minor axis radius (b). The sum a + d is equivalent to the diastolic LV cavity length, which is measured from the apical four-chamber view. (Adapted from Schiller N, Shah P, Crawford M, et al: J Am Soc Echocardiogr 1989;2:358–367. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:389.)

echocardiography. There are theoretical advantages for use of the Simpson's rule algorithm, and this approach is preferable when ventricular shape is distorted, such as with an apical aneurysm. The Simpson's rule approach, also known as the method of discs, is predicated on the fact that the volume of the whole left ventricle (or of any object) may be computed as the sum of individual "slice" volumes. In general, the accuracy of the measurement varies directly with the number of slices:

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V is total volume (cavity or myocardial), A is planimetered area, and T is slice thickness. Myocardial volume is then multiplied by the specific gravity of myocardium to estimate myocardial mass. It is best to compute LV volume from two orthogonal apical views with the LV length divided equally along that length[74] [75] [76] [77] [78] [79] apical four- and two-chamber views at end-diastole should be recorded to maximize ventricular length. The use of the cylinder-hemiellipsoid (area-length) method for calculating the volume component represents a reasonable alternative to the method of discs. The method described by Tortoledo et al[80] allows for the computation of end-diastolic volume from 2D-derived minor- and majoraxis dimension and has been shown to correlate closely with single-plane angiographic volumes: EDV = (Dmax × Lmax × 3.42) − 6.44 where Dmax and Lmax are maximal minor- and major-axis dimensions

derived from apical views.

In general, LV volumes derived from 2D echocardiographic measurements are smaller than those obtained by contrast angiography.[64] [65] There are many explanations for these findings, including foreshortening of the maximal length of the left ventricle on 2D echocardiography; differences in measurement of the LV long axis; and the fact that angiographic contrast material fills intermyocardial interstices, contributing to overall LV cavity volume, whereas echocardiography does not account for this volume.[64] Geometry

Compared with M-mode echocardiography, 2D echocardiography offers improved spatial orientation, because the left ventricle can be sampled in real time at multiple levels. Accordingly, 2D echocardiography may be used to quantify the LV mass and chamber volumes of abnormally shaped ventricles, and, because measurements of LV length are possible, this technique provides more extensive description of LV geometry. Estimates of both the short axis/long axis ratio and the volume/mass ratio[81] [82] [83] [84] are possible with 2D echocardiography. In patients with normal LV mass and function, the short axis/long axis ratio ranges from 0.45 to 0.62.[82] [83]

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In untreated hypertensive patients with normal LV systolic function, the short axis/long axis ratios range from 0.52 ± 0.04 in patients with concentric remodeling to 0.63 ± 0.03 in patients with eccentric hypertrophy.[68] The short axis/long axis ratio also provides information regarding ventricular compensation in valvular heart disease. As in patients with dilated cardiomyopathy, in whom the ventricle becomes more spherical, patients with poorly compensated aortic stenosis and regurgitation (those with low EFs) tend to have higher short axis/long axis ratios. [84] A high ratio in turn alters the relationship of meridional to circumferential stresses, a change in the distribution of afterload that may affect overall pump performance[84] (see Fig. 4-10) . [84]

The end-diastolic volume/mass ratio in normal men and women, as defined by 2D echocardiography, is approximately 0.8.[83] It has been traditionally assumed that the ratio of LV volume to mass is relatively constant from 75

the most basal to the most apical slices of the left ventricle. A study using the technique of ultrafast CT, which can provide approximately eight tomographic slices through the left ventricle, showed that in normal subjects, the volume/mass ratio decreased from approximately 0.8 at the most basal slice, a finding consistent with results of 2D echocardiography, to approximately 0.25 at the most apical slice. LV mass exceeds LV volume at each slice location.[85] It is important to emphasize that 2D echocardiographic methods have limitations that militate against their routine use for quantitation in the clinical setting[64] [65] (Table 4-3) . M-mode echocardiography samples at approximately 1000 frames per second, whereas the frame rate for 2D echocardiography is orders of magnitude less: 30 to 60 frames per second under optimal conditions. There is considerable image degradation when stop frames are used, making precise endocardial definition problematic. Near-field artifact and poor lateral resolution make it difficult to reliably identify endocardium around the entire ventricular perimeter. Apical views often do not yield images of sufficient quality for manual tracing.[86] Computations tend to be tedious. It is likely that digital technology, which has permitted the growth of stress echocardiography, will be routinely used for LV volume quantitation; at present, however, it appears that most 2D quantitation performed clinically is still subjective.[86] [87]

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In view of the limitations discussed earlier, there is considerable interest in the development of online, beat-to-beat volumetric quantitation. One potential solution is the technique of automated boundary detection, which uses integrated backscatter to define a border between echocardiographic picture elements (pixels) assigned to myocardium or LV cavity.[88] [89] [90] Thus, the area of the LV cavity can be displayed for each frame, plotted with respect to time, and the fractional area change computed; the technique may be applied to images obtained from either parasternal or apical windows. Several validation studies have been performed with this technique[88] [89] [90] and have shown an excellent correlation between online LV cavity areas and offline manual planimetry of the corresponding 2D echocardiographic images (Fig. 4-12) . Further software development now permits online estimation of beat-to-beat LV volumes (using the arealength or TABLE 4-3 -- Limitations of Ultrasound Methods for Mass and Volume Quantitation General All methods require high-quality images with good endocardial definition Most methods require geometric assumptions about left ventricular shape and are applicable only to normally shaped hearts M-mode echocardiography Small errors in measurement may lead to large errors in mass/volume determinations May be insensitive to small changes in mass (20–40 g) observed in response to antihypertensive treatment Two-dimensional echocardiography Limited frame rate, making timing of cardiac events difficult Considerable degradation when images are stop-framed Apical images may foreshorten true left ventricular length Tedious, labor-intensive computations Simpson's rule methods), dV/dt, time to peak positive dV/dt, and time to peak negative dV/dt. Software upgrades, such as beat selection and signal averaging, may enhance the application of the automated border detection system for clinical use, which is currently somewhat limited by a significant percentage of technically inadequate studies[86] and other

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technical problems. Assuming these problems will be solved, automated border detection has particular promise for online quantitation of LV volumes obtained by intraoperative transesophageal echocardiography, in view of the generally excellent image quality with this technique. Other automated edge detection systems are in development, and this remains an area of active investigation. Another area of active research is that of three-dimensional (3D) echocardiography (see Chapter 10) . This technique promises to provide the most accurate ultrasound determination of LV volume, mass, and EF, largely because the need for geometric assumptions and on-axis views will be eliminated.[91] [92] [93] [94] Alternative Methods for Quantitation of Left Ventricular Structure and Function In addition to cardiac ultrasound, the clinician may use other noninvasive and invasive techniques to measure LV size and function. A brief review of some of the more commonly used techniques is therefore appropriate. Doppler Echocardiography

Routine Doppler measurements of flow velocity may be combined with echocardiographic dimensional data to determine stroke volume and cardiac output. [94] [95] [96] This technique is known as the time velocity integral (TVI) method. The appeal of this method is that, unlike M-mode and 2D echocardiographic measurements, TVI measurements do not require geometric assumptions about cardiac shape. To compute stroke volume using the TVI method, an integral of the systolic pulsed wave flow envelope in the aortic outflow tract is computed (Fig. 413) . To obtain this velocity spectrum, the transducer is placed in the apical position with the sample volume positioned at the level of the aortic valve annulus. Although the TVI may be obtained in other locations, such as the pulmonary artery or LV inflow, accuracy seems to be best with measurements made in the proximal ascending aorta.[65] The cross-sectional linear dimension of the proximal ascending aorta is obtained in the same approximate location that the pulsed or continuous wave Doppler velocity spectrum is recorded, using the parasternal long-axis window (see Fig. 413) . Stroke volume (SV) is then the product of the TVI and cross-sectional area of the aortic annulus, which is assumed to be circular:

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CSA = π(D/22 ) SV = CSA · TVI

76

Figure 4-12 Technique of automated boundary detection and its application to the study of cardiac volumes and ejection fraction (EF) in clinical practice. Top, A parasternal short-axis image with corresponding enddiastolic and end-systolic areas (EDA and ESA, respectively); the fractional area change for each beat is also displayed below the two-dimensional image. Bottom, In an apical four-chamber view, the corresponding beat-to-beat volume display is shown. From these measurements, the EF can be computed beat to beat. End-diastolic and end-systolic volumes (EDV and ESV, respectively) are given in milliliters.

where CSA is the cross-sectional area of the aortic annulus, D is the linear dimension of the annulus, and TVI is the time velocity integral. Stroke volume and cardiac output obtained by the TVI method correlate well with results of concurrent thermodilution cardiac output determinations in patients who were without left-sided valvular regurgitation.[95] [96] The Doppler TVI method is highly dependent on accurate measurements of aortic annular diameter, because the CSA formula involves squaring the annular dimension; it is also assumed that the Doppler beam is oriented parallel to flow. This method can be particularly useful for following changes in a single patient—beat to beat, or over weeks to months. Doppler echocardiographic assessments of LV function do not depend on measurements of ventricular size (and thus avoid the attendant geometric assumptions and sources of error); they rely on information derived from flow velocities.[96] This information includes measurement of LV stroke volume, cardiac output, and peak flow velocity of aortic ejection, all of which, being ejection phase indices, are dependent on afterload. One approach to the noninvasive assessment of dP/dt has used the continuous wave profile of the mitral regurgitant flow.[97] [98] [99] As we have seen, stroke volume, and thereby cardiac output, may be calculated by measuring the area under the flow velocity contour and multiplying it by the cross-sectional

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77

Figure 4-13 Calculation of cardiac output using the time velocity integral (TVI) method. The continuous wave Doppler-derived TVI (also called velocity time integral [VTI]) is displayed. The cross-sectional area is 3.14 cm2 (π times the square of the annular radius, which is 1 cm2 in this instance) and the TVI is 24.7 cm by planimetry. The stroke volume is 78 cc per beat by equation, yielding a cardiac output of 4.3 L/min at the patient's heart rate of 55.

area of the annulus.[94] [95] Accuracy is dependent on recording velocity parallel to flow and, most importantly, on the aortic diameter measurement used to calculate the cross-sectional area. This method also requires that there be no significant aortic or mitral valve disease. Aortic acceleration and peak flow velocity are both reduced in cardiomyopathy,[94] but this has not received widespread clinical acceptance as a diagnostic tool. Magnetic Resonance Imaging

In many respects, MRI is the ideal method to quantitate LV mass and volume. It combines the attributes of ultrafast CT (noninvasive and permitting true tomographic imaging throughout the entire cardiac volume) with several unique advantages. MRI does not require contrast administration or ionizing radiation, and there is no limitation to image plane selection; thus, the heart may be imaged not only in the familiar contrast ventriculography views but also in the long- and short-axis planes used in standard transthoracic echocardiography. MRI usually provides images with excellent contrast between myocardium and the blood pool so that manual or even semiautomated computerized mass and volume quantitation is possible.[100] For these reasons, MRI has provided the most accurate noninvasive estimates of LV mass and volume to date,[101] even in ventricles distorted by myocardial infarction.[102] A more recent advance, gradient-echo magnetic resonance techniques, displays the heart in cine loop fashion at up to 64 frames per cardiac cycle; this technique can be used to quantitate EF and regional function and to estimate the severity of valvular regurgitation. [103] [104] [105] Although MRI can be used to estimate mass, volume, and EF,[36] [106] [107] ultrasound and radionuclide techniques are currently much more commonly used for this purpose. If technologic advances in MRI lead to shorter scan times and reduced scan costs and permit routine, accurate assessment of coronary anatomy, it is not hard to conceive that this technique will be

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widely used to provide a comprehensive assessment of cardiac structure and function. At present, however, the use of MRI in adult clinical practice is usually confined to answering questions regarding anatomic abnormalities, such as disorders involving the aorta, the pericardium, congenital heart disease, cardiac masses, and RV dysplasia.[108]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Systolic Function As shown in Figure 4-5 , the major factors affecting LV systolic performance and function are preload, afterload, myocardial contractile (or inotropic) state, and heart rate. Nonuniform contraction can also be important; thus, regional variations in mechanical function, as occur in coronary heart disease or even with electronic ventricular pacing, can affect stroke volume. Only if synchronous contraction is present, heart rate is stable, and loading conditions are constant does a change in performance indicate a change in contractility. These traditional concepts relating preload, afterload, and contractility are generally considered in the assessment of an acute response to altered hemodynamic conditions. Thus, an isolated increase in preload is said to produce an increment in performance through the Frank-Starling mechanism, whereas an isolated increase in afterload is said to produce 78

TABLE 4-4 -- Clinical Methods Used to Evaluate Systolic Function Ejection fraction Fractional shortening at endocardium and midwall Stress-shortening relations Pressure-volume analysis a decrease in the stroke volume (or EF) by virtue of the inverse forceshortening relation. Unfortunately, in the intact heart, especially in patients with chronic heart disease, it is virtually impossible to produce an isolated change in preload or afterload. For example, nitrates are classified as vasodilators and agents that primarily affect preload, but the associated decrease in LV volume and arterial pressure leads to a reduction in

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afterload. Likewise, a pure arterial vasodilator also reduces heart size (and preload) by augmenting the stroke volume. It is apparent, therefore, that preload and afterload are intimately related, and that it is an oversimplification to assume that isolated changes in preload or afterload occur in patients with chronic heart disease. Most interventions that produce an acute change in preload or afterload also result in a length-dependent change in intrinsic myocardial contractility, [109] which further complicates the assessment of global systolic function. Therefore, acute changes in preload produce changes in performance through the Frank-Starling mechanism and through this length-dependent activation. The importance of this phenomenon in the chronically enlarged or diseased heart is unknown. It is usually not difficult to detect an acute change in LV performance or contractile function, but it is harder to determine the major mechanism or mechanisms responsible for the change. Chronic changes in LV volume, mass, and geometry are even more difficult to interpret because such changes tend to limit our use of the traditional interrelationships of preload, afterload, and contractility. Indeed, there is no acceptable index of basal contractility that can be used in patients with chronic heart disease, nor can LV end-diastolic pressure or even absolute end-diastolic volume be used as a surrogate for fiber stretch in chronically diseased hearts. For these and other reasons, the evaluation of contractile function and the distinction between a compensated and a decompensated ventricle often rest on empiric observations coupled with analyses based on physiologic principles. In the following section the use and limitations of several clinically useful approaches to the evaluation of contractile function are discussed (Table 4-4) . Ejection Fraction The EF is perhaps the most widely used measure of LV systolic function. This parameter is defined as the change in LV volume (i.e., stroke volume) divided by the initial volume (i.e., end-diastolic volume): EF = (EDV − ESV)/EDV where EDV is end-diastolic volume and ESV is end-systolic volume; these may be obtained by either M-mode or 2D echocardiography. In addition, there are other published algorithms that use minor-axis dimensions and an estimate of long-axis shortening derived from 2D echocardiography to

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derive EF directly.[110] The EF, representing volume strain, is appropriately normalized; it can be used as an index of systolic function that is independent of the size of the patient or the ventricle. The normal ventricle ejects more than half of its end-diastolic volume; the average EF, as determined by 2D echocardiography, varies from 63% to 69%.[81] In patients with coronary disease or idiopathic cardiomyopathy, it is generally conceded that values in the range of 40% to 50% are abnormal but of little clinical significance.[1] However, in patients with mitral regurgitation, an EF in this range may denote significant depression in contractile function.[111] Hemodynamic Determinants of the Ejection Fraction

Acute changes in LV loading conditions are known to exert a major influence on the EF. Thus, an acute increase in preload and/or a decrease in afterload results in a higher EF. By contrast, an acute decrease in preload and/or an increase in afterload reduces the EF. Under such circumstances, it can be difficult to decide whether a change in contractility has occurred. If, however, alterations in load are associated with a change in the EF that is opposite to the expected result, it is possible to conclude that a simultaneous change in contractility (i.e., inotropic state) also occurred. For example, an increased EF in the presence of increased afterload likely represents increased contractility, because an increase in afterload would normally be expected to cause a lower EF. Despite its load sensitivity, the EF can therefore provide useful information, even during acute hemodynamic interventions. In this regard, the concept of preload reserve is important. In patients with chronic heart disease, the EF can be an important index of contractile function, in part because of its sensitivity to increased afterload. As LV dysfunction develops and dilation occurs, afterload tends to increase, as dictated by the Laplace relationship, and the EF falls.[55] Such a decline in the EF can be useful in identifying LV dysfunction very early in the course of a disease; it does not, however, identify the underlying mechanism or mechanisms. Therefore, in patients with chronic heart disease, the EF must be interpreted with consideration of the magnitude and time course of changes in loading conditions that evolve during progression of the disease.[111] For example, very early in the course of aortic regurgitation, LV preload and afterload tend to be increased; these changes affect the EF in opposite directions, and it remains within the normal range. As the ventricle remodels and eccentric hypertrophy develops, the loads

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normalize despite LV enlargement; if myocardial contractility is preserved, the EF remains normal. As the hemodynamic burden increases (or contractile dysfunction develops), the afterload increases and the EF decreases. Thus, 79

even a modest decline in the EF can be an important early marker of LV dysfunction. In decompensated aortic stenosis, LV systolic pressures increase in parallel with an increase in wall stress, as predicted by the Laplace relationship. As wall stress progressively rises, EF decreases. Carabello et al[21] have shown that patients with critical aortic stenosis, congestive heart failure, and decreased EF owing to high levels of wall stress ("afterload mismatch") may anticipate improvement in systolic function following afterload reduction associated with valve replacement[21] [111] [112] (Fig. 4-14) . In contrast, those patients whose reduction in EF is out of proportion to the high levels of wall stress are thought to have developed cardiomyopathic changes in addition to excess afterload; such patients generally do not experience functional improvement after valve replacement.[21] [112] This subgroup of patients may be identifiable by a low transvalvular gradient (usually less than 30 mm Hg) in association with severe stenosis of the aortic valve.[21] In the clinical setting, making the proper diagnosis can be challenging. Because the Gorlin equation is flow dependent, patients with primary LV dysfunction and coexistent (mild) calcific aortic stenosis can be difficult to distinguish from those with LV dysfunction caused by unrelieved severe aortic stenosis. Dobutamine echocardiography is increasingly used to help make this distinction and to assess prognosis.[113] Fractional Shortening and Related Indices The fractional change (percentage) in minor-axis dimension is a widely used index of systolic performance; fractional shortening is usually derived from M-mode echocardiographic tracings (see Fig. 4-8) . This measurement Figure 4-14 Relationship between ejection fraction (EF) and endsystolic stress in patients undergoing cardiac catheterization for critical aortic stenosis and severe congestive heart failure. All patients were free of significant coronary artery disease. Patients falling close to the regression line relating EF to stress (open circles) are thought to have

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LV dysfunction owing to excessive wall stress (afterload). These patients experienced a gratifying functional recovery after aortic valve replacement. In contrast, the four subjects who fell below the regression line (dark circles) have depressed EF beyond that predicted by the level of afterload and are considered to have depressed contractility as well. These patients did not experience functional recovery after valve replacement. (Adapted from Carabello BA, Green LH, Grossman W, et al: Circulation 1980;62:42. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:416.)

is particularly useful because LV circumferential fiber shortening is responsible for most of the stroke volume. In this regard, fractional shortening is similar to the EF; in the absence of focal wall motion abnormalities, the two indices correlate closely, although the absolute values for fractional shortening are obviously less than that for EF. Fractional shortening, measured at the endocardium (FSendo [%]), is

calculated as

FSendo = 100 × (LVIDd − LVIDs )/(LVIDd ) Normal values for FSendo exceed 30%. As is the case with EF, FSendo is

influenced by factors in addition to contractile state and should be interpreted in the light of loading conditions; increases in preload and decreases in afterload increase fractional shortening.

A refinement of fractional shortening, the velocity of circumferential shortening (Vcf ) reflects the mean velocity of ventricular shortening at the level of the LV minor axis, and it is also calculated from M-mode echocardiographic dimensions: Vcf = FSendo /ET where ET is the ejection time derived either from the duration of aortic valve opening, from the period of aortic forward flow (pulsed or continuous wave Doppler), or from a carotid pulse tracing.[65] The Vcf is expressed in circumferences per second (the lower limit of normal is 1.1 c/sec); because Vcf measures the velocity rather than the extent of shortening, it is

theoretically a more sensitive index of contractility than FSendo and may be

an earlier marker of abnormality in chronic disease states. As with the EF and fractional shortening, this parameter is normalized for LV chamber size

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and may be used to make comparisons between patients. Vcf has been

shown to be

80

relatively insensitive to acute changes in preload.[114] [115] However, it is also possible that this preload insensitivity may be a result of acute elevations in preload increasing heart size (and pressure) and thus increasing afterload. Thus, augmentation in afterload may offset the increased shortening caused by the increased preload. A further refinement in Vcf , the rate-corrected

Vcf ,[64] [65] [113] may be obtained by dividing Vcf by the square root of the

preceding RR interval. This index is designed to allow comparison between patients with differing heart rates. The incremental value of velocity of shortening methods (e.g., Vcf , rate-corrected Vcf ), compared with extent of shortening (e.g., fractional shortening) may be marginal.[116]

Standard M-mode measurements also may be used to estimate circumferential fractional shortening at the midwall (FSmw [%]), using the

same standard M-mode echocardiographic measurements. FSmw is

calculated using a modified two-shell cylindrical model.[37] This method assumes constant LV mass throughout the cardiac cycle and does not require the assumption that inner and outer wall thickening fractions are equal.[37] [117] [118] Most important, in contrast to FSendo , FSmw is not

influenced by LV geometry (relative wall thickness) and therefore has particular use in the evaluation of the hypertrophied heart with increased relative wall thickness (see Fig. 4-16) . Normal systolic function includes the excursion of the mitral annulus toward the relatively immobile apex; thus, the long axis of the left ventricle shortens during systole. An assessment of the longitudinal (or long-axis) shortening of the left ventricle can be made using M-mode measurements under 2D echocardiographic guidance.[119] [120] Using the apical window, the transducer is oriented to maximize apical endocardial to mitral annular distance. M-mode tracings are made with the cursor directed through the lateral aspects of the mitral annulus; recordings of multiple cardiac cycles are made on strip chart paper,[118] [120] and mitral annular excursion is normalized for initial diastolic length. Several investigators have used mitral annular excursion and long-axis

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shortening as a descriptor of ventricular systolic function. Keren and LeJemtel [119] showed that the principal systolic mitral annular excursion toward the apex coincides with the systolic component of pulmonary venous flow; this systolic phase of mitral annular motion is markedly attenuated in patients with dilated cardiomyopathy. Jones and Gibson[120] showed that, in the normal left ventricle, mitral annular excursion toward the apex precedes circumferential shortening, leading to a more spherical LV shape early in systole.[120] These investigators also showed that mitral annular descent was reduced in patients with mitral disease who had undergone valve replacement.[120] In patients with "compensated" hypertensive heart disease, that is, LV hypertrophy and normal EF, longaxis shortening is depressed compared with normal controls.[118] Similar findings have been reported using the technique of MRI tagging, as described later.[121] Other ultrasound techniques have been employed in recent years to investigate LV systolic and diastolic function. Doppler tissue imaging applies a modification of pulsed Doppler methods to the assessment of myocardial systolic and diastolic motion.[122] [123] In this way, the velocity of myocardial tissue or of the mitral annulus, and not just the total excursion, may be measured. The velocity of the diastolic mitral annular motion has been applied to the study of LV diastolic function (see Chapter 6) .[122] [123] Nagueh et al[123] have demonstrated that mitral annular velocity information, when coupled with more traditional mitral inflow velocity data, can be used to reliably predict diastolic pressure. Similarly, more qualitative assessment of ventricular function can be obtained using color Doppler imaging.[124] Stress-Shortening Relations On the basis of extensive experimental and clinical experience, the myocardial force-velocity relation provides a framework for evaluating the contractile state and function of the left ventricle. A most important advantage of assessing function with a stress-shortening analysis is that it avoids afterload dependency, the major limitation of the EF alone. Unfortunately, end-diastolic fiber length (or the degree to which the resting fiber is stretched) is difficult if not impossible to measure; LV end-diastolic pressure or volume or even wall stress fails to provide an absolute measure of fiber length. For this reason, length is generally omitted and the simpler force-velocity or stress-shortening relation is used as a substitute for the force-length-velocity relation. Both systolic stress (the force per unit cross-sectional area of myocardium)

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and shortening (fractional change in length or volume) are appropriately normalized and allow accurate comparisons among hearts of different sizes. [125] Therefore, contractile function in pressure overload hypertrophy, volume overload hypertrophy, and dilated as well as hypertrophic cardiomyopathies may be assessed within the framework of the stressshortening relation. A major limitation of the simple stress-shortening analysis is the assumption that differences in resting length do not substantially influence the stress-shortening relation. In this regard, a distinction must be made between acute interventions and chronic steady-state conditions. Changes in fiber length and appropriate use of preload reserve certainly occur during acute or short-term hemodynamic interventions. However, under chronic conditions (e.g., chronic compensated volume overload), this may not be the case.[126] After the acute or subacute phase, when the compensatory remodeling process is complete and chronic changes in LV volume and mass are established, end-diastolic fiber length may not be substantially different from normal.[127] In pressure overload or concentric hypertrophy, end-diastolic sarcomere lengths may even be less than normal.[128] [129] In such hearts, high chamber stiffness apparently limits use of the preload reserve. It appears, therefore, that assumptions about chronic changes in fiber length are unwarranted. Midwall Stress-Shortening Analysis

The analysis of midwall stress-shortening relations may be superior to that of endocardial stress-shortening relations, especially for comparison of contractile state between 81

hearts differing in LV geometry ( Fig. 4-15 and Fig. 4-16 ). The first advantage of midwall measurements is that the (circumferential) stress vector and the shortening transient are oriented in the same direction, because circumferential fibers predominate in the midwall of the LV.[130] [131] Second, the values for midwall (but not endocardial) shortening are consonant with experimental data indicating that myocardial fibers shorten by approximately 15% to 20%. Circumferential midwall strain ranges from 9% ± 2% in the anesthetized, open chest dog (implanted markers[132] ) to 30% ± 7% in conscious humans (MRI tagging).[133] We believe that the experimental results represent an underestimate of strain, but MRI

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techniques likely overestimate true myocardial shortening. All methods indicate that circumferential shortening at the endocardium exceeds that seen at the midwall. Third, significant differences in chamber radius or circumference may be caused by differences in LV relative wall thickness. [37] By contrast, midwall shortening is independent of relative wall thickness. We believe that studies designed to assess myocardial contractile function should ideally be based on midwall stress-shortening data, not on endocardial Figure 4-15 Left ventricular (LV) shortening in normal LV (top) and in concentric left ventricular hypertrophy (LVH) (bottom), illustrating the added insight into systolic function provided by midwall shortening. LV endocardial dimension (LVID), wall thickness (Th), relative wall thickness (RWT), and LV mass are measured in diastole (d). The systolic dimensions (s) are shown at right. The midwall circumference is indicated by the dotted line. Systolic shortening refers to the percent reduction in the circumference that occurs from diastole to systole. FS endo, the percent reduction of the endocardial circumference (dark inner circle) and FS mw, the percent reduction of the midwall circumference (dotted line), are in the normal range. However, concentric LVH (elevated RWTd and LV mass) is associated with an increased value for FS endo, but a diminution in FS mw, compared with normal LV, owing to the nonuniformity of systolic thickening. Myocardial fibers in the inner (subendocardial) layers contribute more to systolic thickening than those in the outer (epicardial) layers; this effect is exaggerated when concentric geometry is present.

shortening parameters, which may be contaminated by altered ventricular geometry. An example of the usefulness of a midwall stress-shortening analysis is shown in Figure 4-17 . The endocardial stress-shortening relation is normal in patients with pressure overload hypertrophy owing to aortic stenosis; thus, LV function is normal. By contrast, the midwall stress-shortening relation is abnormal in approximately one third of the patients, indicating a subtle depression of myocardial function in these individuals. Pressure-Volume Analysis By plotting LV pressure against volume throughout the entire cardiac cycle, a pressure-volume loop can be generated (Fig. 4-18) . The height of the loop is determined by systolic pressure, and its width is determined by stroke volume; thus, the area within the loop is a measure of stroke work. By definition, such loops incorporate end-diastolic and end-systolic volumes; thus, the stroke volume and the EF are displayed. The bottom

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limb of the loop (i.e., the diastolic pressure-volume curve) 82

Figure 4-16 Endocardial and midwall stress-shortening relations in pressure overload hypertrophy. The top panel shows fractional shortening at the endocardium versus circumferential stress in a consecutive series of patients with severe, symptomatic aortic stenosis who were free of segmental wall motion abnormalities. All patients fall within the 95% confidence intervals of the stress-shortening relationship, suggesting normal contractile function. In contrast, the bottom panel shows midwall shortening versus circumferential stress in the same population. A substantial portion (approximately one third) of these patients demonstrates a diminution in contractility by the midwall analysis.

describes ventricular diastolic compliance. Therefore, the pressure-volume loop can provide a simple yet comprehensive description of ventricular pump function. [134] Such loops can be generated from a variety of techniques that provides ventricular volume data in conjunction with LV pressure. [135] [137] Online, beat-to-beat determinations of LV volumes with automated edge detection can be combined with LV pressure measurements to yield real-time pressure-volume loops, useful in both clinical and research settings[137] [138] [139] (Fig. 4-19) . Pressure-dimension loops derived from M-mode echocardiographic data are adequate surrogates for pressurevolume loops, and they provide the added advantage of simplicity and widespread availability. If only the systolic portion is of interest, calibrated carotid pulse tracings may be substituted for intraventricular pressure, and the data can be obtained entirely noninvasively.[43] By manipulating LV volume and/or arterial pressure, multiple coordinates of the maximal ratio of pressure to volume or dimension (which occurs near end-ejection) can be obtained; these coordinates exhibit a nearly linear direct relation. The slope of this relation (Emax ) is relatively insensitive to

acute changes in loading conditions. The relation shifts upward and to the left during positive inotropic interventions, and it shifts downward to the right when the ventricle is depressed; the slope of the relation generally increases with the former and decreases with the latter ( see Fig. 4-18 and Fig. 4-19 ).

This end-systolic index of contractility is sensitive to acute changes in contractility, but its reliability is diminished in chronically diseased hearts, especially dilated hearts. In large ventricles the end-systolic pressure-

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volume curve can be displaced down and to the right (depressed Emax ), in

the absence of a depressed contractility. For this reason, Emax should be

normalized for heart size,[140] [141] [142] as illustrated in Figure 1-19 . In this example of chronic aortic regurgitation, there is modest LV enlargement, the end-systolic volume is less than 60 mL/m2 , the EF is normal, and the total stroke volume is high. Such data indicate that the ventricle is compensated, albeit larger than normal. However, the depressed slope of the end-systolic pressure-volume relation inappropriately suggests depressed contractility. These disparate conclusions can be reconciled if the effect of chamber dilation on Emax is considered.[140] [141] [142] Thus, if the slope is normalized for chamber size, it approximates that seen in the normal heart.

Recognizing this limitation, end-systolic stress-volume or stress-dimension relations should not be a major criterion for the diagnosis of chronic contractile dysfunction. Certainly, it is not useful as a measure of basal contractility and it has limited applicability in comparisons among normal and diseased hearts. The raw pressure-volume or stress-dimension data provide important diagnostic information and, with few exceptions, the simple measurement of the end-systolic volume or dimension identifies a depressed ventricle. An example of the usefulness of echocardiography pressure-dimension loops is shown in Figure 4-20 . This example illustrates the effect of mitral valve replacement on LV size and function in compensated and decompensated chronic mitral regurgitation. In compensated mitral regurgitation the chamber is enlarged but the end-systolic dimension is only 42 mm, systolic stress is minimally increased, and the fractional shortening is normal (35%). After valve replacement the stress-dimension loop returns to near normal. In decompensated mitral regurgitation the end-diastolic and end-systolic volumes are markedly increased and fractional shortening is low (26%). After mitral valve replacement there is persistent LV enlargement and a further decline in shortening. A similar analysis has been used in patients with aortic regurgitation.[143] (See also Chapter 18.)

83

Figure 4-17 Left ventricular pressure-volume (P-V) loops. The dashed

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line indicates a normal ventricle. An acute decrease in contractile state is shown; the loop is displaced to the right, and the end-systolic P-V line shifts downward and to the right. The effect of an acute increase in contractile state is illustrated by the line on the left; the slope of the end-systolic P-V line is increased (the corresponding loop is not shown). (From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:418.) Figure 4-18 Pressure-volume loops with inferior vena caval occlusion at baseline and with 3 µg/kg/min of dobutamine infusion in an intact canine model. Volume was assessed online with transesophageal echocardiographic border detection using a Simpson's rule algorithm. End-systolic elastance (Ees ), or the slope of the end-systolic P-V relation, increased with positive inotropic modulation, which is consistent with increased contractility. (Courtesy of Dr. John Gorcsan III.) Figure 4-19 LV pressure-volume loops and end-systolic pressure volume lines illustrate the effects of chronic aortic regurgitation on ventricular size and function. Moderate ventricular enlargement is present, ejection fraction (EF) is normal, and stroke volume (SV) is high. Such data are consistent with compensated aortic regurgitation. However, the slope of the end-systolic P-V relation (Emax ) is reduced. This apparent inconsistency may be resolved by considering the effect of chamber size on Emax . If the slope is normalized for chamber size (end-diastolic volume), the result indicates that Emax is similar in the two ventricles. (Adapted from Shen WF, Roubin G, Choong CYP, et al: Circulation 1985;71:31–38. From Aurigemma GP, Gaasch WH, Villegas B, Meyer TE: Curr Probl Cardiol 1995;20:420.)

84

Figure 4-20 Left ventricular (LV) stress-dimension loops in two cases of mitral regurgitation, before (Preop) and after (Post) mitral valve replacement. In the left panel the preoperative loop indicates compensated ventricular function; the end-diastolic dimension is 6.5 cm, the end-systolic dimension is 4.2 cm, systolic stress is minimally elevated, and fractional shortening is normal (35%). After valve replacement the end-diastolic dimension and end-systolic wall stress return to normal, but fractional shortening decreases (29%). In the right panel the preoperative loop indicates a decompensated ventricle; the end-diastolic and end-systolic dimensions are markedly increased (7.3 cm and 5.4 cm, respectively) and fractional shortening is low (26%). After valve replacement there is persistent LV enlargement and a further decline in fractional shortening. These examples illustrate the LV response to mitral valve replacement in

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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101. Maddahi J, Crues J, Berman DS, et al: Noninvasive quantification of left ventricular myocardial mass by gated proton nuclear magnetic resonance imaging. J Am Coll Cardiol 1987;10:682–692. 102. Shapiro EP, Rogers WJ, Beyar R, et al: Determination of left ventricular mass by

magnetic resonance imaging in hearts deformed by acute infarction. Circulation 1989;79:706–711. 103. Utz JA, Herfkens RJ, Heinsimer JA: Cine MR determination of left ventricular

ejection fraction. AJR Am J Roentgenol 1987;148:839–849. 87

104. Aurigemma G, Reichek N, Schiebler M, Axel L: Evaluation of mitral

regurgitation by cine magnetic resonance imaging. Am J Cardiol 1990;66:621–625. 105. Aurigemma G, Reichek N, Schiebler M, Axel L: Evaluation of aortic

regurgitation by cardiac cine magnetic resonance imaging: Planar analysis and comparison to Doppler echocardiography. Cardiology 1991;78:340–347. 106. Cranney G, Lotan C, Dean L, et al: Left ventricular volume measurements using

cardiac axis nuclear magnetic resonance imaging. Circulation 1990;82:154–163. 107. Aurigemma GP, Davidoff A, Silver K, Boehmer J: Left ventricular mass

quantitation using single-phase cardiac MRI. Am J Cardiol 1992;70:259–262. 108. Carlson MD, White RD, Trohman RG, et al: Right ventricular outflow tract

ventricular tachycardia: Detection of previously unrecognized anatomic abnormalities using cine magnetic resonance imaging. J Am Coll Cardiol 1994;24:720–727. 109. Allen DG, Kentish JC: The cellular basis of the length tension relation in cardiac

muscle. J Mol Cell Cardiol 1985;17:821–828. 110. Quinones MA, Waggoner AD, Nelson JG, et al: A new simplified and accurate

method for determining ejection fraction with two dimensional echocardiography. Circulation 1981;64:744–752. 111. Ross J Jr: Afterload mismatch in aortic and mitral valve disease: Implications for

surgical therapy. J Am Coll Cardiol 1985;5:811–826.

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112. St. John Sutton M, Plappert T, Spiegel A, et al: Early post-operative changes in

LV chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: A prospective twodimensional echocardiographic study. Circulation 1987;76:77–89. 113. DeFilippi CR, Willett DL, Brickner ME, et al: Usefulness of dobutamine

echocardiography in distinguishing severe from non-severe valvular aortic stenosis in patients with depressed left ventricular function and low transvalvular gradients. Am J Cardiol 1995;75:191–194. 114. Colan SD, Borow KM, Neuman AS: The left ventricular end-systolic wall stress-

velocity of fiber shortening relation: A load independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715–724. 115. Quinones MA, Gaasch WH, Alexander JK: Influences of acute changes in

preload, afterload, contractile state, and heart rate on ejection and isovolumic indices of myocardial contractility in man. Circulation 1976;53:293–300. 116. Aurigemma GP, Meyer TE, Sharma M, et al: Evaluation of extent of shortening

versus velocity of shortening at the endocardium and midwall in hypertensive heart disease. Am J Cardiol 1999;83:792–794. 117. Shimizu G, Zile M, Blaustein AS, Gaasch WH: Left ventricular chamber filling

and midwall fiber lengthening in patients with left ventricular hypertrophy: Overestimation of fiber velocities by conventional midwall measurements. Circulation 1985;71:266–272. 118. Aurigemma GP, Silver KH, Fox MA, et al: Depressed midwall and long axis

shortening in hypertensive left ventricular hypertrophy with normal ejection fraction. J Am Coll Cardiol 1995;26:195–202. 119. Keren G, LeJemtel T: Mitral annulus motion: Relation to pulmonary venous and

transmitral flows in normal subjects and in patients with dilated cardiomyopathy. Circulation 1988;78:621–629. 120. Jones CR, Gibson D: Functional importance of the long axis dynamics of the

human left ventricle. Br Heart J 1990;65:215–220. 121. Palmon L, Reichek N, Yeon S, et al: Intramural myocardial shortening in

hypertensive left ventricular hypertrophy with normal pump function. Circulation 1994;89:122–131. 122. Sohn DW, Chai IH, Lee DJ, et al: Assessment of mitral annulus velocity by

Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am

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Coll Cardiol 1997;30:474–480. 123. Nagueh SF, Middleton KJ, Kopelen HA, et al: Doppler tissue imaging: a

noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527–1533. 124. Sutherland GR, Stewart MJ, Groundstroem KWE, et al: Color Doppler

myocardial imaging: A new technique for the assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 125. Mirsky I, Pasternac A, Ellison RC: General index for the assessment of cardiac

function. Am J Cardiol 1972;30:483–491. 126. Ross J Jr: Adaptations of the left ventricle to chronic valvular overload. Circ Res

1974;35:64–70. 127. Ross J Jr, Sonnenblick EH, Taylor RR, et al: Diastolic geometry and sarcomere

lengths in the chronically dilated canine left ventricle. Circ Res 1971;28:49–56. 128. Sonnenblick EH: Correlation of myocardial ultrastructure and function.

Circulation 1968;38:29–44. 129. Laks MM, Morady F, Swan HJC: Canine right and left ventricular cell and

sarcomere lengths after banding the pulmonary artery. Circ Res 1969;24:705–710. 130. Greenbaum R, Ho S, Gibson D: Left ventricular fibre architecture in man. Br

Heart J 1981;45:248–263. 131. Streeter D, Spotnitz H, Patel D: Fiber orientation in the canine left ventricle

during diastole and systole. Circ Res 1969;24:339–346. 132. Villareall FJ, Lew WYW, Waldman LK et al: Transmural myocardial deformation

in the ischemic canine left ventricle. Circ Res 1991;68:368–381. 133. Clark NR, Reichek N, Bergey P, et al: Circumferential myocardial shortening in

the normal human left ventricle. Assessment by magnetic resonance imaging using spatial modulation of magnetization. Circulation 1991;84:67–74. 134. Sagawa K, Maughan L, Suga H, Sunagawa K: Cardiac Contractility and the

Pressure-Volume Relationship. New York, Oxford University Press, 1988. 135. Magorien DJ, Shaffer P, Bush CA, et al: Assessment of left ventricular pressure-

volume relations using gated radionuclide angiography, echocardiography and

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micromanometer pressure recordings. Circulation 1983;67:844–852. 136. McKay RG, Aroesty JM, Heller GV, et al: Left ventricular pressure-volume

diagrams and end-systolic pressure-volume relations in human beings. J Am Coll Cardiol 1984;3:301–312. 137. Gorcsan J III, Gasior TA, Mandarino WA: Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressure-area relations. Circulation 1994;89:180–190. 138. Gorcsan J III, Denault A, Gasior TA, et al: Rapid estimation of LV contractility

from end systolic relations by echocardiographic automated border detection and femoral artery pressure. Anesthesiology 1994;81:553–562. 139. Katz WE, Gasior TA, Reddy SC, Gorcsan J III: Utility and limitations of biplane

transesophageal echocardiography for estimation of LV stroke volume. Am Heart J 1994;128:389–396. 140. Sagawa K: The ventricular pressure-volume diagram revisited. Circ Res

1978;43:677–680. 141. Bogen DK, Ariel Y, McMahon TA, Gaasch WH: Measurement of peak systolic

elastance in intact canine circulation with servo pump. Am J Physiol 1985;249:H585– H593. 142. Berko B, Gaasch WH, Tanigawa N, et al: Disparity between ejection and end

systolic indexes of left ventricular contractility in mitral regurgitation. Circulation 1987;75:1310–1319. 143. Gaasch WH, Carroll JD, Levine HJ, et al: Chronic aortic regurgitation: Prognostic

value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio. J Am Coll Cardiol 1983;1:775–782. 144. Gottdiener JS, Livengood SV, Meyer PS, et al: Should echocardiography be

performed to assess the effects of antihypertensive therapy? Test-retest reliability of echocardiography for measurement of left ventricular mass and function. J Am Coll Cardiol 1995;25:424–430. 145. Dahloff B, Pennert K, Hanson L: Reversal of left ventricular hypertrophy in

hypertensive patients: A meta-analysis of 109 treatment studies. Am J Hypertens 1992;5:95–110.

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88

Chapter 5 - Quantitative Evaluation of Regional Left Ventricular Systolic Function Florence H. Sheehan MD

Two-dimensional (2D) echocardiography is well suited to the assessment of regional left ventricular systolic function for both clinical and research applications. Every region of the ventricle can be examined at high spatial and temporal resolution, allowing a more comprehensive visualization than with other imaging modalities. Furthermore, echocardiography is portable, safe, and relatively inexpensive, so serial studies can be obtained without risk to the patient to follow disease progression or response to therapy. Quantitative methods have been developed for measurement of systolic function both for diagnosis and for evaluation of treatment efficacy and prognosis in patients with ischemic heart disease. These methods also allow analysis of the structure-function relationship of the left ventricle and mitral valve, of asynchrony in the timing of contraction, and of the heart's compensatory response to disease processes. Thus, echocardiographic examination offers high informational content for both clinical and research applications.

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Semiquantitative Assessment of Regional Systolic Function In clinical practice, visual assessment provides a rapid evaluation of regional systolic function. In each imaging plane, the ventricular contour is divided into several segments. Each segment is assigned a numeric value that indicates its degree of asynergy. Methodology Segmentation of Ventricle

Several schemata have been devised for dividing the ventricle into 14 to 20 segments.[1] [2] The American Society of Echocardiography's most recent recommendation is for a 16-segment model (Fig. 5-1) .[2] The goal is to obtain sufficient detail to characterize the pattern of dysfunction 89

Figure 5-1 Sixteen-segment model for visual assessment of regional wall motion, recommended by the American Society of Echocardiography. A, anterior; AL, anterolateral; AS, anteroseptal; PL or IL, postero-or inferolateral; I or P, inferior or posterior; IS or PS, infero- or postero-septal; RV, right ventricle; L, lateral; S, septal. (From Schiller NB, Shah PM, Crawford M, et al: Am Soc Echocardiogr 1989;2:358–367.)

in patients with ischemic heart disease without overburdening the clinician. The locations of the segments follow the perfusion territory of the three major epicardial arteries (Fig. 5-2) to facilitate the diagnosis of ischemic dysfunction. Wall Motion Score

The severity of dysfunction is scored visually in each segment. The recommended standard assigns a score of 1 for normal contraction or

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hyperkinesis, 2 for hypokinesis, 3 for akinesis, 4 for dyskinesis, and 5 for aneurysmal segments. [2] Some investigators use the system developed for angiography by Herman and Gorlin,[3] which assigns 1 for normal motion, 2 for mild or moderate hypokinesis, 3 for severe hypokinesis or akinesis, 4 for dyskinesis, and 5 for aneurysmal segments. Gibson et al[4] recommended evaluating wall thickening as well as motion in scoring segmental function because of reports that wall motion varies widely in normal subjects. However, wall thickening evaluation is not included in the American Society of Echocardiography's recommendation for regional function assessment.[2] Hyperkinesis can be distinguished from normal motion and may be assigned a negative value (e.g., -1) to indicate that its contribution to global function is opposite to that of segments with depressed function.[5] A global wall motion score is then calculated by summing or averaging the readings in all of the segments. The region of infarction can be evaluated separately from the noninfarct region by averaging the scores in the appropriate subset of segments. [6] Validation Comparison with Other Imaging Modalities

In clinical validation studies, the echocardiographic score agreed exactly with the score obtained from contrast ventriculograms in 44% of segments; agreement within one functional class was seen in 68% to 88% (Table 5-1) [7] [8] [9] [10] [11] [12] that is, agreement is higher for distinguishing normal from abnormal contraction than in identifying grades of abnormality. Comparable results were obtained in comparisons of radionuclide ventriculography versus 2D echocardiography (see Table 5-1) .[9] [13] In a significant minority of patients, however, the discordance is two or three classes. In one study, the global wall motion score by 2D echocardiography and angiography correlated with r = .70.[11] Factors Affecting Diagnostic Accuracy

Many factors influence the apparent accuracy of qualitative assessment of wall motion. Obvious direct factors are image quality and correct positioning of the image plane relative to the left ventricle. Another important factor is the difference between imaging modalities. Unlike contrast and radionuclide ventriculography, 2D echocardiography is tomographic, producing images of discrete slices of the heart; therefore, the different modalities do not obtain exactly comparable views of each

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segment. The training and experience of the observer are also important, both in recognizing normality and in differentiating classes of abnormality. Even with adequate training, significant intra- and interobserver variability exists in visual assessment. In general, variability increases with the number of grades. Exact agreement within and between observers ranges from 81% to 95%.[14] [15] [16] [17] However, allowance of a one-grade error (e.g., combining normal with hypokinesis or dyskinesis with aneurysm) improves intra- and interobserver agreement to 98% to 99%. These variability rates are comparable to those reported for the 90

Figure 5-2 Regions of single-vessel infarct asynergy. The maximum predicted area of infarct akinesis or dyskinesis and adjacent, noninfarct hypokinesis is depicted for each coronary artery. The ventricular model is based on 11 segments evaluated from short-axis sections obtained at the level of the mitral valve, papillary muscles, and apex. The mitral and papillary level sections were each divided into five segments. LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery. (From Stamm RB, Gibson RS, Bishop HL: Circulation 1983;67:232– 244.)

visual assessment of wall motion from contrast ventriculograms.[18] [19] To minimize the impact of observer variability, most studies report readings made by consensus between two or more observers. Variability reduces the sensitivity of qualitative assessment in diagnosing abnormality or detecting change in function. In patients studied after bypass surgery, wall motion in the revascularized segments improved significantly from baseline values when measured quantitatively, but they did not improve significantly when assessed visually.[20] Nevertheless, the global wall motion score has been repeatedly shown to predict survival in patients with acute or chronic myocardial infarction.[11] [21] Other clinical applications TABLE 5-1 -- Diagnostic Accuracy of Semiquantitative Echocardiography Analysis: Agreement Analysis: Agreement with Other with Other Imaging Modalities No. of Patients Echo Views No. of Classes

% Concordance ±1 COMPLETE CLASS Reference

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Comparison with contrast ventriculography 105 4 SAX, 1 apical 66 2 apical 24 2 parast, 2 apical 47 2 parast, 2 apical 47 2 parast, 2 apical 50 3 SAX, 3 LAX 20 2 parast, 2 apical Comparison with radionuclide ventriculography 24 2 parast, 2 apical 39 Subcostal

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2: normal vs. abnormal 4: nl, hypo, ak, dys

— 94

2: nl/hypo, ak/dys

—

87 Kisslo et al[7] 100 Ohuchi et al[8] 68 Hecht et al [9]

2: normal vs. abnormal 4: nl, hypo, ak, dys

—

5: nl, hypo, ak, dys, aneur 2: normal vs. abnormal

44

2: nl/hypo, ak/dys

—

69

—

79 Freeman et al[10] 94 Freeman et al[10] 88 Shiina et al[11] 77 Lundgren et al[12]

64 Hecht et al [9]

5: hyper, nl, hypo, 86 98 Ginzton et ak, dys al[13] ak, akinesis; aneur, aneurysm; dys, dyskinesis; hypo, hypokinesis; LAX, long axis (include apical views and parasternal long-axis view); nl, normal; parast, parasternal; SAX, short axis. are diagnosis of acute infarction in patients with nondiagnostic electrocardiograms, estimation of infarct size, and prediction of complications of infarction.[4] [22] [23]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of Regional Systolic Function Overview of Calculable Parameters As a tomographic imaging modality, 2D echocardiography allows delineation of both the endocardial and epicardial contours of the left ventricle. Consequently, it is 91

possible to calculate not only those parameters reflecting endocardial displacement, such as are used to analyze contrast ventriculograms, but also parameters based on measuring wall thickness. For clinical applications, the most commonly measured parameters are wall motion and wall thickening. The velocity of wall motion can also be measured by analyzing the Doppler signals generated by myocardial tissue. For research, other parameters of interest include midwall shortening, epicardial motion, shape, and wall stress. These measurements can be performed not only in two dimensions, within the plane of imaging, but also in three dimensions and even in four dimensions, with time. Through multiplanar image acquisition, echocardiography provides more complete visualization of the left ventricle than can be provided by either radionuclide or contrast ventriculography. Methods have been developed for three-dimensional (3D) reconstruction of the endocardium and epicardium and for performing 3D analysis of left ventricular dimensions, shape, and regional and global function (see Chapter 10) . Unlike with other imaging modalities, the visibility of landmarks on echocardiogram images (e.g., the papillary muscles, valve planes, and right ventricular septal insertion) helps to localize functional defects on the ventricle. From a multiplanar analysis of function, an estimate of infarct size can be derived by mapping the location of the dysfunctional region on the endocardial surface.

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The analysis of function, both regional and global, measures the alteration of the left ventricle between two time points in the cardiac cycle. For clinical purposes, the contours at end-diastole and end-systole are generally compared. Some investigators have also studied the extent of contraction at specific phases such as during isovolumic contraction or relaxation.[24] Frame-by-frame analysis through the cardiac cycle provides information on the synchrony of regional function. This can be taken to the "fourth dimension" by performing 3D analyses of the left ventricle at multiple time points through the cardiac cycle. Four-dimensional analysis is feasible with currently available fast computer technology and is being undertaken for teaching purposes. Application to clinical medicine will require automated border detection (see Chapter 7) to relieve the labor and tedium associated with analyzing so many images. Wall Motion Wall motion analysis measures the displacement of the left ventricular endocardium. To normalize for patient-to-patient differences in heart size, the measured motion is divided by the left ventricular dimension at enddiastole. The resulting unitless shortening fraction is analogous, on a local and linear level, to the global volume ejection fraction. Unlike the ejection fraction, however, wall motion may have negative values, which indicate paradoxical outward motion during systole. Implicit Assumptions

There are two major assumptions implicit in wall motion analysis. The first is that a one-to-one correspondence can be made from anatomic points on the left ventricular contour at end-diastole to the same points at end-systole. Second, the location of the patient relative to the imaging equipment remains stable. In fact, both assumptions are compromised in 2D image analysis. Nevertheless, the methods developed for wall motion analysis attempt to deal with these sources of imprecision. Methods for Wall Motion Analysis

Because it is not possible to track specific points on the left ventricle over time, there is no gold standard for judging the accuracy of methods for measuring wall motion. As a consequence, there is a plethora of methods, all of which model rather than measure wall motion. Almost all methods available for analysis of wall motion from echocardiogram images were developed initially for contrast ventriculograms. Ventriculograms have

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only one clearly visible landmark—the aortic valve—although some investigators attempt to identify the apex as a second landmark even though it is not an anatomic structure. Because the aortic valve is the only structure whose motion can be tracked over time, all other points on the ventricle have to be identified by their distance from the aortic valve. Echocardiograms display more anatomic landmarks, but they have not been used to make additional correspondences between the endocardial contour at end-diastole and end-systole, probably because the descent of the base toward the apex during systole moves different "slices" of the ventricle into and out of the imaging plane, so that the landmarks cannot be tracked over time. Most wall motion analysis methods for echocardiography employ a radial coordinate system. Motion is assumed to proceed from all points on the endocardial contour toward a single point, the center of area (Fig. 5-3) . There is little evidence supporting this assumption, although some data suggest a multicentric motion pattern.[25] However, the radial approach seems inherently suited to analysis of short-axis images. The radial method has also been applied to contours from apical views.[26] In methods based on a rectangular coordinate system, motion is measured along hemiaxes constructed at intervals along and perpendicular to the long axis of the ventricle. Rectangular coordinate system methods are applied only to apical views.[27] [28] [29] The apex is the least well visualized part of the contour; therefore, construction of a coordinate system based on identification of the apex may be subject to variability. One author justified the coordinate system approach by its similarity at the apex to a method derived by tracking endocardial landmarks felt to represent trabeculae.[30] The concept in these two methods is that endocardial displacement at the apex results from apical obliteration as the lateral walls contract toward the long axis. However, a study that also tracked endocardial landmarks found that apical wall motion proceeds toward the base, that is, 90 degrees off from the direction dictated by the first endocardial landmark method.[31] An angiographic analysis of the motion of surgically implanted metallic markers also reported that apical wall motion proceeds toward the base.[32] Thus, the 92

Figure 5-3 Method used for analysis of regional left ventricular

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contraction in a schematic of a short-axis two-dimensional echocardiographic image. The junction between the posterior right ventricular free wall endocardium and right ventricular septal endocardium was chosen as a landmark and a line drawn to the farthest point on the lateral left ventricular wall epicardium. From the midpoint of this line (1–7), 12 equidistant radii are drawn to separate the image into 12 cavity and wall segments. Percentage area change of each cavity segment and percentage thickening of the wall along each radius during systole are calculated. Solid lines, end-diastole; interrupted lines, end-systole. (From Pandian NG, Skorton DJ, Collins SM, et al: Am J Cardiol 1983; 51:1667–1673. Reprinted with permission from Excerpta Medica Inc.)

rectangular coordinate system, endocardial landmark, and midwall marker methods produce radically different descriptions of the direction of endocardial displacement at the apex. Only part of this discrepancy can be explained by the differing motions of the endocardium versus the midwall, which become separated during systole owing to relatively greater thickening of the inner myocardium.[33] Little of the discrepancy can be attributed to left ventricular torsion that rotates different layers of myocardium to different extents around the long axis of the left ventricle.[34] The Figure 5-4 Centerline method for regional wall motion analysis. Left, End-diastolic (ED) and end-systolic (ES) endocardial contours of the left ventricle from the apical long-axis echocardiographic view with the centerline midway between the two contours. Right, One hundred equidistant chords (not all shown) are constructed perpendicular to the centerline and numbered counterclockwise from the anterior aortic valve. The motion at each chord is normalized by the end-diastolic perimeter to yield a dimensionless chord fractional shortening. (From Wohlgelernter D, Cleman M, Highman A, et al: J Am Coll Cardiol 1986;7:1245–1254. Reprinted with permission from the American College of Cardiology.)

disagreement between these studies illustrates the current lack of knowledge and forms the justification for modeling rather than attempting to measure regional wall motion, at least until more definitive results can be obtained. Two methods have been developed for modeling wall motion without using a coordinate system. Gibson et al[35] divide the end-diastolic contour into a number of evenly spaced points and measure the distance from each to the nearest point on the end-systolic contour. In the centerline method, a centerline is drawn midway between the end-diastolic and end-systolic contours. Motion is measured along 100 chords evenly spaced along and

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perpendicular to the centerline and normalized by the end-diastolic perimeter length (Fig. 5-4) .[36] [37] [38] [39] Because they make no assumptions concerning the geometry of the left ventricular contour, both methods can be applied to chambers of diverse shapes. For example, the centerline method has been used to measure wall motion in the right ventricle as well as from different views of the left ventricle, unaffected by distortions of ventricular shape resulting from disease processes. Wall Motion Parameters

Motion can be measured in one dimension as the linear distance between the end-diastolic and end-systolic contours and normalized to yield a shortening fraction. Alternatively, function can be measured in regions of the left ventricle: the change in the area of a region between end-diastole and end-systole normalized by the end-diastolic area yields a regional ejection fraction (Fig. 5-5) . Studies have shown that such an area parameter is less subject to variability in delineating the endocardial contour, probably because the variability at individual contour points is averaged out over the region.[29] [40] [41] The principal drawback to regional assessment lies in the definition of the regions. Although the perfusion territories of the major epicardial coronary arteries have been mapped,[42] studies have shown that dysfunction in 93

Figure 5-5 Schematic of diastolic and systolic left ventricular outlines subdivided into octants, showing different approaches to measuring regional contraction. A, regional area change; H, hemiaxis shortening; P, segmental endocardial perimeter contraction. Similar measurements can be made for other approaches of segmenting the ventricular contour. (From Moynihan PF, Parisi AF, Feldman EL: Circulation 1981;63:752–760.)

patients with ischemic heart disease may extend beyond the defined territory of the stenosed artery.[5] [43] [44] [45] [46] [47] This result may be due to multivessel disease, border zone dysfunction, and/or variable coronary anatomy. In patients with multiple critical stenoses or infarctions, there may be multiple regions of dysfunction that run together and cannot be distinguished from each other.[5] The only distinguishing feature about border zone dysfunction is that it is less severe than dysfunction in the central ischemic region.[48] [49]

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The impact of variable coronary anatomy on the measurement of regional left ventricular function is significant, because dysfunction may be underestimated if the central ischemic region straddles two adjacent segments, each of which also containing some normally contracting myocardium.[36] One solution to this problem is to measure wall motion at many discrete points around the ventricular contour and then average the motion of points lying within the region of interest. This approach is flexible enough to adjust for variable coronary anatomy while retaining the advantage of lower variability for regional analyses, and it has been applied successfully using the centerline method to analyze function in the center of, on the periphery of, and remote from the ischemic region.[36] [50] It is important to note that the motion of multiple points from different locations on the contour cannot be averaged validly unless the motion values have comparable distributions. For wall motion, the normal mean and standard deviation vary by location on the ventricle (see "Definition of Normal Values"). One solution is to convert the shortening fraction values to a Z score (i.e., to units of standard deviations from the mean of a normal reference population).[41] After conversion, a value of zero indicates normal motion, positive values indicate hyperkinesis, and negative values indicate hypokinesis. The magnitude of the wall motion value indicates the clinical significance of the abnormality. These standardized wall motion values can be averaged over regions and compared among different regions and different patients. Validation Using Empirical Criteria

The various methods for wall motion analysis have been "validated" clinically using empirical criteria. The principal criteria are high sensitivity and specificity in distinguishing patients with diseased hearts from normal subjects. The problem with this approach is that the demonstrated diagnostic accuracy depends not only on the parameter but also on the patient populations used for testing. For example, the diagnostic accuracy of a new method will appear to be much higher if the diseased patients have myocardial infarction than if they merely suffer from chronic stable angina, simply because the latter have near-normal function. For this reason, the relative merits of the various methods of wall motion analysis are best assessed from comparative studies of two or more methods. Most comparisons have been made on contours drawn from contrast ventriculograms (Table 5-2) . These studies have shown that the radial and centerline methods have higher diagnostic accuracy than methods based on a rectangular coordinate system. One study of 2D echocardiograms in the

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subcostal view reported that the centerline method is less likely to diagnose abnormality in normal subjects than the radial method.[26] In contrast, another echocardiographic study found that a rectangular coordinate system approach yielded higher diagnostic accuracy than either the radial or centerline methods.[28] The homogeneity of the normal group is the second empirical criterion. A narrow normal range, reflected by a small standard deviation, enhances sensitivity in diagnosing TABLE 5-2 -- Comparison of Sensitivity and/or Specificity of Methods of Wall Motion Analysis in Detecting Regional Dysfunction Methods RadialED COM > radialES COM, LA

Reference Papapietro et al[122]

RadialLA > radialES COM, ED + ES COM

Karsch et al *

Radial > area > rectangular Area, radialmidwall >> radialED + ES COM ,

Karsch et al * Lorente et al †

rectangular in anterior MI RadialED + ES COM , radialmidwall >>

Lorente et al †

rectangular, area in inferior MI Radialmidwall > rectangular > radialED + ES Colle et al ‡ COM

Area > radialLA , rectangular

Gelberg et al[41]

Centerline, rectangular >> radialmidwall

Sheehan et al §

Centerline = radialmidwall = rectangular

Lamberti et al

Centerline >> radialmidwall

Ginzton et al[26]

Radialmidwall > radialLA , radialES COM ,

Ingels et al ¶

rectangular Rectangular > centerline, radial Assmann et al[28] A >> B, C indicates that method A was significantly better than methods B and C, and that B and C do not differ from each other; A > B indicates method A was better than method B but not compared statistically; Area

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specifies that regional ejection fractions were measured; Radialmidwall

refers to the method of Ingels et al; Centerline refers to the centerline method of Sheehan et al; ED COM, origin at end-diastolic center of mass; ES COM, origin at end-systolic center of mass; ED + ES COM, origin of each contour at that contour's center of mass; LA, origin at midpoint of long axis; MI, myocardial infarction.

*Clin Cardiol 1980;3:123. †Int J Cardiol 1985;7:361. ‡Arch Mal Coeur 1982;75:395. §In Sigwart U, Heintzen PH, (eds): Ventricular Wall Motion. Stuttgart, Georg Thieme Verlag, 1984, p 139. In Computers in Cardiology. Long Beach, Calif., IEEE Computer Society, 1985, p 467. ¶Circulation 1980;61:966.

94

abnormality (Fig. 5-6) . For example, in calculating sample size for a clinical trial, the number (n) of patients per group is proportional to the square of the standard deviation (σ):

One way to evaluate a method quickly is to divide the value for the normal mean by the normal standard deviation. If the quotient is greater than 2, then akinesis is unlikely to lie within the normal range (defined as the mean ± 2 SD). If akinesis differs from the normal mean by less than 2 SD, then a patient's motion must be dyskinetic or aneurysmal to be considered definitely abnormal. Such a method is relatively insensitive to lesser degrees of dysfunction. Additional considerations in selecting a method of wall motion analysis are its ability to focus on a user-defined region of interest and its applicability to other chambers of the heart or to particularly distorted ventricular

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contours. The importance of these considerations depends on the intended application. Effect of Cardiac Translation on Wall Motion Analysis

The second assumption implicit in wall motion—that the heart's position is stable—is particularly problematic for 2D echocardiography. During systole, the left ventricle rotates about its long axis and translates anteriorly. [51] [52] There is no easy way to distinguish contraction from the translational motion of the heart. Several empirical methods have been proposed to "correct for" translation by realigning the end-systolic contour relative to the end-diastolic contour (Fig. 5-7) . For contrast ventriculography, Figure 5-6 Effect of variability on diagnostic accuracy. Bottom, Probability distribution functions for a normal (—) and disease (---) population. When the variability of the measurement is low and the standard deviation (SD) is narrow, virtually no overlap exists between the two groups. Top, When variability is greater, as indicated by a higher SD, the overlap between the same two populations increases from 11% to 68%. (From Sheehan FH: Measurement of left ventricular function from contrast angiograms in patients with coronary disease. In Brundage B [ed]: Comparative Cardiac Imaging-Function, Flow, Anatomy, Quantitation. Rockville, Md, Aspen Publications, 1990, pp 101–118.)

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Figure 5-7 Reference systems. The method of reregistration of the contours is shown on the left; the resulting superimposition of contours is shown on the right. Top, Fixed external reference system. There was no realignment of the drawn outlines between extension of radii from (in this example) the enddiastolic center of the area. Middle, Floating reference system with translation. The center of area in end-diastole and the center of area in end-systole were superimposed. Bottom, Floating reference system with translation and rotation. The centers of area in end-diastole and end-systole were superimposed for translation. The long axis from the center of the area to the apex at end-diastole was superimposed over the long axis in end-systole for rotation. □, end-diastolic center of area; •, endsystolic center of area. (From Schnittger I, Fitzgerald P, Gordon E, et al: Circulation 1984;70:242–254.)

realignment methods have no theoretical advantage over using a fixed reference system (i.e., analyzing the motion of the endocardial contour relative to the image frame [53] ) and may even worsen the reproducibility of the analysis.[40]

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For echocardiographic analysis, the question of realignment has not been definitively answered because of conflicting evidence. There are data to show that use of a fixed reference system may cause artifactual hypokinesis in a normal heart[54] however, using a floating reference (i.e., realigning) may present a dysfunctional segment as normal.[54] Parisi et al[55] found that fixed and floating reference systems yield equal accuracy in detecting the presence of wall motion abnormalities, but the fixed reference system was superior for localizing the abnormality. Schnittger et al[56] performed a detailed analysis of several methods for correcting for translation and rotation. They reported that the optimal analysis method differs by view. In the apical four-chamber view, correction for translation by superimposing the center of mass in the enddiastolic and end-systolic contours yielded the highest sensitivity and specificity in distinguishing patients with diseased hearts from normal subjects. However, in the short-axis view at the papillary muscle level, optimal results were obtained with a fixed reference. Zoghbi et al[57] reaffirmed the superior performance of the fixed over the floating reference analysis for the short-axis view, but they found that realignment using an epicardial centroid yielded the best correlation between wall motion and regional wall thickening. The need for realignment in the four-chamber view was reiterated by Force et al,[54] who found that patients with normal function studied after bypass surgery developed artifactual septal hypokinesis when analyzed using a fixed reference system. Feneley et al[58] [59] also found that a fixed reference causes artifactual dyskinesis in the septum when measured from short-axis images in patients with right ventricular volume overload or after bypass surgery. Wall Thickening In analyzing wall thickening, the thickness of the myocardium is measured at two or more time points in the cardiac cycle, then the measurements are compared. The thickness change is normalized by the end-diastolic dimension, as for wall motion. Normal myocardium thickens during systole. Dysfunctional myocardium exhibits decreased thickening or even thinning. Because each measurement of wall thickening is made from a single time point, thickening analysis is independent of artifact owing to cardiac translation. For this reason, many investigators prefer thickening for analyzing regional systolic function.[60] Experimental Basis

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The validity of wall thickening as a parameter of regional systolic function was initially demonstrated in experimental animals. In a series of acute and chronic studies, Ross and Franklin[61] showed a linear relationship between wall thickening and subendocardial fiber shortening measured using implanted ultrasonic crystals. Heikkila and Nieminen[62] reported that wall thickening is preferable because of its larger signal and lower variability compared with epicardial segment shortening. The accuracy of wall thickness measurements from echocardiograms was established initially using M-mode imaging of postmortem specimens.[62] The accuracy of wall thickening measurements from 2D echocardiograms has been validated for the calculation of ventricular mass.[63] [64] Subsequently, several investigative groups demonstrated 96

the feasibility of noninvasive regional wall thickening analysis by 2D echocardiography [44] [55] , [65] [66] and explored the potential clinical usefulness of this method for diagnosis of infarction, estimation of infarct size, and assessment of recovery and response to treatment. Measurements of wall thickening obtained from analyzing 2D echocardiograms are higher than those obtained using implanted ultrasonic crystals. This discrepancy is due to placement of the crystals in the subendocardium, whose movement underestimates true endocardial excursion.[63] Implicit Assumptions

Two assumptions are made in analysis of regional wall thickening. The first assumption is that wall thickness is measured along a vector orthogonal to the myocardial wall; that is, the imaging plane should be orthogonal to the wall and thickness should be measured in a radial direction within that plane, because analysis at oblique angles overestimates wall thickness. Some investigators advocate 3D analysis to ensure orthogonality.[67] In practice, the problem of oblique imaging pertains primarily to magnetic resonance imaging and computed tomography, which image in parallel planes, rather than to echocardiography, which offers greater flexibility in selecting each imaging plane. Nevertheless, this potential source of error should not be overlooked. The second assumption is the same as for wall motion: that a one-to-one correspondence be made between points on the ventricular contour at enddiastole and at end-systole. Actually, a strict correspondence is not possible

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because different slices of ventricle are imaged in systole and diastole owing to the translational motion of the heart through the imaging plane and the descent of the base toward the apex.[51] [52] However, the methods developed to date provide an estimated correspondence that has served well for both clinical and research applications. Figure 5-8 Measurement of wall thickening by the centerline method. The epicardial and endocardial contours of the left ventricular wall are displayed at end-diastole (left) and end-systole (right). Thickness is measured as the length of each of 100 chords constructed perpendicular to and evenly spaced along a line in the center of the myocardial wall (not shown), midway between the epicardial and endocardial contours. The end-diastolic endocardial contour is reproduced on the end-systolic plot to illustrate the extent of endocardial wall motion. (Redrawn from Sheehan FH, Feneley MP, DeBruijn NP, et al: J Thorac Cardiovasc Surg 1992;103:347–354.) Methods for Analyzing Regional Wall Thickening

Two methods are used for wall thickening analysis. The radial method measures wall thickness along radii extending from an origin usually located at the center of area, or at the midpoint of an anatomically defined diameter.[29] [51] [54] This method is most suitable for analyzing short-axis views with their near-circular contours, but it has also been applied to apical views.[68] In the centerline method, a centerline is drawn midway between the endocardial and epicardial contours. Wall thickness is measured along chords constructed perpendicular to and evenly spaced along the centerline (i.e., in the direction of the local radial vector[38] [69] [70] ) (Fig. 5-8) . In both methods the correspondence between end-diastole and end-systole relies on even distribution of points around the ventricular contour. No attempt has yet been made to anchor the point numbering system to available anatomic landmarks other than those used to define the start and end of the border. In short-axis views, border tracing usually begins at the junction of the right ventricle and septum, because the papillary muscles are not visible at all levels. In apical views, the border begins and ends at the valve planes. Wall thickening may be affected by cardiac motion if the wall thickness measurements are not performed independently at each time point. For example, Pandian et al[51] measured wall thickening using a radial coordinate system defined at end-diastole and superimposed on the end-

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systolic contours. In a patient with marked translational motion, the origin of this coordinate system may deviate from the center of the end-systolic contour. However, these investigators measured the translation and rotation of short-axis "slices" and found that the mean rotation in their 12 normal subjects was 1.0 ± 7.6 degrees counterclockwise, and translation averaged 1.7 ± 21.4 mm to the right and 6.7 ± 37 mm anteriorly. Realignment to correct for translation and rotation did not alter the mean or range of normal thickening.[51] Force 97

et al[54] reported that rotation in the dog averages 3.5 degrees and also recommended against corrective realignment. However, it is not clear how much translation affects wall thickening measurements in patients with diseased hearts. Comparison of Wall Motion and Wall Thickening Several studies have been performed that compare wall motion, wall thickening, and other parameters. Because no test has yet been developed for anatomic validation of methods for wall motion analysis, the comparisons with wall thickening have used empirical criteria. In deciding between these two parameters, theoretical and practical considerations are also worthy of attention. Theoretical Considerations

When the left ventricle is modeled as a thick-walled cylinder contracting radially and longitudinally, it can be shown mathematically that wall thickening, midwall shortening, and longitudinal axis shortening are related, but internal radius shortening (i.e., wall motion) is significantly influenced by the degree of left ventricular hypertrophy.[71] In ventricles with normal wall thickness, wall motion and wall thickening correlate closely.[72] However, the relative contribution of wall thickening, but not of wall motion, to ventricular power during ejection increases with increasing hypertrophy.[73] Thus, for example, wall motion may be inappropriately elevated in patients with hypertrophy owing to chronic valvular disease or cardiomyopathy. The discordance between wall motion and either wall thickening or midwall fiber shortening, both of which do not display hyperkinesis in these patients, is related to the relative wall thickness (compared with the chamber radius).[71] [74] [75] Thus, analysis of regional wall thickening more accurately reflects the functional status of

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hypertrophied ventricles than does endocardial wall motion. TABLE 5-3 -- Heterogeneity of Wall Motion and Wall Thickening in Normal Subjects *

N 10 10 12 12 12 10 14 14 14 9 9 9 9

% Wall % Wall Motion Thickening MEAN COEF. MEAN COEF. ± SD OF VAR. ± SD OF VAR. Reference Method View Hemiaxis SAX 30 ± 7 0.29 — — Moynihan shortening mitral et al[29] Hemiaxis SAX 35 ± 0.36 — — Moynihan shortening papillary 13 et al[29] Radius SAX 44 ± 0.39 52 ± 0.52 Pandian et shortening mitral 17 27 al[51] Radius SAX 49 ± 0.39 53 ± 0.43 Pandian et shortening chordal 19 23 al[51] Radius SAX 53 ± 0.34 53 ± 0.45 Pandian et shortening papillary 18 24 al[51] Radius SAX 24 ± 5 0.21 18 ± 0.72 Sandor et shortening papillary 13 al[76] Area change SAX 39 — — — Haendchen mitral et al[78] Area change SAX 56 — — — Haendchen papillary et al[78] Area change SAX 61 — — — Haendchen apical et al[78] Area change SAX 61 ± 0.16 38 ± 0.45 Ren et al[77] mitral 10 17 Area change 4CH: 69 ± 0.23 37 ± 0.38 Ren et al[77] apex 16 14 Area change 4CH: 62 ± 0.26 25 ± 0.40 Ren et al[77] postlateral 16 10 Area change 4CH: 70 ± 0.19 35 ± 0.43 Ren et al[77] septum 13 15

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4CH, apical four chamber; Coef. of Var., coefficient of variation (calculated as standard deviation/mean); N, number of subjects; SAX, short axis; SD, standard deviation. *Table displays representative data only from cited references; for complete data, see reference.

In addition to being independent of the degree of hypertrophy, wall thickening analysis is independent of translational artifact; therefore, no empirical realignment needs to be performed to correct for cardiac translation or rotation, and patients can be evaluated serially before and after bypass surgery without having to adjust for the effect of pericardiectomy on septal motion. The disadvantage of measuring wall thickening is that it does not reflect the contribution of epicardial motion to stroke volume.[57] Practical Considerations

Wall thickening analysis requires delineation of the epicardial contours as well as the endocardial contours. This doubling of work is not merely time consuming but also introduces additional opportunity for error. Imaging must be performed with the intent to quantify regional wall thickening, so that care is taken to include the epicardium within the scan sector throughout the cardiac cycle. Empirical Comparisons

The final arbiter between wall motion and wall thickening, each with its theoretical advantages and practical disadvantages, is performance. Because diagnostic accuracy is intimately related to normal variability, several investigators have performed comparative studies (Table 5-3) .[29] , [51] [69] [76] [77] [78] In general, although both akinesis and the absence of wall thickening are rare in normal subjects, wall thickening is more heterogeneous (i.e., has a higher coefficient of variation). The normal range, defined as mean ± 2 standard deviations, is more likely to encompass 0% thickening than 0% motion. The higher wall thickening variability is due in large part to point-to-point differences in end-diastolic wall thickness and can be reduced by using the end-diastolic perimeter length to normalize the observed change in wall thickness.[69]

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In diagnosing myocardial infarction, both parameters perform well (see "Diagnosis of Myocardial Infarction" 98

and "Assessment of Infarct Size"). Wall motion is slightly more sensitive in detecting dysfunction (96% vs. 93%), and wall thickening is slightly better in identifying normally functioning regions (100% vs. 83%) (Table 5-4) . In clinical studies, wall thickening has proved to be more sensitive in detecting dysfunction.[77] [79] For estimation of infarct size, both parameters yield comparable results (Table 5-5) . Tissue Doppler Imaging of Myocardial Velocity Low-velocity Doppler signals returned by myocardial tissue can be analyzed to assess regional ventricular function without the need for border delineation. [80] The velocities are presented visually using color coding, but they can also be quantified. The M-mode format provides higher temporal resolution. For accuracy 2D tissue Doppler imaging should be performed at a frame rate fast enough to capture changes in velocity.[80] Although it is a form of mapping rather than imaging, the pulsed wave Doppler mode allows peak velocity to be measured with high temporal and spatial resolution within the sample volume.[81] The accuracy of velocity measurements by tissue Doppler imaging has been validated in phantoms against M-mode echocardiography, in experimental animals by comparison with sonomicrometry, and in normal subjects versus M-mode.[80] [82] [83] The artifactual velocity contributed by the heart's translational motion can be canceled by computing a myocardial velocity gradient as the difference TABLE 5-4 -- Accuracy of Regional Systolic Function Analysis in Dia Myocardial Infarction Diagnosis Study Group Human: 37 acute MI Human:

Locatio SENSITIVITY SPECIFICITY Accurac Method Threshold (%) (% (%) Semiquantitative Abnormal 100 — 9

Semiquantitative Hypo, ak,

—

—

9

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26 TMMI, 6 SEMI Human: 66 acute MI Human: 20 MI, 18 normal Human: 20 MI, 18 normal Human: 20 MI, 18 normal Human: 15 MI Human: 48 acute MI Human: 18 angina, 12 SEMI Human: 18 angina, 12 SEMI Human: 32 angina, 33 acute MI Dog: 27 Dog: 27

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dys

Semiquantitative Hypo, ak, dys

—

—

9

Area change

<2 SD

95

89

—

Hemiaxis shortening

<2 SD

85

78

—

Perimeter shortening

<2 SD

90

72

—

Semiquantitative Hypo, ak, dys Semiquantitative Hypo, ak, dys

90

54

—

—

—

9

Semiquantitative Akinesis

50

100

—

Semiquantitative Severe hypo

83

100

—

Semiquantitative Abnormal

94

84

—

Area change

<2 SD

77

83

7

Wall thickening <2 SD

81

100

8

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— Human: 9 Wall motion <2 SD 100 — TMMI 6 Wall motion <2 SD 33 — — SEMI 9 Wall thickening <2 SD 89 — — TMMI 6 Wall thickening <2 SD 83 — — SEMI 6 Epicardial <2 SD 0 — — SEMI motion Human: Semiquantitative Hypo, ak, 94 — 9 95 acute dys MI Human: Semiquantitative Hypo, ak, 100 — — 31 TMMI dys 9 Semiquantitative Hypo, ak, 56 — — SEMI dys Dog: 24 Wall thickening ≤0 71 100 — MI, 5 nl Dog: 24 Wall motion ≤0 63 80 — MI, 5 nl Human: Semiquantitative Hypo, ak, 100 — 9 32 acute dys MI Human: Semiquantitative Hypo, ak, — — 8 73 TMMI dys Human: Semiquantitative Hypo, ak, 93 — 7 92 acute dys MI ak, akinesis; dys, dyskinesis; hypo, hypokinesis; MI, myocardial infarctio normal; SD, standard deviation; SEMI, subendocardial MI; TMMI, transmu between the endocardial and epicardial velocities normalized by the local wall thickness. [84] This correction, however, can only be applied to the anterior and posterior segments in the parasternal short-axis view, whose motion parallels the direction of the ultrasound beam.

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The normal range differs between the base and apex, the anterior and posterior walls, and the endocardium, midwall, and epicardium regardless of whether it is measured in M-mode as a tissue velocity, in 2D as a myocardial velocity gradient, or by pulsed wave Doppler as a peak velocity.[84] [85] [86] Variability is not lower than for other echocardiographic indices of ventricular function.[87] Several clinical applications have been proposed[88] even though the technology is limited to ventricular segments lying within ± 15 degrees of the incidence angle. In apical views, tissue Doppler imaging captures only longitudinal shortening. Tissue velocities measured from the apex failed to correlate with visual wall motion scores in infarct patients, although the velocity gradient between base and apex did reflect the number of dysfunctional segments. [89] A more recent study indicated that velocity measurement by pulsed Doppler improves diagnostic accuracy of viability assessment by dobutamine stress echocardiography.[90] In contrast, another study found this mode unable to discriminate control versus scar tissue when systolic velocity was measured, although diastolic velocities proved to be useful. [91] Clinical acceptance of tissue Doppler imaging is currently inhibited by the lack of consensus or standardization among the various acquisition and quantification modes. This modality's greatest contribution may be to applications for which it offers unique information. For example, 2D tissue Doppler acceleration 99

TABLE 5-5 -- Evaluation of Myocardial Infarction by Two-Dimensio Study No. of Echo Group Subjects Timing View Method Estimation of infarct size Dog 25 5.5 hr 1 Semiquant LAX +3 SAX Human 20 2–4 4 Semiquant days SAX Human 29 2–4 4 Semiquant days SAX

Infarct Size Threshold Parameter Hypo, ak, Tc99 dys

Hypo, ak, Thallium 201 dys Hypo, ak, Tc99 dys

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Human

60

Human

15

Human

48

Dog

20

Dog

20

Dog

24

Dog

24

Dog

27

Dog

27

Dog

10

Human

61

Dog

11

Human

20

<12 hr 3 LAX +5 SAX Varied 3 SAX <12 hr 3 apical 2 hr 1 LAX +3 SAX 48 hr 1 LAX +3 SAX 20 min 2 SAX 2 days 2 SAX Varied 3 SAX Varied 3 SAX 6 hr 4 SAX <12 hr 4 LAX +3 SAX 6 hr 3 SAX +3 apical <1 yr 3 SAX

Semiquant

Hypo, ak, Peak CK-MB dys

Semiquant

Ak, dys

Semiquant

Hypo, ak, Peak CK-MB dys <0 Histopatholog

Wall thickening

Postmortem

Wall thickening

<0

Histopatholog

Wall thickening Wall thickening Area change

<0

Histopatholog

<0

Histopatholog

<2 SD

Histopatholog

Wall thickening Semiquant

<2 SD

Histopatholog

Semiquant

Hypo, ak, Peak CK dys

Semiquant; endocardial surface map

Abnormal Histopatholog

Semiquant; endocardial

Abnormal Postmortem

Abnormal Histopatholog

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+ 2 surface map apical Dog 10 72 hr 5 Radial SAX shortening at ES Dog 10 72 hr 5 Radial SAX shortening over cardiac cycle Correlation with the size of the risk region Dog 24 20 min 2 Wall SAX thickening Dog 24 2 days 2 Wall SAX thickening Dog 10 6 hr 4 Semiquant SAX Dog 11 3 hr 4 Wall motion SAX Dog 11 3 hr 4 Wall motion SAX Dog 11 3 hr 4 Circumference SAX Dog 11 3 hr 4 Wall motion SAX over cardiac cycle Wall Dog 12 2 hr 1 SAX thickening: referenced to contrast defect Dog 12 2 hr 1 Wall SAX thickening: COM method

<15%

Histopatholog

<15%

Histopatholog

<0

Angiography

<0

Angiography

Abnormal Echo contrast <10%

Echo contrast

<20%

Echo contrast

Ak, dys

Echo contrast

<95% CI

Echo contrast

<95% CI

Echo contrast

<95% CI

Echo contrast

Risk Study No. of Echo Group Subjects Timing View Method

Infarct Size Threshold Parameter ESTIM

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Dog

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18

60 min 1 Wall <95% CI Microsphere SAX thickening Dog 16 60 min 1 Wall <2 SD Microsphere SAX motion Dog 16 60 min 1 Wall <95% CI Microsphere SAX motion Dog 16 60 min 1 Wall Dys Microsphere SAX motion Dog 16 60 min 1 Wall <2 SD Microsphere SAX thickening Wall <95% CI Microsphere Dog 16 60 min 1 SAX thickening Dog 16 60 min 1 Wall Dys Microsphere SAX thickening ak, akinesis; CI, confidence interval; CK, creatine kinase; CK-MB, creati COM, center of mass (method of realignment for translation); Corr. Coef., c dys, dyskinesis; ES, end-systole; hypo, hypokinesis; LAX, long axis; SAX, deviation; SEE, standard error of estimate; semiquant, semiquantitative anal Tc 99m pyrophosphate scintigraphy. * Percentage circumference.

100

imaging can localize the onset of mechanical contraction for electrophysiology testing. [92] Epicardial Motion The motion of the epicardium can be measured as a parameter of regional systolic function by applying methods for wall motion analysis to the epicardial contour. Compared with endocardial motion, however, epicardial motion is much lower in magnitude,[76] [78] [79] because thickening of the wall during systole contributes about half of what is measured as endocardial displacement.[93] Because measurement of epicardial motion is subject to the same sources of error and variability as endocardial motion, its lower

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magnitude results in an unfavorably high coefficient of variation,[76] which may explain its low sensitivity in detecting the presence of myocardial infarction.[79] Shape Analysis It has long been established that the left ventricle becomes more spherical when it dilates and decompensates.[94] [95] This compensatory mechanism allows a more even distribution of regional stress and improves ventricular efficiency. More recently it has been recognized that similar changes occur on a regional level in patients with recent myocardial infarction. Measurement of the magnitude of these changes provides information on the mechanism, magnitude, and time course of remodeling and its effect on prognosis. Global Shape

The analysis of global left ventricular shape is performed using general mathematical models. Most commonly, the ventricle is assumed to be elliptic, and its degree of sphericity is assessed by determining the ratio of the long-axis length to the short-axis diameter.[96] This parameter is subject to variability in measuring the axis lengths. Other parameters of global shape have also been developed, such as the ratio of the end-diastolic volume to the volume of a sphere with equivalent long-axis length, the ratio of the end-diastolic volume to the volume of the sphere with equivalent surface area, or the following ratio[97] [98] [99] 4π(Area)/(Perimeter2 ) In an experimental heart failure model, shape measurements based on axis length and area-to-perimeter ratios were less sensitive to incipient ventricular decompensation than the volume-to-surface area ratio.[99] Regional Shape

In patients with regional dysfunction (e.g., secondary to myocardial infarction), the left ventricular contour may develop regional abnormalities in curvature. [97] Curvature is a major determinant of wall tension, and changes in ventricular shape have been attributed to acute elevation in stress at the time of infarction; remodeling redistributes these stresses to improve efficiency. [100] [101] Analysis of regional curvature has been shown to provide diagnostic information when measured from contrast

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ventriculograms.[102] However, relatively little investigation has been performed in measuring regional curvature from 2D echocardiograms. [103] This lack of investigation may be because the apparent shape of the left ventricle in 2D echocardiography is greatly influenced by the imaging plane and is therefore dependent on the skill and care of the sonographer acquiring the images. It may be preferable, when analyzing echocardiograms, to measure regional shape using a method that is relatively insensitive to oblique imaging. One approach is to compare the lengths of the contour segments between the papillary muscles in the shortaxis view (Fig. 5-9) . This simple but effective method has proved useful for studying ventricular remodeling in patients with myocardial infarction. [104] Expansion (lengthening) of the infarct region is accompanied by thinning of the myocardium; therefore, the ratio of wall thickness in the diseased and normal regions provides another parameter of left ventricular geometry.

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Imaging and Image Analysis for Quantification Image Acquisition Technique

Unlike contrast ventriculography, in which the view angles are fixed, 2D echocardiography relies on the skill Figure 5-9 Method of measuring the expansion index and thinning ratio, shown in a midventricular section from a patient with anterior infarction and asynergy. Segment lengths were measured between midpoints of papillary muscle landmarks. a, average thickness of asynergic zone; b, average thickness of nonasynergic zone; LV, left ventricle; RV, right ventricle; x, endocardial length of asynergy-containing segment; y, endocardial length of segment without asynergy. Expansion index, x/y; thinning ratio, a/b. (Copyrighted and reprinted with the permission of Clinical Cardiology Publishing Company, Inc., and/or the Foundation for Advances in Medicine & Science, Inc. From Jugdutt BI, Michorowski BL: Clin Cardiol 1987;10:641–652.)

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of the sonographer in locating the desired anatomic slice in each patient. It is important to locate the various "standard" views with precision, reduce heterogeneity in the normal population, enhance diagnostic accuracy, and reduce variability between repeated studies in the same patient. The quality of quantitative analysis improves if the person performing image acquisition also performs the analysis. A sonographer with experience in quantification can recognize images that will be difficult to analyze and will enhance them as much as possible during acquisition. The American Society of Echocardiography has published recommendations concerning imaging for quantitative analysis of the endocardial contour. [2]

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Additional attention also may be needed to ensure visualization of the epicardium (e.g., increasing depth to ensure that the epicardium and anatomic landmarks are visible within the sector scan throughout the cardiac cycle and increasing lateral gain to improve edge definition along walls parallel to the beam). In patients with poor endocardial edge definition, intravenous injection of a contrast agent (e.g., albumin microbubbles) opacifies the chamber and improves endocardial depiction. [105]

An electrocardiographic rhythm strip should be acquired and recorded with the image to facilitate selection of a normal sinus beat (not following a premature beat) for analysis. Analog versus Digital Imaging

Echocardiograms are traditionally recorded on videotape at 30 frames per second. Because of the nature of analog imaging, only half of the scan lines are laid down at this rate; the other half of the lines, which alternate between the first set, are recorded 1/60 second later. Thus, each image frame consists of two half-resolution fields offset by 1/60 second. In analog-to-digital conversion, the convention is to treat each frame as a single image, regardless of the component fields. Digital images have a resolution of 256 × 256 or 512 × 512 pixels. Using the higher format retains the original image's resolution, but it requires four times as much computer memory. In practice, digitization at the 256 × 256 pixel resolution produces acceptable results. Digitization is necessary for quantitative analysis and facilitates comparison of serial studies.[106] As the speed of computer workstations increases and the price of digital memory decreases, the use of digital imaging will increase to take advantage of these benefits. This scenario is best exemplified by imaging systems intended for exercise echocardiography, which acquire and display up to four cine loops at a time, so that small changes in wall motion can be more easily appreciated. The same technology can be used to compare serial studies on the same patient. Networking between computers will allow images to be accessed from different locations in the hospital. Indeed, it may be possible in the near future to transmit and receive cardiac images over long distances for consultations. Image Analysis

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Frame Selection

When the objective is to select a representative cardiac cycle of images for quantitative analysis, the principal consideration is to find a beat in which the endocardial and epicardial contours are clearly visible throughout the cardiac cycle. In general, images acquired near end-expiration are clearer because there is less respiratory motion artifact and less lung interposition between the transducer and the heart. During inspiration, the beat-to-beat variability is higher than at end-expiration, especially at the apex (Fig. 510) .[107] The electrocardiographic rhythm strip assists in selecting a normal sinus beat or a beat of average RR interval in patients with atrial fibrillation. The end-diastolic frame is that with maximum cavity area and generally lies on or one frame after the R wave. The end-systolic frame is that with minimum cavity area. Identification of end-systole may be difficult in patients with asynchronous wall motion, because the timing of minimum cavity area may differ between views. End-systole can be identified from the second heart sound if a phonocardiogram is recorded during imaging. [108] Alternatively, the average time of minimum cavity area can be determined from reviewing all views and then applied to each view by noting its timing on the electrocardiogram. Border Tracing

The objective of border tracing is to delineate the left ventricular endocardial and epicardial contours. The endocardial edge is the interface between the bright echoes at the edge of the myocardium and the darker region of the ventricular cavity. Deciding where the endocardium lies among the bright echoes may be difficult, particularly when the contour is roughened by trabecular reflections. Contributing to the roughness is the relatively poorer resolution parallel to the echo beam. Studies in postmortem hearts have shown that tracing the leading edge of the endocardial echoes reduces underestimation of the cavity area compared with tracing the innermost black-white border.[109] In practice, this approach is associated with unacceptable variability, because the leading edge of the wall nearest to the transducer is separated from the trailing edge at the lumen by the bright border pixels.[109] [110] Some investigators suggest that the trailing edge of the nearer wall be traced and then corrected using image processing techniques to approximate the leading edge. [110] Along walls parallel to the echo beam, phantom studies have shown that accuracy is greatest when the midpoint of the leading edge is traced.[109]

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By convention, the papillary muscles are included in the cavity (Fig. 5-11) . It is recommended that the trabeculae also be included in the cavity, for two reasons. First, this is the approach used for analyzing contrast ventriculograms, which have a high accuracy for volume determination.[111] Indeed, the reported underestimation of volume by 2D echocardiography techniques may be related in part to inclusion of trabeculae with the myocardium in 102

Figure 5-10 Variability in the analysis of regional wall motion. Top, The effect of respiration on variability in 10 normal subjects. The regional ejection fraction between two consecutive beats from an inspiratory phase (variability Insp) is compared with the variability between two beats from the end-expiratory phase of two consecutive respiratory cycles (variability Exp). The variability is expressed as the mean of the absolute differences. In addition, the mean values for regional ejection fraction are presented from the second of the two consecutive beats from the inspiratory phase (mean Insp) and from an end-expiratory phase (mean Exp). Bottom, Variability in regional left ventricular function as measured at end-expiration in 20 normal subjects. The intraobserver, interobserver, and interbeat variability in regional ejection fraction are expressed as the mean of the absolute differences. In addition, the 10th to 90th percentile range for the regional ejection fraction in normal subjects is presented. Note that the interbeat variability is comparable to the intraobserver and interobserver variability. REF, regional ejection fraction. (From Assmann PE, Slager CJ, van der Borden SG, et al: J Am Soc Echocardiogr 1990;3:478–487.)

earlier studies.[112] Second, the borders traced for volume analysis can be applied to analysis of regional function as well. If trabeculae are traced, the borders of the endocardium are extremely noisy, and the resulting measurements of wall motion or wall thickening suffer from wide point-topoint variability. Some automated border detection programs have been developed. [113] As these methods become available commercially, it is important to remember that the physician ultimately must take responsibility for verifying that the border is drawn correctly. One image processing technique does not attempt to define a continuous endocardial contour such as a human observer would trace, but rather detects all blood-tissue interfaces lying within a user-defined region of interest.[114] Because the process can be performed in real time, the displacement of the interfaces through the cardiac cycle can be computed. Using color coding, an image is generated

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representing regional wall motion.[115] The method has been validated for measurement of volume and ejection fraction; for wall motion assessment its segmental analysis does not differ more from the consensus of two human observers than the humans do from each other.[115] Assistance from Digital Workstations

Digital workstations were initially developed for acquisition and display of image loops for exercise echocardiogram interpretation. With the increased interest in quantitation, workstation software is currently available for reviewing images and tracing the borders of the left ventricle and other structures. A properly programmed digital workstation can assist image analysis in a number of ways.

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Figure 5-11 (color plate.) Border tracing. In the initial tracing of the endocardial contour, the papillary muscles are included with the chamber, which produces a smooth contour for analyzing wall motion and wall thickening. Then the papillary muscle borders are traced separately and can be inserted for calculation of left ventricular volume. The epicardial contour is also shown. Cine Loop.

Few images are of such high quality that they can be analyzed entirely from a single stopped frame; therefore, it is essential to be able to review the full cardiac cycle in cine loop format, because watching wall motion helps to identify the endocardial and epicardial borders. The ability to watch wall motion is particularly important in analyzing images of borderline quality. Sometimes it is helpful to toggle quickly between the frame being analyzed and the preceding or following frame to look for a flash of movement that might help to identify an elusive border. Having control over the gray scale and contrast level also may assist in identifying a dim border segment. Review of the cine loop should be available not only before tracing but also during tracing so that the border can be traced in segments as they are identified. Cine loop review is also needed to double-check the tracing, which is most easily accomplished by alternately hiding and displaying the border while viewing the images. Tracing and Editing.

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There are two main methods of tracing: continuous drawing and dot entry. Continuous drawing allows direct delineation of complex border shapes, but it requires good hand-eye coordination. With dot entry, the spaces between the dots are filled in using spline curves. Dot entry is easier for the user and faster over regions that have a simple shape. However, in highly curved regions, the spline curve may not put the border where it was intended; in this case, the border would need to be edited. The workstation software should allow editing of any part of the traced border. Programs that allow selected border segments to be stretched in or out to a new position ("rubber banding") are easier to use than programs that delete the border segment and redraw it, because the latter requires more steps, and connecting the new segment smoothly to the raw ends of the remaining original border is difficult. As a final check, the observer should turn off the border overlay, review the cine loop again, and then turn the overlay back on to confirm the accuracy of the border placement. A custom program developed at the University of Washington allows the user to enter additional points on the border to demarcate segments whose definition is of low confidence. This customized option may help in the subsequent data interpretation. These warning points can also be used to omit the affected segments from regional function analysis. The ability to retain partial borders for analysis makes maximum use of the data by reducing the number of patients whose studies are rejected. The use of digital workstations does not reduce the fatigue associated with image analysis. Paying careful attention to details such as ambient lighting, ergonometrically sound furnishings, and periodic rest periods helps to maximize observer attention to detail and improve accuracy. Because of the possibility of fatigue, observers should not trace more than four hours per day on a regular basis. Variability Many factors affect the accuracy of quantitative image analysis and the precision or repeatability of a measurement. One must be aware of these sources of variability so that measures can be taken to minimize their impact. Beat-to-Beat Variability

Because patients are living, breathing subjects, there is variability between

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different cardiac cycles. This variability can be minimized by averaging over multiple consecutive cardiac cycles. Sandor et al[76] reported that threebeat averaging reduced the normal standard deviation for wall motion and wall thickening by 34% and 38%, respectively. Variability is higher during inspiration than expiration; end-expiratory cardiac cycles are least subject to motion artifact (see Fig. 5-10) . [107] Intraobserver and Interobserver Variability

In general, variability is higher for wall thickening than wall motion.[51] [69] [77] This difference is due mostly to point-to-point variability in enddiastolic wall thickness, because normalization of thickness change by enddiastolic perimeter length reduces variability to that of wall motion.[69] Variability in measuring wall thickening can also be reduced if thickness change is normalized by the end-diastolic wall thickness computed over a local region rather than at a discrete point on the ventricular contour.[70] The magnitude of inter- and intraobserver variability is low, ranging from 5% to 10% of the mean measurement for both wall motion and wall thickening, and it is not significantly higher than the variability between consecutive cardiac cycles (see Fig. 5-10) .[57] [77] , [107] [116] Pandian et al[51] reported intraobserver variability exceeding 50% of the mean for wall thickening, perhaps because the 104

beat and frame selection were not held constant between repeated tracings. Variability in measuring regional function is highest at the apex.[52] Pertinent to methods that use a coordinate system based on anatomic landmarks, the intra- and interobserver variability for landmark identification is 4.4% and 3.5% of the ventricular circumference, respectively.[44] Study-to-Study Variability

Echocardiography is the imaging modality most suitable for serial studies (e.g., to follow a patient's response to treatment), because it is safe, portable, and inexpensive. Study-to-study variability is low for 2D echocardiography, ranging from 7% to 15%.[16] [56] Some of the contributing factors cannot be controlled, such as changes in hemodynamic or emotional state. In stable patients, however, day-to-day changes in heart rate and blood pressure are small and do not significantly affect measurement of the ejection fraction.[117] Variability is 5% between studies acquired by different

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sonographers but analyzed by the same observer, which is lower than the 7% variability for images acquired by the same sonographer but analyzed by different observers.[117]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Research Applications Two-dimensional echocardiography is particularly useful as a research tool because of its large informational content. Regional function can be assessed qualitatively or measured quantitatively in terms of endocardial wall motion, wall thickening, or epicardial motion. From wall thickness measurements it is possible to measure mass, wall stress, and even regional stroke work, a parameter of local oxygen consumption.[165] To this list can be added 108

measurement of left ventricular shape, a major determinant of stress and function. The ability to clearly visualize the valve allows assessment of the relationship between valvular and ventricular function.[166] [167] [168] Frameby-frame analysis can be performed to analyze the synchrony of regional function through the cardiac cycle.[116] [169] By infusing echo contrast or performing tissue characterization analysis, the functional status of the myocardium can be related to its perfusion and pathology.[170] [171] By incorporating knowledge of spatial position and orientation of imaging planes, the 2D data can be used to create 3D reconstructions of the left ventricle,[172] which provide a more comprehensive view of this complex organ and allow for more detailed and accurate analysis of spatial relationships. Thus, left ventricular volume can be measured without geometric assumptions concerning its shape, wall thickness can be measured without error from oblique imaging, and shape can be better appreciated in three dimensions. These tools facilitate research to improve understanding of the pathophysiology of the disease process, the mechanisms by which the left ventricle attempts to compensate, and the beneficial effect of therapeutic interventions. However, it is important for investigators interested in applying these techniques to understand the limitations of the method as

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well as its potential benefits. It is generally known that spatial resolution within the imaging plane is higher in the direction of the echo beam than parallel to it. It is equally important to understand that spatial resolution is lowest orthogonal to the imaging plane: the so-called slice thickness owing to finite beam width causes inaccuracy in delineating complex curved surfaces.[173] [174] The temporal resolution, up to 30 frames per second, allows for comparisons of end-diastole to end-systole and analysis of asynchrony,[116] [169] but it may not be adequate for patients with high heart rates (e.g., infants). Two-dimensional echocardiography has been used to acquire the end point measurements in several clinical trials. For example, echocardiographic assessment of wall motion was performed to evaluate functional recovery after angioplasty or thrombolytic therapy for acute myocardial infarction and after coronary artery bypass surgery for angina.[17] [175] [176] [177] Other applications are to test drugs for side effects and to study the effects of anesthetics and surgical procedures.[178] [179] In general, however, echocardiography has not been considered the imaging modality of choice for clinical trials. This fact may be due to poor echogenicity in up to 25% of patients, usually as a result of coexistent lung disease. Another reason may be the reliance on skill, training, and reproducibility of sonographers in acquiring images in comparable imaging planes between patients. New technologic advances in imaging equipment may alleviate this problem in the future, for example, by displaying the position of each imaging plane online to actively assist in properly orienting each acquisition.[180] [181] [182] These sources of data loss and variability are greater than for other imaging modalities, but they are more than compensated for by the much greater informational content of echocardiographic examinations. It can be anticipated that echocardiography will be increasingly employed for clinical investigation in the future.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

References 1. Edwards WD, Tajik AJ, Seward JB: Standardized nomenclature and anatomic basis

for regional tomographic analysis of the heart. Mayo Clin Proc 1981;56:479–497. 2. Schiller, NB, Shah PM, Crawford M, et al: Recommendations for quantitation of the

left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of TwoDimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358–367. 3. Herman MV, Gorlin R: Implications of left ventricular asynergy. Am J Cardiol

1969;23:538–547. 4. Gibson RS, Bishop HL, Stamm RB, et al: Value of early two dimensional

echocardiography in patients with acute myocardial infarction. Am J Cardiol 1982;49:1110–1119. 5. Stamm RB, Gibson RS, Bishop HL, et al: Echocardiographic detection of infarct-

localized asynergy and remote asynergy during acute myocardial infarction: Correlation with the extent of angiographic coronary disease. Circulation 1983;67:233–244. 6. Bourdillon PDV, Broderick TM, Sawada SG, et al: Regional wall motion index for

infarct and noninfarct regions after reperfusion in acute myocardial infarction: Comparison with global wall motion index. J Am Soc Echocardiogr 1989;2:398–407. 7. Kisslo J, Robertson D, Gilbert B, et al: A comparison of real-time, two-dimensional

echocardiography and cineangiography in detecting left ventricular asynergy. Circulation 1977;55:134–141. 8. Ohuchi Y, Kuwako K, Umeda T, Machii K: Real-time, phased-array, cross-sectional

echocardiographic evaluation of left ventricular asynergy and quantitation of left ventricular function: A comparison with left ventricular cineangiography. Jpn Heart

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1980;21:1–15. 9. Hecht HS, Taylor R, Wong M, Shah PM: Comparative evaluation of segmental

asynergy in remote myocardial infarction by radionuclide angiography, twodimensional echocardiography, and contrast ventriculography. Am Heart J 1981;101:740–749. 10. Freeman AP, Giles RW, Walsh WF, et al: Regional left ventricular wall motion

assessment: Comparison of two-dimensional echocardiography and radionuclide angiography with contrast angiography in healed myocardial infarction. Am J Cardiol 1985;56:8–12. 11. Shiina A, Tajik AJ, Smith HC, et al: Prognostic significance of regional wall

motion abnormality in patients with prior myocardial infarction: A prospective correlative study of two-dimensional echocardiography and angiography. Mayo Clin Proc 1986;61:254–162. 12. Lundgren C, Bourdillon PDV, Dillon JC, Feigenbaum H: Comparison of contrast

angiography and two-dimensional echocardiography for the evaluation of left ventricular regional wall motion abnormalities after acute myocardial infarction. Am J Cardiol 1990;65:1071–1077. 13. Ginzton L, Conant R, Brizendine M, et al: Exercise subcostal two-dimensional

echocardiography: A new method of segmental wall motion analysis. Am J Cardiol 1984;53:805–811. 14. Bhatnagar SK, Al-Yusuf AR: Significance of early two-dimensional

echocardiography after acute myocardial infarction. Int J Cardiol 1984;5:575–84. 15. Loh IK, Yzhar C, Beeder C, et al: Early diagnosis of nontransmural myocardial

infarction by two-dimensional echocardiography. Am Heart J 1982;104:963–968. 16. Deutsch HJ, Curtius JM, Leischik R, et al: Reproducibility of assessment of left

ventricular function using intraoperative transesophageal echocardiography. Thorac Cardiovasc Surg 1993;41:54–58. 17. Otto C, Stratton JR, Maynard C, et al: Echocardiographic evaluation of segmental

wall motion early and late after thrombolytic therapy in acute myocardial infarction: The Western Washington Tissue Plasminogen Activator Emergency Room Trial. Am J Cardiol 1990;65:132–138. 18. Chaitman BR, DeMots H, Bristow JD, et al: Objective and subjective analysis of

left ventricular angiograms. Circulation 1975;52:420–425.

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19. Wexler LF, Lesperance J, Ryan TJ, et al: Interobserver variability in interpreting

contrast left ventriculograms (CASS). Cathet Cardiovasc Diagn 1982;8:341–355. 109

20. Lazar HL, Plehn JF, Schick EM, et al: Effects of coronary revascularization on

regional wall motion. J Thorac Cardiovasc Surg 1989;98:498–505. 21. Kan G, Visser CA, Koolen JJ, Dunning AJ: Short and long term predictive value of

admission wall motion score in acute myocardial infarction. A cross sectional echocardiographic study of 345 patients. Br Heart J 1986;56:422–427. 22. Nixon JV, Narahara KA, Smitherman TC: Estimation of myocardial involvement

in patients with acute myocardial infarction by two-dimensional echocardiography. Circulation 1980;62:1248–1255. 23. Horowitz RS, Morganroth J, Parrotto C, et al: Immediate diagnosis of acute

myocardial infarction by two-dimensional echocardiography. Circulation 1982;65:323–329. 24. Gibson DG, Prewitt TA, Brown DJ: Analysis of left ventricular wall movement

during isovolumic relaxation and its relation to coronary artery disease. Br Heart J 1976;38:1010–1019. 25. Goodyear AVN, Langou RA: The multicentric character of normal left ventricular

wall motion. Implications for the evaluation of regional wall motion abnormalities by contrast angiography. Cathet Cardiovasc Diagn 1982;8:225–232. 26. Ginzton LE, Berntzen R, Lobodzinski S, et al: Computerized quantitative segmental wall motion analysis during exercise: Radial vs. centerline left ventricular segmentation. In Ripley KL (ed): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1985, pp 157–160. 27. Rein A, Sapoznikov D, Lewis N, et al: Regional left ventricular ejection fraction

from real-time two-dimensional echocardiography. Int J Cardiol 1982;2:61–70. 28. Assmann PE, Slager CJ, van der Borden SG, et al: Comparison of models for

quantitative left ventricular wall motion analysis from two-dimensional echocardiograms during acute myocardial infarction. Am J Cardiol 1993;71:1262– 1269.

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29. Moynihan PF, Parisi AF, Feldman EL: Quantitative detection of regional left

ventricular contraction abnormalities by two-dimensional echocardiography: I. Analysis of methods. Circulation 1981;63:752–760. 30. Slager CJ, Hooghoudt TEH, Serruys PW, et al: Quantitative assessment of regional

left ventricular motion using endocardial landmarks. J Am Coll Cardiol 1986;7:317– 327. 31. Caiani EG, Cerutti S: Analysis of left ventricular wall motion using dynamic

alignment. Comput Cardiol 2000 (in press). 32. Ingels NB Jr, Mead CW II, Stinson EB, Alderman EL: A new method for

assessment of left ventricular wall motion In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1978, pp 57–61. 33. Homans DC, Sublett E, Lindstrom P, et al: Subendocardial and subepicardial wall

thickening during ischemia in exercising dogs. Circulation 1988;78:1267–1276. 34. Young AA, Kramer CM, Ferrari VA, et al: Three-dimensional left ventricular

deformation in hypertrophic cardiomyopathy. Circulation 1994;90:854–867. 35. Gibson DG, Sanderson JE, Trail TA, et al: Regional left ventricular wall movement

in hypertrophic cardiomyopathy. Br Heart J 1978;40:1327–1333. 36. Sheehan FH, Bolson EL, Dodge HT, et al: Advantages and applications of the

centerline method for characterizing regional ventricular function. Circulation 1986;74:293–305. 37. Wohlgelernter D, Cleman H, Highman A, et al: Regional myocardial dysfunction during coronary angioplasty: Evaluation by two-dimensional echocardiography and 12 lead electrocardiography. J Am Coll Cardiol 1986;7:1245–1254. 38. McGillem MJ, Mancini GBJ, DeBoe SF, Buda AJ: Modification of the centerline

method for assessment of echocardiographic wall thickening and motion: A comparison with areas of risk. J Am Coll Cardiol 1988;11:861–866. 39. Ginzton, LE: Stress echocardiography and myocardial contrast echocardiography.

Cardiol Clin 1989;7:493–509. 40. Sheehan FH, Stewart DK, Dodge HT, et al: Variability in the measurement of

regional ventricular wall motion from contrast angiograms. Circulation 1983;68:550– 559.

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41. Gelberg HJ, Brundage BH, Glantz S, Parmley WW: Quantitative left ventricular

wall motion analysis: A comparison of area, chord and radial methods. Circulation 1979;59:991–1000. 42. Jugdutt BI, Hutchins GM, Bulkley BH, Becker LC: Myocardial infarction in the

conscious dog: Three-dimensional mapping of infarct, collateral flow and region at risk. Circulation 1979;60:1141–1150. 43. Kerber RE, Marcus ML, Ehrhardt J, et al: Correlation between

echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion. Circulation 1975;52:1097–1104. 44. Lieberman AN, Weiss JL, Jugdutt BI, et al: Two-dimensional echocardiography

and infarct size: Relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog. Circulation 1981;63:739–746. 45. Wyatt HL, Meerbaum S, Heng MK, et al: Experimental evaluation of the extent of myocardial dyssynergy and infarct size by two-dimensional echocardiography. Circulation 1981; 63:607–614. 46. Pandian NG, Kyoanagi S, Skorton DJ: Relations between 2-dimensional

echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. Am J Cardiol 1983;52:1318–1325. 47. Hutchins GM, Bulkley BH, Ridolfi RL, et al: Correlation of coronary arteriograms

and left ventriculograms with postmortem studies. Circulation 1977;56:32–37. 48. Homans DC, Asinger R, Elsperger KJ, et al: Regional function and perfusion at the

lateral border of ischemic myocardium. Circulation 1985;71:1038–1047. 49. Buda AJ, Zotz RJ, Gallagher KP: Characterization of the functional border zone

around regionally ischemic myocardium using circumferential flow-function maps. J Am Coll Cardiol 1986;8:150–158. 50. Sheehan FH, Doerr R, Schmidt WG, et al: Early recovery of left ventricular

function after thrombolytic therapy for acute myocardial infarction: An important determinant of survival. J Am Coll Cardiol 1988;12:289–300. 51. Pandian NG, Skorton DJ, Collins SM, et al: Heterogeneity of left ventricular

segmental wall thickening and excursion in 2-dimensional echocardiograms of normal human subjects. Am J Cardiol 1983;51:1667–1673. 52. Assmann PE, Slager CJ, Dreysse ST, et al: Two-dimensional echocardiographic

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analysis of the dynamic geometry of the left ventricle: The basis for an improved model of wall motion. J Am Soc Echocardiogr 1988;1:393–405. 53. Clayton PD, Jeppson GM, Klausner SC: Should a fixed external reference system

be used to analyze left ventricular wall motion? Circulation 1982;65:1518–1521. 54. Force T, Kemper A, Perkins L, et al: Overestimation of infarct size by quantitative

two-dimensional echocardiography: The role of tethering and of analytic procedures. Circulation 1986;73:1360–1368. 55. Parisi A, Moynihan P, Folland E, Feldman C: Quantitative detection of regional

left ventricular contraction abnormalities by two-dimensional echocardiography. II. Accuracy in coronary artery disease. Circulation 1981;63:761–767. 56. Schnittger I, Fitzgerald P, Gordon E, et al: Computerized quantitative analysis of

left ventricular wall motion by two-dimensional echocardiography. Circulation 1984;70;242–254. 57. Zoghbi WA, Charlat ML, Bolli R, et al: Quantitative assessment of left ventricular

wall motion by two-dimensional echocardiography: Validation during reversible ischemia in the conscious dog. J Am Coll Cardiol 1988;11:851–860. 58. Feneley M, Farnsworth A, Shanahan M, Cheng V: Mechanisms of the

development and resolution of paradoxical interventricular septal motion after uncomplicated cardiac surgery. Am Heart J 1987;114:106–114. 59. Feneley M, Gavaghan T: Paradoxical and pseudoparadoxical interventricular septal

motion in patients with right ventricular volume overload. Circulation 1986;74:230– 238. 60. Kittleson MD, Knowlen GG, Johnson LE: Early and late global and regional left

ventricular function after experimental transmural myocardial infarction: Relationships of regional wall motion, wall thickening, and global performance. Am Heart J 1987;114:70–78. 61. Ross J Jr, Franklin D: Analysis of regional myocardial function, dimensions, and

wall thickness in the characterization of myocardial ischemia and infarction. Circulation 1976;53:I88–I92. 62. Heikkila J, Nieminen MS: Echoventriculography in acute myocardial infarction.

IV. Infarct size and reliability by pathologic anatomic correlations. Clin Cardiol 1980;3:26–35.

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110

63. Feneley M, Hickie J. Validity of echocardiographic determination of left

ventricular systolic wall thickening. Circulation 1984;70:226–232. 64. Weiss RJ, Buda AJ, Pasyk S, et al: Noninvasive quantification of jeopardized

myocardial mass in dogs using 2-dimensional echocardiography and thallium-201 tomography. Am J Cardiol 1983;52:1340–1344. 65. Nieminen M, Parisi AF, O'Boyle JE, et al: Serial evaluation of myocardial

thickening and thinning in acute experimental infarction: Identification and quantification using two-dimensional echocardiography. Circulation 1982;66:174– 180. 66. Heikkila J, Tabakin BS, Hugenholtz PG: Quantification of function in normal and

infarcted regions of the left ventricle. Cardiovasc Res 1972;6:516–531. 67. Beyar R, Shapiro EP, Graves WL, et al: Quantification and validation of left

ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach. Circulation 1990;81:297–307. 68. Erbel R, Schweizer P, Meyer J, et al: Sensitivity of cross-sectional

echocardiography in detection of impaired global and regional left ventricular function: Prospective study. Int J Cardiol 1985;7:375–389. 69. Sheehan FH, Feneley MP, DeBruijn NP, et al: Quantitative regional wall

thickening analysis by transesophageal echocardiography. J Thorac Cardiovasc Surg 1992;103:347–354. 70. Yang P, Otto C, Sheehan F: The effect of normalization in reducing variability in

regional wall thickening. J Am Soc Echocardiogr 1997;10:197–204. 71. Dumesnil J, Shoucri R, Laurenceau J, Turcot J: A mathematical model of the

dynamic geometry of the intact left ventricle and its application to clinical data. Circulation 1979;59:1024–1034. 72. Sasayama S, Franklin D, Ross J Jr, et al: Dynamic changes in left ventricular wall

thickness and their use in analyzing cardiac function in the conscious dog: A study based on a modified ultrasonic technique. Am J Cardiol 1976;38:870–879. 73. Azancot I, Masquet C, Bourthoumieux A, et al: Myocardial hypertrophy, rate of

change of free wall thickness and directional components of ventricular power in man.

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J Physiol (Paris) 1981;77:695–703. 74. Aurigemma GP, Silver KH, McLaughlin M, et al: Impact of chamber geometry and

gender on left ventricular systolic function in patients >60 years of age with aortic stenosis. Am J Cardiol 1994;74:794–798. 75. Dong SJ, MacGregor JH, Crawley AP, et al: Left ventricular wall thickness and regional systolic function in patients with hypertrophic cardiomyopathy: A threedimensional tagged magnetic resonance imaging study. Circulation 1994;90:1200– 1209. 76. Sandor T, Henschke C, Risser TA, et al: Quantitative analysis of left ventricular

wall motion and thickness using two-dimensional echocardiography. Int J Biomed Comput 1983; 14:431–439. 77. Ren JF, Kotler Mn, Kakki, AH, et al: Quantitation of regional left ventricular

function by two-dimensional echocardiography in normals and patients with coronary artery disease. Am Heart J 1985;110:552–560. 78. Haendchen RV, Wyatt HL, Maurer G, et al: Quantitation of regional cardiac

function by two-dimensional echocardiography. I. Patterns of contraction in the normal left ventricle. Circulation 1983;67:1234–1245. 79. Henschke CI, Risser TA, Andor T, et al: Quantitative computer-assisted analysis of

left ventricular wall thickening and motion by 2-dimensional echocardiography in acute myocardial infarction. Am J Cardiol 1983;52:960–964. 80. Miyatake K, Yamagishi M, Tanaka N, et al: New method for evaluating left ventricular wall motion by color coded tissue doppler imaging: In vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 81. Isaaz K, Thompson A, Ethevenot G, et al: Doppler echocardiographic

measurement of low velocity motion of the left ventricular posterior wall. Am J Cardiol 1989;64:66–75. 82. Gorcsan J III, Strum DP, Mandarino WA, et al: Quantitative assessment of

alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography: Comparison with sonomicrometry and pressure-volume relations. Circulation 1997;95:2423–2433. 83. Donovan CL, Armstrong WF, Bach DS: Quantitative Doppler tissue imaging of the

left ventricular myocardium: Validation in normal subjects. Am Heart J 1995;130:100–104.

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84. Uematsu M, Miyatake A, Tanaka N, et al: Myocardial velocity gradient as a new

indicator of regional left ventricular contraction: Detection by a two-dimensional tissue doppler imaging technique. J Am Coll Cardiol 1995;26:217–223. 85. Palka P, Lange A, Fleming AD, et al: Doppler tissue imaging: Myocardial wall

motion velocities in normal subjects. J Am Soc Echocardiogr 1995;8:659–668. 86. Galiuto L, Ignone G, DeMaria AN: Contraction and relaxation velocities of the

normal left ventricle using pulsed-wave tissue Doppler echocardiography. Am J Cardiol 1998;81:609–614. 87. Vinereanu D, Khokhar A, Fraser AG: Reproducibility of pulsed wave tissue

Doppler echocardiography. J Am Soc Echocardiogr 1999;12:492–499. 88. Rambaldi R, Poldermans D, Vletter WB, et al: Doppler tissue imaging in the new

era of digital echocardiography. G Ital Cardiol 1997;27:827–839. 89. Jamal F, Derumeaux G, Douillet R, et al: Analysis and quantification of

longitudinal contraction of the left ventricle in myocardial infarction. Value of Doppler myocardial tissue imaging. Arch Mal Coeur Vaiss 1999;92:315–322. 90. Rambaldi R, Poldermans D, Bax JJ, et al: Doppler tissue velocity sampling

improves diagnostic accuracy during dobutamine stress echocardiography for the assessment of viable myocardium in patients with severe left ventricular dysfunction. Eur Heart J 2000;21:1091–1098. 91. von Bibra HV, Tuchnitz A, Klein A, et al: Regional diastolic function by pulsed

Doppler myocardial mapping for the detection of left ventricular ischemia during pharmacologic stress and perfusion testing: A comparison with stress echocardiography and perfusion scintigraphy. J Amer Coll Cardiol 2000;36:444–452. 92. Yin L-X, et al: Ventricular excitation maps using tissue Doppler acceleration

imaging: Potential clinical application. J Amer Coll Cardiol 1999;33:782–787. 93. Gould KL, Lipscomb K, Hamilton GW, Kennedy JW: Relation of left ventricular

shape, function and wall stress in man. Am J Cardiol 1974;34:627–634. 94. Burton AC: The importance of the shape and size of the heart. Am Heart J

1957;54:801–810. 95. Dodge HT, Frimer M, Stewart DK: Functional evaluation of the hypertrophied

heart in man. Circ Res 1974; 34–35(suppl II), II122–II127.

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96. D'Cruz IA, Aboulatta H, Killam H, et al: Quantitative two-dimensional

echocardiographic assessment of left ventricular shape in ischemic heart disease. J Clin Ultrasound 1989;17:569–572. 97. Gibson DG, Brown DJ: Continuous assessment of left ventricular shape in man. Br

Heart J 1975;37:904–910. 98. Lamas GA, Vaughan DE, Parisi AF, Pfeffer MA: Effects of left ventricular shape

and captopril therapy on exercise capacity after anterior wall acute myocardial infarction. Am J Cardiol 1989;63:1167–1173. 99. Tomlinson CW: Left ventricular geometry and function in experimental heart

failure. Can J Cardiol 1987;3:305–310. 100. Bogen DK, Rabinowitz SA, Needleman A, et al: An analysis of the mechanical

disadvantage of myocardial infarction in the canine left ventricle. Circ Res 1980;47:728–741. 101. Mitchell GF, Lamas GA, Vaughan DE, Pfeffer MA: Left ventricular remodeling

in the year after first anterior myocardial infarction: A quantitative analysis of contractile segment lengths and ventricular shape. J Am Coll Cardiol 1992;19:1136– 1144. 102. Mancini GBJ, DeBoe SF, Anselmo E, LeFree MT: A comparison of traditional

wall motion assessment and quantitative shape analysis: A new method for characterizing left ventricular function in humans. Am Heart J 1987;114:1183–1191. 103. Sawada H, Fujii J, Takata H, et al: Quantitation of regional left ventricular wall motion by curvature: Two dimensional echocardiographic analysis. J Cardiogr 1986;16:789–798. 104. Jugdutt BI, Michorowski BL: Role of infarct expansion in rupture of the ventrical

septum after acute myocardial infarction: A two-dimensional echocardiographic study. Clin Cardiol 1987;10:641–652. 105. Crouse LJ, Cheirif J, Hanly DE, et al: Opacification and border delineation

improvement in patients with suboptimal endocardial border definition in routine echocardiography: Results of the phase III Albunex Multicenter trial. J Am Coll Cardiol 1993;22:1494–1500. 111

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106. Feigenbaum H: Digital echocardiography in myocardial infarction. Aust NZ J

Med 1992;22:521–526. 107. Assmann PE, Slager CJ, van der Borden SG, et al: Quantitative echocardiographic

analysis of global and regional left ventricular function: A problem revisited. J Am Soc Echocardiogr 1990;3:478–487. 108. Moynihan PF, Parisi AF, Folland ED, et al: A system for quantitative evaluation

of left ventricular function with two-dimensional ultrasonography. Med Instrum 1980;14:111–116. 109. Conetta DA, Geiser EA, Skorton DJ, et al: In-vitro analysis of boundary

identification techniques used in quantification of two-dimensional echocardiograms. Am J Cardiol 1984;53:1374–1379. 110. Garcia E, Gueret P, Bennett M, et al: Real time computerization of two-

dimensional echocardiography. Am Heart J 1981;101:783–792. 111. Dodge HT, Sandler H, Ballew DW, Lord JD Jr: The use of biplane

angiocardiography for the measurement of left ventricular volume in man. Am Heart J 1960;60:762–776. 112. Helak JW, Reichek N: Quantitation of human left ventricular mass and volume by

two-dimensional echocardiography: In vitro anatomic validation. Circulation 1981;63:1398–1407. 113. Geiser EA, Wilson DC, Wang DA, et al: Autonomous epicardial and endocardial

boundary detection in echocardiographic short-axis images. J Amer Soc Echocardiogr 1998;11:338–348. 114. Vandenberg BF, Rath LS, Stuhlmuller P, et al: Estimation of left ventricular

cavity area with an on-line, semiautomated echocardiographic edge detection system. Circulation 1992;86: 159–166. 115. Lang RM, Vignon P, Weinert L, et al: Echocardiographic quantification of

regional left ventricular wall motion with color kinesis. Circulation 1996;93:1877– 1885. 116. Gillam LD, Hogan RD, Foale RA, et al: A comparison of quantitative

echocardiographic methods for delineating infarct-induced abnormal wall motion. Circulation 1984;70:113–122. 117. Himelman RB, Cassidy MM, Landzberg JS, Schiller NB: Reproducibility of

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quantitative two-dimensional echocardiography. Am Heart J 1988;115:425–431. 118. Brutsaert DL: Nonuniformity: A physiologic modulator of contraction and

relaxation of the normal heart. J Am Coll Cardiol 1987;9:341–348. 119. Azancot I, Vannier D, Vannier A, et al: Utilisation of a minicomputer for analysis

and database management of hemodynamic parameters for routine and research applications. In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1979, pp 441–444. 120. Huhmann W, Duangphung K: Left ventricular wall motion. A comparison of six

evaluation methods. Z Kardiol 1980;69:818–826. 121. Karsch KR, Lamm U, Blanke H, Rentrop KP: Comparison of nineteen

quantitative models for assessment of localized left ventricular wall motion abnormalities. Clin Cardiol 1980;3:123–128. 122. Papapietro SE, Smith LR, Hood WP Jr, et al: An optimal method for angiographic

definition and quantification of regional left ventricular contraction. In Ripley KL, Ostrow HG (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1978, pp 293–296. 123. Falsetti HL, Marcus ML, Kerber RE, Skorton DJ: Quantification of myocardial

ischemia and infarction by left ventricular imaging. 1981;63:747–751. 124. Rozanski A, Diamond GA, Forrester JS, et al: Alternative referent standards for

cardiac normality. Ann Intern Med 1984;101:164–171. 125. Gerstenblith G, Grederiksen J, Yin FCP, et al: Echocardiographic assessment of a

normal adult aging population. Circulation 1977;56:273–278. 126. Tennant R, Wiggers CJ: Effect of coronary occlusion on myocardial contraction.

Am J Physiol 1935;112:351–361. 127. Gould KL, Lipscomb K, Hamilton GW: Physiologic basis for assessing critical

coronary stenosis. Am J Cardiol 1974;33: 87–94. 128. Schwarz F, Flameng W, Thiedemann K-U, et al: Effect of coronary stenosis on

myocardial function, ultrastructure and aortocoronary bypass graft hemodynamics. Am J Cardiol 1978;42:193–201. 129. Sheehan FH, Brown BG, Dodge HT, et al: Quantitative analysis of the

relationship between coronary artery stenosis and regional left ventricular wall

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motion. In Sigwart U, Heintzen PH (eds): Ventricular Wall Motion. Georg Thieme Verlag, Stuttgart, 1984, pp 198–205. 130. McMahon MM, Brown BG, Cukingnan R, et al: Quantitative coronary

angiography: Quantitation of the critical stenosis in patients with unstable angina and single-vessel disease without collaterals. Circulation 1979;60:106–113. 131. Sheehan FH, Mathey DG, Schofer J, et al: Factors determining recovery of left

ventricular function following thrombolysis in acute myocardial infarction. Circulation 1985;71:1121–1128. 132. Harrison DG, Ferguson DW, Collins SM, et al: Rethrombosis after reperfusion

with streptokinase: Importance of geometry of residual lesions. Circulation 1984;69:991–999. 133. Braunwald E, Rutherford JD: Reversible ischemic left ventricular dysfunction:

Evidence for the "hibernating myocardium." J Am Coll Cardiol 1986;8:1467–1470. 134. Cohen M, Charney R, Hershman R, et al: Reversal of chronic ischemic

myocardial dysfunction after transluminal coronary angioplasty. J Am Coll Cardiol 1988;12:1193–1198. 135. Heger JJ, Weyman AE, Wann LS, et al: Cross-sectional echocardiography in

acute myocardial infarction: Detection and localization of regional left ventricular asynergy. Circulation 1979;60:531–538. 136. Nieminen M, Heikkila J: Echoventriculography in acute myocardial infarction II:

Monitoring of left ventricular performance. Br Heart J 1976;38:271–281. 137. Meltzer RS, Woythaler JN, Buda AJ, et al: Two dimensional echocardiographic

quantification of infarct size alteration by pharmacologic agents. Am J Cardiol 1979;44:257–262. 138. Visser CA, Lie KI, Kan G, et al: Detection and quantification of acute, isolated

myocardial infarction by two dimensional echocardiography. Am J Cardiol 1981;47:1020–1025. 139. Weiss JL, Bulkley BH, Hutchins GM, Mason SJ: Two-dimensional

echocardiographic recognition of myocardial injury in man: Comparison with postmortem studies. Circulation 1981;63:401–408. 140. Visser CA, Kan G, Lie KI, et al: Apex two dimensional echocardiography:

Alternative approach to quantification of acute myocardial infarction. Br Heart J 1982;47:461–467.

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141. O'Boyle JE, Parisi AF, Nieminen M, et al: Quantitative detection of regional left

ventricular contraction abnormalities by 2-dimensional echocardiography: Comparison of myocardial thickening and thinning and endocardial motion in a canine heart. Am J Cardiol 1983;51:1732–1738. 142. Van Reet RE, Quinones MA, Poliner LR, et al: Comparison of two-dimensional

echocardiography with gated radionuclide ventriculography in the evaluation of global and regional left ventricular function in acute myocardial infarction. J Am Coll Cardiol 1984;3:243–252. 143. Widimsky P, Gregor P, Cervenka V, Visek V: Two-dimensional

echocardiography in acute transmural and non-transmural myocardial infarction. Cor Vasa 1984;26:12–19. 144. Pandian NG, Skorton DJ, Collins SM, et al: Myocardial infarct size threshold for

two-dimensional echocardiographic detection: Sensitivity of systolic wall thickening and endocardial motion abnormalities in small versus large infarcts. Am J Cardiol 1985;55:551–555. 145. Aebischer N, Bise AC, Gabathuler J, Lerch R: Prognostic value of bidimensional

echocardiography in the acute phase of myocardial infarct. Schweiz Med Wochenschr 1985;115:1641–1646. 146. Widimsky P, Kopsa P, Cervenka V, et al: The possibility of non-invasive

identification of occluded coronary artery in acute myocardial infarction. Cor Vasa 1986;28:428–437. 147. Horowitz RS, Morganroth J: Immediate detection of early high-risk patients with

acute myocardial infarction using two-dimensional echocardiographic evaluation of left ventricular regional wall motion abnormalities. Am Heart J 1982;103:814–822. 148. Ideker RE, Behar VS, Wagner GS, et al: Evaluation of asynergy as an indicator of

myocardial fibrosis. Circulation 1978;57:715–725. 149. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB: The wavefront

phenomenon of ischemic cell death. Circulation 1977;56:786–794. 150. TIMI Research Group: Immediate vs delayed catheterization and angioplasty

following thrombolytic therapy for acute myocardial infarction. J Am Med Assoc 1988;260:2849–2858. 151. Kemper AJ, O'Boyle JE, Sharma S, et al: Hydrogen peroxide contrast-enhanced

two-dimensional echocardiography: Real-time in vivo delineation of regional

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myocardial perfusion. Circulation 1983;68:603–611. 112

152. Nishimura RA, Tajik AJ, Shub AC, et al: Role of two-dimensional

echocardiography in the prediction of in-hospital complications after acute myocardial infarction. J Am Coll Cardiol 1984;4:1080–1087. 153. Guyer DE, Foale RA, Gillam LD, et al: An echocardiographic technique for

quantifying and displaying the extent of regional left ventricular dyssynergy. J Am Coll Cardiol 1986; 8:830–835. 154. Wilkins GT, Southern JF, Choong CY, et al: Correlation between

echocardiographic endocardial surface mapping of abnormal wall motion and pathologic infarct size in autopsied hearts. Circulation 1988;77:978–987. 155. Mann DL, Foale RA, Gillam LD, et al: Early natural history of regional left

ventricular dysfunction after experimental myocardial infarction. Am Heart J 1988;115:538–546. 156. Kaul S, Pandian NG, Gillam LD, et al: Contrast echocardiography in acute

myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis. J Am Coll Cardiol 1986;7:383–392. 157. Maroko PR, Libby P, Ginks WR, et al: Coronary artery reperfusion. I. Early

effects on local myocardial function and the extent of myocardial necrosis. J Clin Invest 1972;51:2710–2716. 158. Mock MB, Ringqvist I, Fisher LD, et al: Survival of medically treated patients in

the Coronary Artery Surgery Study (CASS) Registry. Circulation 1982;66:562–568. 159. Schwartz RS, Ilstrup DM, Vlietstra RE, et al: Weighted ventriculographic wall

motion score for improved survival prediction in patients with coronary artery disease. Cathet Cardiovasc Diag 1989;18:79–84. 160. Nishimura RA, Reeder GS, Miller FA Jr, et al: Prognostic value of predischarge

2-dimensional echocardiogram after acute myocardial infarction. Am J Cardiol 1984;53:429–432. 161. Shah PK, Pichler M, Berman DS, et al: Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol

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1980;46:915–921. 162. Bishop HL, Gibson RS, Stamm RB, et al: Role of two-dimensional

echocardiography in the evaluation of patients with ventricular septal rupture postmyocardial infarction. Am Heart J 1981;102:965–971. 163. Jugdutt BI: Identification of patients prone to infarct expansion by the degree of

regional shape distortion on an early two-dimensional echocardiogram after myocardial infarction. Clin Cardiol 1990;13:28–40. 164. Tischler MD, Niggel J, Borowski DT, LeWinter MM: Relation between left

ventricular shape and exercise capacity in patients with left ventricular dysfunction. J Am Coll Cardiol 1993;22:751–757. 165. Nakano K, Sugawara M, Kato T, et al: Regional work of the human left ventricle

calculated by wall stress and the natural logarithm of reciprocal of wall thickness. J Am Coll Cardiol 1988;12:1442–1448. 166. Kono T, Sabbah HN, Rosman H, et al: Left ventricular shape is the primary

determinant of functional mitral regurgitation in heart failure. J Am Coll Cardiol 1992;20:1594–1598. 167. Boltwood CM, Tei C, Wong M, Shah PM: Quantitative echocardiography of the

mitral complex in dilated cardiomyopathy: The mechanism of functional mitral regurgitation. Circulation 1983;68:498–508. 168. Alam M, Rosenhamer G: Atrioventricular plane displacement and left ventricular

function. J Am Soc Echocardiogr 1992;5:427–433. 169. Weyman AE, Hogan TD Jr, Gillam LD, et al: Importance of temporal

heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia. Circulation 1984;70:102–112. 170. Skorton DJ, Melton HE Jr, Pandian NG, et al: Detection of acute myocardial

infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray-level distributions. Circ Res 1983;52:36–44. 171. Armstrong WF, Mueller TM, Kinney EL, et al: Assessment of myocardial

perfusion abnormalities with contrast-enhanced two-dimensional echocardiography. Circulation 1982;66:166–173. 172. Geiser EA, Lupkiewicz SM, Christie LG, et al: A framework for three-

dimensional time-varying reconstruction of the human left ventricle: Sources of error and estimation of their magnitude. Comput Biomed Res 1980;13:225–241.

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173. Geiser EA, Skorton DJ, Conetta DA: Quantification of left ventricular function by two-dimensional echocardiography: Consideration of factors restricting image quality. Am Heart J 1982;103:905–910. 174. Garrison JB, Weiss JL, Maughan WL, et al: Quantifying regional wall motion and

thickening in two-dimensional echocardiography with a computer-aided contouring system. In Ostrow HG, Ripley KL (eds): Computers in Cardiology. Long Beach, Calif, IEEE Computer Society, 1977, pp 25–35. 175. Presti CF, Gentile R, Armstronf WF, et al: Improvement in regional wall motion

after percutaneous transluminal coronary angioplasty during acute myocardial infarction: Utility of two-dimensional echocardiography. Am Heart J 1988;115:1149– 1155. 176. Touchstone D, Beller GA, Nygaard TW, et al: Effects of successful intravenous

reperfusion therapy on regional myocardial function and geometry in humans: A tomographic assessment using two-dimensional echocardiography. J Am Coll Cardiol 1989;13:1506–1513. 177. Bourdillon PDV, Broderick TM, Williams ES, et al: Early recovery of regional

left ventricular function after reperfusion in acute myocardial infarction assessed by serial two-dimensional echocardiography. Am J Cardiol 1989;63:641–646. 178. Nakashima Y, Maldareli W, Oka Y, Sisto DA: Evaluation of the effects of

different cardioplegic techniques on left ventricular function during coronary artery bypass surgery using transesophageal echocardiography. Cardiovasc Surg 1993;1:587–593. 179. Slavik JR, LaMantia KR, Kopriva CJ, et al: Does nitrous oxide cause regional

wall motion abnormalities in patients with coronary artery disease? Anesth Analg 1988;67:695–700. 180. King DL, Harrison MR, King DL Jr, et al: Improved reproducibility of left atrial

and left ventricular measurements by guided three-dimensional echocardiography. J Am Coll Cardiol 1992;20:1238–1245. 181. Sheehan FH: Measurement of left ventricular function from contrast angiograms

in patients with coronary disease. In Brundage BH (ed): Comparative Cardiac Imaging—Function, Flow, Anatomy, Quantitation. Rockville, Md, Aspen Publications, 1990, pp 101–118. 182. Kloner RA: Coronary angioplasty: A treatment option for left ventricular

remodeling after myocardial infarction? J Am Coll Cardiol 1992;20:314–316.

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113

Chapter 6 - Left Ventricular Diastolic Function Clinical Utility of Doppler Echocardiography Mikel D. Smith MD

Left ventricular diastolic function is recognized as an important contributing factor in the pathophysiology of many common cardiovascular diseases. The clinical manifestations of cardiomyopathy, hypertension, and coronary artery disease are often the result of abnormalities of left ventricular filling. Diastolic dysfunction may be present prior to, or concomitant with, systolic dysfunction. Although treatments are often aimed at improving left ventricular contractile performance, they may conflict with appropriate therapy for diastolic abnormalities. Recently, attention has been increasingly directed toward the diagnosis, evaluation, and treatment of diastolic dysfunction. Although catheterization measurements of diastolic performance remain the standard, these invasive parameters have proved technically challenging and tedious to acquire. In recent years, a large body of literature has accrued describing various Doppler echocardiographic techniques for assessing diastolic function. These methods have given new insight into the flow dynamics of the left ventricle, mitral valve, and pulmonary veins and have allowed a more practical noninvasive assessment of diastolic function. Several features of Doppler flow patterns have emerged as having

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important diagnostic and therapeutic implications. This chapter reviews the state of the art in the Doppler echocardiographic assessment of left ventricular diastolic function, relates these methods to the physiology of left ventricular filling, and describes the use of these techniques in clinical decision making.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Physiology of Diastole Definition. Traditionally, diastole has been described as the portion of the cardiac cycle that begins with aortic closure (S2 ) and ends with mitral closure (S1 ). Importantly, this definition includes the isovolumic relaxation phase. Normal diastolic function may be clinically defined as the ability of the left ventricle to accommodate an adequate filling volume to maintain cardiac output while operating at a low pressure. Phases of Diastole. For descriptive purposes, the diastolic period can be divided into four stages (Fig. 6-1) . [1] After systolic ejection is complete and left ventricular 114

Figure 6-1 Schematic of intracardiac pressures and volumes to define the four stages of diastole. The periods of isovolumic relaxation, rapid filling, slow filling (diastasis), and atrial filling are shown. See text for description. AVC, aortic valve closure; AVO, aortic valve opening; LV, left ventricle; MVC, mitral valve closure; MVO, mitral valve opening. (From Zile M: Mod Concepts Cardiovasc Dis 1989;58:67.)

pressure falls below aortic pressure, the aortic valve closes. This marks the beginning of isovolumic relaxation, which subsequently ends at mitral valve opening. During this interval, pressure continues to fall at a rapid rate, while ventricular volume remains constant. Events occurring during this phase have been attributed mainly to myocardial relaxation and have been shown to be an energy-requiring process. At this time, myofibrils return to their resting state from the contracted state. The left ventricular cavity changes in geometry, while volume remains constant.

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When left ventricular pressure falls below left atrial pressure (crossover point) the mitral valve opens, and the rapid filling phase begins. The peak rate of filling is directly related to the magnitude of the left atrial-left ventricular pressure gradient. Even though relaxation continues, the rapid increase in left ventricular volume counterbalances this effect and results in a gradual rise in pressure. Physiologically, this appears to represent a complex interaction between left ventricular suction (active relaxation),[2] and passive viscoelastic properties of the myocardium (compliance). As relaxation slows and the atrium empties, the atrioventricular pressure gradient gradually dissipates, and this phase of left ventricular filling ends. The third phase of diastole consists of passive filling during diastasis. In this period, the left atrial and ventricular pressures are nearly equal, so filling is mainly the result of pulmonary venous flow, with the left atrium essentially acting as a passive conduit. The amount of filling is directly proportional to left ventricular compliance. The final phase of diastole is atrial contraction. This active process contributes approximately 15% of left ventricular filling in normal subjects and possibly more in patients in various disease states. This phase is most affected by left ventricular stiffness and external pericardial restraint (as a resistance to left atrial ejection), atrial contractility, and left atrial-left ventricular synchrony (i.e., the PR interval). This final phase of diastole is terminated with the subsequent rise in ventricular pressure and mitral valve closure. The last three phases after mitral valve opening have also been termed auxotonic relaxation, since left ventricular volume continues to increase, although pressure changes are variable.[3]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Invasive Measures of Diastolic Function From the description just given, it should be evident that no single parameter can be derived that will adequately describe diastolic performance. Left ventricular filling is the result of a variety of complex forces, including myocardial relaxation, ventricular suction, ventricular stiffness, viscoelastic properties of the myocardium, erectile filling of the coronary arteries, atrial contraction, ventricular interdependence, and pericardial restraint. To understand the role of Doppler echocardiographic information in assessing diastolic function, it is necessary to have a working knowledge of other conventional methods. Traditionally, catheterization-based methods for studying diastolic events have focused on evaluation of the relationship between left ventricular pressure and volume. Because of the dynamic nature of diastole, measurements have been derived to describe the function of the ventricle during its isolated phases. The indices of function have centered on the evaluation of relaxation, filling, or compliance (Fig. 6-2) . As shown, these measurements are not interchangeable and, like Doppler descriptors, describe different phenomena during the sequential phases of diastole. They may also be variably influenced by changes in factors such as load or heart rate (Table 6-1) . Hemodynamic indices describing early diastolic events include peak -dP/dt, the time constant of isovolumic left ventricular pressure decay or tau (τ), the isovolumic relaxation time (IVRT), and the half-time of ventricular pressure decline (T1/2 ).[4] [5] Peak -dP/dt. Just after aortic valve closure and early during the isovolumic phase, left ventricular pressure falls exponentially. The maximal rate of this rapid pressure decline (peak -dP/dt) can be obtained with high-fidelity,

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micromanometer-tipped catheters in the ventricular cavity. This value is taken as the lowest value of the first derivative of left ventricular pressure (see Fig. 6-2) and typically yields values in the range of 2000 ± 400 mm Hg per second for normal subjects.[6] [7] The index becomes decreased (less negative) with impaired relaxation due to ischemia. [7] However, the peak dP/dt is dependent on sympathetic tone and absolute aortic pressure and reflects properties of left ventricular relaxation at a single point in time.[8] [9] Tau. Weiss' group and others[7] , [9] [9] have proposed the use of a time constant of relaxation (tau, τ) to describe pressure fall throughout isovolumic diastole. The measurement 115

Figure 6-2 Schematic showing the relationship of pressures, rate of pressure change (dP/dt), volumes, and Doppler transmitral and pulmonary venous flows. The portion of the cardiac cycle and index of diastolic function are shown in block letters and include tau, isovolumic relaxation time (IVRT), peak -dP/dt, peak filling rate (PFR), rapid filling fraction (RFF), and atrial filling fraction (AFF) along with the corresponding Doppler measures of transmitral and pulmonary venous flow. The derivation of these indices is described in the text, and the characteristics and limitations of these parameters are listed in Table 6-1 . Kv, modulus of chamber stiffness.

assumes a monoexponential decay in left ventricular pressure from aortic closure (taken as peak -dP/dt) to an arbitrary point 5 mm Hg above enddiastolic pressure (approximating mitral valve opening). The pressure values are converted to a logarithmic scale and fitted to a straight line (Fig. 6-3) . The negative reciprocal of the slope of this line represents the exponential decay time constant (TL) and is expressed in milliseconds. Normal values for tau range from 25 to 40 msec. Higher values represent reduced early diastolic distensibility due to relaxation at excessively slow rates. Tau may be relatively load independent[6] but does not describe events during any phases of ventricular filling. Nevertheless, the time constant of relaxation remains an accepted standard and widely used invasive descriptor of left ventricular diastolic function. Chamber Stiffness. Catheterization methods have also been derived for pressure-volume events

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during filling. The assessment of diastolic mechanics in the catheterization laboratory requires highly accurate determinations of both pressure and volume. The simultaneous recording of these values allows the calculation of compliance as the rate of change in volume per rate of change in pressure, dV/dP (Fig. 6-4) . The reciprocal of this value, dP/dV (called chamber stiffness), is usually derived by obtaining pressures at different volumes, measured at end-diastole. Since this relationship is exponential for the left ventricle, the rate of change is calculated from a single point and represents the instantaneous slope of the tangent to this curve. Chamber stiffness values are preload dependent, so that an increase in volume from point A to point B will result in an increase in chamber stiffness (see Fig. 64A) . However, when dP/dV is plotted against pressure, a linear relationship exists for a given ventricle (see Fig. 6-4B) . The slope of the line describing chamber stiffness versus pressure is called the modulus of chamber stiffness, or Kv. Although Kv is relatively independent of pressure and volume, comparison between ventricles of different volume must be normalized for chamber stiffness (i.e., VdP/dV). The reciprocal dV/VdP represents specific chamber compliance. Normal values for Kv range from 0.010 to 0.025, and dV/VdP data generally fall between 0.015 and 0.045.[10] Although often difficult to acquire, these values are descriptive of events occurring in late diastole and define the passive components of ventricular filling. The values have not been validated for acute conditions, making comparisons among patients somewhat impractical.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Radionuclide Descriptors of Filling Contrast ventriculography and radionuclide angiography have been used to describe the volume changes that occur with ventricular filling.[11] When volumes are calculated and plotted over time, the resultant curve can readily define the rapid filling, diastasis, and atrial contraction phases of diastole (see Fig. 6-2) . The first derivative of this time-activity curve (dV/dt) describes the peak filling rate and time to peak filling rate. Other available measurements include the atrial filling fraction and early or rapid filling fraction. In summary, there are a number of time-honored methods for describing left ventricular diastolic function. Catheterization methods have the advantage of combining pressures with volume but are tedious, often define only a single point in time, and are load dependent. Although these elegant indices can provide significant insight regarding the physiology of ventricular diastole, their practical application to individual patients remains limited.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Doppler Echocardiographic Indices of Diastolic Function Isovolumic Relaxation Time Dynamic left ventricular relaxation begins at the time of peak systolic pressure.[12] The process continues as ventricular pressure falls below aortic pressure, ejection ceases, and the valve closes. Left ventricular pressure continues to fall even as volume remains constant during the isovolumic phase of diastole but prior to mitral valve 116

TABLE 6-1 -- Description and Limitations of Conventional Diastolic Function Indices Index Description Limitations Catheterization -dP/dt First derivative of LV pressure Sympathetic tone and decay during IVRT afterload dependent No filling data Tau (τ) Time constant of exponential No filling data decay of LV pressure during isovolumic period Kv Modulus of LV chamber Requires multiple stiffness measured at endpressures/volumes diastole Normalized for volume Radionuclide Peak filling Maximal slope of filling curve No pressures

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rate Rapid filling Fraction of early, late filling fraction, atrial filling fracture Transmitral Doppler IVRT Continuous wave Doppler across MV, aortic valve; time between aortic closure, MV opening Peak E, Ei Peak A, Ai

Early filling velocities and integrals Late filling velocities and integrals

No data during IVRT

Age dependent

No filling data Preload dependent Age dependent

Limited by atrial function, heart rate, and rhythm Deceleration Deceleration time from peak E Preload dependent time to baseline velocity Pulmonary vein Doppler Peak S, Si Forward flow velocities from Age and preload atrial relaxation and MV dependent annulus motion Mitral regurgitation Peak D, Di Forward flow velocities due to Age and preload LV relaxation dependent S/D Systolic fraction; ratio (%) Age and preload from Si /Di dependent Atrial reversal

Reverse flow due to atrial contraction

Age dependent

Limited by atrial function, LV compliance A, atrial filling velocity; Ai , integral of atrial filling velocity; D,

diastolic velocity; Di , integral of diastolic velocity; E, early filling

velocity; Ei , integral of early filling velocity; IVRT, isovolumic relaxation

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time; Kv, modulus of left ventricular chamber stiffness; LV, left ventricular; MV, mitral valve; S, systolic velocity; Si , integral of systolic velocity.

Figure 6-3 The derivation of the time constant of relaxation (tau) from left ventricular (LV) pressure recordings. A, Plot of LV pressure over time. The solid line represents the monoexponential decay during the isovolumic period. B, Plot of the log of these LV pressure values over time. The reciprocal of the slope of this line represents tau (TL ) expressed in milliseconds. A, slope of the line; TL , tau.

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Figure 6-4 Derivation of the modulus of chamber stiffness from pressure and volume recordings in the left ventricle. A, Pressure/volume plot for the left ventricle is shown in a hatched line. Pressures are obtained at two separate volume states (A and B). The slope of the tangent of this line at these points represents stiffness, dP/dV. B, The stiffness values at points A and B plotted versus pressure, which gives a straight (dashed) line. The slope of this line is called chamber stiffness, Kv.

opening. M-mode echocardiography with simultaneous phonocardiography traditionally has been used to assess the length of this period between aortic closure and mitral opening.[13] With the aortic closure sound (phono) recorded on a separate channel from but with the same time sweep as mitral leaflet opening (M-mode echo), the aortic closure-mitral opening time interval (representing IVRT) can be readily measured. The IVRT has been described for normal subjects and for subjects in various disease states, including hypertrophic cardiomyopathy and ischemic heart disease.[14] [15] Generally, as relaxation becomes impaired, the IVRT is prolonged, with normal values approximating 65 ± 20 msec.[16] More recently, the phonocardiographic method has been replaced by a continuous wave Doppler echocardiographic method. In this technique, the continuous wave beam is directed from the apical five-chamber view across the region between the aortic outflow tract and the mitral inflow tract (Fig. 6-5) . The Doppler echocardiographic spectrum in this position includes aortic valve flow with valve closure and the onset of mitral inflow, so that

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the aortic closure-mitral opening interval can be determined. Comparisons of Doppler IVRT with catheterization measurements of this time period have shown reasonable correlations.[17] Notably, nuclear scintigraphy conventionally includes the IVRT in the early filling phase, since the volume/count technique is unable to distinguish isovolumic changes.[11] [18] [19]

The IVRT has been demonstrated to be shortened in restrictive cardiomyopathy, probably because of high left atrial pressures resulting in early mitral opening.[20] Although the IVRT describes a limited portion of early diastole, abnormalities of this index have been described as a noninvasive predictor of ventricular diastolic dysfunction in doxorubicininduced cardiomyopathy.[21] However, measurement of the IVRT as the sole predictor of diastolic function is limited, since no information on ventricular filling is provided (see Table 6-1) . Transmitral Flow The use of pulsed Doppler echocardiography to describe events of left ventricular filling is based on the assumption that transmitral blood flow velocities are representative of volumetric flow.[22] According to the law of conservation of mass, true volumetric transmitral flow is equal to the velocity of flow times the area of the orifice (F = A × V). Thus, the dynamic nature of the mitral orifice during diastole plays a role in producing the flow profile. Although the mitral cross-sectional area remains Figure 6-5 Technique for measurement of isovolumic relaxation time by continuous wave Doppler with the beam directed between the aortic outflow tract and mitral inflow. The interval between aortic valve closure (valve click) and onset of mitral flow can be measured in milliseconds (arrow).

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Figure 6-6 Normal pulsed wave Doppler recording taken from mitral valve tips showing peak E (early) and A (late) diastolic flows as well as a low-velocity flow during diastasis (L wave). The integrated area under the early peak (Ei ) and late peaks (Ai ) can be measured, as can the deceleration time (DT).

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relatively constant in size at the annulus level, the diastolic area of flow constantly changes at the leaflet tips.[23] The Doppler velocity profile, therefore, does not represent a direct recording of volumetric flow but is proportional to the atrioventricular pressure gradient, according to the modified Bernoulli equation: P1 − P2 = 4(V2 ), one of the main

determinants of transvalvular blood flow.[24] [25] True volumetric flow rates can be derived when combined with valve area measurements, although a significant benefit of this step in assessing diastolic function has not been well established.

The typical pulsed wave Doppler transmitral spectral pattern is shown in Figure 6-6 . The two phases of forward flow in early diastole and late diastole can be readily identified by their triangular shape and are separated by a brief period of diastasis. The early phase, or E wave, represents flow during the rapid filling phase, while the second peak, or A wave, represents transmitral flow occurring as a result of atrial contraction. The E and A waves are two well-defined peaks within the spectrum and usually display a linear upslope and downslope that can be measured as acceleration and deceleration, respectively, in centimeters per second.[2] Other conventional measurements include the peak E and A velocities, as well as the integrated areas within each phase, Ei and Ai . At slower heart rates, the E and A waves are separated by low, flat velocities during diastasis. These velocities are more readily recorded using low wall filter settings and sweep speeds of 50 or 100 mm per second. Occasionally, a separate distinct and positive inflow wave is seen immediately after the E wave; this wave has been designated the L wave (see Fig. 3-6) . It is thought to represent pulmonary venous flow passing through the left atrium, which acts as a conduit during this period.[26] Studies performed to compare transmitral velocities with ventricular cineangiography have found a significant correlation for both early and late phases. [17] [27] , [28] Studies by Friedman et al[11] and Spirito et al [19] demonstrated similar findings for Doppler versus radionuclide techniques. However, filling time intervals between Doppler and these methods have not correlated well, in part because of the inclusion of IVRT by nuclear methods but not by Doppler echocardiography.[11] Normative data from Doppler transmitral velocities have been reported mainly as control data for studies of various disease states.[29] [30] [31] [32] [33] [33] A normal peak E wave velocity is in the range of 70 to 100 cm per second,

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with a peak A wave of 45 to 70 cm per second, resulting in an E/A ratio of 1.0 to 1.5. The normal deceleration time (DT) for the E wave is 160 to 220 msec. Table 6-2 gives a summary of normal values from various echocardiography laboratories as taken from the literature. The recording methods and the populations sampled vary considerably among centers. Therefore, normative data should be established for each laboratory using standard examination and measurement techniques so that individual subjects can be evaluated against control subjects. Abnormal Transmitral Flow Patterns

Although the ranges for normal values are wide and Doppler parameters are affected by a variety of hemodynamic and physiologic factors, patients with proven diastolic dysfunction have been shown to demonstrate characteristic abnormalities in the spectral flow profile. Rarely is a single finding diagnostic of a specific disease process, but constellations of abnormalities tend to be present for a given pathophysiologic condition.[34] Thus, three distinct clinical patterns of abnormal transmitral flow have been described. [34] [35] [36]

The first pattern consists of a prolonged IVRT and deceleration time with a reduced peak E and an increased peak A wave velocity (Fig. 6-7) . These findings have been associated with normal early diastolic filling pressures and are attributed to impaired left ventricular relaxation.[35] [37] The delay in relaxation directly lengthens the IVRT and produces a smaller atrioventricular gradient in early diastole. The effect is a reduced E wave velocity with a more Figure 6-7 Impaired relaxation pattern of Doppler transmitral flow. A reduced E wave velocity, prolonged deceleration time (DT), and predominant flow during atrial contraction (A) are characteristic of this pattern.

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TABLE 6-2 -- Normal Values Reported for Transmitral Flow b

Study

Age Sample Subjects Range Volume Peak E Ei Peak A Ai (N) (yr) Location (cm/sec) (cm) (cm/sec) (cm) E/A

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Takenaka, et al[14]

16 19–60 Tips

60 ± 9

— 38 ± 8

Gardin, et al[56]

52 21–78 Midleaflet

54 ± 12

— 47 ± 11

Graettinger et al[31]

47 12–14 Tips

Maron et al

35

73 ± 12 6.5 39 ± 7 ± 1.4 69 ± 12 — 27 ± 7

29

[96]

Bryg et al [42]

Gardin et al

Highest recorded

33 30–49 Highest 62 ± 14 recorded

— 33 ± 7

18

— 46 ± 13

50

Highest 59 ± 14 recorded

10 24–29 Annulus 108 ± 10

— 58 ± 15

12 30–49 Annulus 103 ± 16

— 71 ± 17

10 50–68 Annulus 91 ± 16

— 80 ± 15

8 21–30 Tips

66 ± 11

— 41 ± 7

18 61–70 Tips

45 ± 10

— 55 ± 11

[32]

Douglas et al[30]

17 29–60 Annulus 62 ± 9

— 40 ± 8

— 1.52 ± 0.25 — 1.06 ± 0.35 2.2 1.37 ± ± 0.5 0.2 — 2.7 ± 0.7 — 2.0 ± 0.6 — 1.2 ± 0.4 — 1.98 ± 0.53 — 1.52 ± 0.36 — 1.07 ± 0.41 — 1.6 ± 0.31 — 0.82 ± 0.34 — 1.61 ± 0.39

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Appleton et al[35]

40 22–60 Tips

Hatle et al

20 27–63 Tips

1.5 ± 0.32 1.1 ± 0.3 0.89 ± 0.4 0.87 ± 0.17 86 ± 16 13 ± 56 ± 13 5.5 1.6 2.9 ± ± 1.1 0.5 84 ± 18 — 61 ± 14 — —

40 25–65 Tips

86 ± 16

[115]

Drinkovic et al[28]

Pearson et al[89]

24 42–76 Annulus 68 ± 12 8.6 ± 1.8 62 20–66 Tips 64 ± 10 8.9 ±2

48 ± 11 3.6 ± 1.0 59 ± 8 5.3 ± 1.1 Annulus 47 ± 13 6.1 52 ± 10 4.3 ± ± 1.5 0.9 18 65–84 Annulus 58 ± 15 — 69 ± 17 —

[107]

— 1.6 ± 0.5 Kitzman et 10 21–32 Tips 82 ± 12 11 ± 43 ± 10 4.1 1.85 [29] al 2.6 ± ± 1.2 0.25 10 62–73 Tips 56 ± 13 7.9 59 ± 14 5.5 0.92 ± ± ± 2.2 1.2 0.4 25 25–45 Tips 74 ± 8 — 38 ± 3.2 2.5 1.96 Cacciapuoti [33] ± ± et al 0.7 0.2 25 46–65 Tips 73 ± 7 — 38 ± 3 2.4 1.82 ± ± 0.6 0.25 25 66–85 Tips 70 ± 5 — 62 ± 3.1 2.6 1.28 ± ± 0.5 0.24 A, atrial filling velocity; Ai , integral of actual filling velocity; E, early fil Klein et al

— 56 ± 13

[36]

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filling velocity; IVRT, isovolumic relaxation time. gradual downslope (or prolonged deceleration time). The increased peak A wave velocity and Ai are likely the result of diminished early diastolic flow

with a higher left atrial residual volume at the time of atrial contraction.[35]

A second transmitral flow pattern has been termed restrictive (Fig. 6-8) . The characteristics of this pattern are a short (or normal) IVRT and reduced deceleration time, along with increased E wave and diminished A wave Figure 6-8 Restrictive pattern of Doppler transmitral flow. The high early velocity (E), short deceleration time (DT), and diminished atrial velocity (A) are typical of this pattern.

velocities.[20] [36] Thus, filling is predominantly shifted to the rapid filling phase in early diastole and is thought to be due to a high cross-over pressure at the time of mitral valve opening in the presence of a relatively nondistensible left ventricle. The result is a high early velocity of transmitral flow but with rapid equilibration of the atrioventricular pressures and an abrupt cessation of flow (short deceleration time). Late diastole is characterized by diminished atrial transport caused by high left ventricular pressures, poor atrial function, or both.[20] [36] A third pattern has been termed normalized or pseudonormal.[35] This pattern has characteristics of normal transmitral velocities but results from counterbalancing influences of both abnormal relaxation and restrictive forces. This pattern represents an intermediate pattern between the two ends of the pathologic spectrum and may be viewed as a transition from one pattern to another.[34] An example of a pseudonormal pattern is shown in Figure 6-9 . The pseudonormal flow pattern shows nearly equal E and A wave velocities, with a deceleration time that is either normal or shortened. The fact that flow patterns can be seen to change over time within individual patients has caused concern that transmitral Doppler tracings alone may not be used to 120

Figure 6-9 Pseudonormal pattern of Doppler transmitral flow. Nearly equal E and A velocities, with a slightly prolonged deceleration time

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(DT), are shown.

identify diastolic dysfunction.[38] [39] Indeed, it is currently recognized that patients with a pattern of impaired relaxation may convert to "normal" (pseudonormal) as a result of increased mitral regurgitation, hypervolemia, or increased ventricular stiffness resulting from progression of the underlying disease. These physiologic changes can all potentially produce an increased E wave and more rapid deceleration slope. Similarly, the restrictive pattern may be affected by lowering preload.[40] [41] The ability of Doppler flow patterns to mutate as a result of changes in load compromises the use of these recordings from a single examination to assess diastolic function. Thus, serial studies, along with available clinical or direct hemodynamic information, may be beneficial in sorting out findings in individual patients. In addition, studies of Doppler recordings of pulmonary vein flow have contributed to knowledge in this area. Physiologic Factors Affecting Transmitral Flow

A number of physiologic variables have been shown to influence the pattern of flow across the mitral valve during diastole; these include age, heart rate, heart rhythm, loading conditions, systolic function, atrial function, and phases of respiration. The complex interplay of these parameters results in the final spectral Doppler echocardiographic signal. It is therefore important to consider each of these factors to interpret the clinical relevance of the Doppler echocardiographic findings. Age.

Age has been found to be an important determinant of the transmitral flow profile.[32] [42] In studies of normal populations, the peak E wave and integrated E wave (Ei ) velocities have been shown to decrease with advancing age from 20 to 75 years. The peak A and Ai velocities increase

with age, resulting in a decreased E/A ratio.[43] Furthermore, the IVRT and deceleration time have been demonstrated to be progressively longer with age. Thus, Doppler examination of normal, young patients may resemble the restrictive pattern, whereas patients with advanced age often show findings compatible with impaired relaxation. It has been proposed that these changes are due to the development of left ventricular hypertrophy, since wall thickness and mass are known to increase over time in the normal population.[44] An increase in hypertrophy

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and myocardial stiffness could lead to delayed relaxation and result in prolonged IVRT, decreased E wave, and longer deceleration time. This development of a "physiologic state of hypertrophy" remains hypothetical, since Doppler echocardiographic characteristics were not dependent on blood pressure or left ventricular mass in these studies.[29] Heart Rate.

Changes in heart rate affect the resulting transmitral flow pattern by several mechanisms. As heart rate increases and the diastolic interval is shortened, the A wave begins to encroach on the preceding E wave. Studies of patients with dual-chamber pacemakers have shown a decreased E wave peak velocity and Ei , with concomitant increases in A waves with heart rates up to 90 beats per minute. [45] The increase in atrial contribution may be due to a reflex increase in myocardial contractility (the Bowditch phenomenon); a rise in left atrial pressure; or, more simply, the result of higher atrial volume at the onset of atrial systole due to elimination of diastasis.

Similarly, in normal volunteers with atrial pacing via a transesophageal electrode, the peak A wave was seen to increase by a mean value of 8 cm per second for each increment of 10 beats per minute in heart rate.[46] Most studies have shown that at rates greater than 100 beats per minute, the E and A waves become fused, making conventional measurements of peak velocities, velocity integrals, and acceleration or deceleration unobtainable in most cases (Fig. 6-10) . Heart Rhythm.

Changes in atrioventricular synchrony due to alterations in the PR interval, atrial fibrillation, or ectopic rhythms can cause dramatic changes in Doppler transmitral flow. A prolongation of the PR interval usually results in a reduced E wave component, possibly due to more complete atrial emptying and a reduced diastolic time interval, especially during the rapid filling period. Atrial ectopic rhythms and heart block may provide a variety of E and A wave profiles depending on the timing of atrioventricular dyssynchrony (Fig. 6-11) . Atrial fibrillation results in an absence of organized A wave velocities, with variable E waves, depending on the length of the preceding RR interval. Loading Conditions.

Loading conditions have a substantial impact on the Doppler transmitral flow pattern. The most important variable appears to be the left ventricular

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preload, which can have a profound effect on E wave velocities. A study by Choong et al[40] first demonstrated that the administration of nitroglycerin reduced the peak Figure 6-10 Fusion of the E and A waves due to increased heart rate. The peak early (arrow) and late velocities remain distinguishable.

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Figure 6-11 Doppler transmitral flow in a patient with atrial fibrillation. The tracing shows variability in peak E wave velocities depending on RR interval. No A wave velocities are present.

E, Ei , and deceleration rates of the rapid filling phase without significant

changes in A wave parameters. Most importantly, these changes were noted to resemble the pattern of impaired relaxation, even though there was no hemodynamic evidence for diastolic dysfunction. The mechanism for these changes is felt to be related to a decreased left atrium—left ventricle pressure gradient at the time of mitral valve opening ("cross-over pressure"), which results in lower E wave velocities. [47] Other studies using a tilt table or lower body negative pressure have substantiated these findings.[48] Conversely, increasing preload by volume expansion in a canine model has been shown to result in an increased peak E wave velocity, with a lesser effect on the A wave. [49] Of all hemodynamic parameters evaluated, left atrial pressure was the most significant determinant of peak E wave values. Systolic Function.

Left ventricular systolic function also affects the transmitral flow rate during the rapid filling phase. Studies in dogs[50] and humans[51] have shown that left ventricular end-systolic volume is indirectly correlated with peak E wave velocity. Thus, in the presence of systolic dysfunction or increased afterload, the early diastolic velocities can be expected to be reduced, with deceleration time prolonged. These important studies make it clear that one must take volume status and loading conditions into account before classifying patients into categories of diastolic dysfunction. Obviously, patients evaluated in an

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echocardiographic laboratory may be subject to extremes of load and volume due either to the underlying disease process or to treatment with vasoactive drugs. Careful consideration of these circumstances must be given to individual patients during analysis of the Doppler data. Atrial Function.

The size and functional status of the left atrium itself may contribute to changes in the Doppler transmitral flow profile. For example, it has been noted that the reduced atrial contractility (or "atrial stunning") that occurs after cardioversion of patients with atrial fibrillation or flutter results in a reduced peak A-wave velocity.[52] Thus, despite restoration of sinus rhythm, the atrial transport function (and A wave component) of diastole may remain impaired for weeks after cardioversion.[52] , [53] Theoretically, any acute process affecting atrial function (e.g., inflammation, scarring, or infarction) could produce similar abnormalities in transmitral flow. Respiration.

The physiologic intrathoracic pressure changes that occur during normal breathing produce minor changes in transmitral flow. As a result of negative pressures—and, consequently, enhanced peripheral venous return—developed during inspiration, right heart and transtricuspid flows predominate.[54] [55] Concurrently, the transmitral velocity spectrum yields reduced peak E wave velocities in the range of 5% to 10%.[55] Since little or no change is seen in the corresponding A wave, the E/A ratio may fall slightly under that seen in normal circumstances. These changes are compatible with known physiologic reduction of left ventricular preload during inspiration. However, in situations of acute right heart strain or pericardial tamponade, the effect of respiration on transmitral flow has been shown to be much more dramatic. To minimize respiratory changes, most laboratories record the transmitral spectral Doppler echocardiogram with the patient in held, shallow endexpiration. Technical Considerations of Transmitral Flow Measurements Two-Dimensional Imaging Plane.

Doppler recordings of transmitral flow must be performed in a standardized fashion for consistency. Since the Doppler equation includes a term for angle of incidence (cos theta), the technique for recording transmitral flow

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velocities is optimally performed from the apical window (four-chamber, two-chamber, or long-axis views). Most laboratories use the four-chamber view because of its orthogonal relationship to the major diameter of the mitral annulus. Pulsed Wave versus Continuous Wave Doppler.

Because of its superior temporal and range resolution, pulsed wave Doppler echocardiography is the preferred technique for recording transmitral flow. Although the continuous wave method may ensure that the highest velocities are recorded, these signals may arise from other locations along the interrogating beam path (i.e., from aortic insufficiency) rather than via diastolic transmitral flow. In addition, the pulsed wave signal provides a "cleaner" outer border that readily lends itself to tracing peak velocities and slopes. However, the continuous wave Doppler technique is required for obtaining the IVRT, as previously described. Sample Site.

Studies in the literature differ according to optimal location of the pulsed wave sample volume. Some investigators have recommended placing the sample volume near the center of the mitral annulus, just on the ventricular side, using two-dimensional imaging for positioning. This scheme has the advantage of being more reproducible among patient studies and providing a better evaluation of the atrial component.[56] Recordings made between the mitral leaflet tips yield higher velocities of flow and a better assessment of the rapid filling phase.[57] [58] Since no clear consensus currently exists, each laboratory must establish a protocol for recording and analysis, as the spectral profiles often differ at these locations (Fig. 6-12) . As shown in Table 6-2 , normal values are sample site dependent, and published studies must be read carefully if the methods are to be reproduced.

122

Figure 6-12 Pulsed wave Doppler transmitral flow recordings from the two most commonly used sample sites. Top, Spectral pattern recorded from mitral valve leaflet tips shows nearly equal E and A wave components. Bottom, Recording from mitral valve annulus level demonstrating a smaller E wave and predominant A wave. Modal Velocity.

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Flow through the normal mitral orifice with normal cardiac output remains essentially laminar and has a blunt profile.[59] Thus, the border of the pulsed wave velocity spectrum generally exhibits very little spectral dispersion, since at any given instant the red cell targets within the region of interest are moving at nearly the same speed and direction. However, the border does show a finite width. The darkest portion of this band represents the modal velocity and has been suggested as the best location for tracing or measuring the spectrum, as it should be less susceptible to changes in gain. [56]

E and A Waves.

At slower heart rates, the early (E) and late (A) contributions to left ventricular filling can be readily identified, as well as the lower velocities occurring during diastasis (if wall filters are kept low). However, at heart rates above 100 beats per minute, the individual E and A waves often become fused,[46] making measurements of Ei and Ai difficult. At higher

heart rates (around 130 beats per minute), peak velocities may not be readily discriminated and appear as a single large wave (see Fig. 6-10) . Various approaches have been taken to this problem. For example, the E and A waves can be measured by extrapolating the descending and ascending slopes, respectively, through the merged portion of velocity spectrum. Another approach involves dropping a perpendicular line from the point of convergence. Our experience suggests that integrated timevelocity values may be less reliable in this setting and that perhaps only peak velocity values should be used, since these usually remain distinctly visible. The E wave deceleration time can usually be obtained by extrapolating the visible portions of the downslope to the baseline. If Ei and

Ai are to be measured, a convention should be adopted for the laboratory. It should be noted that use of these different methods may account for differences in time-velocity integrals and time intervals between separate examinations and centers. Diastasis.

The velocities recorded between the E and A waves represent the ventricular filling that occurs during diastasis. Normally these velocities are low and represent a very small contribution to overall volume of flow. Indeed, if wall filters are increased to eliminate noise around the baseline, the velocity spectrum during the period may be completely eliminated. Since this portion of the Doppler spectrum may be helpful in understanding

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pulmonary vein flows, the wall filters should be adjusted as low as possible to eliminate noise and yet preserve the outer border of the spectrum during this time period. Deceleration Slope versus Deceleration Time.

Measurements of the descending limb of the transmitral E wave have been reported in terms of both deceleration slope (cm per second squared)[14] [60] and time (msec).[35] [36] The slope is defined by the rate of decline from the peak velocity, whereas deceleration time describes the time interval between peak velocity and the point of intercept of the decay slope (or extrapolated slope) with the baseline. Although these parameters have both been used to describe relaxation events in early diastole, they are not equivalent. The deceleration slope is influenced by and directly related to peak E velocity, whereas deceleration time has the advantage of being more independent of the E velocity.[34] Pulmonary Vein Flow Normal Patterns

Doppler echocardiographic recordings of flow within the pulmonary venous system have been obtained using both transthoracic and transesophageal windows. [61] These spectral patterns have yielded important insight into the physiology of left ventricular filling and diastolic function. The pattern of flow is largely determined by transmitral flow and left atrial function. A typical example of pulsed wave Doppler recording of pulmonary vein velocities is shown in Figure 6-13 . The pattern consists of two forward waves and one reverse (below the baseline) wave. One forward wave occurs during systole (S) and coincides with left atrial relaxation immediately after atrial contraction. The systolic wave occasionally demonstrates two separate components at slow heart rates; these may be distinguished by a notch in the upslope (see Fig. 6-13B) . The early component (SE ) is thought to result from atrial relaxation, and the late systolic wave (SL ) has been described as originating from movement of the mitral annulus toward the apex.[61] [62]

The other forward wave occurs during diastole (D) and coincides with the early transmitral flow and ventricular filling but is delayed by approximately 50 msec.[26] In this

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123

Figure 6-13 Normal Doppler pulmonary vein flow tracings using transthoracic (A) and transesophageal (B) techniques. A, Nearly equal systolic (S) and diastolic (D) waves and a small reverse flow at enddiastole (Ar). B, Transesophageal recording demonstrates laminar flow with well-defined early (SE ) and late (SL ) systolic waves.

context, the diastolic flow can be viewed as produced by ventricular relaxation, resulting in forward pulmonary vein flow, with the left atrium acting as a conduit after mitral valve opening. With short RR intervals, the systolic and diastolic waves may merge, resulting in a single forward-flow wave. Thus, depending on heart rate and rhythm, the pulmonary vein velocities above the baseline may be recorded as monophasic, biphasic, or triphasic.[26] Reverse flow can often be recorded as a small, brief velocity signal below the baseline during atrial contraction (just after the P wave). This wave has been variously designated the pulmonary vein A (PVa) or atrial reversal (Ar) wave and represents retrograde pulmonary vein flow (see Fig. 6-13) . It is usually larger when the atrial afterload is high from left ventricular hypertrophy or restrictive/constrictive processes.[34] [63] Some workers have termed the systolic and diastolic forward waves as J and K waves [26] [64] or X and Y waves, respectively.[65] Although labeling of the pulmonary vein velocity has not yet been standardized as for transmitral flow, most recent investigators have used the S and D designations. This format has the advantage of being readily associated with timing within the cardiac cycle. However, the J and K terminology is more easily associated with the L wave of transmitral flow during diastasis and thus is preferred in some laboratories. Other authors have named these as X and Y waves to correspond to the x and y descent of the pulmonary capillary wedge pressure tracings. In this scheme, the atrial reversal velocity is called the Z wave.[66] Measurements

As with the transmitral flow, the conventional assessment of pulmonary vein velocity waves has included the measurement of peak velocities, as well as the time velocity integral for S (Si ) and D (Di ). The ratio of the

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systolic to diastolic components has also been described by peak S/peak D or expressed as the systolic fraction (percent) by the following equation[63] [66]

The peak Ar velocity, velocity time integral, and duration (Adur , in milliseconds) have also been defined.[41] [63] [66]

Fewer studies of normative data are available for pulmonary vein flow than for transmitral Doppler data. Table 6-3 lists the mean (±SD) values reported from a number of important series in the literature for reference. However, as indicated, some of these investigations were performed in patients undergoing catheterization or elective operations and thus may not reflect values obtained during a routine echocardiographic examination. In general, the S wave is predominant in normal patients, with peak velocities ranging from approximately 40 to 60 (±15) cm per second and time velocity integrals of 15 ± 5 cm. The SE component is usually smaller than SL, with peak velocities of 30 to 40 (±10) cm per second. The diastolic wave has been measured in the range of 35 to 45 (±15) cm per second with a velocity integral of around 7.5 to 9.5 (±4) cm. The ratio of peak S to peak D has been described in normal subjects as 1.3 to 1.5 (±0.3), with a systolic fraction of 60 to 68 (±10%). The peak A wave is normally the smallest of the velocity components at -22 to -32 (±10) cm per second, with integrated values of 2 ± 1 cm. The Ar duration has been found to be helpful in the clinical interpretation of pulmonary vein flow and is approximately 137 ± 31 msec. Abnormal Patterns of Pulmonary Vein Flow

The alterations in transmitral waveforms seen in various cardiac disease states and loading conditions and with aging have also been described for pulmonary vein velocities.[34] , [41] Since pulmonary vein tracings provide additional information about atrial filling and function, these patterns have been used in conjunction with transmitral flows to better define abnormalities of ventricular filling. In patients with impaired left ventricular relaxation, the pulmonary vein

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flow during early diastole (D) becomes smaller, corresponding to decreased E wave velocities at the transmitral site, both being related to a slower rate of ventricular relaxation. As a result, pulmonary vein flow is shifted toward the systolic phase (S) and results in a 124

TABLE 6-3 -- Normal Values Reported for Pulmonary Vein Flow by Pu

Study Keren et al[62] Keren et al[26] Nishimura et al[41] * Kuecherer et al[66] * Castello et al[61]

Age Patients Range Peak S Si Peak D Di Fra (N) (yr) Technique (cm/sec) (cm) (cm/sec) (cm) (% 13 1–83 TTE 44 ± 10 — 53 ± 15 — — 12

26–49 TTE

48 ± 8

— 49 ± 11

—

—

19

45–80 TEE

41 ± 13

— 33 ± 14

—

—

60

35–78 TEE

19

20–65 TEE

41 ± 13 9.2 32 ± 15 ±4 52 ± 15 12 ± 44 ± 14 4.4

12

TTE

Kuecherer et al[65] Arakawa et al[71]

12

33–60 TTE

44

17–70 TEE

Rossvoll and Hatle

28

15–75 TTE

5.2 66 ± ±3 — 7.8 ± 4.4 50 ± 14 11 ± 41 ± 6 2.5 — 1.5 ± 3.1 63 ± 18 — 46 ± 12 — 68 ± —

12.8 — ± 3.3 56 ± 12 — 40 ± 13

— 68 ±

— 65 ±

[63] †

Brunazzi et al[67] †

96

40

TTE

48 ± 13 11.7 57 ± 10 12.7 47 ± ±4 ±2

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41–50

50 ± 11 12.5 46 ± 11 11.4 54 ± ±4 ±2 51–60 55 ± 12 13.3 40 ± 9 10.5 56 ± ±3 ±4 61 60 ± 10 15.1 36 ± 14 9.7 61 ± ±4 ±4 Ar, atrial reversal velocity; Adur, atrial reversal duration; Di , integral of d

systolic velocity; Si , integral of systolic velocity; D, diastolic velocity; TEE echocardiography; TTE, transthoracic echocardiography.

* During coronary artery bypass grafting. † Undergoing diagnostic catheterization with normal pulmonary wedge pressure.

higher peak S, Si , and systolic fraction (Fig. 6-14A and B) . The effect on

the Ar wave is variable, depending on left ventricular distensibility at atrial contraction.[34] [63] If left ventricular compliance remains low, the Ar remains normal or small; however, if compliance is diminished, the Ar wave can become dramatically increased, reflecting Figure 6-14 Transmitral (A) and pulmonary vein flow (B) in a hypertensive patient with impaired relaxation. The transmitral pattern reveals typical peak A greater than peak E and prolonged deceleration time. Pulmonary vein flow shows a predominant systolic (S) wave and a small or absent Ar wave. C and D, Corresponding tracings from a patient with similar history. The transmitral pattern again shows a prolonged deceleration time and prominent A wave, while the pulmonary vein flow demonstrates a large Ar wave and prominent S wave.

more reflux into the pulmonary veins due to a resistance to forward emptying during atrial contraction (see Fig. 6-14C and D) . The pseudonormal pattern is thought to represent a transition between impaired relaxation and restrictive phases and is associated with a normal transmitral flow. Patients 125

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Figure 6-15 Patient with a pseudonormal transmitral flow (A) and corresponding pulmonary vein recording (B). As atrial compliance has become reduced, the pulmonary vein flow demonstrates smaller forward velocities during systole and predominant diastolic flow (D).

in this category often have had progressive increases in left atrial volume and pressure due to decreasing left ventricular compliance over time. Because atrial compliance often becomes gradually reduced in this setting, the pulmonary venous flow during systole (S) is reduced owing to decreased atrial relaxation. Thus, the diastolic (D) wave may become predominant, with Si /Di less than 1 and systolic fraction less than 50%. A characteristic feature to this pattern is also a larger Ar wave, reflecting reduced ventricular compliance (Fig. 6-15) .

The features of pulmonary vein velocity waveforms in patients with restrictive physiology are a small S wave and a large D with an abrupt cessation of flow. The Ar wave size and duration are variable depending on the state of left atrial function. If left atrial contractility is preserved, the pulmonary vein A may be very large and prolonged. However, if left atrial failure has occurred due to chronic dilation, the Ar may become diminutive (Fig. 6-16) . A summary of the combined characteristics of transmitral and pulmonary vein flow changes commonly seen in various disease states is shown in Table 6-4 .[34] Estimation of Left Atrial Pressure

A relationship between pulmonary venous flow variables and mean left atrial or left ventricular diastolic pressures Figure 6-16 Transmitral recording in a patient with restrictive transmitral flow pattern (A) and corresponding pulmonary vein flow (B) from an apical transthoracic approach. Both demonstrate evidence of high velocities during early diastole (arrows). The pulmonary vein recording shows virtually no forward systolic flow and a small or absent Ar wave.

has been described.[63] [66] [67] [68] Kuecherer et al[66] compared pulmonary vein flow variables as well as mitral inflow with mean left atrial pressure (LAP) in 47 consecutive patients undergoing cardiovascular surgery and transesophageal echocardiography. The pulmonary vein systolic fraction correlated best with LAP (r = -.88; SEE = 3.5 mm Hg). The relationship between the two parameters was described by the following equation:

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LAP = 35 − 0.39 × (systolic fraction) The authors believed that the shift from predominant systolic flow to diastolic flow seen with rising left atrial pressure was most likely due to decreased left atrial compliance.[66] Retrospective evaluation of the data also suggested that a systolic fraction less than 55% was 91% sensitive and 87% specific for predicting a mean left atrial pressure of 15 mm Hg or greater. A similar study using transthoracic pulmonary venous flow recordings was reported by Brunazzi et al[67] in 116 consecutive patients undergoing elective catheterization that included measurements of pulmonary capillary wedge pressures (PCWP). The systolic fraction was again noted to correlate best, with r = -.88 and SEE = 3.1 mm Hg. A success rate of 83% was reported in recording 126

TABLE 6-4 -- Characteristic Doppler Findings in Various Stages of Diastolic Dysfunction

E/A DT, msec IVRT, msec S/D AR, cm/sec Vp ,

Normal (young) >1 <220

Normal (older) ≥1 <220

Delayed Pseudonormal Restrictive Relaxation Filling Filling <1 1–2 >2 >220 150–200 <150

<100

<100

>100

60–100

<60

<1 <35

≥1 <35

≥1 <35

<1 ≥35

<1 ≥25

>55

>45

<45

<45

<45

>8

<8

<8

<8

cm/sec Em , >10

cm/sec AR, pulmonary venous peak atrial contraction reversed velocity; DT, early left ventricular filling deceleration time; E/A, early-to-atrial left

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ventricular filling ratio; Em , peak early diastolic myocardial velocity;

IVRT, isovolumic relaxation time; S/D, systolic-to-diastolic pulmonary venous flow rate; Vp , color M-mode flow propagation velocity.

Modified from Garcia MJ, Thomas JD, Klein AL: J Am Coll Cardiol 1998;32:872. pulmonary vein flow from the transthoracic window, and the authors suggested that a systolic fraction of less than 36% percent predicted a mean PCWP of 18 or greater, with a 90% sensitivity and 85% specificity. Rossvoll and Hatle[63] have demonstrated a strong relationship between systolic fraction and the pre-A wave left ventricular end-diastolic pressure (LVEDP). A systolic fraction less than 40% was predictive of LVEDP greater than 18 mm Hg (r = -.70). These investigators also found that the pulmonary A wave duration (Adur ) was frequently prolonged, whereas the transmitral A wave was significantly shortened in patients with increased LVEDP. The difference ([PV − Adur ] − [M − Adur ]) in milliseconds

correlated best with LVEDP (r = -.68). A longer duration of the pulmonary vein A wave than transmitral A wave predicted LVEDP greater than 15 mm Hg with a sensitivity of 85% and specificity of 79%. This study was also recorded using the transthoracic approach in 45 patients undergoing diagnostic catheterization. Factors Affecting Pulmonary Vein Flow

As with transmitral recordings, a number of physiologic factors may affect the pulmonary vein Doppler echocardiographic velocity profile. Age.

Studies of normal subjects with a wide age range have demonstrated that the diastolic components are diminished and the systolic velocities are increased with advancing age.[69] [70] [71] A trend toward a larger atrial flow reversal wave has also been noted, perhaps reflecting abnormalities of left ventricular diastolic performance as part of the normal aging process. Loading Conditions.

The volume of pulmonary venous flow occurring during systole is dependent on preload—that is, with preserved myocardial contractility and increasing preload (i.e., volume loading), the atrial preload will also

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increase, resulting in increased pulmonary venous systolic flow. This increase in S and S/D has been observed in human studies in the operating room[65] and in canine experiments.[72] A direct correlation between both systolic and diastolic forward flows and cardiac output has also been found. [41]

The effect of afterload was studied by Nishimura et al.[41] Patients given phenylephrine in the operating room exhibited variable responses in pulmonary vein flow patterns. Those with a dramatic rise in PCWP (>50%) showed an increase in diastolic pulmonary vein velocities, and a middiastolic flow wave (L) became apparent. Mitral Regurgitation.

Changes in transmitral and pulmonary vein velocity profiles have been found to be useful clinical markers for the estimation of severity of mitral insufficiency. Castello et al[73] found a significantly lower peak S/D velocity ratio (0.4 ± 1.3) in patients with moderate to severe regurgitation compared with patients with less regurgitation (1.4 ± 0.5, P < .0001). This trend toward "systolic blunting" was more remarkable as regurgitation worsened. In patients with severe mitral regurgitation, the systolic flow was reversed (retrograde) into the pulmonary veins. The presence of reversed systolic flow was identified as a sensitive (90%) and specific (100%) marker for severe regurgitation in the 75 patients evaluated.[73] Similar results were reported by Klein et al.[74] An equally high sensitivity and specificity for reversed systolic flow was noted, and the pattern subsequently returned to normal after operative repair in 22 patients. Thus, significant mitral regurgitation may alter the phasic appearance of pulmonary venous flow, with a progressive increase in the diastolic (D) wave component for increasing grades of insufficiency. Technical Considerations in Pulmonary Vein Flow Recordings Transesophageal versus Transthoracic Methods.

The pulmonary vein flow spectrum is generally of superior quality when recorded from the transesophageal window. The transesophageal window has been described as especially helpful in recording reversed flow during atrial contraction (Ar) and in separating the two components of forward systolic flow (SE and SL) (see Fig. 6-13) .[73] Indeed, the transthoracic method may be limited in these areas, yielding Ar recordings of acceptable quality in the minority of patients studied.[69] [73]

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When the transthoracic four-chamber view is used, the right upper (medial) pulmonary vein is recommended for sampling. Spectral data from this site correlate well with velocities recorded from the same vein using the transesophageal technique.[73] The use of color flow or newly available echocardiographic contrast agents may help in identifying the location of the pulmonary vein orifice and in improving Doppler signal intensity from transthoracic studies.[73] Although 127

the esophageal window normally allows imaging of all four pulmonary veins, the upper veins are preferred for sampling because they provide a more parallel flow angle for Doppler interrogation.[70] The advantages of the transesophageal study must be weighed against those of patient discomfort to determine the need for this procedure in each clinical instance. Sample Position.

The ideal position for sampling pulmonary vein velocities and analyzing waveforms is 0.5 to 1 cm from the pulmonary vein orifice into the left atrium.[73] Sampling at greater depths results in spectral broadening, decreased diastolic flow velocities, and loss of phasic characteristics of systolic flow.[64] Pulmonary Vein Size.

One potential factor affecting reproducibility of pulmonary vein inflow velocities is variation of the vein orifice size during the cardiac cycle. Studies of vein dimensions and flow in both dogs and humans have not demonstrated this to be a substantial factor under physiologic conditions.[75] However, in comparisons between mitral and pulmonary vein flow velocities, this factor must certainly be considered.[41]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Applications of Doppler Techniques for Assessing Diastolic Function Transmitral and Pulmonary Vein Recordings: A Combined Approach From the preceding discussion, it should be clear that no single noninvasive or catheterization-derived parameter can be used to describe the complex nature of diastolic function. As with systolic measures of performance, there are general descriptors (e.g., ejection fraction) and more specific measurements (e.g., Vmax , dP/dt, and mean velocity of circumferential

fiber shortening [Vcf ]) that define the process of contractility in greater

detail. Each measurement must be evaluated in the context of the clinical situation so that modifiers such as age, loading conditions, and volume status can be included.

Since the 1980s, diastolic dysfunction has become increasingly recognized as an important part of many clinical syndromes.[76] [77] [78] [79] Consequently, Doppler echocardiography has been recognized as a readily available tool for evaluating left ventricular filling and has given the clinician a method for better understanding these events. However, it must be recognized that the diagnosis of diastolic abnormalities is not routine and requires significant effort and knowledge, even for the experienced echocardiographer. In specific disease states, Doppler variables have provided a conceptual framework for understanding pathophysiology without necessitating cardiac catheterization. Recordings of transmitral and pulmonary vein flows, along with isovolumic relaxation time, should be evaluated in context with other two-dimensional echocardiographic information to best apply these techniques (see Table 6-4) . For example, in the assessment of left ventricular filling, the thickness, cavity size, and systolic function, as well as left atrial size, should be assessed. In other settings, the Doppler

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data may provide more subtle clues that are helpful in distinguishing restrictive from constrictive processes. Thus, although the Doppler information represents a significant advance in the field, its use for detecting abnormal hemodynamics may still be considered part of the "art of medicine." [80] More recent studies also suggest that these noninvasive indices may give insight regarding the prognosis of various heart diseases. [81] Therefore, the following section reflects an attempt to give illustrative case examples of the use of Doppler in various cardiac problems. The cases include a discussion of relevant literature regarding the use of Doppler in these areas; further details can be found in subsequent chapters as noted. Case Examples and Literature Review Hypertensive Heart Disease (Pressure Load Left Ventricular Hypertrophy)

A 74-year-old woman with a history of hypertension presented to the clinic with complaints of dyspnea on exertion. Specifically, for the past 6 months she has had difficulty climbing stairs, carrying laundry, and vacuuming the house. Physical examination revealed a blood pressure of 170/110 with a heart rate of 90 beats per minute. There was no jugular venous distention or evidence of pulmonary congestion. Trace pedal edema was present. The left ventricular impulse was sustained, the carotid pulses were normal, and a grade 2/6 systolic ejection murmur was heard along the left sternal border. A 12-lead electrocardiogram revealed high voltage and secondary ST-T wave changes compatible with left ventricular hypertrophy. Twodimensional echocardiography with Doppler was performed to evaluate left ventricular function. Interpretation.

The Doppler transmitral flow recording from this patient is shown in Figure 6-17 and exhibits several features characteristic of patients with hypertension and left ventricular hypertrophy. The spectral profile shows a reduced E wave, prolonged deceleration time, and predominant A wave. The peak E/A ratio is less than 1.0, and the deceleration time was measured to be 200 msec. The IVRT was also found to be prolonged at 150 msec (see Fig. 6-17B) . These features are consistent with the pattern of impaired relaxation. The reduced velocities of early filling reflect the loss of ability of the

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hypertrophied ventricle to relax quickly and develop a negative pressure gradient ("suction") after mitral opening. The prolonged deceleration time shows that the process of relaxation continues well into diastole, while the increased peak A velocities and Ai show that the atrial volume remains high in late diastole and that atrial contractility is preserved in this case. Although a similar pattern may also be seen in healthy elderly patients, the magnitude of prolongation of deceleration time and IVRT are helpful in distinguishing this as abnormal relaxation. A prolonged IVRT has been reported to be a sensitive sign of this condition, independent of heart rate.[82]

128

Figure 6-17 A, Transmitral pulsed wave recording of a patient with hypertensive heart disease showing delayed deceleration time at 200 ms (arrow) and A greater than E. B, The isovolumic relaxation time (IVRT) (dashed lines) was prolonged at 150 msec. C, Pulmonary vein recordings in the same patient showing absent D wave and prominent Ar velocities suggesting reduced left ventricular (LV) compliance.

The Doppler pulmonary vein flow (see Fig. 6-17C) demonstrates a reduced D component (corresponding to a smaller transmitral E wave) and more prominent S wave (due to larger atrial stroke volume). However, if left ventricular compliance is reduced, a prominent Ar wave may also be seen. [83]

Literature Review.

Several studies of adult patients with hypertensive left ventricular hypertrophy have found this constellation of abnormalities to be present and statistically to be significantly different from findings in control subjects (see Chapter 32) .[84] [85] [86] [87] The pattern of impaired relaxation has also been reported in patients with concentric left ventricular hypertrophy due to aortic stenosis,[88] hypertensive hypertrophic cardiomyopathy of the elderly,[89] and hypertrophy due to obesity heart syndrome.[90] [91] Further evidence that the pathophysiology is related to hypertrophy is available from longitudinal studies in which regression is associated with reversion of this pattern to normal. Progressive improvement in E/A velocities have been demonstrated over 3 to 6 months in patients treated with angiotensin-converting enzyme inhibitors[92] [93] and in patients undergoing aortic valvuloplasty.[94] These effects may be due to

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the direct reduction of afterload or the inhibition of connective tissue protein and collagen production by these drugs.[92] The classic example of impaired relaxation shown (see Fig. 6-17) is not always seen in patients with hypertensive left ventricular hypertrophy. Indeed, patients with high left atrial pressures may have a normal or "pseudonormalized" transmitral flow pattern.[35] [95] Elevated filling pressures result in a higher cross-over pressure gradient in early diastole, resulting in a larger E wave, while left ventricular end-diastolic pressures become elevated to result in smaller atrial contribution. For example, the pseudonormal pattern has also been reported in patients with aortic stenosis and systolic dysfunction[88] and those with chronic hypertension with eccentric hypertrophy.[85] The presence of significant mitral regurgitation may also elevate early filling velocities and result in a normal pattern. However, these exceptions should be apparent from clinical or echocardiographic information. Some authors have suggested that the transmitral flow profile can be used to help choose antihypertensive therapy [95] that is, when delayed relaxation is present, patients are more likely to benefit from a slower heart rate (e.g., beta blockers). Conversely, patients with elevation of diastolic filling pressures may be more likely to respond to diuretics or vasodilator therapy. Clearly, more clinical trials are necessary to assess drug effects on diastolic function and Doppler velocity patterns. Hypertrophic Cardiomyopathy

The diastolic Doppler transmitral velocity profile in patients with hypertrophic cardiomyopathy is variable (see Chapter 27) . Most patients have some evidence of diastolic dysfunction when compared with control subjects. Studies by Maron et al[96] and Lewis et al[97] showed that more than 80% of patients with hypertrophic cardiomyopathy, including those without symptoms or obstruction, had at least one abnormal index of transmitral flow. Typically, the abnormalities were similar to those described for hypertensive hypertrophy: a reduced E velocity, larger A wave component, and prolonged IVRT and deceleration time. These data are concordant with results of nuclear studies of left ventricular filling in patients with hypertrophic cardiomyopathy. Bonow et al[98] described reduced filling during the rapid filling phase, with more filling occurring during atrial systole. However, other investigators have shown that patients with this disorder may present with normal (or pseudonormal) flow profiles.[14] [33] Subgroup analyses in these studies suggest that this pattern may result from mitral regurgitation, a common associated finding.

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Dilated Cardiomyopathy

A 52-year-old man with a long history of an "enlarged heart," diagnosed as idiopathic dilated cardiomyopathy, 129

has been treated with digoxin and diuretics. He presented to the clinic with a history of medical noncompliance and excessive salt and water intake for 3 weeks. Echocardiograms in the past revealed four-chamber enlargement, a dilated hypocontractile left ventricle with thin walls, and an estimated ejection fraction of 30%. Physical examination showed elevated neck veins, bibasilar rales, a pulsatile enlarged liver, and dependent edema to the knees. A grade 2/6 pansystolic murmur was heard at the apex. A two-dimensional echocardiographic and Doppler study was performed to evaluate left ventricular function and rule out pericardial effusion (Fig. 618) and compared with a study performed 1 year earlier. Interpretation.

The tracings in Figure 6-18 demonstrate a number of important findings that can be helpful in the diagnosis and management of this patient. The earlier recording (see Fig. 6-18A) shows a transmitral pattern similar to that shown in Figure 6-7 . The delayed deceleration time and predominant A wave suggest impaired relaxation. However, the spectral Doppler scan now has changed to reflect a restrictive pattern (see Fig. 6-18B) . As the disease process has continued, ventricular compliance has decreased, despite a lack of any evident change in systolic performance. A rising left atrial pressure (higher preload) has resulted in a predominant E component, while the A wave has diminished due to deteriorating contractility and a more noncompliant left ventricle (higher atrial afterload). Most importantly, the availability of serial tracings greatly aids in this assessment of worsening diastolic dysfunction. Literature Review.

Several studies have evaluated left ventricular filling patterns in patients with congestive heart failure due to dilated cardiomyopathy (see Chapter 26) .[81] [99] [100] [101] [102] The combined data suggest that patients with this disorder may present with any of the patterns within the spectrum of

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diastolic abnormalities. Lavine and Arends [100] found that patients with dilated cardiomyopathy and normal left ventricular filling pressures had a prolonged IVRT and reduced E/A ratio, while those with pulmonary capillary pressures greater than 15 mm Hg demonstrated an increased peak E and E/A (2.1 ± 0.4). The two patient groups had similar ages, left ventricular dimensions, and degrees of systolic dysfunction. Mitral regurgitation appeared to be one factor accounting for increased E velocities. Similarly, Takenaka et al[103] found that dilated cardiomyopathy patients without mitral regurgitation typically had a pattern of abnormal relaxation, Figure 6-18 Transmitral flow recordings in a patient with dilated cardiomyopathy. The earlier recording (A) shows a slightly delayed deceleration time and A greater than E, suggesting an impaired relaxation pattern. Transmitral flow recording 1 year later (B) shows markedly an increased E wave and a near-absent A wave typical of the restrictive pattern. Conversion to this pattern suggests a higher preload and has been associated with a poorer prognosis.

whereas patients with mitral regurgitation had a "normalized" pattern. Subjects in the mitral regurgitation group differed from normal subjects in having a shorter deceleration time. Vanoverschelde et al[101] also found the pattern of left ventricular filling to be closely related to both left atrial pressure and the presence of significant mitral regurgitation. Because the majority of patients with dilated cardiomyopathy are studied while on medications, drug effects must also be considered. A study by Makhoul et al[104] demonstrated a direct relationship between PCWP changes induced by intravenous isosorbide dinitrate and the transmitral E/A ratio. The E/A ratio was initially high (restrictive pattern) and was reduced by more than 50% after nitrates in nearly all patients with class IV congestive heart failure. Perhaps the most important clinical information obtainable from Doppler tracings in patients with dilated cardiomyopathy and heart failure relates to functional status and prognosis. Studies by Vanoverschelde et al[101] and Xie et al[105] have demonstrated a clear relationship between transmitral flow pattern and New York Heart Association functional class. Patients with increased peak E velocities or shortened deceleration, or both, had poorer treadmill performance compared with those who had a pattern of impaired relaxation. These clinical data support the idea that the restrictive pattern represents increased preload and abnormal left ventricular compliance.

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Studies by Xie et al[81] and Werner et al[99] have shown the restrictive filling pattern to predict a higher mortality rate in patients with systolic dysfunction. Both series found that patients with a deceleration time of 140 msec or less and an E/A ratio 2.0 or greater had a 2-year survival rate of approximately 50%, compared with heart failure patients with reduced ejection fractions but without this pattern who had a survival rate greater than 90%. Although some authors have correlated an increased peak E wave and higher mortality rate with the degree of mitral regurgitation, [101] two 1994 studies[81] [99] showed no significant difference in this parameter. Thus, the pattern of short IVRT, predominant early diastolic filling (by transmitral peak E wave and pulmonary vein D waves), and a prominent Ar wave and dilated left atrium may all reflect a stage of severely decreased left ventricular compliance and high filling pressures.[34] Findings of this nature may have direct clinical applications, such as encouraging more aggressive medical treatment or consideration of earlier evaluation for heart transplantation.

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In summary, patients with systolic dysfunction, ventricular dilation, and clinical evidence of heart failure may be heterogeneous in their Doppler transmitral or pulmonary venous flow patterns. However, interpretation of these tracings can be extremely helpful if the clinical setting is considered. [102] [106]

Constrictive Pericarditis versus Restrictive Cardiomyopathy

A 38-year-old man presented with severe dyspnea on exertion, worsening over the past year. An earlier evaluation had revealed normal pulmonary function and "no evidence of cardiac disease," based on normal systolic function. Physical examination revealed elevated jugular venous pressure with Kussmaul's sign and pulsus paradoxus of 15 mm Hg; blood pressure was 90/60. The liver was palpably enlarged, with evidence of ascites and 3+ peripheral edema. There were no audible murmurs or gallops. A Doppler echocardiographic examination was obtained to evaluate left ventricular function and to rule out a constrictive or restrictive process. Interpretation.

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The spectral Doppler tracings from this patient are shown in Figure 6-19 . The findings are typical for the "restrictive" transmitral flow pattern: a short IVRT, a high-velocity peak E wave (>100 cm per second) with abrupt cessation of flow and, therefore, extremely short deceleration time (120 msec). The A wave component is nearly absent, with a peak velocity of less than 35 cm per second, and resultant peak E/A of 2.2. The Ei /Ai ratio is also increased at 2.4. The dramatic shift of flow to early diastole along with abrupt cessation of the E wave is compatible with the "dip and plateau" pattern seen in right and left ventricular pressure tracings in patients with constrictive pericarditis. The beat-to-beat variation in E wave size is noteworthy and corresponds to changes during respiration frequently seen with constrictive

Figure 6-19 Spectral Doppler transmitral flow in a patient with constrictive pericarditis. The tracing shows high peak E velocity greater than 100 cm/sec and small A component barely visualized because of high heart rate. The beat-to-beat variation in E wave size shows a greater than 50% change during inspiration (arrows). This finding may be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy.

physiology, but less often with restrictive cardiomyopathy. Literature Review.

Appleton, Hatle, and Popp have published several studies describing the typical Doppler echocardiographic features of patients with restrictive cardiomyopathy. [20] [107] These series included patients with systemic infiltrative disorders (e.g., amyloidosis and Fabry's disease) and postcardiac transplant patients.[107] Comparison of these patients with normal subjects and with a group with coronary artery disease led to the initial description of the patterns of transmitral flow: impaired relaxation, "normalized," and restrictive.[35] Comparison of flow velocity patterns with invasive hemodynamic data showed correlations between transmitral E wave and left ventricular filling pressure (r = .59), and between IVRT and the rapid filling wave (r = -.72). Klein et al[36] demonstrated similar Doppler findings in a large group of 53 patients with biopsy-proven cardiac amyloidosis. This study found the restrictive pattern to be most associated with advanced stages of the disease. Pulmonary vein flows were also recorded by transthoracic echocardiography in 29 patients and showed that those with advanced disease had markedly decreased peak systolic (S) filling and increased diastolic (D) filling compared with normal subjects.

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Atrial systolic function was believed to remain intact (despite left atrial enlargement), since the Ar wave was prominent in 10 patients. A follow-up study of 63 consecutive patients with biopsy-proven cardiac amyloidosis from the same center has shown a high 1-year mortality rate in patients with the restrictive pattern (51%) compared with those who had a deceleration time greater than 150 msec (8%; P < .001). The combination of shortened deceleration time and increased peak E/peak A ratio greater than 2.1 was the most predictive of a high-risk group, whereas the E/A ratio alone exhibited the single best correlation with survival.[108] Fewer clinical data are available from patients with constrictive pericarditis. A study by Hatle et al[107] compared seven patients with constrictive pericarditis, 12 with restrictive cardiomyopathy, and 20 normal subjects. Both constrictive and restrictive groups demonstrated a shorter transmitral deceleration time during held breathing at end-expiration, compared with control subjects. However, during normal inspiration, the patients with constriction showed marked increases in IVRT (50%) and decreases in peak E wave velocity (mean, -33%; all patients, greater than 25%), and these changes were small in the restrictive and control groups (see Fig. 6-19) . Indeed, no patient in the restrictive group had a greater than 15% change in either variable. The transtricuspid flow velocity changes of an increased peak E wave and a peak A wave with shortened deceleration time were also much larger in the constrictive pericarditis patients. The respiratory variation was not seen in five patients who underwent repeat studies after pericardial stripping. The authors theorized that the dramatic changes in transmitral and transtricuspid flow seen during inspiration likely were due to displacement of the interventricular septum and ventricular interdependence in patients with constriction who have a fixed total cardiac volume. Conversely, patients 131

with restrictive cardiomyopathy have a marked reduction in left ventricular compliance that remains relatively constant regardless of the respiratory phase.[107] Thus, patients with abnormalities in ventricular filling due to restrictive muscle disease or pericardial constriction may be readily identified by the "restrictive" Doppler transmitral filling pattern. These data suggest that careful study of diastolic transmitral and transtricuspid velocity during the

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phases of respiration may also be used to separate these groups. Although these results are promising, larger series are needed to confirm these findings. Pericardial Effusion and Cardiac Tamponade

Abnormalities in left ventricular filling have been described in patients with cardiac tamponade. A preliminary report from Pandian et al[109] first described alterations in flow velocity across all four cardiac valves; these alterations coincided with the phases of respiration. The primary study was carried out in a canine model but also included three patients who had documented tamponade physiology and underwent pericardiocentesis. The authors noted an increase in transtricuspid flow velocities and concomitant decrease in transmitral peak E and A waves (-42%) during inspiration. Appleton et al[110] studied seven patients with tamponade compared with 14 patients who had effusion due to malignancy, cardiac surgery, myocardial infarction, chronic renal failure, or cardiac transplantation. The patients with tamponade and severe hemodynamic alterations had a significant change in transmitral filling indices when the first Doppler beat of expiration was compared with the first beat of inspiration: peak E (−43 ± 9%), peak A (−25 ± 12%), IVRT (85 ± 14 msec), Ei (−52 ± 10%), and Ai (−28 ± 22%). Similar decreases were noted in aortic velocities, whereas transtricuspid and transpulmonic flows increased during inspiration. The variation was eliminated after pericardial drainage. Half of the group of patients without tamponade also showed respiratory variations compared with control subjects, but not of the magnitude seen in patients with tamponade. The authors concluded that the Doppler flow abnormalities seen with effusion are extremely sensitive to changes in pericardial pressure and should be viewed as a continuum.

In an animal model described by Gonzales et al,[111] significant respiratory variation in Doppler parameters was noted to occur at low intrapericardial pressures and preceded the echographic findings traditionally associated with clinical tamponade (i.e., right atrial inversion[112] and right ventricular diastolic collapse[113] ). It was concluded that the Doppler findings are sensitive and persist throughout all stages of tamponade but are not predictive of pericardial pressures or the severity of hemodynamic compromise. Picard et al[114] demonstrated similar findings using aortic and pulmonic flow velocities in animals. Their report did not include mitral or tricuspid Doppler data but acknowledged that the E and A waves tended to

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merge in tamponade because of associated tachycardia, and that the transtricuspid Doppler interrogation was often difficult because of compression of the right heart chambers. These limitations may also prove substantial in patients with severe clinical cardiac tamponade. Myocardial Ischemia

Several studies have demonstrated that acute coronary occlusion results in diastolic dysfunction (see Chapter 12) . Most studies have used Doppler indices recorded before and during angioplasty in patients with angina[15] [115] [116] as the clinical model for evaluating the effects of ischemia on diastolic function. Wind et al[115] reported an increased proportion of left ventricular filling during late diastole and a decreased E/A ratio in 34 patients with normal global systolic function who underwent Doppler echocardiographic examination 1 day before and 1 day after coronary angioplasty for angina. These findings were thought to be consistent with impaired relaxation, as previously reported from radionuclide scans in coronary angioplasty patients.[117] The authors provided indirect evidence that the abnormal diastolic indices were due to a prolongation of IVRT, although this was not directly measured. Labovitz et al[116] investigated 32 patients during coronary angioplasty and found that evidence of diastolic left ventricular dysfunction was the earliest change during coronary occlusion with the balloon, preceding electrocardiographic changes, chest pain, or systolic wall motion abnormalities. Impaired relaxation was the pattern most often exhibited and occurred within 15 seconds of balloon inflation but returned to baseline by 15 seconds after deflation. Masuyama et al[118] also found a reduction in peak E-wave velocities and E/A ratio in serial Doppler echocardiographic studies of patients undergoing percutaneous transluminal coronary angioplasty to be a strong predictor of significant coronary restenosis. The most complete comparison of hemodynamic and Doppler indices of diastolic function in patients with coronary disease has been performed by Stoddard et al.[15] Their study evaluated the relationship of chamber stiffness and relaxation (tau) to the traditional transmitral indices in 35 patients undergoing diagnostic catheterization for chest pain. Subjects without coronary artery disease and with normal relaxation were found to have a direct correlation between increasing chamber stiffness and enhanced early filling velocities. Conversely, the group with coronary

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disease showed a significant indirect correlation between impaired relaxation and decreased peak E velocity. Although their findings differ from those of previous studies in that a variety of patterns of transmitral flow were found, they are consistent with early observations by other investigators.[119] The authors concluded that chamber stiffness has a greater influence than relaxation on the pattern of diastolic filling in patients without coronary disease. In contrast, abnormal relaxation appears to be the predominant factor influencing the Doppler pattern in patients with coronary disease and an abnormal tau value. El-Said et al[120] studied the effects of ischemia on left ventricular filling using Doppler transmitral flow recordings 132

during dobutamine stress echocardiography. Their data showed marked decreases in peak E velocities (-22%) and time to peak E acceleration (28%) in ischemic subjects, whereas 10 control subjects had an increase in both values (+33% and +75%, respectively; P < .0001). There was no overlap in the percentage change from baseline to peak dobutamine stress values between normal subjects and patients who had documented singlevessel coronary disease. The authors also found diastolic abnormalities to be more sensitive than induction of wall motion abnormalities for detecting coronary stenoses. Thus, the transmitral Doppler pattern of impaired relaxation appears to be the type most often seen in association with acute (or induced) myocardial ischemic syndromes. Fewer data exist for patients with chronic coronary artery disease or previous myocardial infarction. Fujii et al[121] showed a reduced E/A ratio and prolonged deceleration time to be common in patients with a history of infarction, regardless of location. Other studies comparing inferior with anterior infarct patients have suggested that transtricuspid Doppler echocardiographic recordings may be more sensitive in demonstrating abnormal filling and high right ventricular end-diastolic pressures.[122] One study also suggests a significant relationship among infarct size, degree of systolic dysfunction, and restrictive transmitral flow patterns.[123] This pattern is seen more often in coronary artery disease patients with a worse functional class and poorer prognosis.[81] [105] However, larger studies specifically designed to assess the clinical applicability of Doppler filling patterns in this population are currently not available.

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Another active area of investigation is the use of Doppler echocardiographic techniques to assess changes in left ventricular relaxation produced by commonly used cardioactive drugs. Myreng and Myhre[124] first reported enhanced relaxation and a shift in left ventricular filling toward early diastole in 20 patients given oral verapamil. The patients studied had documented coronary artery disease and showed baseline transmitral filling patterns that did not differ from those of control subjects. After verapamil administration, an increased peak E velocity and E/A ratio and shortening of IVRT were seen. The authors have reported a similar "normalization" of transmitral flow in coronary disease patients after beta blocker treatment.[125] However, the effects of calcium and beta blockade on diastolic function remain controversial.[126] Caramelli et al[127] concluded that the shift in transmitral flow to early diastole can be attributed to effects on heart rate and an increase in pulmonary wedge pressure in a study of 32 patients with anterior wall infarction who were given intravenous atenolol. Nishimura et al[128] have also shown an increase in peak filling rate and a concomitant rise in left ventricular end-diastolic pressure after intravenous verapamil, with no consistent change in tau in 20 patients with coronary artery disease and preserved left ventricular function. Thus, although the use of Doppler echocardiographic methods for assessing pharmacologic effects on diastolic function remains promising, peak filling rates alone should not be used as a marker for improved relaxation. Pulmonary Hypertension

The role of the pericardium and right ventricular function in left heart filling have been recognized from elegant animal studies by Ross,[129] Sonnenblick,[130] and Glantz and coworkers.[131] [132] Patients with primary pulmonary hypertension have also been found to have abnormal left ventricular filling by Doppler echocardiography. [133] Essentially, these patients have been described as having a redistribution of transmitral flow to late diastole, with low E/A ratio (often <0.5), and prolongation of the IVRT. Louie et al[133] have shown this finding to be related to distortion of the left ventricular geometry caused by flattening of the interventricular septum. A subsequent study from the same center showed that patients with right ventricular volume overload (from severe tricuspid insufficiency) had a normal IVRT and reduced atrial component.[134] These effects were related to differences in timing of leftward septal displacement in patients with an intact pericardium. These and other studies[135] point out the importance of diastolic ventricular interaction as a determinant of filling, which may have

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profound effects on relaxation and early diastole (see Chapter 33) . Post-Cardiac Transplantation

The noninvasive evaluation of the transplanted heart has become an integral part of the long-term follow-up of post-cardiac transplantation patients (see Chapter 30) . An increase in left ventricular mass, decreased volume, and evidence of reduced systolic function have all been described in patients who have acute or chronic rejection.[136] [137] [138] Doppler abnormalities of diastolic function have also been described.[137] [139] [140] [141] [142] In a large series of patients, Valantine et al[141] evaluated 64 patients undergoing hemodynamic and Doppler echocardiographic studies as part of the routine follow-up 1 to 13 years (mean, 5 years) after cardiac transplantation. Ten patients were found to have strikingly abnormal (restrictive) transmitral flow patterns. This group had a higher incidence of rejection as the only identifiable clinical difference. Restrictive filling also was associated with impaired systolic performance. Preliminary data comparing Doppler parameter recordings with endomyocardial biopsy findings have shown a relationship between transtricuspid (right ventricular IVRT) and transmitral (left ventricular IVRT) flow patterns and degree of rejection as assessed microscopically.[141] [143] Although preliminary, these data encourage the notion that, in the future, noninvasive examination of transplant patients may help to define which chronic transplant patients have a low likelihood of rejection and thus avoid the need for repeated biopsies.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Newer Doppler Echocardiographic Approaches to Diastolic Function Two-Dimensional Left Ventricular Volume Methods Echocardiographic methods have been described to assess the time course of diastolic changes in left ventricular 133

Figure 6-20 (color plate.) Recording of left ventricular (LV) volume curves (A) using acoustic quantitation. This method allows a real-time assessment of area or volumes and rate of change (B) within a region of interest. The technique provides curves similar to those of radionuclide angiography for assessing the contributions of early and late filling.

volume and dimension.[144] [145] M-mode methods are limited by the need for geometric assumptions to calculate volume and inaccuracies introduced by regional wall motion differences. Traditional two-dimensional techniques require off-line manual tracing of imprecise borders from multiple stillframe images. The frame rate produced at usual scanning depths (around 30 per second) is also slow relative to the instantaneous changes that occur during the isovolumic time period. As a result of these problems, alternative methods have been developed. Research in this area has led to the development of computer-assisted automated border detection algorithms.[146] [147] By differentiating between ultrasound backscatter from myocardium and low-energy reflectances from blood within the left ventricular cavity, these systems can track the motion of the endocardial edge throughout the cardiac cycle. Commercially available programs currently include a real-time assessment of area, volumes, and rate of change within a region of interest (Fig. 6-20) . The accuracy of this method compares well with manual edge tracing and has

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been validated in studies using radionuclide and cineangiographic standards. [148] [149] The main advantage of these methods of quantitation is the on-line availability of data. Comparisons between Doppler and acoustic quantitation in diastolic measurements of the rapid filling and atrial filling phases have shown significant correlations. [150] Therefore, this method has potential uses in evaluating left ventricular filling. However, the technique is gain dependent and requires significant operator experience to acquire reproducible data, especially in patients with characteristics that lead to less than ideal image quality.[151] Noninvasive Measurement of Tau The rate of left ventricular pressure decline has remained a reference standard for the assessment of the relaxation phase of diastole, but its measurement is invasive and requires the use of high-fidelity catheters. A new method has been developed to noninvasively measure tau using continuous wave Doppler spectral recordings of mitral regurgitation.[152] [153] The method involves tracing the deceleration phase of the mitral regurgitant spectral signal and applying the Bernoulli equation to obtain the instantaneous pressure gradient between the left ventricle and the left atrium (Fig. 6-21) . The derivation of tau from this velocity curve has been validated in both animal[152] and human[153] studies using simultaneous catheterization data for corroboration. Although the technique necessitates offline computer analysis of tracings and is not applicable in patients without a complete mitral regurgitant envelope, the results are promising, showing good correlations with results of invasive methods. Additional clinical studies are needed to determine the feasibility of this technique in clinical practice. Color M-Mode Doppler Echocardiography Several investigators have described a new method for relating ventricular inflow velocities to left ventricular relaxation.[154] [155] [156] [157] This method uses color M-mode Doppler echocardiography from apical windows, directed along the longitudinal axis of inflow from mitral valve to apex. The recording typically shows the two waves (early filling and atrial contraction) of flow propagation from the base toward the apex (Fig. 6-22) . The slope of the early filling wavefront has been shown to represent the presence of intraventricular gradients produced from active recoil (suction) of the ventricular myocardium.[156] [158] The velocity of streamlined

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flow propagation into the ventricle (Vp ) is therefore described along the Mmode line by the slope of the color wavefront, in centimeters per second. Measurements of Vp have now been successfully obtained using either the leading edge (transition from black to color) or by tracing along any isovelocity line. More reproducible measurements can be obtained by (1) adjusting 134

Figure 6-21 A, Simultaneous mitral regurgitation Doppler velocity curve and high-fidelity left ventricular (LV) pressure curve. The time constant of relaxation (tau) is calculated from the LV pressure curve using a semilogarithmic model. B, Digitized Doppler velocity curve at 3 msec intervals in which the velocities have been converted to pressure using the modified Bernoulli equation. This new method has been described for the noninvasive assessment of tau. (From Nishimura RA, Schwartz RS, Tajik AJ, Holmes DR: Circulation 1993;88:148.)

the color scale or baseline shift to produce color aliasing, (2) tracing the slope of the first aliasing velocity line, (3) tracing the slope from the mitral leaflet tips to a position 4 cm distally into the left ventricle, and (4) avoiding intracavity flow originating before mitral opening.[159] The method may not be applicable to patients with tachycardia, arrhythmia, or heart block. Young, healthy individuals generally have Vp greater than 55 cm per second, whereas older people have Vp greater than 45 cm per second.[159] Patients with abnormal Figure 6-22 (color plate.) Color M-mode Doppler recording of diastolic flow toward the apex from the four-chamber view. The patient had severe left ventricular (LV) systolic dysfunction and a restrictive transmitral flow pattern. The inflow propagation of velocities (Vp ) is indicated by the slope of the color change during early diastole (dotted white line). The measured slope in this patient was abnormally low at 30 cm/sec.

transmitral filling patterns such as delayed relaxation, restrictive or pseudonormal, will generally have Vp less than 45 cm per second. Thus,

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when combined with other Doppler parameters, measurement of early filling by color M-mode may be useful in distinguishing pseudonormal from normal patterns (see Table 6-4) .[159] This method appears to be less affected by preload than transmitral or pulmonary vein flow.[160] For example, a "pseudonormal" transmitral flow pattern can be produced by increased left atrial pressure in otherwise normal patients. A blunted S wave is commonly seen in young people (especially athletes) in whom the left atrium is functioning as a "passive conduit" and can masquerade as restrictive cardiomyopathy. These situations may be clarified by examining the color M-mode slope during the early filling phase. Another important potential use for color M-mode is in the differential diagnosis of restrictive cardiomyopathy versus constrictive pericarditis.[161] Since color M-mode describes the early inflow of the blood column along the longitudinal axis, this will be rapid in constrictive physiology, whereas filling toward the apex is delayed in restriction. Doppler Tissue Imaging Another promising technique for the noninvasive evaluation of diastolic function involves the direct recording of mitral annulus motion. The technique was first described using M-mode echocardiography[162] but has since evolved to the use of pulsed-wave Doppler spectral recordings, with the sample volume located on the posterolateral portion of the mitral annulus or in the adjacent myocardium.[163] Imaging is usually performed from the apical four-chamber view to minimize the effects of translation 135

and rotation of the heart, while maximizing the longitudinal excursion of the annulus and base. Since tissue Doppler echocardiography involves the assessment of motion of the strong signal reflections (myocardium), the high pass filters are bypassed. Low gain amplification is also used to eliminate the weaker blood flow signals. The result is a triphasic signal with forward velocity toward the apex during systole, and two "away" signals during the early (Em) and the atrial (Am) phases of diastole (Fig. 6-23) . Thus, the diastolic signal appears as a mirror image of the transmitral inflow pattern. The Em wave is also referred to as Ea (for annulus) or E' in the current literature.

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In normal subjects, the Em wave is larger than the Am component, but the ratio falls with age. In restrictive or hypertrophic cardiomyopathies, the early myocardial relaxation phase has been shown to be reduced to less than 8 cm per second. In constrictive pericarditis, the Em values are greater than 8 cm per second, which allows separation of these two groups despite similar tramsmitral flow patterns[164] (see Table 6-4) .[159] A recent study by Sohn et al[165] has shown Em values from tissue Doppler echocardiograms to correlate well with tau as measured during catheterization and to be relatively unaffected by preload changes induced by volume infusion and nitroglycerin. Patients with pseudonormal filling were separated from normal by an Em velocity of less than 8.5 cm per second and an Em/Am ratio less Figure 6-23 Patterns of mitral annulus velocity as recorded by Doppler tissue imaging, with sampling of the septal side of the mitral annulus from the apical view. Note the changes in pattern from normal to restrictive physiology, along with corresponding transmitral flows. The Doppler tissue image may be helpful in differentiating pseudonormal from normal and restrictive transmitral flow patterns. (From Sohn, et al. J Am Coll Cardiol 1997;30:479.)

than 1, with a sensitivity of 88% and a specificity of 67%. Thus, the combination of transmitral flow patterns and color M-mode and tissue Doppler measurements may be helpful in distinguishing patients in various stages of diastolic dysfunction (see Table 6-4) . Estimation of Left Ventricular Filling Pressures As described previously, various Doppler echocardiographic indices of transmitral and pulmonary vein flow have been combined to predict left atrial pressure. Similarly, by combining transmitral E wave velocities with a preload-independent parameter such as the velocity of motion of the lateral mitral annulus (Ea), a reasonable estimate of left atrial pressure can be obtained. Nagueh et al found that an E/Ea ratio of greater than 10 correlated well with a mean pulmonary capillary wedge pressure of greater than 15 mm Hg.[166] The correlation coefficient was 0.87 in 60 patients who had hemodynamic measurements, with the relationship described by the following equation: PCWP (mm Hg) = 1.24[E/Ea] + 1.9 The authors proposed that left ventricular filling pressure can be estimated (with a 95% confidence level of

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± 7.6 mm Hg) from these two simple Doppler measurements. These findings have recently been confirmed by Ommen et al.[167] Their study consisted of 100 consecutive patients who underwent catheterization with micromanometer-tipped catheters and simultaneous Doppler measurements. A ratio of E/E' (or E/Ea) greater than 15 identified patients with elevated LVEDP greater than 12 mm Hg, whereas an E/E' ratio less than 8 accurately predicted normal pressures. Patients with ratios between 8 and 15 had widely variable ventricular diastolic pressures. The authors also noted that, in their experience, adequate signals were more often obtained from the medial or septal portion of the annulus. Although there are currently few such data available, these early and well conducted investigations are highly suggestive that the combination of tissue Doppler and mitral inflow velocities can be used to noninvasively estimate left ventricular filling pressures.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Diastolic dysfunction of the left ventricle has been increasingly appreciated as an important factor in the syndrome of clinical heart failure. The need for noninvasive methods to assess left ventricular filling has led to Doppler echocardiography as a means for describing these events. After a decade of research, it is clear that various patterns of abnormal filling are readily recognized from transmitral and pulmonary vein flow velocity recordings. Although obtaining optimal measurements requires care and diligence on the part of the operator, these data can be obtained in the majority of patients. Further studies of long-term follow-up are needed to determine whether prognostic information can be obtained from Doppler data in subsets of patients. The importance of response of Doppler echocardiographic patterns to drug therapy in patients with heart failure has also not been adequately evaluated. Clearly, this is an active area of investigation and a field in evolution that promises to provide further insight into the pathophysiology and mechanisms of heart disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

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65. Kuecherer HF, Kusumoto F, Muhiudeen IA, et al: Pulmonary venous flow patterns

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99. Werner GS, Schaefer C, Dirks R, et al: Prognostic value of Doppler echocardiographic assessment of left ventricular filling in idiopathic dilated cardiomyopathy. Am J Cardiol 1994;73:792. 100. Lavine S, Arends D: Importance of the left ventricular filling pressure on diastolic

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[abstract]. J Am Coll Cardiol 1993;21:41A. 144. Upton MT, Gibson DG: The study of left ventricular filling from digitized

echocardiograms. Prog Cardiovasc Dis 1978;20:359. 145. Shimizu G, Zile MR, Blaustein AS, Gaasch WH: Left ventricular chamber filling

and midwall lengthening in patients with left ventricular hypertrophy: Overestimation of fiber velocities by conventional midwall measurements. Circulation 1985;71:266. 146. Geiser EA, Conetta DA, Limacher MC, et al: A second generation computer-

based edge detection algorithm for short-axis, two-dimensional echocardiographic images: Accuracy and improvement in interobserver variability. J Am Soc Echocardiogr 1990;3:79. 147. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular

function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313. 148. Gorcsan J III, Schulman DS, Koch L, et al: Echocardiographic automated border

detection derived left ventricular ejection fraction: Comparison with radionuclide angiography [abstract]. Circulation 1991;84(Suppl II):II-585. 149. Sapin PM, Kwan OL, Xie GY, et al: The assessment of left ventricular filling

dynamics using an on-line automatic border detection algorithm: Comparison with cineangiography. Echocardiography 1995;12:559. 150. Chenzbraun A, Pinto FJ, Popylisen S, et al: Comparison of acoustic quantification

and Doppler echocardiography in assessment of left ventricular diastolic variables. Br Heart J 1993;70:448. 151. Smith MD, Xie G, Sapin PM, et al: Factors affecting the determination of left

ventricular area by acoustic quantitation [abstract]. J Am Coll Cardiol 1992;19:199A. 152. Chen C, Rodriquez L, Levine RA, et al: Noninvasive measurement of the time

constant of left ventricular relaxation using the continuous-wave Doppler velocity profile of mitral regurgitation. Circulation 1992;86:272. 153. Nishimura RA, Schwartz RS, Tajik AJ, Holmes DR: Noninvasive measurement of

rate of left ventricular relaxation by Doppler echocardiography: Validation with simultaneous cardiac catheterization. Circulation 1993;88:146. 154. Brun P, Tribuoilloy C, Duval AM, et al: Left ventricular flow propagation during

early filling is related to wall relaxation: A color M-mode Doppler analysis. J Am Coll Cardiol 1992;20:420.

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155. Stugaard M, Smiseth DA, Risoe C, Ihlen H: Intraventricular early diastolic filling

during acute myocardial ischemia: Assessment by multigated color M-mode Doppler echocardiography. Circulation 1993;88:2705. 156. Curtois M, Ludbrook PA: Intraventricular pressure gradients during relaxation

and filling. In Gaasch WH, Le Winter MM (eds): Left Ventricular Diastolic Dysfunction and Heart Failure. Philadelphia, Lea and Febiger, 1994, p 150. 157. Greenberg NL, Vandervoort PM, Thomas JD: Estimation of diastolic

intraventricular pressure gradients from color M-mode Doppler spatiotemporal velocities: Analytical Euler equation solution. Los Alamitos, CA, Computers in Cardiology 1994, IEEE Computer Society Press, 1995, p 465. 158. Greenberg NL, Vandervoort PM, Thomas JD: Instantaneous diastolic transmitral

pressure differences from color Doppler M-mode echocardiography. Am J Physiol 1996;271:H-1267. 159. Garcia MJ, Thomas J, Klein AL: New Doppler echocardiographic applications for

the study of diastolic function. J Am Coll Cardiol 1998;32:865. 140

160. Takatsuji H, Mikami T, Urasawa K, et al: A new approach for evaluation of left ventricular diastolic function: Spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography. J Am Coll Cardiol 1996;27:365. 161. Rodriguez L, Ares MA, Vandervoort PM, et al: Does color M-mode flow

propagation differentiate between patents with restrictive vs. constrictive physiology? J Am Coll Cardiol 1996;27:268A. 162. Gibson DG, Prewitt TA, Brown DJ: Analysis of left ventricular wall movement

during isovolumic relaxation and its relation to coronary artery disease. Br Heart J 1976;38:1010. 163. Isaaz K, Munoz del Romeral L, Lee E, Schiller NB: Quantitation of the motion of

the cardiac base in normal subjects by Doppler echocardiography. J Am Soc Echocardiogr 1993;6:166. 164. Garcia MJ, Rodriguez L, Ares MA, et al: Differentiation of constrictive

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pericarditis from restrictive cardiomyopathy: Assessment of left ventricular diastolic velocities in the longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108. 165. Sohn DW, Chai IH, Lee DJ, et al: Assessment of mitral annulus velocity by

Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474–80. 166. Nagueh SF, Middleton KJ, Kopelen HA, et al: Doppler tissue imaging: A

noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527. 167. Ommen SR, Nishimura RA, Appleton CP, et al: Clinical utility of Doppler

echocardiography and tissue Doppler imaging in the estimation of left ventricular filling presures: A comparative simultaneous Doppler-catheterization study. Circulation 2000;102:1788.

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141

Chapter 7 - Two-Dimensional Echocardiographic Digital Image Processing and Approaches to Endocardial Edge Detection Hans G. Bosch MSc Johan H.C. Reiber PhD

Digital image processing techniques nowadays can be found in any ultrasonography machine or offline analysis system. Moreover, ultrasonography machines have evolved from mainly analog, video-type technology into fully digital, computer-like systems. Digital image storage and digital processing of echocardiographic images, both for image enhancement and for analysis, are widely practiced. Some forms of automated image analysis and automated border detection (ABD) techniques (also known as edge detection, border delineation, or edge finding) are commercially available. However, automated border detection is still in the process of development. Many issues remain to be solved, but important breakthroughs can be expected soon. Automated border detection can potentially supply the echocardiologist with quantitative, less subjective tools for research and clinical practice. However, ultrasonography is a difficult imaging modality for interpretation, for both humans and computers. Frequently, unrealistic expectations as

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well as unfounded denunciation of the possibilities of image processing and automated analysis are encountered. In this chapter, we want to provide the clinician with some insight into the background of different techniques and supply some practical guidelines for 142

the choice and use of techniques and their possibilities and limitations.

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Digital Image Processing and Endocardial Edge Detection: Why and When? Digital image processing concerns all manipulation of images by a computer. In a more limited sense, it refers to enhancement or analysis of images. Image enhancement aims at improvement of images, for visual interpretation or for further automated analysis. This can range from a simple contrast adjustment up to sophisticated filtering. The user can apply these when all or parts of an image need improved visualization. Image analysis generally involves the derivation of some quantitative measures or parameters from images. In a narrower sense, this often refers to automatic localization and outlining (edge detection, border detection) of certain structures. In echocardiography, the left ventricular (LV) endocardium is of prime interest. Outlining of the LV endocardial border is necessary for quantitative measurements of LV cavity area and calculation of volume, local wall displacement and velocity, and so on. Combination with the epicardial border allows calculation of wall thickness and LV mass. Besides quantitative measurements based on delineated areas or caliper distances, visual estimation of parameters (such as ejection fraction) or semiquantitative classification (e.g., wall motion scoring for stress echocardiography) still plays an important role in clinical practice. Eyeballing can be done fast, without much ado, and some experts reach an admirable accuracy. In general, however, it is inaccurate, irreproducible, and hard to learn.[1] Visual estimation of quantifiable measures should be discouraged for any purpose beyond a rough classification, whenever a quantitative alternative is present. Quantitative analysis is advisable when repetitive interpretations are done, when more subtle differences are sought, when interpretation experience is limited, and whenever scientific research is the goal.

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The classic method of outlining the borders is manual drawing. Any ultrasonography machine or offline analysis system has facilities for this, using a mouse, trackball, or similar device. Manual drawing, however, is known to have high inter- and intraobserver variability; it is strenuous and time consuming for the operator and requires expertise and dexterity. Drawing of all frames in the cardiac cycle, over multiple cycles and over multiple stages (as in stress echocardiography), is especially hard to perform practically, in terms of both consistency and workload. Automated Border Detection (ABD) in principle can provide solutions to these problems. Potentially, any measurement that requires manual drawing of borders or indication of landmark points may benefit from automated detection techniques. Moreover, if ABD can be performed online and in real time, it opens possibilities for real-time monitoring of parameters such as LV area and volume. Procedures such as stress echocardiography that currently rely totally on visual scoring of wall motion and comparison between different stages could benefit enormously from automated analysis; the lack of quantification and the large inter- and intraobserver and interinstitution variabilities[2] are perceived as important limitations. No practical automated method for stress echocardiographic analysis is available yet, but some promising developments are described here.

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Digital Image Storage, Communication, and Compression The basis of digital image processing and analysis is the availability of images in digital form. Digital image storage and related subjects are discussed in more detail in the chapters on the digital echocardiography laboratory; in this chapter, an overview of properties of importance for image processing is given. The generation of ultrasonographic images, including ultrasound physics, radiofrequency signal processing, scan conversion, and the instrumentation of ultrasonography machines, is beyond the scope of this chapter. Excellent descriptions on these subjects can be found in many handbooks.[3] [4] [5] [6] Digital Images Digital images are bitmaps, large rectangular matrices of dots or pixels (picture elements) in which the brightness (or color) at each position is represented by a numeric (digital) value. Brightness level is also referred to as intensity or gray value. Typical sizes for echo images are 640 × 480 × 24-bit, equivalent to an NTSC color image, or 768 × 576 × 8-bit for a PAL black and white image. NTSC and PAL are U.S. and European video standards. This should be read as 640 columns by 480 rows of pixels (width X height), 24 bits per pixel. The composing colors red, green, and blue are each coded by 8 bits, giving 256 levels per color, allowing 16.8 million color combinations. A cineloop or movie is a sequence of such images, typically at a frame-rate of 30 or 25 images per second. A digital representation makes it possible to store images as data files and process these in a computer—hence, digital image processing. Analog images, as they are used in TVs and VCRs, consist of a continuously varying electrical signal (the video signal) that represents the brightness along horizontal lines in the image. Such a signal is subject to noise and degradation when it is transmitted over a line or stored on a VCR tape. On the other hand, digital images do not degrade when copied, transmitted, or stored for longer periods. Digital images can be stored on digital media such as floppy disks,

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MOD, CD-ROM, or DVD, transported over networks, stored in large databases, and linked with any other patient information. The main drawback is still the huge amount of data storage that is involved—a single VCR tape of 2 hours carries the equivalent of about 200 gigabytes of uncompressed color images. With image compression and selection, we can limit the storage requirements considerably, but still we cannot use digital storage simply instead of a VCR now. Inside the ultrasonography system, echo images are 143

always created as digital images. Frame-rates and image size can be very different from the typical video values. For display on a monitor and recording on VCR, these digital images are converted into an analog video signal. Not all ultrasonography machines support the storage or communication of digital images, and some can only store single frames, not cineloops. For digital image processing and analysis, digital images are a prerequisite. If only analog video output or VCR tape is available, it is possible to redigitize the analog signal with the help of computer devices named frame grabbers or video digitizers. Note that this introduces unwanted image deterioration in the form of noise and jitter, loss of spatial and temporal detail, loss of separation between image, graphics and color overlays, and loss of additional information such as calibration and patient information. Storage Formats and Image Communication DICOM

The current method of choice for digital image storage and exchange is DICOM (Digital Imaging and Communications in Medicine [7] ). DICOM 3.0 is a generally accepted international standard for medical images proposed by the DICOM committee, a cooperation of professional organizations such as the American College of Radiology, the American College of Cardiology, and the European Society of Cardiology and experts from the medical imaging industry and standardization organizations such as the National Electrical Manufacturers Association. Originally developed for radiography, DICOM now encompasses extensions for most image modalities, including ultrasonography, magnetic resonance imaging, computed tomography, x-ray angiography, and nuclear imaging. The

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DICOM standard is still being extended and improved to better support stress echocardiography, three-dimensional echocardiography, ultrasonography, and others. DICOM should improve the exchangeability of all medical image data. As its name implies, DICOM is a communication standard rather than a file format—it defines the way in which medical imaging devices such as ultrasonography machines, Picture Archiving and Communications Systems (PACS) servers, and printers communicate to transport, store, retrieve, find, or print images and associated patient information. All major manufacturers have committed themselves to support DICOM; eventually, this should allow easy networking in multivendor environments, workable PACS systems, and easy and transparent offline viewing and analysis. Ultimately, this may lead to the digital integrated patient record, which should contain the full patient file, including patient history, laboratory reports, images of all modalities, and other information. DICOM covers every detail of medical image handling, for a multitude of imaging modalities and uses, all captured in substandards that are defined by subcommittees and working groups. Therefore, DICOM is a very complicated standard: the full description covers several thousands of pages.[8] A very readable explanation of DICOM for echocardiographers is given by Thomas. [9] Note that the statement that devices are "DICOM compliant" is rather meaningless; DICOM defines a multitude of services and imaging modalities. For each piece of equipment, a DICOM Conformance Statement defines precisely which services are supplied and supported for what modalities and to what extent. For ultrasonography, it is good to know that image loop storage is not a part of the standard US (ultrasound) modality, but of the later defined US-MF (Ultrasound-MultiFrame) modality. To verify interoperability between devices, the conformance statements should be compared—not a simple job for a novice in DICOM.[10] Proprietary Formats

Several manufacturers still use or support their own proprietary formats for storage of digital image runs with associated patient and image information. Such formats include HP-TIFF or DSR,[11] DEFF[12] (both TIFF extensions), and VINGMED. Although these digital formats may be adequate or even have certain advantages in a single-vendor environment, they may complicate exchange with other departments or hospitals, use of PACS, offline analysis systems, and so on. General Purpose Formats

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Other widely used general-purpose image formats are BMP, TIF, GIF, and JPEG. These are often used for export of screen shots or single images for use in reports, presentations, and papers. These formats generally lack the possibility for storage of image loops (movies) and additional patient information. For movies, AVI, MPEG, and QuickTime are popular formats. These are also general-purpose formats without possibilities for storage of associated data. Image Compression For reducing the data storage requirements, image compression can be employed. A distinction should be made between lossless and lossy image compression. For lossless compression techniques (such as Run Length Encoding [RLE], Lossless JPEG, or various general-purpose file compression techniques such as LZW [used in the ubiquitous ZIP or TAR]), reversing the compression will produce a perfect copy of the original image. Unfortunately, lossless compression generally only reduces file sizes by a factor of 2 to 5. Lossy compression can reach much higher compression ratios (up to 20 to 100) at the cost of a certain amount of image degradation, generally by eliminating information for which the eye is least sensitive. This degradation may be very acceptable visually (JPEG factor 20 has been found to produce only diagnostically nonsignificant degradation[13] ), especially when compared with the degradation associated with VCR storage. However, the compression 144

artifacts may certainly influence digital image processing and analysis. Severely lossy compression is not advisable for archiving or when digital image postprocessing is foreseen. Lossy compression techniques include Lossy JPEG, fractal and wavelet compression, and MPEG, a popular compression scheme for movies. DICOM currently supports RLE and JPEG (lossless and lossy) compression. MPEG and JPEG 2000 compression schemes have been proposed as extensions to the standard.

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Digital Image Processing Digital image processing[14] [15] is a science by itself and cannot be discussed here in great detail. Medical image processing is a thriving subdiscipline with many applications and innovations that have become valuable tools in the hands of the clinician. Several good handbooks on medical image processing, with special attention to ultrasonography, are available.[16] [17] [18] [19]

Image Enhancement: Level Manipulations, Filtering Image enhancement deals with the improvement of images, either for visual interpretation or as a preprocessing for analysis. Most of the techniques described here are available in any general-purpose program for manipulating digital images, such as photo editors, as well as on most ultrasonography machines and offline analysis programs. The simplest class of operations is level manipulations: operations that change the brightness level or color of each pixel without considering any neighboring pixels. These operations are also known as lookup-table (LUT) operations, because the original brightness of the pixel is simply used to look up the new value in a conversion table. Operations of this class include brightness level manipulations and pseudocoloring. Brightness Level Manipulations

This class includes all one-to-one conversions of image brightness levels (input) to display brightness levels (output), either linear or nonlinear. Examples are digital contrast/brightness adjustments, image inversion, gamma correction, and histogram-based conversions. The histogram H(I) of an image is a function that describes, for each brightness level I, the number or percentage of pixels in the image that have this brightness level. Histogram-based conversions include histogram stretching, a linear contrast stretch between the minimum and maximum values of I (or certain

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percentiles) in the histogram; and histogram equalization, a nonlinear transformation that redistributes the gray levels I so that a flat histogram is obtained, increasing the contrast in brightness ranges with many pixels and reducing the contrast in less frequented ranges. Some examples are given in Figure 7-1 . Note that many level manipulations may result in clipping ( See Fig. 7-1C,D , and E ) and in reduction of the effectively used number of brightness levels. The extreme example is thresholding (see Fig. 7-1E) , in which all brightness levels above a threshold are set to white, and all below to black. Pseudocolors

Pseudocoloring involves a direct conversion of brightness levels to a color scale, generally labeled with fancy names such as Rainbow, Ocean, or Harvest. As the eye is more sensitive to color differences than to intensities, this may reveal subtle contrast differences. It can be visually pleasing but it is highly suggestive, as it clusters similar gray values into color groups. Because brightness levels in ultrasonography by themselves do not represent any physical property (see the section on problems and pitfalls) and are highly dependent on gain, signal attenuation, and time gain control, among other factors, the borders that are suggested visually by these colors have no practical significance.[20] This technique is also applied sometimes to highlight brightness values above some threshold with a color, such as during injection of contrast material. Similar objections apply in such a case. Filtering

Filtering is the generic name for image operations that consider neighborhoods of pixels and deal with the spatial or temporal aspects of the image. Filtering operations include noise reduction, smoothing or blurring, and sharpening or edge enhancement. Smoothing or low-pass filtering (e.g., uniform, Gaussian) is used in many ABD methods (see later discussion) to reduce the speckle noise and get more or less homogeneous regions; highpass edge enhancing or detection filters (e.g., Sobel, Laplacian) are often used to find (candidate) border points. Note that most smoothing methods change the positions of edges and cannot differentiate between noise and weak signals. High-pass filters tend to be very sensitive to noise. In general, filtering does not improve the appearance of ultrasonographic images without simultaneously removing valuable information. Smoothing and sharpening filters may be available on your ultrasonography machine for real-time use: keep the above-mentioned caveats in mind when using this

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option. Many more complex forms of postprocessing exist, including median filters, temporal smoothing, morphologic operators such as opening and closing, region growing, matched filters, texture analyses, wavelet transforms, and Fourier and cosine transforms, all of which have been used as parts of ABD methods. Most of these have little practical value by themselves. Image Interpretation: The Interpretation Pyramid The interpretation of highly complex information like medical images is an extremely complicated task. We humans 145

Figure 7-1 Image brightness conversions (look-up table operations) and their results. A, Identity: no change; B, inversion; C, increased contrast (note clipping, C); D, decreased brightness; E, thresholding; F, histogram equalization.

146

Figure 7-2 The image interpretation pyramid.

tend to underestimate it considerably: for us, vision is a very natural process that we perform instantly and automatically. From the study of human perception, we know that vision is anything but a simple, straightforward process. Think of the many well-known optical illusions: there is a lot of hidden interpretation going on. In the interpretation of images, a certain number of information abstraction levels can be distinguished. This is generally known as the image interpretation pyramid (Fig. 7-2) . The levels of this pyramid give us more insight into the mechanisms of different automated techniques and their limitations. A good analogy is found in the interpretation of handwriting or spoken language. This analogy is described in Table 7-1 . For interpretation of a written text, one has to know about the alphabet, spelling, vocabulary,

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syntax, and semantics, and ultimately about the subject of the text, the intentions of the source, and adornments such as humor, sarcasm, and metaphors. These last aspects concern real-world knowledge that has nothing to do with language—it refers to the domain that the text is discussing. In practice, this is not just a simple bottom-up TABLE 7-1 -- Abstraction Level Hierarchy Associated Level General Speech Image Cardiac Operations 0 Raw data Samples Pixels Pixels Image generation 1 Features Amplitude, Intensity, Intensity, Preprocessin filtering, frequency texture, texture, feature gradients gradients extraction 2 Structures Phonemes Edges, Edges, Linking, regions regions merging, matching, clustering 3 Objects Words World Cardiac Model entities, structures relaxation, borders, (lumen, border objects endocardium finding, valve) classification 4 Object sets Sentences Scene Cardiac Scene scene modeling, interobject relationships 5 Interpretation Significance Scene Interpretation High-level interpretation and interpretatio diagnosis expert systems, rul process of combining letters into words into sentences into significance. Text can be fragmented; there are imperfections such as misspellings and ambiguities, unknown words, and missing domain knowledge that necessitate interactions and feedback between all levels, and even guessing, to come to a consistent interpretation.

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Cardiac Image Interpretation

In image interpretation, we have a similar hierarchy. At the basis, we find the raw image information (pixels). Going up, we encounter image features such as local texture and gradients; structures such as regions (groups of adjacent pixels with similar properties) and edges (lines of sudden change, between regions); objects such as a square or a person; and a scene, such as a football match. At the top we have significance, such as finding out who's winning; this requires very specific knowledge on behavior of the players and audience, rules of the play, and so on.

147

Interpretation of medical images, especially of a complex, dynamic organ like the heart, is still more difficult, as it requires expert knowledge about the three-dimensional anatomic structures in the heart, their dynamic behavior, pathology and anatomic variability between patients, and the intricacies of the imaging modality involved. This last point specifically is not to be underestimated for ultrasonography. Again, interpretation is not a simple bottom-up process. Missing or ambiguous information, disturbances such as noise and artifacts, and higher-level knowledge of anatomy, physiology, and pathology are involved and necessitate feedback and interactions between levels. Clearly, very different sorts of knowledge are applied at each level to come to a valid interpretation, and only the lower levels have to do with image properties: higher levels concern sizes and shapes of cardiac parts, anatomic models of the heart, physiology, congenital or pathologic conditions, and so on. Automated border detection systems generally have very limited knowledge at the higher interpretation levels, and resolve this in one of three ways, as follows: 1. They use simplifying assumptions regarding the objects. For example, the left ventricle is a dark, round object in the middle of the image; the endocardial contour is convex, the endocardium is the strongest edge in the image, the cardiac wall will not move more than x pixels per frame. Most of such assumptions will hold only to some extent or are overly general. 2. They limit themselves to a subset of the problem domain, for aspects like cross sections (e.g., only midpapillary short-axis), image quality

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(no dropouts, low noise), anatomy (e.g., no congenital defects), or imaging equipment or settings (scale, gain, frequency). 3. They require the user to handle the high-level aspects by initializing, steering, or correcting the system. The level of knowledge that a certain system applies, the validity of its assumptions, and the ease of interaction for the user determine the "intelligence" and practical value of the system. Rules for a Well-Behaved Automated Border Detection Method

No practical system can do without the intervention of the user. Ideally, there is only one desired and necessary interaction; in cases in which there is room for multiple interpretations, the user should have the final decision. In practice, a computer system can never have all the high-level knowledge that the physician has, and it requires the physician's intervention to handle these blind spots. Systems with little high-level knowledge and models, however, rely heavily on the user to handle their shortcomings and mistakes (USER = Universal Solution for Error Recovery). With these limitations in mind, we can formulate a few criteria for a good and well-behaved ABD method. 1. The method should generate "correct" contours. Because this judgment may be subjective (in the light of multiple possible interpretations), a system should be able to adapt to the expert user's general ideas about correct contours. 2. The contours should be reproducible; this seems obvious for an automatic system, but almost all systems require some type of user interaction (setting of certain parameters, indicating some start point or region, selection of the images to be analyzed, corrections), which will lead to some variability in results. This inter- and intraobserver difference should possibly be smaller than the considerable inter- and intraobserver variabilities associated with similar manual work. 3. The method should be user-friendly; it should only address the user for high-level expert decisions. It should not require him or her to handle "stupid" mistakes or do repetitive corrections. Some implications are as follows: • It should not generate physically or anatomically impossible solutions; unlikely solutions should be marked as such. It should supply alternative hypotheses (when relevant). • It should not override user-drawn contours, for example, unless

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specifically asked to (apart from clean-up of minor imperfections). • It should allow for easy, intelligent, minimized control and correction (the intent of the correction should be applied throughout the whole image set).

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Automated Border Detection in Echocardiography Problems and Pitfalls of Border Detection in Ultrasonography Ultrasonography is a particularly difficult imaging modality for interpretation. Outsiders mostly find it hard to interpret, contrary to other tomographic modalities such as computed tomography and magnetic resonance imaging. Ultrasonography suffers from several specific drawbacks, which also impede automated analysis. 1. There is no simple physical relation between pixel intensity and any physical property of the tissue visualized, in contrast to the LambertBeer law for radiography or the Hounsfield units for computed tomography. In ultrasonography, images are formed by sound reflection and scattering, resulting in a combination of interference patterns (ultrasound speckle patterns) and reflections at tissue transitions. Different tissues are often distinguishable only by subtle differences in texture (speckle patterns) or behavior of texture over time, rather than by different intensity values. 2. Ultrasonographic image information is very anisotropic and positiondependent, as reflection intensity, spatial resolution, and signal-tonoise (S/N) ratio are very dependent on both the depth and the angle of incidence of the ultrasound beam, as well as on the user-controlled time gain compensation (depth gain) settings. Even the definition of the border position may be direction-dependent (leading edge or trailing edge borders[20] ). 148

3. Image disturbances can occur, such as artifacts caused by side lobes, reverberations, lateral and radial point spread functions, and significant amounts of random noise. Many of these problems are associated with high gain settings, which are often necessary in obese or older patients.

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Speckle noise can be seen as an artifact as well; although it is an inherent part of ultrasound imaging, it often veils anatomic details. 4. Missing information can occur, such as dropouts (for structures parallel to the ultrasound beam), shadowing (behind acoustically dense structures), scan sector limitations, and limited echo windows. Stillframe images generally miss some information; the human eye compensates for this when viewing a sequence of images. It resolves ambiguities and interpolates the missing parts by exploiting the temporal behavior of structures and texture, which allows discrimination between noise, artifacts, and anatomy. 5. Problems can arise that are caused by the limited temporal resolution and the scanning process. The sequential scanning of lines combines information from different time moments into one image. For quickly moving structures, this may lead to spatial distortion. When the scan frame-rate is not synchronous with the video frame-rate of 25 or 30 images per second, sharp transitions between "old" and "new" scan line information may appear in still images. These effects are stronger for lower scan frame-rates. 6. Two-dimensional ultrasonography generally lacks spatial reference information. No exact spatial localization of the cross-sectional plane is known. In three-dimensional techniques such as magnetic resonance imaging or computed tomography, this information is often employed in model positioning for the detection. In cardiac ultrasonography, the choice of the imaged cross section depends both on the skill and precision of the sonographer and on the available echo window, which is limited by ribs or other structures. Apart from volume measurement errors, this may also result in detection problems if the ABD method relies on assumptions of shape, distance between epicardium and endocardium, and the presence or absence of other structures such as valves or papillary muscles. Practical Considerations for Automated Border Detection Practical considerations for appropriate border detection (either automatic or manual) are listed in Table 7-2 , subdivided into three categories. Acquisition and Image Quality

The primary requirement for any analysis, whether automated, manually traced, or visual, is optimal image quality. If the border cannot be seen, it can only be guessed at (more or less intelligently). Therefore, one should optimize image quality, standardize system settings, and reduce variability

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in settings and cross sections. Select a depth such that the object of interest fits well TABLE 7-2 -- Practical Considerations for Automated Border Detection Acquisition and image quality Optimize border visualization Limit variation in system settings (gain, power, time gain control, lateral gain control) Limit variation in cross sections (use landmarks) Proper region of interest/depth High frame-rate Digital storage (preferably lossless); no filtering No spatial/temporal subsampling or small regions of interest for storage Border definitions and consistency Inventory of desired calculations Standardize border drawing definitions: Inclusion or exclusion of papillary muscles, trabecular structures, valves, etc. Position of edges: leading, peak, trailing Exclusion criteria and special cases: Image quality: foreshortening, dropouts, artifacts, noise Pathologies: hypertrophy, dilation, cardiac masses, etc. Congenital deformations, etc. Assess inter- and intraobserver variabilities: To test standardization To check errors against study goal, estimate patient population size for significance Include acquisition protocol? Choice of detection technique Check specifics of technique against problem: Cross sections Cardiac objects (left ventricle, right ventricle, endocardium, epicardium)

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Border definitions Single frame, ED/ES, full-cycle, multicycle Real-time online or offline with corrections Dependence on image quality, artifacts, settings Amount and types of user interaction Is manual analysis a practical alternative? inside the scan sector and fills most of it. Try to adjust acoustic power, overall gain, time gain control, or lateral gain control such that the endocardium is best and most homogeneously visualized. Remember that stop-frame images are much harder to interpret than moving sequences; individual frames may be much less pleasing than the cineloop suggests. Since most detection methods do not use interframe relationships, they actually use single frames and suffer from the higher uncertainty. A high frame-rate (at least 25 frames per second) is advisable, both for full-cycle analysis or for proper selection of end-diastolic (ED) and end-systolic (ES) frames in case of ED/ES analysis. For image storage, use digital images whenever possible—do not store images on videotape to redigitize later. Avoid lossy compression with high compression rates, image subsampling (resolution reduction), and temporal subsampling (frame rate reduction). When selecting a region of interest for storage, make sure that it will contain the object completely over the full time range. Contour Definitions and Consistency

Before attempting manual or automated detection, make sure that proper criteria are defined for the desired contours. This may depend on the desired calculations to 149

be performed from the contour. Trabecular structures, papillary muscles, or valves can either be included or excluded for certain calculations (LV volume, regional wall motion, LV mass). Many points need to be standardized: whether leading, maximum, or trailing edges are drawn; what to do in case of foreshortening, dropout, and so on.[20] [21] When possible, perform inter- and intraobserver comparisons and try to reach consensus before starting a large study. In some cases, this should include the image acquisition, to assess inter- and intraoperator variability in the choice of

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cross section, ultrasonographic system settings, and other factors. Choice of Detection Technique

When considering an automated technique for border detection, it is wise to check the following against the specifications of the automated method: the cross sections involved, the object to be detected (e.g., left ventricle, right ventricle, atrium); single-frame, ED/ES, full-cycle or multicycle analysis; the brand and type of echo machine used; the type of contour to be found (blood-tissue border or other, such as epicardium); online or offline availability of the detection; possibilities for user correction of the boundaries (in offline case); dependency on system gain, image quality, and common artifacts such as dropouts or noise; and amount of user interaction needed. In case no suitable automated technique is found for a certain analysis, manual measurements may (or may not) provide a practical alternative. Overview of Automated Border Detection Methods Ever since the invention of echocardiography, methods have been devised for the automated analysis of these images. Literally hundreds of methods have been reported,[22] [23] most of which have only academic value.[24] [25] We do not try to present a complete taxonomy here and limit ourselves to the main directions of research. We refrain from any comparisons on reported success scores, as there are no standard test data sets for this purpose, nor standard test criteria. It is also difficult to compare the type and extent of user interaction, reproducibility, and so on. Any success scores reported depend very much on the chosen inputs and their quality. Because of lack of a gold standard, contours are generally judged by an expert or compared with contours manually drawn by one or more experts, or derived values such as area or volume are compared with some alternative measurement. Most of these values are hard to compare between studies. A rough measure for the worth of a method could be the number of patients on which it has been tested. Methods that have been tested on fewer than 10 patients probably have no practical value (although their academic value may be high): no matter how naive the method, one can always find a few images on which it will work. A listing of a representative cross section of reported techniques is given in Table 7-3 . For each level, the most basic technique is given first. This one is often applied by methods that focus on other levels. Not surprisingly, older techniques generally operate on a lower level. Of level 5, few true

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examples currently exist. The terms "knowledge-based," "intelligent," and "model-driven" are widely misused, even for the most basic techniques at any level. Feature-Based Method: Integrated Backscatter Method, Advantages, and Limitations

The clinically most widespread method for ABD is by far HewlettPackard's Acoustic Quantification (AQ[26] ), which is installed in several Hewlett-Packard (Philips) ultrasonography machine models (Fig. 7-3) . AQ is not an ABD system in the strict sense as described previously, because it merely does a blood/border/tissue pixel classification (by thresholding) on the basis of the integrated backscatter energy of the radiofrequency ultrasound signal. Therefore, it falls into the lower hierarchical levels of the image interpretation pyramid. However, its use of the radiofrequency data, the online real-time applicability, and widespread availability make it a valuable tool. A real-time lumen area plot and area change (dA/dt) plot can be generated, as well as a real-time frame-to-frame monoplane volume calculation. When used with care in images of good quality, it can give very nice results. However, AQ also suffers from some serious drawbacks, [27] [28] which can be summarized as follows: • The AQ borders are very sensitive to image quality (noise, dropouts) and gain settings (time gain control, lateral gain control), and often difficult to control for the user. Cardiac cycle-dependent intensity changes can influence area change calculations.[27] • AQ uses a fixed, user-drawn region of interest within which the blood pixels are counted. Parts of the ventricle (the valve plane and/or septum) tend to move in and out of such a region throughout the cycle, resulting in considerable measurement errors because of missed parts of the ventricle or included parts of the atrium and the other ventricle. • It is mostly impossible to eliminate tissue parts within the ventricle (valve, papillary muscle, and trabecular structures) or to exclude dropout regions from the ventricle, and noise and artifacts may cause serious problems, especially in difficult patients. Reported success scores in larger patient populations vary widely. • The contours are very noisy, which can be expected for a thresholding-type technique; this implies that they are not directly suitable for regional wall motion calculations. A procedure for extracting and postprocessing these contours has been reported.[29] • The method is real time by nature, as it uses the radiofrequency

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signal, which is available only during image acquisition. Apart from representing a unique advantage, this feature also means that the method cannot be used offline, nor can the same images be reanalyzed with different settings. Whenever radiofrequency data can be stored, this limitation will be resolved. Figure 7-3 (color plate.) Acoustic quantification on Philips (HewlettPackard) equipment. (Courtesy Philips Medical Systems Ultrasound, Andover, Mass.)

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TABLE 7-3 -- Overview of Automated Border Detection Methods at Different Abstraction Levels Level Name Basic Technique(s) 1. Heavy smoothing for Preprocessing noise/speckle reduction[68] Contrast stretching Histogram equalization

2. Edge or region detection

Advanced Techniques Spatiotemporal smoothing[69]

Morphologic filters[70] Texture filters: inverse difference moment[71] wavelet transforms[72] Fourier-based filters[73] Radiofrequency data processing: integrated backscatter (AQ) [26] Global or local thresholding Advanced edge detectors: [69] [74] Marr-Hildreth[77] [78] Canny[79] [80] [81] rank-based operator[82] Simple edge detectors such Pattern or profile matching[51] as difference-of-boxes[65] [75] [76]

Matched filters[83] arc filters [40]

Region detection: region growing[73] fuzzy clustering;

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resolution pyramids; neural nets; Markov random fields [84]

3. Geometric Implicit models: e.g., radial objects or search for candidate points, [68] models interpolation/linking, smoothing/shape filtering

Classification of edge points by fuzzy reasoning[78]

Dynamic Programming optimization[42] [80] [85] [86] [87] Simulated annealing[81] selforganizing maps (SOM, Kohonen)[82] Snakes/balloons/active contours/deformable contours, etc.[75] [79] [80] , [88] Active shape models (ASM) [51] [52]

4. Anatomic None or implicit: Hardstructure or coded scene models Manually positioned

User-drawn

Single geometrical shape models—2D, 2D + T, 3D, 3D + T: Model positioning/landmark finding techniques: row/column sums,[76] [78] arc filters,[40] template matching; Hough transform [81] fuzzy logic[72] Shape parameters (2D + [23] T) 3D shape neural nets[89] Composite models (several objects and their relation, e.g., ventricles and septum)—2D, 2D + T, 3D, 3D + T: Point distribution models [53]

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Multiple active contours[79] Fuzzy neural nets (2D)[90] Adaptation of models to image and user[23]

5. None Interpretation, high-level knowledge User intervention: correction Use of patient group derived of contours, etc models: neural nets,[70] SOM, [82] geometrical eigenvariations (PDM)[51] [53] Learning behavior over all cases analyzed Rule-based analysis Pathology awareness Multiple hypothesis generation 2D, two-dimensional; 3D, three-dimensional; PDM, Point Distribution Models; T, time.

Most of these problems are exemplary for a low-level method that does not use any geometric models or knowledge about cardiac anatomy. Apart from these drawbacks, the use of radiofrequency data supplies superior basic information for blood-tissue classification and may well serve as a basis for higher-level developments, especially when the digital radiofrequency data become available for offline postprocessing. The use of harmonic imaging (see later discussion) has been shown to improve AQ border delineation[30] [31] but does not eliminate most of these problems. A spin-off of AQ is known as color kinesis[32] [33] (Fig. 7-4) . This technique is in essence a method of presenting the time sequence of AQ contours in a single image, by color-coding the lumen area for each time frame and superimposing the images. This method renders a rainbow-like lumen in which each color represents some time-offset from ED. Provided there is little global heart translation, this can give a good impression of wall motion patterns in systole or diastole, especially when these motions are analyzed per region.[33] [34] [35] Of course, all limitations of AQ apply here as

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well, plus the concern of overall heart translation, making this technique also challenging to apply accurately.

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Figure 7-4 (color plate.) Color kinesis image on Philips (HewlettPackard) equipment. (Courtesy Philips Medical Systems Ultrasound, Andover, Mass.) Clinical Use

Acoustic Quantification has been applied in clinical studies for many purposes, especially for looking at left ventricular function (lumen area, volume, and fractional area change). Studies on right ventricular function have been reported as well.[36] Combination of AQ data with invasively measured ventricular pressure has been reported,[37] allowing pressure-area and pressure-volume loops to be constructed, which may hold promise for the assessment of LV mechanical performance. Color kinesis has been used for studying wall motion patterns in several patient groups, systolic and diastolic function, regional wall motion in stress echo, and other parameters.[35] [38] [39] Structure-Based Method: Matched Filters As an example of a structure-based method, we highlight the method by Geiser and Wilson and their group[24] , [40] [41] for automatically detecting endocardial and epicardial borders in short-axis echocardiograms. The method is based on matched filters that respond to arclike structures. The first step applies a filter that responds to the bright epicardial-pericardial interface at the posterior wall. Subsequently, other circular structures along the wall are detected and, after update of the LV center estimate, redetected (an example of high-to-low level feedback). This gives an estimate of epicardial position, which is used as a region of interest. Radial edge detectors are used to locally adjust epicardial edges and to estimate the (relatively strong) anteroseptal endocardial edge. From the estimated wall thickness, the border search is further limited and final endocardial and epicardial edge estimates are found (Fig. 7-5) . This method seems practically useful (it has been validated on a large set of quality-selected patients), and it is clever in the sense that it uses feedback

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between a high-level model of a short-axis cross section and low-level feature data. From a theoretical viewpoint, it is vulnerable because of the cascade of dependent steps, each of which may fail and cause the process to break down. Much of the applied geometrical and expert knowledge (such as the order of strength of expected features) seems to be coded into the steps of the algorithm rather than being captured in a general model. Such an approach may be hard to extend to other views or to certain pathologic conditions that break the assumptions, as this requires redesigning the algorithm. Object-Based Method: Echo-CMS Method

As an example of an object-based (pattern- and geometric model based) ABD method, we describe the Echo-CMS system (MEDIS Medical Imaging Systems, Leiden, The Netherlands) that was developed in our laboratory. The system has been designed for practical use, with the main intent of quantifying endocardial wall motion and lumen volume frame-toframe. A relatively simple circular model-based Dynamic Programming approach is used for short-axis views.[28] [42] An LV center point is indicated by the user, defining a circular model and region of interest in which the strong endocardial edge is found by Dynamic Programming using first derivatives and smoothness and distance constraints. The found border is used as a model in neighboring frames to allow frame-to-frame analysis. In the different long-axis views (apical four-chamber, two-chamber, and parasternal long axis), a more elaborate semiautomated pattern-based approach is used.[23] [43] For the analysis of one or more complete beats (Fig. 7-6A) , one ED and ES contour must be manually drawn (Fig. 7-6B) . Next, three landmark points characterizing the position of the LV (apex and mitral valve attachment points, which are the end points of the contour) are extracted from the contours and interpolated or extrapolated linearly over the cycles. The user is required to inspect these markers over the cycles and may then redefine, if necessary, intermediate positions where the true position deviates from the estimated position. Now, the automated contour detection is started. From the manually drawn ED and ES contours, models are extracted describing the geometrical shape of the ventricle over the cycle and the intensity profiles in a neighborhood of the drawn contours. All models (phase, pose, geometry, and edge profiles) are interpolated over the cycle and extrapolated over other cycles ( see Fig. 7-6C, D andE ). The resulting geometry models are positioned over the images ( Fig. 7-7A and B ), which are resampled along straight lines perpendicular to the models.

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For each point of all scan lines (see Fig. 7-7C, left) , a cost value is calculated representing the likelihood of this point as a contour point: unlikely points will have high costs. The cost is calculated from a combination of edge detectors, match differences with the edge profile models, and local edge reliability measures. Through this rectangular array of cost values (see Fig. 7-7C, center) , an optimal connective path is determined using a Dynamic Programming approach. Cumulative costs for all connective paths are calculated, applying position-dependent penalties for deviation from a straight path. In this way, local stiffness of 152

Figure 7-5 (color plate.) Short-axis border detection with arc filters. Top, Short-axis echocardiographic images at end-diastole and endsystole. Bottom, automatically generated borders at end-diastole and end-systole. (From Sheehan F, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M, Fitzpatrick JM (eds): Handbook of Medical Imaging, vol 2. Medical Image Processing and Analysis. Bellingham, Wash, SPIE—The International Society for Optical Engineering, 2000, p 609.)

parts of the border is modeled. The path with overall lowest cost is selected as optimal (see Fig. 7-7C, right) and by inversion of the resampling process converted into a new contour (see Fig. 7-7D) . After detection of all contours (see Fig. 7-6F) , the user may apply any corrections by overdrawing part of a contour. Consecutively, all models are updated with the extra user-defined information, which is interpolated and extrapolated over the sequence, followed by a redetection of all non-manual contours. In short, this method uses full-cycle models for the two-dimensional pose, shape, and local stiffness properties of the wall and for the intensity profiles of the edges. Case-specific and user-specific information is incorporated by collecting information from all user-defined contours. Drawbacks are the need for two manually defined borders and the marker manipulations. Clinical Use

This method has been applied in studies on wall motion patterns for pacemakers[44] [45] and systolic function.[46] [47] [48] The system has some very strong features, including tracking of structures other than blood-tissue borders (user-defined positions); temporal and spatial coherence; and basic

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knowledge of LV anatomy and appearance. For research purposes, it has been shown to be a valuable tool, but at the moment it is mainly focused on frame-to-frame or multibeat analyses of wall motion patterns. For ED/ES analyses, it offers no extra benefits, as the ED/ES contours need to be defined manually. Population Model-Based Method: Active Appearance Models Great promise is held by a new class of techniques called Active Appearance Models (AAMs). These techniques were originally developed by Cootes and coworkers[49] [50] for facial recognition and medical image analysis, as an extension of the active shape model (ASM[51] [52] [53] ) approach. We have recently applied AAMs to magnetic resonance imaging [54] and echocardiography [55] with very promising results. These techniques derive the typical shape and appearance of an echocardiogram from a large 153

Figure 7-6 Echo-CMS semiautomated border detection procedure. A, Electrocardiogram (ECG) and original images; B, manual drawing of two contours and inspection of markers; C, generation of pose models (landmarks); D, generation of shape models; E, generation of profile models (match patterns); F, automatically detected contours. Figure 7-7 Echo-CMS dynamic programming border detection. A, Original image; B, image with landmarks and shape model; C, scan value matrix (left), cost value matrix (middle), and detected path (right); D, image with detected contour.

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Figure 7-8 Active appearance model: average four-chamber images of left ventricle from 65 patients, at different moments in the cardiac phase. A, End-diastole; B, mid-systole; C, end-systole; D, end of rapid filling; E, start of atrial filling.

set of example images with expert-drawn contours. Principal Component Analysis (PCA) on a point distribution model extracts the average organ shape and the principal variations (so called eigenvariations) of shape. By

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warping all examples to the average shape, an average image (Fig. 7-8) and principal image variations (Fig. 7-9) can be found. By applying another PCA, simultaneous shape and intensity, eigenvariations are modeled in an Appearance Model. Such an appearance model can synthetically generate "probable" echocardiographic images similar to the variations shown in Figure 7-9 . By deforming the model Figure 7-9 (color plate.) Active appearance model eigenvariations: Top to bottom: eigenvariations 1 to 4 of four-chamber left ventricle at end-diastole. Left to right: average minus 3 standard deviations, average, average plus 3 standard deviations. Note the simultaneous shape and intensity variations.

along the characteristic model eigenvariations, using a gradient descent minimization of the difference between the synthetic and the real image, the desired structure can be found (Fig. 7-10) . This can be done fast and fully automatically with good results. This technique has some significant advantages: it models both average organ shape and all variations over a population of examples; it models the complete organ Figure 7-10 Active appearance model matching results on end-systolic left ventricular four-chamber image. A, Image with initial model; B, intermediate iteration; C, final matching result.

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appearance, including typical artifacts; it captures the expert's definition of proper border definition; it can model complex shapes (e.g., LV endocardium plus LV epicardium, right ventricle, valves); it is not limited to blood-tissue borders; and it is easily customizable for different types of images. Limitations of this technique are its dependence on the training data, the selected population of examples, and the quality of the expert contours.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Promise In the near future, serious improvements in the applicability of ABD can be expected. Some instrumental developments will have important effects, and the ABD methods themselves will improve. Impact of Instrumental Developments Harmonic Imaging

Any technical measure that improves visual image quality is likely to improve ABD as well. This is certainly true for harmonic imaging. Originally intended to be used in combination with contrast, harmonic imaging has been shown to improve endocardial visualization in twodimensional echocardiography[56] without contrast as well.[30] It has also been shown to improve endocardial tracking by AQ as rated visually,[30] and by correlating AQ EF measurements to x-ray ventriculography.[31] AQ with harmonic imaging still underestimates absolute volumes and can be technically difficult to perform. Note that harmonic imaging will not improve image quality in all cases, and that it sometimes results in a very grainy image. ABD techniques that rely on image texture may be influenced, but others should certainly benefit from harmonic imaging. Tissue Doppler, Strain Imaging

Tissue Doppler imaging can supply real-time information on tissue velocity in the direction of the ultrasound beam, and thus in itself is a method for quantification of motion.[57] [58] [59] [60] The derived strain rate imaging[61] and strain imaging [62] [63] techniques provide an estimate of local tissue strain, but their practical value remains to be established. For certain purposes, this may become an alternative to border motion detection approaches, but the one-dimensionality of the measurement limits its use considerably. Tissue Doppler information could also well be included in ABD techniques, as it provides clues both on presence and local speed of tissue. ABD might

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supply additional (transversal) motion information. Three-Dimensional and Four-Dimensional Ultrasonography

In principle, three-dimensional image acquisition may provide superior input data for ABD. Border positions can be detected more reliably if information from neighboring slices can be used: spatial continuity, like temporal continuity, may provide additional clues in difficult-to-interpret cases. Furthermore, real volumes can be calculated from three-dimensional data instead of monoplane or biplane estimates. However, the triggered acquisition of such image sets may introduce motion artifacts. Threedimensional smoothing and cut-plane interpolations may also influence border positions. This modality will probably benefit most from an inherently three-dimensional or four-dimensional model-based detection technique. Momentarily, real-time three-dimensional ultrasonography (Volumetrics, Durham, NC) is becoming available[64] [65] this eliminates triggering problems and motion artifacts, but image quality is still limited. With improvement of image quality, real-time 3D echocardiography may become an important substrate for ABD. Contrast

Ultrasonographic contrast agents can be used for luminal opacification to improve visualization of the endocardial border, or for myocardial opacification. Contrary to what is sometimes suggested,[66] it is unlikely that contrast will directly enhance ABD. Although lumen opacification may boost the visual interpretation, application of contrast still has many pitfalls. The transient nature of the opacification, incomplete or inhomogeneous filling of the cavity, shadowing, and local destruction of microbubbles (causing mixing of "white" and "black" blood), especially, make it hard to model the lumen appearance for any detection method. Next-generation contrast agents or special-purpose border detection techniques may provide solutions. Digital Image Storage and Radiofrequency Data

Digital image storage and communication will have a positive effect on general image quality and the availability of additional information (calibration, time, patient age and sex, body surface area, physiologic signals, protocol stages, views) can be a highly important source of a priori information for ABD techniques. As soon as raw radiofrequency information becomes available via digital storage, digital postprocessing of

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these data may provide superior input for ABD methods, effectively combining the strengths of AQ with those of high-level model-based approaches. Developments in Image Processing Model-Based Techniques

As seen in the section on Active Appearance Models, the biggest promises come from new developments in higher-level image processing. These techniques can model the complete appearance of a cardiac echo scene, 156

including patient variabilities. This approach may allow more natural solutions than older, edge-based or geometric model-based approaches. Because both shape variations over a large patient set and image appearance variations can be modeled, these techniques may handle typical artifacts, locally differing edge patterns, and other problems while restricting themselves to probable shapes. Furthermore, it seems possible to separate these models in patient-specific, view-specific, and pathologyspecific parts,[67] allowing more precise and flexible models and opening views to automated classification. The next-generation ABD technique for ultrasonography may well emerge from this family. Intelligent Systems

At the interpretation level, we enter the domain of artificial intelligence. Work in this field, especially in conjunction with image interpretation, is still in its infancy. Many high-level interpretation problems will need techniques from the field of artificial intelligence to be solved: formal reasoning from rule-based expert knowledge; generating multiple hypotheses with measures of confidence; reasoning with pathologic or congenital conditions during detection; checking overall consistency of an interpretation and taking action to resolve conflicts; opportunistically choosing an optimal detection strategy for the image data presented; and learning from operator corrections and actions. Ultimately, such developments may lead to an intelligent "automated image interpretation assistant" for echocardiographers.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Automated border detection for ultrasonography is still undergoing development. Few clinically applicable systems exist, and automation is limited. Positive expectations exist for the future. On the instrumental side, new opportunities will emerge from computer and ultrasonographic hardware improvements, availability of digital images and of raw radiofrequency information, and the perfection of techniques such as harmonic imaging, tissue Doppler imaging, real-time three-dimensional echocardiography, and maybe contrast echocardiography. In the field of ABD, improvements will result from several new technologies at the higher hierarchical levels (especially better three- and four-dimensional geometric modeling, anatomic scene descriptions, and modeling of anatomic interpatient variability and pathologic conditions) and techniques from artificial intelligence.

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References 1. Foster E, Cahalan MK: The search for intelligent quantitation in echocardiography:

"Eyeball," "trackball" and beyond. J Am Coll Cardiol 1993;22:848. 2. Hoffman R, Lethen H, Marwick TH, et al: Analysis of interinstitutional observer

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Schelbert HR, Wolf GL, Brundage BH (eds): Marcus Cardiac Imaging: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1996, p 273. 5. Weyman AE: Physical principles of ultrasound. In Weyman AE (ed): Principles and

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Century: A Primer. Bethesda, Md, American College of Cardiology, Cardiac and Vascular Information Working Group, 1997. 8. DICOM Committee: Digital Imaging and Communications in Medicine (DICOM),

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echocardiographers. J Am Soc Echocardiogr 1995;8:319.

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10. Waitz AS: An echocardiographer's guide to determining whether DICOM disk

interchange can be achieved between two systems. In Kennedy TE, Nissen SE, Simon R, et al (eds): Digital Cardiac Imaging in the 21st Century: A Primer. Bethesda, Md, American College of Cardiology, Cardiac and Vascular Information Working Group, 1997, p 138. 11. Anonymous: Digital Storage and Retrieval (DSR) File Format Specification V 0.18

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2nd ed. Pacific Grove, Calif, International Thomson-Brooks/Cole, 1999. 16. Collins SM, Skorton DJ: Cardiac Imaging and Image Processing. New York,

McGraw-Hill, 1986. 17. Skorton DJ, Schelbert HR, Wolf GL, Brundage BH: Marcus Cardiac Imaging: A

Companion to Braunwald's Heart Disease, 2nd ed. Philadelphia, WB Saunders, 1996. 18. Sonka M, Fitzpatrick JM: Handbook of Medical Imaging, vol 2. Medical Image

Processing and Analysis. Bellingham, Wash, SPIE—The International Society for Optical Engineering, 2000. 19. Thomas JD: Digital image processing. In Weyman AE (ed): Principles and Practice

of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 56. 20. Vuille C, Weyman AE: Left ventricle I: General considerations, assessment of

chamber size and function. In Weyman AE (ed): Principles and Practice of Echocardiography. Philadelphia, Lea & Febiger, 1994, p 575. 21. Nidorf SM, Weyman AE: Left ventricle II: quantification of segmental

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Philadelphia, Lea & Febiger, 1994. 22. Sher DB, Revankar S, Rosenthal S: Computer methods in quantitation of cardiac

wall parameters from two dimensional echocardiograms: A survey. Int J Card Imaging 1992;8:11. 23. Bosch JG, van Burken G, Nijland F, Reiber JHC: Overview of automated quantitation techniques in 2D echocardiography. In Reiber JHC, van der Wall EE (eds): What's New in Cardiovascular Imaging. Dordrecht, The Netherlands, Kluwer, 1998, p 363. 24. Sheehan F, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M,

Fitzpatrick JM (eds): Handbook of Medical Imaging, vol 2. Medical Image Processing and Analysis. Bellingham, WA, SPIE—The International Society for Optical Engineering, 2000, p 609. 25. Geiser EA: Edge detection and wall motion analysis. In Chambers J, Monaghan M

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26. Perez JE, Waggoner AD, Barzilai B, et al: On-line assessment of ventricular

function by automatic boundary detection and ultrasonic backscatter imaging. J Am Coll Cardiol 1992;19:313. 27. Marcus R, Bednarz J, Coulden R, et al: Ultrasonic backscatter system for

automated on-line endocardial boundary detection: Evaluation by ultrafast computed tomography. J Am Coll Cardiol 1993;22:839. 28. Bosch JG, Reiber JH, van Burken G, et al: Automated contour detection and

acoustic quantification. Eur Heart J 1995;16 (Suppl J):35. 29. Chandra S, Garcia MJ, Morehead AJ, et al: Spatiotemporal Fourier filtration of

acoustic quantification endocardial border using carthesian vs. polar coordinate system. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 17. 30. Spencer KT, Bednarz J, Rafter PG, et al: Use of harmonic imaging without echocardiographic contrast to improve two-dimensional image quality. Am J Cardiol 1998;82:794.

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31. Tsujita-Kuroda Y, Zhang G, Sumita Y, et al: Validity and reproducibility of echocardiographic measurement of left ventricular ejection fraction by Acoustic Quantification with Tissue Harmonic Imaging technique. J Am Soc Echocardiogr 2000;13:300. 32. Lang RM, Vignon P, Weinert L, et al: Echocardiographic quantification of regional

left ventricular wall motion with color kinesis. Circulation 1996;93:1877. 33. Mor-Avi V, Vignon P, Koch R, et al: Segmental analysis of color kinesis images:

New method for quantification of the magnitude and timing of endocardial motion during left ventricular systole and diastole. Circulation 1997;95:2082. 34. Vignon P, MorAvi V, Weinert L, et al: Quantitative evaluation of global and

regional left ventricular diastolic function with color kinesis. Circulation 1998;97:1053. 35. Koch R, Lang RM, Garcia MJ, et al: Objective evaluation of regional left

ventricular wall motion during dobutamine stress echocardiographic studies using segmental analysis of color kinesis images. J Am Coll Cardiol 1999;34:409. 36. Helbing WA, Bosch HG, Maliepaard C, et al: On-line automated border detection

for echocardiographic quantification of right ventricular size and function in children. Pediatr Cardiol 1997;18:261. 37. Gorcsan J, Romand JA, Mandarino WA, et al: Assessment of left ventricular

performance by on-line pressure-area relations using echocardiographic automated border detection. J Am Coll Cardiol 1994;23:242. 38. Carey CF, Mor-Avi V, Koch R, et al: Effects of inotropic stimulation on segmental

left ventricular relaxation quantified by color kinesis. Am J Cardiol 2000;85:1476. 39. Mor-Avi V, Spencer KT, Lang RM: Acoustic quantification today and its future

horizons. Echocardiography 1999;16:85. 40. Geiser EA, Wilson DC, Wang DX, et al: Autonomous epicardial and endocardial

boundary detection in echocardiographic short-axis images. J Am Soc Echocardiogr 1998;11:338. 41. Geiser EA, Wilson DC: Automatic center point determination in 2-dimensional

short-axis echocardiographic images. Pattern Recognition 1992;25:893. 42. Bosch JG, Savalle LH, van Burken G, Reiber JHC: Evaluation of a semiautomatic

contour detection approach in sequences of short-axis two-dimensional

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echocardiographic images. J Am Soc Echocardiogr 1995;8:810. 43. Bosch JG, van Burken G, Reiber JHC: Automatic frame-to-frame contour

detection in echocardiograms using motion estimation. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 351. 44. Auricchio A, Ghanem A, Groethus F, et al: Echocardiographic analysis of left ventricular contraction patterns in left bundle branch block and congestive heart failure [abstract]. J Cardiac Failure 1999;5(Suppl 1):3. 45. Breithardt OA, Kramer A, Schiffgens B, et al: Characteristics of left ventricular

contraction patterns and acute changes with multisite pacing in patients with heart failure as assessed by echocardiographic semiautomatic contour detection [abstract]. Eur Heart J 2000;21:351. 46. Fry SJ, Hunziker PR, Bosch HG, et al: Automated echocardiographic confirmation

of regional wall motion abnormalities: Quantitation of continuous LV volume [abstract]. J Am Coll Cardiol 1998;31:56A. 47. Hunziker PR, Schöb L, Lefkovits M, et al: Automatic border detection in

dobutamine stress echo: How do normal and ischaemic segments behave objectively and quantitatively? [abstract]. Eur Heart J 1999;20:618. 48. Hunziker PR, Yuan D, Schöb L, et al: Objective and quantitative stress echo

analysis to diagnose coronary disease using model-based image processing [abstract]. J Am Coll Cardiol 2000;35:413A. 49. Cootes TF, Edwards GJ, Taylor CJ: Active Appearance Models. In Proceedings,

European Conference Computer Vision. Berlin, Springer, 1998;2:484. 50. Edwards GJ, Taylor CJ, Cootes TF: Interpreting face images using Active

Appearance Models. In Proceedings of the 3rd International Conference on Face and Gesture Recognition. Nara, Japan, IEEE Computer Society Press, 1998, p 300. 51. Cootes TF, Hill A, Taylor CJ, Haslam J: Use of active shape models for locating

structures in medical images. Image Vision Computing 1994;12:355. 52. Cootes TF, Taylor CJ, Cooper DH, Graham J: Active shape models: Their training

and application. Comp Vision Image Understanding 1995;61:38. 53. Parker AD, Hill A, Taylor CJ, et al: Application of point distribution models to the

automated analysis of echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 25.

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54. Mitchell SC, Lelieveldt BPF, van der Geest RJ, et al: Segmentation of cardiac MR images: An active appearance model approach. In Proceedings, SPIE Medical Imaging 2000, Image Processing. Bellingham, Wash, SPIE—The International Optical Engineering Society, 2000;3979:224. 55. Bosch JG, Mitchell SC, Lelieveldt BPF, et al: Feasibility of fully automated border

detection on stress echocardiograms by Active Appearance Models [abstract]. Eur Heart J 2000;21:11. 56. van Camp G, Franken PR, Schoors D, et al: Impact of second harmonic imaging on

the determination of the global and regional left ventricular function by 2D echocardiography: A comparison with MIBI gated SPECT. Eur J Echocardiogr 2000;1:122. 57. Isaaz K: What are we actually measuring by Doppler tissue imaging? J Am Coll

Cardiol 2000;36:897. 58. Hunziker PR, Picard MH, Jander N, et al: Regional wall motion assessment in

stress echocardiography by tissue Doppler bull's-eyes. J Am Soc Echocardiogr 1999;12:196. 59. Derumeaux G, Ovize M, Loufoua J, et al: Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging: Characterization of normal, ischemic, and stunned myocardium. Circulation 2000;101:1390. 60. Pasquet A, Armstrong G, Beachler L, et al: Use of segmental tissue Doppler

velocity to quantitate exercise echocardiography. J Am Soc Echocardiogr 1999;12:901. 61. Heimdal A, Stoylen A, Torp H, Skjaerpe T: Real-time strain rate imaging of the

left ventricle by ultrasound. J Am Soc Echocardiogr 1998;11:1013. 62. Armstrong G, Pasquet A, Fukamachi K, et al: Use of peak systolic strain as an

index of regional left ventricular function: Comparison with tissue Doppler velocity during dobutamine stress and myocardial ischemia. J Am Soc Echocardiogr 2000;13:731. 63. Urheim S, Edvardsen T, Torp H, et al: Myocardial strain by Doppler

echocardiography: Validation of a new method to quantify regional myocardial function. Circulation 2000;102:1158. 64. Qin JJX, Jones M, Shiota T, et al: New digital measurement methods for left

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ventricular volume using real-time three-dimensional echocardiography: Comparison with electromagnetic flow method and magnetic resonance imaging. Eur J Echocardiogr 2000;1:96. 65. Takuma S, Zwas DR, Fard A, et al: Real-time, 3-dimensional echocardiography

acquires all standard 2-dimensional images from 2 volume sets: A clinical demonstration in 45 patients. J Am Soc Echocardiogr 1999;12:1. 66. Kamp O, Sieswerda GT, Visser CA: State-of-the-art: Stress echocardiography

entering the next millennium. In Reiber JHC, van der Wall EE (eds): What's new in cardiovascular imaging. Dordrecht, The Netherlands, Kluwer, 1998, p 351. 67. Costen N, Cootes TF, Edwards GJ, Taylor CJ: Simultaneous extraction of

functional face subspaces. In Proceedings, IEEE Computer Vision & Pattern Recognition. Los Alamitos, Calif, IEEE Computer Society Press, 1999, p 492. 158

68. Grube E, Mathers F, Backs B, Luederitz B: Automatische und halbautomatische

Konturfindung des linken Ventrikels im zweidimensionalen Echokardiogramm: Invitro Untersuchungen an formalinfixierten Schweineherzen. Z Kardiol 1985;74:15. 69. Ezekiel A, Garcia EV, Areeda JS, Corday SR: Automatic and intelligent left

ventricular contour detection from two-dimensional echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1985, p 261. 70. Klingler JW, Vaughan CL, Fraker TD, Andrews LT: Segmentation of

echocardiographic images using mathematical morphology. IEEE Trans Biomed Eng 1988;35:925. 71. Montilla G, Barrios V, Roux C, et al: Border detection in echocardiography images

using texture analysis. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 643. 72. Setarehdan SK, Soraghan JJ: Automatic left ventricular feature extraction and

visualisation from echocardiographic images. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1996, p 9. 73. Verlande M, Flachskampf FA, Schneider W, et al: 3D reconstruction of the beating

left ventricle and mitral valve based on multiplanar TEE. In Proceedings, Computers

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in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1991, p 285. 74. Han CY, Lin KW, Wee WG, et al: Knowledge-based image analysis for automated

boundary extraction of transesophageal echocardiographic left-ventricular images. IEEE Trans Med Imaging 1991;10:602. 75. Hozumi T, Yoshida K, Yoshioka H, et al: Echocardiographic estimation of left ventricular cavity area with a newly developed automated contour tracking method. J Am Soc Echocardiogr 1997;10:822. 76. Monteiro AP, Marques de Sa JP, Abreu-Lima C: Automatic detection of

echocardiographic LV-contours: A new image enhancement and sequential tracking method. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1988, p 453. 77. Chu CH, Delp EJ, Buda AJ: Detecting left ventricular endocardial and epicardial

boundaries by digital two-dimensional echocardiography. IEEE Trans Med Imaging 1988;7:81. 78. Feng J, Lin W-C, Chen C-T: Epicardial boundary detection using fuzzy reasoning.

IEEE Trans Med Imaging 1991;10:187. 79. Chalana V, Linker DT, Haynor DR, Kim Y: A multiple active contour model for

cardiac boundary detection on echocardiographic sequences. IEEE Trans Med Imaging 1996;15:290. 80. Dong L, Pelle G, Brun P, Unser M: Model-based boundary detection in

echocardiography using dynamic programming technique. In Proceedings, SPIE Medical Imaging V. Bellingham, Wash, SPIE-The International Society for Optical Engineering, 1991, p 178. 81. Friedland N, Adam D: Echocardiographic myocardial edge detection using an

optimization protocol. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1989, p 379. 82. Belohlavek M, Manduca A, Behrenbeck T, et al: Image analysis using modified

self-organizing maps: Automated delineation of the left ventricular cavity in serial echocardiograms. In Proceedings of the 4th International Conference on Visualisation in Biomedical Computing, VBC '96. Berlin, Springer, 1996, p 247. 83. Detmer PR, Bashein G, Martin RW: Matched filter identification of left-ventricular

endocardial borders in transesophageal echocardiograms. IEEE Trans Med Imaging 1990;9:396.

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84. Herlin IL, Nguyen C, Graffigne C: Stochastic segmentation of ultrasound images.

In Proceedings of the 11th IAPR International Conference on Pattern Recognition A: Computer Vision and Applications. Los Alamitos, Calif, IEEE Computer Society Press, 1992, p 289. 85. Dias JMB, Leitao JMN: Wall position and thickness estimation from sequences of

echocardiographic images. IEEE Trans Med Imaging 1996;15:25. 86. Gustavsson T, Molander S, Pascher R, et al: A model-based procedure for fully

automated boundary detection and 3D reconstruction from 2D echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1994, p 209. 87. Maes L, Delaere D, Suetens P, et al: Automated contour detection of the left

ventricle in short axis view and long axis view on 2D echocardiograms. In Proceedings, Computers in Cardiology. Los Alamitos, Calif, IEEE Computer Society Press, 1990, p 603. 88. Cohen LD: Note on active contour models and balloons. CVGIP Image

Understanding 1991;53:211. 89. Coppini G, Poli R, Valli G: Recovery of the 3-D shape of the left ventricle from

echocardiographic images. IEEE Trans Med Imaging 1995;14:301. 90. Brotherton T, Pollard T, Simpson P, DeMaria A: Echocardiogram structure and

tissue classification using hierarchical fuzzy neural networks. In Proceedings, IEEE Conference on Acoustics, Speech, and Signal Processing. IEEE New York, Computer Society Press, 1994, p 573.

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159

Chapter 8 - Myocardial Contrast Echocardiography Methods, Analysis, and Applications Thomas R. Porter MD Danielle Noll MD Feng Xie MD

Background The use of hand-agitated saline as a source of ultrasonographic contrast was first described in 1968, based on the concept of creating a gas-blood interface for ultrasonic enhancement of blood within the heart. During the following years, bubbles from agitated saline as well as a variety of other substances were used as echocardiographic contrast agents. Because of the large size of the microbubbles, their use was restricted to right heart contrast, when administered via a peripheral vein. This application included the detection of congenital or acquired intracardiac shunts, assessment of right-sided valvular regurgitation, and diagnosis of complex congenital heart defects and pulmonary arteriovenous fistulas. Although color Doppler, echocardiography now provides an easy method of detecting shunts, agitated saline has remained helpful in other areas such as quantifying tricuspid regurgitant velocities. [1] In the past, use of ultrasonographic contrast agents for left-sided imaging, however, could be performed only by direct injection of bubbles into the left atrium or ventricle.

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Initial studies aimed at detecting myocardial contrast used microbubbles produced by hand agitation or solutions containing carbon dioxide gas. Because of the short duration of the contrast, these agents were given either into the aortic root or directly into the coronary artery.[2] [3] [4] [5] [6] Since these studies, however, significant developments have been made in how intravenous microbubbles can be used to study myocardial perfusion. The stimulus for these developments includes an improved understanding of coronary physiology in patients with coronary artery disease, advances in ultrasonographic imaging, and the development of microbubbles that reach the coronary microcirculation after intravenous injection. The purpose of this chapter is to first illustrate the methods used to create ultrasonographic contrast. Second, we examine how these methods have been used to quantify myocardial perfusion, risk area, infarct size, and collateral blood flow with myocardial contrast echocardiography. Finally, 160

Figure 8-1 Effect of incorporating gases with lower diffusivity and solubility into microbubbles. When microbubbles contain only room air (RA) or sulfur hexafluoride (SF), an intravenous injection produces no myocardial contrast compared with baseline (BL). When these microbubbles contain a gas with low diffusivity and solubility such as perfluoropropane (PESDA), intravenous injection produces bright myocardial contrast. (From Porter TR, Xie F, Kilzer K: J Am Soc Echocardiogr 1995;5:710–718.)

the clinical applications of contrast echocardiography are reviewed.

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Characteristics of Microbubbles Microbubbles have to meet numerous physical and chemical standards to reach the left ventricular cavity and myocardium following venous injection. The first requirement is size. Microbubbles of more than 8 µm diameter are filtered from the pulmonary circulation and will not reach the left ventricular cavity.[7] The scattering cross section of a microbubble is related to the sixth power of its radius, and thus the smaller bubbles that reach the left ventricle are less reflective than the bubbles filtered by the pulmonary circulation. To detect the comparatively weak echoes of the bubbles small enough for transpulmonary passage, imaging modalities have been developed that register the more "microbubble-specific" resonant frequencies. The resonant frequency of a microbubble is inversely related to its diameter.[8] Another problem arising with the small microbubble size requirement is surface tension. The internal pressure of gases within microbubbles is increased dramatically as the size of a microbubble decreases to less then 7 µm. Therefore, the gases within the microbubbles are at very high concentrations and rapidly diffuse into blood. This immediately reduces the size and hence the contrast effect, a limitation becoming most evident when attempts are made to obtain myocardial ultrasonographic contrast from an intravenous injection. The transit time required to reach the left ventricular cavity from an intravenous injection is greater than 5 seconds and, therefore, significant amounts of gas will have escaped from the microbubble at this point. Therefore, a second requirement for intravenous microbubbles is to have a method of preventing dissolution after exposure to blood. The gas composition is one of the most important factors for retention of microbubble size in circulation. First-generation contrast agents contained

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room air, which is 78% nitrogen. Since nitrogen rapidly diffuses, these microbubbles survived only seconds.[9] To overcome this problem, slowly diffusing, insoluble gases were incorporated into the microbubbles. This improved the duration of ultrasonographic contrast in blood and even achieved myocardial contrast from an intravenous injection.[10] As shown in Figure 8-1 , by incorporating higher molecular weight gases such as perfluoropropane (molecular weight 188 g/mol) into microbubbles instead of room air, the same intravenous dose of dextrose albumin–coated microbubbles can produce a significantly greater amount of myocardial contrast than the same dose of microbubbles containing room air.

161

A third requirement is safety. Perfluorocarbon-containing microbubbles have been shown to have minimal toxicity in humans. The most frequent side effects noticed with Optison, the first and until now only secondgeneration ultrasonographic contrast agent approved by the Food and Drug Administration (FDA), are headache (5.4%), nausea and vomiting (4.3%), warm sensation or flushing (3.6%), and dizziness (2.5%). [11]

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Ultrasonographic Imaging Techniques Although electromechanical sonication and fluorocarbon gases have rendered the microbubbles more stable, 163

their detection in the myocardium with echocardiographic equipment remained difficult with conventional imaging techniques. The invention of second harmonic imaging, intermittent imaging, harmonic power Doppler and, recently, pulse inversion Doppler and power modulation has dramatically enhanced the myocardial contrast produced from intravenously injected microbubbles. Second Harmonic and Intermittent Imaging Microbubbles in an ultrasonic field have the ability to scatter ultrasound not only linearly but also nonlinearly. At peak incident pressures (above 0.1 megapascals), the microbubbles respond in a nonlinear manner. This physical property is attributable to the fact that gas bubbles are compliant and react to insonification at diagnostic frequencies with compression and rarefaction, thus emitting radial oscillations. The magnitude of compression and rarefaction is not the same with each oscillation, and therefore both linear and nonlinear returning waves occur. [44] The nonlinear responses typically occur in harmonics and can be received and filtered by an appropriate echocardiography system. Since tissue and side lobes exhibit a significantly smaller nonlinear response to ultrasound (Fig. 8-3) , ultrasonic transducers that selectively receive the harmonic frequency produce a much better signal-to-noise ratio and more sensitive detection of microbubbles than conventional imaging.[45] Microbubbles are destroyed by ultrasound when it is transmitted at diagnostic intensities (mechanical indices >0.3). Destruction can be

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reduced by selecting one image out of every one to several cardiac cycles, triggered to the electrocardiogram. This has been referred to as intermittent imaging. When the intermittent ultrasound impulse is at a high intensity (above 0.9 mechanical index), there is a strong and brief nonlinear echo. This transient scattering process is the third mode of action microbubbles show in an ultrasonographic field in addition to linear and harmonic response to ultrasound waves.[46] [47] Interrupting the high-intensity ultrasound for a short period of time allows for replacement of microbubbles, which then produce contrast enhancement for the following (triggered) frame. When microbubbles are administered as a continuous infusion and the ultrasound pulsing interval is incrementally varied, the reappearance of bubbles in the myocardium permits the calculation of mean microbubble velocity and plateau (or peak) myocardial signal intensity.[48] Multiplying these two variables together, one can better estimate myocardial blood flow. Therefore, with a combination of second harmonic and so-called intermittent imaging, it has become possible to noninvasively examine myocardial perfusion in animals and humans using a wide variety of intravenous higher molecular weight microbubbles.[8] [49] [50] [51] [52] (Harmonic) Power Doppler Power Doppler images are based on the integrated power in the Doppler signal instead of its mean frequency Figure 8-3 Illustration of returning signal intensity (indicated by arrow length). Microbubbles have the greatest harmonic signal intensity, but myocardium also has a harmonic response. Fortunately, the side lobe (SL) artifacts have very little harmonic signal intensity and thus do not reduce the image quality of a harmonic image as they do in fundamental images. (From Porter TR: Harmonic ultrasound imaging during routine and contrast-enhance echocardiography. Cardiac Ultrasound Today 1998;4:121.)

shift, as used in conventional color Doppler.[53] The amplitude of the Doppler signal is related to the concentration of scatterers at a particular location. This amplitude is much greater in the presence of microbubbles when compared with the signal of red blood cells.[54] This Doppler signal is more sensitive but, more importantly, is not subject to aliasing and is independent of the angle of insonation. It is, however, subject to flash artifacts, which occur with movement of the heart. Combining power Doppler with intermittent harmonic imaging (harmonic power Doppler) can

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decrease these flash artifacts at the expense of real-time imaging. Harmonic power Doppler has been successfully employed in animal[55] and human myocardial perfusion studies, showing satisfactory concordance in the comparison between echocardiographic and 99m Tc-sestamibi single photon emission computed tomography (SPECT) stress imaging.[56] [57] Low Mechanical Index Imaging Accelerated Intermittent Imaging

As previously mentioned, microbubbles are destroyed when exposed to ultrasound at high power output. Although 164

interrupting the imaging process by taking triggered images helps keep a sufficient concentration of contrast agent in the myocardial capillaries, the dynamic character of the echocardiographic examination cannot be used with triggered or intermittent imaging. If the mechanical index is set low enough to prevent major bubble destruction, while still allowing the microbubbles to resonate, the image acquisition can be performed continuously (because of the higher frame-rate), and real-time data on both wall motion and perfusion can be obtained. This procedure, termed accelerated intermittent imaging, has proven to be extremely helpful, especially during stress echocardiography in humans.[58] [59] Pulse Inversion Doppler and Power Modulation

Another possibility for achieving real-time visualization of myocardial function and perfusion is the application of the recently developed pulse inversion technique. The intention of this new method is the separation of linear and nonlinear scattering using the radiofrequency domain. Alternately positive and negative pulses of identical amplitude are transmitted into the tissue, the sum signal of which is equal to 0 (Fig. 8-4) . The responses of linear scatterers to that kind of pulses, therefore, will be cancelled. On the other hand, the signal from nonlinear scatterers (which do not react to positive and negative pressures in the same way) will be unequal to 0 and can be registered as a bubble-specific response (see Fig. 84) .[60] Although pulse inversion is subject to motion artifacts, pulse inversion Doppler overcomes this by sending multiple pulses of alternating polarity into the myocardium. This allows one to visualize wall thickening and contrast enhancement simultaneously at very low mechanical indices

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(<0.2) while maintaining an excellent signal-to-noise ratio. Initial studies using this technique in humans have demonstrated brilliant myocardial opacification from very small bolus injections of intravenous Optison.[61] [62] Figure 8-4 A depiction of how pulse inversion technology is able to enhance the signal-to-noise ratio from microbubbles at a very low mechanical index (<0.3). By sending pulses of alternating polarity, tissue signals cancel. Microbubbles, however, exhibit a nonlinear response to ultrasound even at these low mechanical indices, and hence the returning signals do not cancel. The resulting returning signal is a pure nonlinear response with almost nonexistent background signal. (Courtesy of Advanced Technology Laboratories, Bothell, Wash.)

Power modulation is another technique that improves the signal-to-noise ratio at very low mechanical indices. This technique, developed by Agilent Technologies (Andover, Mass), is also a multipulse cancellation technique, only here the power of each pulse is varied. The low-power pulses create a linear response, whereas the slightly higher power pulse results in a linear response from tissue but a nonlinear response from bubbles (Fig. 8-5) . The linear responses from the two different pulses (the amplified low-power pulse and the slightly higher power pulse) can be subtracted from each other; the transducer then only sees the nonlinear behavior, which emanates exclusively from the microbubbles. Both pulse inversion Doppler and power modulation can be used at very low mechanical indices to assess myocardial contrast in real time with excellent spatial resolution at higher band-widths.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Application of Ultrasonographic Contrast Via different injection routes, ultrasonographic contrast agents have been used to study various clinical problems in the cardiac catheterization laboratory and operating room, and now in the noninvasive setting (Table 8-2) . Detecting Acute Ischemia/Risk Area With Intracoronary and Aortic Root Injection

Prior to the development of stabilized perfluorocarbon microbubble contrast agents, clinical studies aiming at myocardial perfusion assessment mostly involved administration of air-filled microbubbles in the coronary arteries or aortic root. Bolus injections of air-filled microbubbles have been used to assess infarct size. Since microbubbles only enter regions where capillary integrity is preserved, this approach results in a more direct assessment of viability than definition of the contractile reserve. In several animal and human investigations, intracoronary ultrasonographic contrast injections have successfully delineated the area at risk after acute myocardial infarction, which is defined as the complete transmural extent of the perfusion bed supplied by an occluded coronary artery.[74] [75] [76] These studies have shown that area at risk measured with intracoronary contrast is superior to clinical, electrocardiographic, hemodynamic, or angiographic data in determining actual risk area. TABLE 8-2 -- Specific Clinical Applications of Myocardial Contrast Echocardiography Route of Injection Intracoronary

Clinical Parameters Measured Area at risk

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Perfusion bed size Infarct size Coronary flow reserve Collateral flow Area at risk Infarct size Coronary flow reserve Adequacy of cardioplegic delivery Adequacy of bypass graft perfusion Area at risk Infarct size No reflow Perfusion defect size Myocardial blood volume Myocardial blood flow Red blood cell velocity Subendocardial blood flow

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Figure 8-10 An example of the myocardial ultrasonographic contrast produced with perfluorocarbon-exposed sonicated dextrose albumin (PESDA). A, Short-axis view of the left ventricle in an open chest dog with a left circumflex occlusion before contrast injection. B, Myocardial contrast in the anteroseptal myocardium after intravenous contrast, also illustrating a large contrast defect in the posterolateral left ventricular myocardium. C, After reperfusion, an intravenous injection of this perfluorocarbon-exposed sonicated dextrose albumin produces homogeneous contrast throughout the myocardium. With Intravenous Injection

As previously discussed, intravenous microbubbles encapsulating high molecular weight gases in combination with new imaging techniques have made the noninvasive assessment of myocardial perfusion with

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echocardiography possible. These techniques have already been employed in clinical investigations and extend the findings of contrast studies performed with intracoronary and aortic root injections of contrast material. In several animal experiments, the spatial distribution of hypoperfusion after coronary artery occlusion and reperfusion has been accurately quantified with intravenous myocardial contrast echocardiography (Fig. 810) .[41] [77] [78] [79] Perfusion defects delineated by ultrasonographic contrast were found to correlate well with the extent of wall motion abnormality in the corresponding myocardial segment and postmortem measurement of risk area.[77] Peak myocardial videointensity within the hypoperfused segment following bolus injection of microbubbles has correlated closely with radiolabeled microsphere-derived flow in the infarct area.[41] Continuous infusions of microbubbles have been employed to quantify reductions in myocardial blood flow using the destruction-replenishment techniques described previously.[48] Assessment of the Effect of Myocardial Revascularization Intracoronary and Aortic Root Application

Intracoronary and aortic root injections of air-containing microbubbles have been used to assess the outcome of coronary angioplasty in patients with critical coronary artery stenoses.[80] Mudra et al[81] demonstrated that the half-time of contrast washout from peak myocardial videointensity after intracoronary contrast decreased after successful angioplasty. In their study, this rate of contrast washout from the myocardium returned to abnormal values when restenosis occurred. With intracoronary injection of sonicated albumin, Porter et al[82] described an immediate improvement in antegrade coronary blood flow reserve in a majority of patients who underwent angiographically successful angioplasty. The degree of improvement in diameter stenosis by quantitative angiography correlated closely with the magnitude of improvement in the area under the time intensity curve after intracoronary papaverine injection. Other investigators have demonstrated a correlation between the pressure gradient across a coronary stenosis before and after angioplasty and the degree of improvement in peak myocardial contrast produced by intracoronary contrast.[83] Identification of patients with the "no-reflow" phenomenon has been another important clinical application for intracoronary ultrasonographic contrast. This phenomenon, described first in an animal setting by Kloner et al in 1974,[84] is characterized by a lack of recovery in microvascular

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perfusion although the occluded coronary artery is successfully reopened by angioplasty or thrombolysis. Ito et al[85] were the first to systematically examine myocardial perfusion with intracoronary microbubbles in patients with acute anteroseptal myocardial infarction immediately following restoration of antegrade flow in the left anterior descending artery. Using intracoronary sonicated radiographic contrast, they demonstrated that 23% of the patients had persistent contrast defects (i.e., no reflow) in the area at risk after recanalization. The long-term prognosis of these no-reflow patients was impaired, and there was significant deterioration in regional and global systolic function at follow-up. These findings have been confirmed by other investigators. Visualization of collateral myocardial blood flow before and after revascularization has been demonstrated with intracoronary contrast. In patients with occluded vessels, injection of ultrasonographic contrast material into adjacent coronary arteries can produce myocardial contrast enhancement in the perfusion bed subtended by the occluded vessel.[86] [87] This phenomenon is clinically relevant because it indicates viability of the perfusion bed subtended by the occluded coronary artery.[88] Sabia et al[89] demonstrated that revascularization of an occluded coronary artery after myocardial infarction improved function only when ultrasonographic contrast delivered into the 169

opposite coronary artery resulted in contrast enhancement to the perfusion bed of the occluded artery prior to revascularization.[90] The spatial extent of collateral blood flow as defined by contrast echocardiography correlated closely with improvement in regional function within the infarct zone. These observations suggest that intracoronary contrast echocardiography may be a valuable tool in determining whether revascularization procedures are indicated (Fig. 8-11) . When employed in the operation room during coronary bypass grafting, intracoronary and aortic root injections of ultrasonographic contrast agent have been useful in several aspects. The effectiveness of the saphenous vein graft has been determined by injection of air-filled microbubbles into the cross-clamped aortic root or directly into the graft.[91] [92] [93] Aortic root injections of microbubbles before cardiopulmonary bypass have also guided the sequence of bypassing.[94] The peak myocardial videointensity following intra-aortic contrast-enhanced cardioplegia injections has

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correlated with the eventual improvement in wall motion after bypass grafting.[91] [95] Retrograde (via the coronary sinus) and antegrade cardioplegic delivery have been compared by using myocardial contrast echocardiography. In these small studies, retrograde delivery was found to be superior in providing myocardial perfusion in certain cases.[96] Keller et al[96] investigated the possibility of quantifying myocardial blood flow in the arrested heart during open heart surgery and found that the washout of microbubbles was markedly prolonged during antegrade crystalloid cardioplegia, so that it was no longer correlated with tissue flow (Fig. 812) . The washout delay appeared to be due to albumin microbubble adherence to the venules, suggesting that endothelial damage is caused by the cardioplegic solution.[97] This microvasculature damage could be partly Figure 8-11 Changes in myocardial contrast after intracoronary injection of contrast in both the vessel being dilated (recipient vessel area) and the coronary artery providing angiographic collaterals to the vessel being dilated before and after successful angioplasty in six patients. As can be seen, the amount of recipient vessel area contrast enhanced by the artery supplying collateral flow decreases significantly in most patients immediately after angioplasty. PTCA, percutaneous transluminal coronary angioplasty. (From Grill HP, Brinker JA, Taube JC, et al: J Am Coll Cardiol 1990;16:1594.)

Figure 8-12 Different time intensity curves from the myocardium at the same flow rate demonstrating the effect of the cardioplegia-arrested heart on washout of contrast material. This is markedly different than the washout of contrast material from a beating heart. (From Keller MW, Kaul S, Spotnitz WD, et al: J Am Coll Cardiol 1990;16:1267.)

avoided when cardioplegia was mixed with blood. The greater the amount of blood in the cardioplegic solution, the higher was the observed microbubble transit rate. [98] With Intravenous Injection

By using second-generation contrast agents and intermittent nonlinear detection modalities, several investigators have recently succeeded in detecting the no-reflow phenomenon from intravenous administration of microbubbles in patients with acute myocardial infarction following revascularization. Lepper et al[99] studied myocardial contrast enhancement in patients with acute infarction undergoing angioplasty immediately before

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and 24 hours after recanalization using intravenous perfluorocarboncontaining microbubbles (NC100100; Nycomed Imaging AS) and intermittent harmonic imaging. An improvement of myocardial perfusion within 24 hours after intervention was predictive of functional recovery verified at 4-week follow-up. These investigators found that myocardial contrast imaging performed within an hour after revascularization is likely to lead to an underestimation of the ultimate infarct size. Actual infarct size in this time frame is best assessed following the use of a coronary vasodilatator. [100] Porter et al[101] used intravenous PESDA to identify patients with the noreflow phenomenon following successful restoration of antegrade flow after acute myocardial infarction (Fig. 8-13) . In concordance with previous studies using intracoronary contrast, lack of contrast enhancement in the perfusion bed of the infarct-related artery was predictive of a subsequent lack of recovery in both regional and global myocardial function. There are no human studies evaluating intravenous ultrasonographic contrast imaging for the detection of 170

Figure 8-13 Examples from two different patients who had anteroseptal and apical myocardial infarctions and similar wall motion score indexes following restoration of epicardial flow in the left anterior descending artery. The patient on the right had a persistent perfusion defect (no reflow, arrowheads), whereas the patient on the left demonstrated reflow in the same regions (arrowheads). MI, myocardial infarction. (From Porter TR, Li S, Oster R, Deligonul U: Am J Cardiol 1998;82:1173. Reprinted with permission from Excerpta Medica Inc.)

collateral vessels. However, Mills et al[102] studied the development of coronary collaterals flow in a canine model by examining the spatial and temporal course of a contrast defect following acute coronary occlusion using intravenous echocardiographic contrast and second harmonic intermittent imaging modalities. Thus, intravenous myocardial contrast echocardiography may be useful in assessing myocardial viability in the perfusion beds of patients with occluded coronary arteries. Detection of Coronary Artery Disease With Intracoronary and Aortic Root Contrast Injections

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Early attempts to determine perfusion defects in patients with coronary artery disease were restricted to the catheterization laboratory. Cheirif et al [25] described in a canine model a close correlation between dipyridamole contrast echocardiography and thallium-201 SPECT in assessing the extent of jeopardized myocardium when moderate to severe degrees of coronary stenosis were present. DeFilippi et al[103] compared intracoronary myocardial ultrasonographic contrast enhancement with wall motion responses to dobutamine (contractile reserve) in 35 patients with chronic coronary artery disease. They found that both contractile reserve and myocardial contrast enhancement were predictive of functional recovery in hypokinetic segments following revascularization. Contrast echocardiography with intracoronary Albunex was used to identify myocardial hibernation by Nagueh et al[104] in patients with stable coronary artery disease and left ventricular dysfunction. These investigators reported myocardial contrast echocardiography, thallium-201 SPECT, and dobutamine stress echocardiography to be of comparable sensitivity in predicting functional recovery after revascularization, but specificity was highest with dobutamine stress echocardiography. With Intravenous Contrast Injections and Infusions

Until the last few years, radionuclide scintigraphy has been the diagnostic tool to address myocardial perfusion during stress testing. This method, especially when performed with 99m Tc rather than 201 Tl, provides high sensitivity in identifying patients with coronary artery disease. It is limited, however, by relatively poor spatial resolution and frequent attenuation artifacts. With intravenous perfluorocarbon contrast agents and nonlinear ultrasonographic techniques, detection of underperfused myocardial segments during stress echocardiography has become feasible (Fig. 8-14) . Using intravenous Optison and intermittent harmonic imaging, Kaul et al [105] described a 92% concordance between segmental perfusion scores by myocardial contrast echocardiography and 99m Tc-sestamibi SPECT at rest and during dipyridamole stress. Porter et al[52] likewise indicated a close correlation 171

Figure 8-14 (color plate.) Myocardial contrast produced from 0.3 mL

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intravenous injections of Optison at rest (left) and during dobutamine stress (right) echocardiography in three different patients with significant coronary artery disease in three different coronary artery territories. Ultrasonographic imaging is done with pulse inversion Doppler, and this results in bright myocardial opacification in normal regions at mechanical indexes of 0.2 or less. A, Inducible anteroseptal and apical defect; B, inducible inferior perfusion defect; C, inducible lateral wall contrast defect. All patients were found to have greater than 50% diameter narrowings at coronary angiography in the left anterior descending (A), right coronary artery (B), and left circumflex artery (C), respectively.

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between regional peak myocardial videointensity following intravenous PESDA and radionuclide tracer uptake during dipyridamole stress echocardiography performed with intermittent harmonic imaging. Most recently, Heinle et al[57] used an intravenous Optison infusion and harmonic power Doppler imaging at long pulsing intervals during adenosine stress testing to compare perfusion with 99m Tc-sestamibi SPECT in 123 patients with suspected coronary artery disease. There was an overall concordance between both techniques of 83%; concordance was higher in patients with no or multivessel coronary artery disease. Correlation was also dependent on which coronary territory was involved, with the best agreement occurring in the left anterior descending territory (81%). Agreement was not as good between the two techniques in the left circumflex (72%) or right coronary artery (76%) territories.[57] On a segmental basis, the highest concordance between techniques was in the midanterior septum (82%), whereas there was poor agreement in the basal lateral (51%) and posterolateral (59%) segments. This may be due to the fact that, even with continuous Figure 8-15 An example of an apical perfusion defect in the apical longaxis view (arrowheads) during dobutamine stress (bottom panels) using a continuous infusion of perfluorocarbon containing microbubbles. Under baseline conditions (top panels), no contrast defect was observed at incremental pulsing intervals. At peak dobutamine stress, an apical contrast defect was observed even at the longer 3000 msec pulsing interval. This patient had a totally occluded left anterior descending artery at angiography. DOB, dobutamine; PI, pulsing interval. (From Porter TR: Echocardiography 2000;17:92.)

infusion, assessment of the basal regions is often affected by attenuation. Nonetheless, use of a continuous infusion reduces attenuation artifacts and

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provides more homogeneous myocardial contrast opacification. It also may eventually allow us to clinically quantify myocardial blood flow (Fig. 815) . In patients with coronary artery disease, a noninvasive diagnostic option for the definition of occlusion degree would be particularly helpful. Animal stress echocardiographic studies involving continuous perfluorocarbon microbubble infusion and intermittent harmonic imaging have shown a strong correlation between the severity of a coronary stenosis and the severity of a replenishment contrast defect at peak dobutamine stress.[106] Low mechanical index imaging techniques have recently emerged as a much more practical method of detecting myocardial perfusion abnormalities during stress echocardiography.[58] Cwajg et al[59] used accelerated intermittent imaging and intravenous bolus injections of Optison and PESDA at rest and during dobutamine stress 173

Figure 8-16 (color plate.) An example of real-time myocardial contrast enhancement produced with an intravenous Optison injection (0.3 mL) in one patient at rest (top panels), during intermediate dose dobutamine at 70% predicted maximum heart rate (middle panels), and during peak infusion at more than 85% predicted maximum heart rate (bottom panels). Note that with low mechanical index pulse inversion Doppler echocardiography, myocardial contrast enhancement is seen throughout the cardiac cycle. Note that there was an inducible anteroseptal and apical perfusion defect during stress, which became evident at the intermediate dobutamine infusion stage. ED, end-diastole; ES, end-systole.

echocardiography in 45 patients with known or suspected coronary artery disease. In this study, the real-time assessment of perfusion improved the sensitivity of the test in detecting angiographically significant stenoses by more than 10%.[59] More recent phase II studies have demonstrated the incremental value of myocardial perfusion assessment using accelerated intermittent imaging during exercise testing. [107] With the advent of pulse inversion Doppler echocardiography, low mechanical index imaging during stress echocardiography has higher spatial resolution and improved signalto-noise ratio (Fig. 8-16) . Distribution of Transmural Myocardial Blood Flow Because of the high spatial resolution of ultrasonographic imaging, several investigators have demonstrated differences in the degree of

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echocardiographic contrast produced by an intracoronary or aortic root injection between the subendocardial and subepicardial layers of myocardium. Animal studies even demonstrated after an intracoronary injection of a monosaccharide-based contrast agent (SHU-454) that differences in the transmural distribution of contrast could be detected at different times in the cardiac cycle.[107] Lim et al[108] demonstrated with an intracoronary injection of hand-agitated contrast material in humans that there was a lower subendocardial contrast intensity during pacing in regions supplied by a critical coronary stenosis. Although these findings in humans are promising, subsequent animal studies have not been able to confirm that intracoronary or aortic root injections of ultrasonographic contrast agent can distinguish subendocardial from subepicardial blood flow.[90] These investigators have shown that transmural attenuation of the myocardium caused by the contrast agent creates a false impression of relative decreases in subendocardial contrast. In addition, there are other limitations involved in using ultrasonographic contrast to define transmural differences in ultrasonographic contrast, such as (1) the nonspecific scattering properties of microbubbles, (2) the signalto-noise problems that occur even with epicardial imaging in differentiating the subendocardium from subepicardium, and (3) interference from scattering of microbubbles within the arterioles and venules. These same investigators, however, have demonstrated that the quantitative assessment of myocardial blood flow that can be achieved with a continuous intravenous infusion of microbubbles may also be able to delineate transmural differences. [109] In an open chest canine study, only the endocardial-to-epicardial ratio of the product of the initial contrast replenishment slope and plateau myocardial signal intensity correlated with radiolabeled 174

microsphere measurements, whereas transmural measurements of myocardial blood volume did not.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Other Intravenous Applications of Microbubbles Improved Endocardial Border Delineation Several different intravenous ultrasonographic contrast agents have demonstrated their ability to improve the diagnostic value of echocardiographic examinations in patients with suboptimal imaging conditions. In routine ultrasonographic examinations of patients with poor echocardiographic windows, contrast enhancement of the left ventricular cavity provides better delineation of the endocardial border. Clinically, this could give more information regarding regional and global systolic function that could not be assessed with routine echocardiography. Tissue harmonic imaging by itself has significantly improved endocardial border, often eliminating the need for intravenous ultrasonographic contrast agents filled with room air.[110] During the last few years, studies have shown that intravenous perfluorocarbon-containing microbubbles, because of their consistent left ventricular opacification, have improved border definition in the left ventricle of patients with suboptimal tissue harmonic images (Fig. 8-17) . Figure 8-17 An example of how intravenous perfluorocarbon microbubbles can improve endocardial delineation at end-diastole (DIAS) and end-systole (SYS) when compared with harmonic imaging above in a technically difficult patient. With the addition of intravenous contrast, the previously poorly delineated borders are now well visualized throughout the cardiac cycle. AC, after contrast; BC, before contrast. (From Porter TR: Echocardiography 2000;17:92.)

Optison proved its superiority over Albunex in a multicenter study that included 200 patients with suboptimal baseline pictures.[111] In this trial, full ventricular opacification could be achieved in 87% of the patients using the maximum intravenous Optison dose (5 mL), but only in 36% with optimal Albunex dosing (0.22 mL/kg). In patients with an echocardiogram that was

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nondiagnostic because of poor images, the use of Optison resulted in diagnostic quality images in 74% of all cases, whereas the use of Albunex converted only 26% of poor-quality images to images of diagnostic value. Although the use of Optison increases the costs for routine transthoracic echocardiograms, substantial cost savings could still be made in the examination of patients with poor baseline harmonic image quality, because it would prevent the need for additional diagnostic studies in these situations. [112] Reilly et al[113] recently studied the effect of intravenous Optison injections in harmonic transthoracic echocardiography in the intensive care unit. Their results indicated a significant increase in interpreter confidence in evaluating myocardial segments that could not be analyzed without contrast application. Furthermore, the ability to estimate left ventricular ejection fraction was clearly improved with Optison. To accurately detect wall motion abnormalities during stress echocardiography, clear definition of endocardial borders is of particular importance. Several first-generation ultrasonographic contrast agents such as Albunex, 175

Levovist, and BY 963 have already been studied in pharmacologic and exercise stress tests, and all of the trials described better overall image quality at peak stress with these intravenous agents as compared with standard imaging.[114] [115] [116] [117] [118] [119] Contrast enhancement was especially helpful in interpretation of anterior and lateral wall segments.[119] Malhotra et al[120] most recently compared stress echocardiograms performed with both fundamental and harmonic imaging modalities with and without intravenous Optison contrast in 200 patients. They reported that the combination of harmonic ultrasonography with Optison resulted in the most consistent endocardial border delineation, which significantly exceeded the quality of either fundamental contrast imaging or tissue harmonic imaging alone. Interobserver agreement with Optison and harmonic imaging in this study was 95%. Unfortunately, in none of these studies has there been an analysis of whether improving endocardial border definition affects the sensitivity or specificity of the test when compared to radionuclide imaging or quantitative angiography. Contrast-induced homogeneous opacification of the left ventricular cavity

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could also assist physicians in detecting left ventricular thrombi or tumors [121] [122] and complications of acute myocardial infarction such as myocardial rupture and left ventricular pseudoaneurysm.[123] It has also been used during transesophageal echocardiography to delineate false and true lumen in patients with aortic dissection.[124] Doppler Enhancement Intravenous microbubbles affect Doppler recordings because the scatter from them is much greater than from red blood cells. Microbubbles therefore can increase the signal strength in a Doppler examination markedly, which may be helpful in patients with suboptimal imaging quality. Von Bibra et al[125] described a significant enhancement of spectral and color Doppler and an increase in the signal-to-noise ratio in the quantitative assessment of aortic stenosis, pulmonary venous flow, and mitral regurgitation by intravenous injection of Levovist. Transthoracic pulmonary venous flow velocities have been improved by intravenous contrast enhancement to the point that they are comparable to those obtained with transesophageal imaging. [126] Moreover, intravenous microbubble ultrasonographic contrast was successful in providing a clear spectral signal across stenotic aortic valves, in cases in which the echocardiogram would have been nondiagnostic without contrast enhancement.[127] The gradients determined using contrast-enhanced Doppler signals correlated well with catheterization calculations. [127] Okura et al[128] studied the effect of Albunex in 45 patients with prosthetic aortic valves. They found a significant improvement in transvalvular continuouswave Doppler signal intensity with intravenous Albunex, increasing the frequency of satisfactory Doppler signals from 64% to 93% of patients. In patients with congestive heart failure, Kuecherer et al[129] used intravenous ultrasonographic contrast during exercise to evaluate cardiac functional reserve. They reported close correlation between echocardiographic estimation of systolic pulmonary artery pressure and invasively measured values both at rest and during stress testing. Safety of Myocardial Contrast Echocardiography There are no investigations in large study populations concerning the safety of intra-aortic or intracoronary application of microbubbles. In smaller studies, there have been isolated reports of transient chest pain after intracoronary sonicated albumin.[28] In a study of 18 patients given injections of intracoronary Albunex (commercially available sonicated albumin), 1 mL injections had no effects on systolic or diastolic function.

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However, 2 mL injections did transiently alter diastolic function.[130] The effects of ultrasonographic contrast agents compare favorably with the effects of radiographic contrast agents that transiently affected both systolic and diastolic function. Stabilized gas-containing intravenous microbubbles contained by albumin or lipid shells disrupt during insonication and are also pressure sensitive. The gas that is emitted from the bubble is excreted via the lungs, whereas the components of the shell are metabolized by liver enzymes. Perfluorocarbon gases are not metabolized but only exhaled. The safety of intravenous contrast agents containing high molecular weight gases has been tested in both animals and humans. The results of these studies suggest that perfluorocarbon-exposed sonicated dextrose albumin,[12] Definity,[131] Optison,[132] SonoVue,[133] and NC100100[134] all produce no significant hemodynamic abnormalities or serious side effects. After repeated intravenous application of Albunex over several months in 12 patients, there was no evidence of an immune reaction, such as IgE or IgG antibodies, and there were no adverse effects on left and right heart hemodynamics.[135] Animal studies have demonstrated bioeffects resulting from the interaction between microbubbles, low-frequency ultrasound, and tissue. Although both hemolysis and platelet lysis have been described in animal studies, to date these effects have not been observed in the clinical setting.[136] [137] Therapeutic Application of Microbubbles and Ultrasound A number of studies indicate that ultrasound microbubbles not only enhance the diagnostic value of an echocardiographic examination, but may also be used for therapeutic purposes. Drug Delivery

The fact that microbubbles are destroyed by the ultrasound beam has led to the study of their potential role in depositing adherent drugs or genes to an "ultrasound-targeted" organ.[138] Skyba et al[139] studied the intravascular destruction of perfluorocarbon-containing microbubbles 176

and the bioeffects of this process in the isolated spinotrapezius muscle of rats. With just one sweep of a diagnostic ultrasound transducer (2.3 MHz), microbubble destruction was observed that caused local microvessel

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rupture. When the bubbles were mixed with colloidal particles, these particles were also "microinjected" into the interstitial space. The degree of microbubble destruction and resulting "drug delivery" was directly related to the mechanical index used.[140] Porter et al[141] demonstrated that perfluorocarbon-exposed sonicated dextrose albumin microbubbles bind large quantities of synthetic antisense oligonucleotides. These oligonucleotides are synthetic gene products that can be used to inhibit the translation of messenger RNA into proteins and enzymes that regulate pathologic processes such as neointimal hyperplasia following vascular injury. Their experiments indicated that external diagnostic ultrasound released the synthetic antisense into the insonified kidney if the antisense oligonucleotide was given intravenously bound to PESDA. In a recently published study, recombinant adenovirus containing β-galactosidase was attached to the surface of intravenously injected perfluorocarbon-containing albumin microbubbles and successfully targeted to the myocardium of rats by diagnostic ultrasound at a high mechanical index (1.5). Postmortem analysis showed β-galactosidase transgene expression in the myocardium after ultrasound antigene delivery, but no expression of the transgene in the control groups that had received Figure 8-18 (Figure Not Available) (color plate.) Echocardiographic delivery of microbubbles containing galactosidase (AdCMV-β-Gal). A, Short-axis view of rat heart reveals galactosidase staining 4 days after ultrasonic destruction of microbubbles carrying recombinant adenovirus containing β-galactosidase. B, Fast red stain of a 7 µm section from heart in A shows nuclear localization of galactosidase staining (× 20). C, Representative section from a control rat showing no galactosidase staining. D, Microscopic section from same control rat showing no galactosidase staining. (From Shohet RV, Chen S, Zhou Y-T, et al: Circulation 2000;101:1554, with permission.)

microbubbles alone, virus alone, or virus plus ultrasound (Fig. 8-18) (Figure Not Available) .[142] Targeted intramyocardial gene delivery has also been reported in vivo with lipid-encapsulated microbubbles. [143] Thrombolysis

Several investigators have examined the potential of high-energy ultrasound alone to dissolve thrombi in vitro as well as in an animal setting. Transcatheter ultrasound was able to reduce thrombus weight and possibly recanalize occluded femoral arteries.[144] Since this process involves cavitation, more recent investigations have focused on whether microbubbles could potentiate this phenomenon. When combined with intravenous perfluorocarbon microbubbles, low-

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intensity, high-frequency ultrasound significantly increased the thrombolytic effect of urokinase in vitro. Even more importantly, ultrasound plus perfluorocarbon-containing microbubbles alone proved to be equivalent to urokinase in degree of thrombus dissolution. Therefore, it appeared that ultrasound and microbubbles could produce a localized clot lysis similar to a fibrinolytic agent without a systemic lytic state.[145] Invasive clot dissolution with therapeutic ultrasound and PESDA alone has been successfully tested in animal experiments. In a study involving 10 rabbits, iliofemoral arteries received 177

Figure 8-19 (Figure Not Available) Case example of angiography of both iliofemoral arteries following thrombotic occlusion of the iliac arteries (A and B). The right iliac artery was treated with intravenous perfluorocarbon-exposed sonicated dextrose albumin (PESDA) and transcutaneous ultrasound, resulting in recanalization after 30 minutes of therapy (C). The control side, treated with PESDA alone, remained occluded (D). (From Birnbaum Y, Luo H, Nagai T, et al: Circulation 1998;97:130, with permission.)

transcutaneous ultrasound treatment on one side and no ultrasound treatment on the other after an acute artery thrombotic occlusion. PESDA was given intravenously. After ultrasound treatment, all arteries that had received PESDA and ultrasound were recanalized by angiography, but none of the arteries treated with PESDA alone were patent (Fig. 8-19) (Figure Not Available) . Ultrasound alone also was unable to recanalize any of the thrombosed vessels.[146] Although more investigation on this field is required, the combination of ultrasound and microbubbles may turn out to be a promising alternative to the established thrombolytic strategies because of its ability to localize treatment to just the desired area. Detecting Inflammation

According to several experimental studies, albumin microbubbles used for ultrasonographic contrast enhancement persist in the myocardium in regions undergoing ischemia followed by reperfusion. The reason for this prolonged persistence is not exactly known yet. There is evidence, however, that endothelial glycocalyx damage and the presence of inflammatory extracellular matrix increase microbubble adherence to vascular endothelium.[147] [148]

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Lindner et al[149] hypothesized that during the early inflammatory response after reperfusion, activated leukocytes adherent to the venular endothelial surface may bind microbubbles and therefore prolong their transit. Using tumor necrosis factor-α injection in an animal setting, they have shown that both lipid and albumin microbubbles attach to activated leukocytes. The binding of the albumin microbubbles was mediated by β2 -integrins while the interaction between leukocytes and lipid microbubbles involved the complement pathway.[149] In a subsequent investigation, the involved leukocytes were identified to be mostly neutrophils and monocytes. Lipid and albumin microbubbles were phagocytosed by these cells and remained acoustically active for up to 30 minutes. During this time, they responded to ultrasound and could be detected in vivo after microbubbles from the blood pool had already vanished (Fig. 8-20) (Figure Not Available) .[150]

These findings describe the potential of microbubbles to noninvasively assess inflammation and may even lead to a possibility for drug delivery to the affected organ system. Furthermore, since albumin-coated microbubbles adhere to sites where vascular endothelial damage occurs, 178

Figure 8-20 (Figure Not Available) Effects of single pulses of ultrasound (P1 through P4 ) at different peak negative acoustic pressures on phagocytosed albumin-coated microbubbles. Note that neutrophil cell membrane disruption and distortion occurred at higher peak negative pressures (- 1600 kPa). BL, baseline. (From Lindner JR, Dayton PA, Coggins MP, et al: Circulation 2000;102:531, with permission.)

this may be a method of targeting the delivery of drugs bound to the microbubble without ultrasound. For example, we have recently demonstrated that PESDA microbubbles can concentrate the delivery of the antisense to the c-myc protooncogene to balloon-injured sites in the coronary artery and thus prevent neointimal hyperplasia.[151]

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Summary The use of intravenous microbubbles for perfusion imaging is now a realtime reality. Future multicenter studies will demonstrate whether there is an incremental clinical benefit to examining myocardial perfusion during stress echocardiography and in acute coronary syndromes. Intravenous microbubbles also have a potential therapeutic role in the areas of targeted drug delivery, enhancing thrombolysis, and detecting inflammation.

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183

Chapter 9 - Interaction of Ultrasound with Tissue, Approaches to Tissue Characterization, and Measurement Accuracy Roy W. Martin PhD

The purpose of this chapter is to provide insight into what happens when a beam of ultrasound is launched into the body. What are the factors that affect this interrogating energy? How does it interact with the tissue and return reflected information to us? What can contaminate this returned information? What influences the accuracy of the information, and how may we further use information that is present in the signal but has largely been ignored? The answers to these questions provide understanding of common problems encountered daily (such as imaging artifacts and concern about the accuracy of measurements we make from these images). Furthermore, they also provide understanding of methods that extend beyond conventional imaging, such as feature extraction, border detection, and tissue characterization. The thrust of this chapter is to provide insight into basic fundamentals and then to apply those fundamentals to aid in understanding some tissue characterization methods, the recent developments in harmonic imaging, and several measurement errors.

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Beam Patterns Ideally, we'd like to generate an infinitely narrow pencil beam of ultrasound that could be swept rapidly through the tissue, thereby interrogating all the regions of interest. Unfortunately, as we currently understand the physics of the problem, ultrasound energy doesn't allow this; instead of being narrow like laser beams, the beams are more like broad flashlight beams. Furthermore, the intensity is not uniform within and throughout the beam. This lack of a narrowness and uniformity leads to measurement errors and can contribute to artifacts. In addition, we would ideally like to be able to generate infinitely short pulses of ultrasound energy, but this is also only approximated in practice. Short pulses are easier to generate than narrow beams and therefore are not addressed in the chapter. Aperture The general term aperture refers to an opening through which radiation passes. In ultrasound transducers, aperture refers to the active surface of the transducer that emits or receives ultrasound waves. The behavior of these waves is similar to that of a plane wave passing through a hole that is the same size and shape as the active surface of the transducer; therefore, the use of the term has evolved. Several examples of commonly used apertures are shown in Figure 9-1 . With respect to the wavelength λ of the ultrasound, the size of the aperture of the ultrasound transducer is responsible for the overall beam pattern. The focusing and excitation patterns provide further modification to this general pattern. The wavelength of the sound is equal to the speed of sound c, in the media adjacent to the transducer divided by the ultrasound frequency f (i.e., λ = c/f). For example, because the average value of the speed of sound in tissue is 1540 m per second, then at 3 MHz, λ = 0.5 mm. Consider a circular aperture as shown in Figure 9-1A . If the radius of the aperture, a, is much less than the wavelength, the beam pattern is very

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broad, whereas if the aperture radius is much greater than the wavelength, the beam is narrower in the region referred to as the far field. In addition, other features of the beam patterns are influenced by the radius-towavelength size. A radius of approximately 10 times the wavelengths has been found to be a good compromise (i.e., a/λ = 10). The beam 184

Figure 9-1 Geometry of various apertures of transducers used in medical ultrasound. A, circular disc; B, square; C, rectangle; D, annular array; E, square array aperture; F, rectangular array aperture; G, annular aperture; H, small rectangular aperture. Note that D is composed of an assemblage of annular apertures such as G and that E and F are composed of sets of small rectangular apertures such as H.

patterns for three ultrasound frequencies at which this ratio is constantly maintained are shown in Figure 9-2 . [1] [2] The different patterns in the near field and far field of the transducer are seen in Figure 9-3A . Regions of increasing and decreasing pressure isocontours are present in the near field. This near-field effect is due to wavelets from various regions of the aperture arriving at different phases at several points in the near field. Consequently, these wavelets add and subtract depending on their relative Figure 9-2 Beam pattern (3 dB below the axial value) is shown for three circular apertures where a/λ = 9.7. The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). The ultrasound frequencies and radius of each aperture (from left to right) are 5, 3.5, and 2 MHz and 0.3, 0.43, and 0.75 cm, respectively. Note that the point along the z-direction where the beam is the most constricted for each aperture is known as its near-far field transition. Points closer to the aperture are in the near field, whereas further points are in the far field. (Data from Weyns A: Ultrasonics 1980;18:183–188.)

phase with respect to each other. In the far field, this phenomenon is not present because they are all of the same relative phase. In the transition region between the near field and the far field, the beam pattern becomes much narrower and there are no pressure fluctuations because of little difference in the phase of arriving wavelets. The distance at which this transition occurs (the extent of the near field) can be calculated easily for a

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disc transducer[3] [4] as near-field distance = a2 λ. In the far field the beam pattern increases progressively with distance because of the uniform spreading of the propagating energy. The excitation of the transducer with a short (instead of a continuous) tone burst reduces the complexity of the pattern in the near held (see Fig. 9-3B) . A common method of increasing the resolution in a portion of the imaging region is to introduce focusing into the transducer. The modification of a flat disc aperture to a curved aperture is illustrated in Figure 9-3C .[2] [5] The effect is like "pulling" the center of the flat aperture to the left, which also pulls the transition of the near field to far field to the left while decreasing the diameter of the beam in this region. A further effect is increasing beam divergence in the far field. The more the aperture is "pulled" to the left, the sharper the focusing becomes (i.e., the narrower the beam, the closer the focused region is to the transducer, and the greater the divergence of the beam in the far field) (Fig. 9-4) . Square and rectangular apertures ( see Fig. 9-1B and Fig. 9-1C , respectively) have beam patterns (Fig. 9-5) somewhat different from those of the disc-type of transducer (see Fig. 9-2) . First, symmetry is lost. The pattern is the same along the x-z–plane as the y-z–plane at the origin of the x-y–plane. However, at diagonal points, the pattern differs from the axial plane patterns. The rectangular aperture even differs at the x-z– to the y-z– planes. The near field, the distance to the transition, and the far fields all differ because the aperture distance to wavelength varies for these cases. The diagonal varies even further. Arrays The arrays that are commonly used have properties similar to those of the apertures discussed earlier. The structure of the arrays is illustrated in Figure 9-1 ( see Fig. 9-1D , an annular array; Fig. 9-1E , a square array; and Fig. 9-1F , a rectangular array). The annular array is composed of annular elements, such as the element illustrated in Figure 9-1G , and the square and rectangular arrays are composed of elements as illustrated in Figure 91H . The overall beam pattern considerations of an array are determined by the overall size of the array.[4] Therefore, if the radius-to-wavelength ratio of the annular array (see Fig. 9-1D) is the same as that of a solid disc (see Fig. 9-1A) , then the beam patterns are very similar (e.g., patterns such as those of Fig. 9-2 , Fig. 9-3A , and Fig. 9-3B ). A like consideration applies to the square and rectangular arrays ( see Fig. 9-1E versus Fig. 9-1B and

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Fig. 9-1F versus Fig. 9-1C , respectively). The individual elements of the arrays have their own beam patterns, but an assemblage of multiple array elements gives the overall aperture pattern. It is of interest to consider the miniature element in Figure 9-1H . The 185

Figure 9-3 The 3-dB isocontours for beam patterns along a plane passing through the axis of the transducers. On the left the edge view of the transducer on this plane is illustrated. A, Continuous wave pattern for a disc transducer. B, Beam pattern for the transducer in A but resulting from a very short tone burst of excitation (e.g., two cycles). C, Transducer surface that has been made curved (e.g., spherical curvature) showing how applying such a curvature changes the beam pattern from a flat disc (dotted pattern) to a more focused pattern of the curved surface disc. The arrows indicate the direction the pattern changes as a flat transducer becomes spherical. (Data from Weyns A: Ultrasonics 1980;18:183–188, 219–223.)

pattern of this rectangle element is similar to the pattern of Figure 9-1C except that the dimensions with respect to the wavelength are different. The vertical length of the array element (see Figure 9-1H) Figure 9-4 Beam pattern (3 dB below the axial value) for three circular apertures where a/λ = 9.7. The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). Right, for a disc transducer; center and left, for spherically focused transducers with the same aperture size as the disc. The radius of the spherical surface for the left pattern is much less than the radius for the center figure, thus increasing the focusing effect. (Data from Weyns A: Ultrasonics 1980;18:219–223; and Kossoff G: Ultrasound Med Biol 1979;5:359–365.)

is the same as the vertical length of Figure 9-1C ; therefore, the beam patterns in the vertical direction are the same. However, the horizontal width of the element (see Figure 9-1H) is very small in contrast to the horizontal width of the square or rectangle aperture of Figure 9-1B or Figure 9-1C . Therefore, in a horizontal plane the beam Figure 9-5 Beam pattern (3 dB below the axial value) for a square aperture (left) and a rectangular aperture (right). The apertures lie in the x-plane and y-plane at the base, and the ultrasound energy radiates vertically in this illustration (z-direction). For the rectangular aperture

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(right), the near-field to far-field transition distances are different along the x-axis versus the y-axis. Also, beam pattern spreading is different in the far field. (Data from Weyns A: Ultrasonics 1980;18:183–188.)

186

pattern transition of the near field to the far field occurs very close to the face of the element, and the far-field pattern diverges greatly and almost immediately in front of the face of the element. In fact, for a proper array, the element has a beam pattern that is so broad (approaching 180 degrees in angle) that its pattern overlaps with the patterns of all the other elements of the array. This overlap allows the array to have an overall pattern nearly identical to that of a solid aperture of the same size as the array. The real difference between an array and a single-element transducer is that each element in the array is connected to the electronic system, and therefore individual control of the timing associated with the transmission and reception of ultrasound is possible. For example, during transmission from an annular array, a beam of ultrasound energy is launched that focuses at a point similar to that discussed for a curved surface (see Fig. 9-3C) . This action is accomplished by exciting the outer element of the array first and then progressively exciting each annular element slightly later as one moves toward the center of the array. The real advantage is that the focus point can be electronically controlled by varying the respective time delays between elements. The greater the delay, the sharper the focus. During reception, by delaying the signals received by each element in a similar but inverse manner (across the array), one can achieve focusing comparable to transmission focusing. These signal delays are instituted before all the signals from each array element are combined to represent the A-line echo. However, the receiving situation is even more advantageous than transmission. Because the amount of delay imposed across the array can be varied continually as the signals are received, tracking the propagating wave is possible; that is, the receiving focus can move and remain pinpointed on the position of the transmitted burst of energy as it propagates away from the transducer. This action is called dynamic focusing and provides a narrower receiving beam over a much larger axial length than that which occurs without such focusing. It is worth noting that during the transmission of a burst or pulse of ultrasound, the focal point can be set only when the beam is launched. Therefore, only a fixed focal point can be used for transmission, but a dynamically tracking focus can be used

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during reception. Many systems use multiple transmissions, varying the focal point each time and using only the information received from each focal region, thereby blending the transmissions to make a composite received line. This approach, however, slows down the scanning rate, as each line requires several transmissions. This method is widely used in noncardiac scanning, in which a high imaging rate is not so important. Therefore, when multiple focusing positions, or zones, can be set (as is possible with some ultrasound machines), one must check that the frame rate is still fast enough for the desired purpose. Further electronic "tricks" can be employed to improve the beam pattern in modern ultrasound instruments. For example, rather than use the whole array when imaging near the transducer, one may use a smaller group of elements for that zone, which increases resolution in the near region. A further improvement is to use for each focusing zone the number of elements that gives the best resolution (e.g., a small group for the focusing zone nearest the transducer, a somewhat increased size for the next zone, and similar increasing sizes for each zone located farther from the transducer). Other improvement methods include apodization, tissue aberration correction, and synthetic apertures. A similar discussion to the annular array, regarding using delays across the array for focusing, also applies to square and rectangular arrays. However, the focusing pairs of elements are located an equal distance (but opposite) from the horizontal center line of the array, and they are not connected together as in the annular array. Furthermore, because each element can be controlled electronically in addition to focusing the array, one can also steer the beam to produce electronic scanning of a region. This electronic scanning is in contrast to the annular array, which must be mechanically swept to interrogate a region of tissue. Electronic scanning is accomplished by adding a linearly increasing delay to the elements, proceeding from one side of the array to the other. This action allows launching and receiving a beam at an angle with respect to the face of the array. The amount of delay used, or the slope of this linearly increasing delay across the array, determines the amount of the steering angle produced. Therefore, to perform a sector scan, one changes the slope of delay profile across the array between scan lines, proceeding to scan from one side of the sector to the other. A shortcoming of the square or rectangular arrays discussed is that electronic focusing occurs only in the horizontal direction ( see Fig. 9-

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1E and Fig. 9-1F ) because there is no electronic control in the vertical or elevational direction. In contrast, the annular array produces symmetric focusing around the axis, thereby usually producing markedly improved resolution. Consequently, there has been interest in designing rectangular arrays that have some or complete control of the beam pattern in the elevation direction as well. Two-dimensional (2D) or 11/n dimensional arrays are being employed for focusing in the elevational direction. (The 1/n implies that some amount of an array is distributed in the elevation direction, but it is less than a full assemblage of elements compared with the lateral direction.) The simplest designs have been referred to as 11/2 dimensional arrays, arrays in which a small division of the aperture has been made in the vertical direction (Fig. 9-6A) . It is not necessary to have separate transceivers for each vertical element here because it is possible to electrically wire together elements that are symmetrically displaced around a horizontal center line. For example, in Figure 9-6A , the vertically displaced elements associated with row 1 can be electrically connected together, as can elements labeled 2 in the figure. (Note: Only the individual elements in a column can be thus connected or the ability to sector scan would be lost.) By connecting elements in this manner, one can use phasing delays between numbers 1, 2, and the center element to produce focusing in the vertical direction at any of the horizontal steered angles, thereby improving the spatial resolution of the beam. In order to accomplish this, one needs only three times as many transceivers, even though the number of elements in the array has been increased five times. Of course, more than five elements can be used in a column 187

Figure 9-6 Two styles of array design offering added electronic beam control in comparison with the arrays of Figure 9-1 . A, So-called 11/2 dimension array offering electronic focusing in the vertical or elevational direction as well as full scanning control in the horizontal or lateral direction. B, Two-dimensional array offering complete three-dimensional beam scanning.

to provide even greater improvement, giving rise to the 1/n nomenclature. The complete 2D array of Figure 9-6B allows complete control of the beam in three-dimensional (3D) space if each element is connected to a

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transceiver and the delay control for each element is provided in the ultrasound system.[6] The problem is that achieving 3D resolution equivalent to current 2D imaging requires many elements and transceivers. For example, a 64-element array and a 3D scanning system equivalent to a 2D array would need 64 × 64 (or 4096) elements, as well as electric connecting wires, transceivers, and delay control elements. The fabrication and cost of such a system are formidable, but they may be less so in the future. A less complicated electronic system, using a 2D array, has been clinically tested for producing biplane images.[7] With this latter approach, the array elements are connected through a multiplexing method to a standard 2D scanning system in such a way that sector scanning can be performed in the horizontal plane; then the array is switched so scanning can occur in the vertical plane. Undoubtedly, numerous permutations of approaches between a full array and multiplexing of the array will emerge in the near future.

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Ultrasound Properties of Tissue There are four main acoustic or ultrasound properties of tissue: the velocity of propagation, acoustic impedance, attenuation, and the scattering of ultrasound. The first three of these are discussed in this section; the following section is dedicated to a more in-depth discussion of scattering. Velocity, impedance, and scattering are interrelated, and they all relate to the various constituents of different types of tissue as well. These parameters for most tissues have been measured,[8] [9] [10] but the published values vary greatly. This variation is due to differences in measurement methods, conditions of measurement (e.g., frequency, temperature), species tested, and tissue conditions (e.g., excised, fresh, fixed). Velocity of Propagation The velocity of propagation is fundamental to all ultrasound assessments. The commonly used average velocity of tissue at 37°C is 1540 m per second, which is used by most ultrasound machines for displaying calibration markers. Of course, individual tissues vary from this value, as illustrated in Table 9-1 . An approximate range of soft tissue variation for most tissue of usual concern with ultrasound is ±5%. The speed of sound also varies with the temperature of the tissue. Generally, most tissues have a small increase in speed as the temperature increases (a positive temperature coefficient); however, fat tissue has been found to have the opposite effect—a decrease in velocity occurs as temperature increases. [11] For in vitro experiments it is valuable to use water solutions that have the same speed of sound at room or body temperature that tissue has at body temperature. Speed regulation can be accomplished by varying the salinity of the water, as listed in Table 9-1 .[12] The speed of sound, c, in homogeneous media is given by the equation c = (β/ρ)1/2

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where β is the bulk modulus of the media and ρ is the density.[4] The stiffer a material, the greater its bulk modulus. It is generally believed that the bulk modulus varies more than density, and that it is therefore the primary factor accounting for the variation in velocity. Acoustic Impedance The second parameter, acoustic impedance, z, is related to velocity and density: z = ρc = ρ(β/ρ)1/2 = (βρ)1/2 Among other things, acoustic impedance is a useful parameter for assessing the amount of reflection and transmission that can occur at the boundary of two layers of tissue. The acoustic reflection coefficient Rc , which is defined as the ratio of reflected acoustic pressure pr to the incident acoustic

pressure pi on the boundary, is given as pr /pi = Rc = (z2 − z1 )/(z1 + z2 )

where z1 is the acoustic impedance of the first medium and z2 is the impedance of the second medium.[4]

The transmission coefficient Tc is defined as the ratio of the acoustic

pressure transmitted pt into the second medium with respect to the acoustic pressure incident on the boundary from the first medium[4] pt /pi = Tc = 1 + Rc

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TABLE 9-1 Impedance Velocity Density * (106 Temperature Other 3 Material (m/s) (kg/m ) kg/m-s) (°C) Conditions

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Air

343

Lung (bovine)

570 gv 360

Lung 640 gv (bovine) Lung 710 gv (bovine) Lung 830 gv (bovine) Lung 860 gv (bovine) Water 1482 [14] Water 1476 Water 1497 Water 1488 Water 1509 Water 1540

1.2

0.000415

20

0.21

22

430

0.28

22

540

0.38

22

640

0.53

22

720

0.62

22

998 [89] 1.48 [14, 89]

20 22 37 22 37 22

38

0% salinity [4] 0% salinity [4] 0.9% salinity [12] 0.9% salinity [12] 4.62% salinity [12] 3.10% salinity [12] 44% hematocrit [88] 40% hematocrit [88] Peritoneal, 1–7 MHz [16] Stomach, 5 MHz [11] Breast [14]

37

Orbital, 6–7 MHz

Water

1540

37

Blood

1556 [88] 1579 [88] 1580

23

Blood

Fat (bovine) Fat 1412 (canine) Fat 1435 (human) Fat 1462

1055 [89] 918

1.67 [88, 89] 1.45

Atmospheric pressure [4] 66% inflated, 0.55 MHz [89, 90] 60% inflated, 0.55 MHz [89] 49% inflated, 0.55 MHz [89] 64% inflated, 0.55 MHz [89] 32% inflated, 0.55 MHz [89] 0% salinity [14]

37 20 37

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(human) Liver (human) Liver (human) Liver (canine) Spleen (canine) Kidney (canine) Muscle (canine) Muscle (human)

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1584 [16] 1607 [16] 1596

1064 [89] 1064 [89]

1.69 [16]

20

[14] 1–7 MHz [16]

1.71 [16]

37

1–7 MHz [16]

37

5 MHz [11]

37

5 MHz [11]

37

5 MHz [11]

37

Skeletal, 5 MHz [11] Cardiac, perpendicular to fiber, 5 MHz [92] Cardiac, parallel to fiber, 5 MHz [92] Pig, age 5 mo, 15 MHz [91] Achilles, perpendicular to fiber, 5 MHz [30] Achilles, parallel to fiber, 5 MHz [30] Skull, outer table [93] Skull, inner table [93]

1601 1569 [11] 1593

1040 [89]

1.63 [11, 89]

1530

1052

1.61

18

Muscle 1555 (human)

1052

1.64

18

1094

1.87

25

1050

1.75

20

1050

2.12

20

1880

5.43–5.68

37

1910

4.56–5.52

37

*

*

Skin 1710 (porcine) Tendon 1670 (bovine) *

Tendon 2020 (bovine) *

Bone (human) Bone (human)

2890– 3020 2389– 2390

*Formalin fixed. gv, group velocity; [], reference number.

Attenuation

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The third parameter, attenuation, is defined as the loss in the amplitude of an acoustic signal as it propagates. This parameter is responsible for the decrease in the echo signal strength at greater imaging depths, and it is why time-varying gain compensation is used in almost all ultrasound machines. It has been observed that the amplitude of a wave decreases with distance in a logarithmic manner. This phenomenon was first observed with light and has been credited to Beer, Lambert, and/or Bourgher (not necessarily in that order). (Various texts and literature seem confused about whom to credit, and they refer to it as the Beer law, the Lambert law, or various combinations of their names [e.g., Beer-Lambert-Bourgher law].) The phenomenon can be described as follows: For a propagating acoustic pressure wave, if the pressure at point 1 is defined as p1 and the pressure at point 2 a further distance l (in centimeters) from the first point is defined as p2 , then the attenuation between the two points can be given by p2 = p1 e−αl where α is the attenuation coefficient defined in nepers per centimeter (Np/cm), or just cm-1 . Alternative units for the attenuation coefficient (αdB ) are decibels per

centimeter and directly relate acoustic pressure and distance to attenuation, p1 /p2 l = αdB . It is easily shown using logarithms that αdB (dB/cm) =

8.686α (Np/cm), which is a useful constant, because the attenuation coefficients are often given both ways. Finally, it is worth pointing out the relationship of attenuation with respect to intensity of ultrasound. The intensity I of an ultrasound wave has units of watts per centimeter squared and is defined as the average power of a wave per unit area (in centimeters squared). The intensity is related to the amplitude of the acoustic pressure p in most cases by the following equation: I = p2 /2z where z is the acoustic impedance as defined earlier. Therefore, for a propagating wave, the intensity at point 1, I1 , is related to the intensity at a point 2, I2 , located a distance l away by the following equation:

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I2 = I1 e−2αl The difference from the acoustic pressure equation is the 2 in the exponent.

189

The attenuation coefficient by itself does not separate out various mechanisms responsible for the loss of energy from the propagating wave. In order to provide further distinction, the attenuation coefficient has been defined to describe the scattering loss from the wave and the absorption of energy from the wave. The scattering directs energy in other directions, and the absorption describes the amount of energy in the wave turned into heat. The coefficient α is then defined as α = αs + αa , where αs is due to scattering and αa is due to absorption. One has to be careful in taking

coefficients from the literature because the distinction is not always made. Particularly in early work, the attenuation was called the absorption coefficient, because researchers did not realize that the scattering effect entered into their results. In fact, it is difficult to measure these effects in isolation. The next two important aspects of attenuation are that it is temperature- and frequency-dependent. Most tissues (not bone) have a negative temperature coefficient. [13] [14] Fat, as discussed later, has a high negative coefficient. All tissues have a strong frequency effect, with the attenuation coefficient varying directly with a power of frequency. For example, α = afb , where f is the frequency and a and b are constants. The power term b varies from 1 to as high as 4; the latter number is for αs , when scatters are much smaller than the wavelength (as discussed later in the scattering section). Most tissues have a coefficient b ranging between 1 and 2. The b (power of the exponent) attenuation factor for water is 2, because absorption is related to the viscosity of the water and the square of the velocity of particle motion. Absorption in tissue is believed to be related to the relaxation processes in the tissue,[15] but this is still not fully understood. The high dependence of the attenuation on frequency is why high-frequency transducers are not used to image deep in the body. The depth in the body at which one can image is inversely related to the ultrasound frequency used. This fact is emphasized by the expression of the attenuation coefficient as α/f in much of the literature. In considering the attenuation as a function of frequency,

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from the excellent compiled data,[9] [10] it is useful to fit a polynomial function to several of the tissues in which the simple expression (α = afb ) does not provide an adequate fit. The results of this equation and the simpler expression for attenuation for several tissues are given in Table 92 . Note: These fitted equations apply only in the specified frequency range designated; if applied out of that range they may provide erroneous results. TABLE 9-2 -- Approximate Ultrasound Attenuation Coefficients Material Air

Lung Water Blood

Fat

Liver Muscle Skin Bone

α(Np/cm) 1.86 × 10-13 f2

Comments Dry, 1 atmosphere

1.98 × 10-13 f2 + 6.36 × 10-7 f + 3.47 Canine, 1–5 MHz

Kinsler et al

8.1 × 10-15 f2 9.77 × 10-16 f2 + 1.09 × 10-9 f -6.22 × 10-15 f2 + 2.45 × 10-7 f 0.127

[4]

45% Goss et al[9] hematocrit, 2–50 MHz Pig back, 2– Gammell et 20 MHz al[13] Taniguchi et al[95] Goss et al[9]

1.3 × 10-7 f

[10]

Goss et al[9]

2.0 × 10-7 f 1.59 × 10-16 f2 + 2.55 × 10-8 f 0.0195 -4.01 × 10-19 f3 + 2.16 × 10-12 f2 4.12 × 10-7 f

Reference Tempest and Parbook[94] Goss et al[9]

[10]

2.0–10 MHz Goss et al[9] [10]

0.25–3.5 MHz

Goss et al[9] [10]

Fat seems to be a special tissue that is worth discussing briefly because it probably is responsible for the fuzziness of transcutaneous echocardiograms in many people. The reported measurements for fat are

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puzzling because of the dispersed range of attenuation values reported.[8] [9] [10] This variation may be partially caused by differences in measurement techniques. However, the attenuation of fat is known to exhibit a strong temperature dependence, and if the temperature at which the attenuation measurements were made is not reported it is difficult to make comparisons. For example, it has been shown that attenuation of excised mammalian fat samples at body temperature is much less than that taken at room temperature.[13] [16] Furthermore, the freshness of the specimen, the species and breed of the donor, and the region in the body from which the specimen is required may also play an important role in the value of attenuation measured. [13] Finally, because of the energy storage function of adipose tissue and the variation in lipid concentrations in adipocytes (adipose cells) in relationship to the degree of obesity,[17] the nutritional state of the donor could also affect the attenuation measurements obtained within a given species and region of the body. In general, the major fat tissue, white adipose tissue, is known to consist of cells 25 to 200 µ in diameter, composed of weight of 60% to 80% lipid, 5% to 30% water, and 2% to 3% protein. From 90% to 99% of the lipid is triglyceride. [18] These adipose cells are held in "grapelike" aggregates by connective tissue called lobules.[19] The cell sizes have been correlated with the degree of obesity (hypertrophic obesity). [17] In some tissue regions (hyperplastic obesity) the number of the cells correlates more strongly with obesity. For example, a general trend in male humans is hypertrophic obesity in the abdominal regions, whereas female humans show hyperplastic obesity in the subcutaneous femoral and gluteal fat depot regions.[20] The average size of adipocytes in pigs and sheep has been reported to be greater in the omental and the perirenal regions than in the subcutaneous region, whereas in humans the reverse has been found.[17] Cell diameters ranged from 25 to 180 µ in adult pigs ready for market.[17] As discussed later, the size of a scatter with relationship to the wavelength of the sound can affect the frequency dependence of the scattering. Therefore, the nutritional state and location of the fat may affect its attenuation properties. The other interesting constituents of tissue are water and collagen. Water and collagen tend to have opposite 190

effects on ultrasound attenuation. Water content generally reduces

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attenuation, whereas collagen increases attenuation.[21] [22] [23] [24] [25] Because water itself has a low attenuation in contrast to tissue, it is reasonable to expect that as the water content increases, the attenuation coefficient decreases. Fields and Dunn[26] in 1973 were the first to relate how the prominent differences in values of modulus between collagen and muscle may apply to the ultrasound echo properties of tissue. They pointed out that the low-frequency elasticity constant of collagenous fibers from tendon is about 1000 times greater than that of other tissues (e.g., 109 dyne/cm2 for collagenous fibers versus 105 to 107 dyne/cm2 for smooth muscle, [27] 2 × 108 dyne/cm2 for human calcaneal tendinous, and 5 × 104 dyne/cm2 for dog abdominal muscle).[28] From the above relationship of the bulk modulus β to acoustic impedance (z = [βρ]1/2 ) and velocity (c = [β/ρ]1/2 ), it is easily realized that tissue highly distributed with collagen may have sharp changes in z and c, which would produce high inhomogeneity in acoustic properties, thereby leading to a tissue with high scattering. An example of this is the highly collagenous tissue in the submucosa of the intestine. The submucosa produces much higher echogenicity than the muscle in the wall. [29] However, measurements of the modulus of fixed bovine flexor tendon at 5 MHz have revealed values of 45.1 × 109 dyne/cm2 in the direction of fiber orientation and 30.8 × 109 dyne/cm2 perpendicular to the fibers,[30] which were found to be only factors of 1.8 and 1.3 greater than the values in fixed human myocardium, with the fibers respectively oriented. One would expect higher ratios based on the low-frequency measurements of bulk modulus and the fact that only 1% (wet weight) of the myocardium is collagen, whereas 30% (wet weight) of the tendon is collagen. [30] The high modulus of the myocardium may be due in part to the fixation process, but it may also explain why the myocardium is both echogenic and attenuative. A high degree of scattering can produce a high attenuation coefficient, because attenuation is composed of both scattering and absorption. Goss and O'Brien[31] in 1979, using a 100-MHz acoustic microscope, measured the velocity of propagation in mouse tail tendons and found an average value of 1733 ± 56 m per second; this is in the range that Hoffmeister et al [30] found in 1994 for cross-fiber tendon velocity. Two other specific tissues, bone and lung tissue, also affect transcutaneous cardiac imaging. The attenuation of lung tissue has been found to vary with the degree of inflation,[32] [33] [34] and of course it is highly attenuative even with low inflation (see Table 9-2) . Both velocity and attenuation have been found to increase with increasing mineral content in bone.[35]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Scattering One of the most important events in ultrasound interrogation is the scattering of the propagating energy from its initial pathway as it encounters various structures. This event is important for several reasons, but foremost is that the scattered energy is detected in medical ultrasound imaging. Clearly, the more a region tends to scatter ultrasound, the more hyperechoic it is (all other things being equal). Therefore, understanding scattering is important in understanding what is actually measured, as well as in estimating what can be measured in a particular situation. The complexity of scattering is directly related to the complexity of the structure being investigated. Some of the initial understanding was provided by Lord Rayleigh[36] as early as 1877, but today research in scattering continues. Considerable insight into scattering can be obtained by first considering scattering from a single particle in a homogenous medium. As the mechanical properties of the particle with respect to the surrounding medium vary, so does the scattering. Further, the size of the particle with respect to the wavelength of the interrogating sound is very important. When the size of the particle is very large with respect to the wavelength, the particle reflects like a smooth surface. A second useful area for deliberation is scattering from a surface both smooth and rough, but this is not discussed here. Third, it is useful to consider tissue as a structure in which (1) the velocity of propagation varies some fractional amount with distance, and (2) each point in the tissue has identical acoustic properties over only a finite length (a correlation length). These three cases are simplifications of what occurs at all sites in the body, but they provide helpful insight for understanding the more complex situations. Some useful terms have grown out of the radar and sonar literature and have been applied to medical ultrasound in order to provide quantitative descriptions: Scattering cross σs = Ps /Ii with units of area (e.g., section

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σd (theta) = R2 Is (theta)/Ii

Backscattering cross σ = R2 I (180°)/I b s i section Backscattering coefficient

ηb = R2 Is (180°)/Ii V

cm2 ); with units of area per solid angle; with units of area per solid angle (e.g., cm2 /Sr); and with units of area per volume-solid angle or 1/length-solid angle (e.g., cm-1 Sr-1 )

where Ii is the ultrasound intensity incident on the particle; Ps is the average

power scattered from the particle; R is the radial distance from the particle to an observation point (where R is considered to be in the far field of the scatter); theta is the angle between the direction the sound is scattered and the direction the sound is propagating; Is (180 degrees) is the scattered intensity in the back direction (i.e., theta = 180 degrees); and V is a unit volume (e.g., cm3 ).

Each of these terms has a physical meaning. The scattering cross section σs describes the amount of cross-sectional area needed in the incident beam to contain as much power as is scattered by the object (i.e., power = area × intensity). The differential scattering cross section relates the incident intensity to the intensity scattered per unit solid angle in the direction described by the angle theta. The backscattering cross section relates the incident intensity to that scattered opposite to the direction the beam is 191

propagating (i.e., back, theta = 180 degrees). Most ultrasound instruments detect only backscattered signals, not those scattered at other angles. The radial distance R appears in the last two equations because we are relating two intensity terms, and we assume the scattered intensity is uniform over some small solid angle (consistent with the far-field approximation of an aperture). There is a directional or angular factor in the equations because scattering in a particular direction (e.g., the back direction) may be different from scattering in other directions; therefore, the units are area per solid

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angle, where the solid angle is defined in the units of steradians (Sr). Finally, these first two terms have worked well in radar and sonar, in which there are usually single objects in a homogenous medium producing the scattering. However, when one tries to apply these terms to tissue, a rather nonhomogeneous medium, the term backscattering coefficient ηb was

developed. This term relates the back directional scattering cross section σb to a volume or region rather than a single particle; hence ηb = σb per unit

volume, which takes on the expression related to Is (180 degrees)/Ii with the units of 1/length-solid angle (e.g., cm-1 Sr-1 ). Scattering from a Single Particle Scattering from a small fixed sphere in a fluid was first studied by Rayleigh. Small was defined as a sphere with a radius a where the circumference of the sphere, 2πa, divided by the wavelength λ is much less than 1 (i.e., ka = 2πa/λ <<1). In this equation, k is the wave constant = 2πf/c; f is the frequency of the wave; and c is the velocity of propagation. In the Rayleigh range, the differential scattering cross section has been shown for elastic spheres to be given by σd = 0.11 k4 a6 [{(κe + κ)/κ} + {3(ρe + ρ)/(2ρe + ρ)}cos (theta)]2 where, respectively, κ and ρ are the compressibility and density in the fluid, κe and ρe are the compressibility and density in the sphere, and theta is the

angle between the direction of the incident ultrasound energy and the direction of the scattered intensity, which for backscattering is 180 degrees. The red blood cell with a radius of about 4 µ is an example of a particle that is small compared with the wavelength for frequencies below 61 MHz (ka 1 at that frequency) and therefore falls into the Rayleigh scattering region. Therefore, the red blood cell can be approximated as an elastic sphere, and the equation for the scattering cross section in the Rayleigh region for elastic spheres can be applied in the back direction. The compressibility for plasma and a blood cell,[37] respectively, are κ and κe = 40.9 and 34.1 × 10−−12 cm2 /dyne, and the density ρ and ρe = 1.021 and

1.092 g/cm3 . Further, for backscattering, because cos (180 degrees) = −1, then σb = 6 × 10−−3 k4 a6 and k = 2πf/c (where f is the frequency and c is the velocity of propagation), the backscattering cross section is proportional to

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the fourth power of the frequency and the sixth power of the radius. Therefore, the scattering of blood is very dependent on frequency. The ratio of the backscattering cross section to the geometric cross section of the sphere (area of a circle of radius a) is given as σ/πa2 = 2.8(ka)4 This normalized relationship is plotted in Figure 9-7 on the left side of the graph. When ka → 1 there is often a resonance effect in which σ/πa2 oscillates above and below 1 as ka approaches, equals, and becomes greater than 1. For large scatters, the values of ka > 1, the value of σ/πa2 → 1 (if the sphere is infinitely stiff); that is, the scattering cross section becomes equal to the geometric cross section. Therefore, when ka << 1, the surface of the sphere appears as a flat surface with respect to wavelength, and the scattering becomes the same as reflection from a flat surface. For spheres with other values of compressibility, but large enough so the duration of the burst of ultrasound is over before the wave passes from the front of the particle to the back, σ/πa2 → [(z2 − z1 )/(z1 + z2 )]2 , where z1 is the acoustic impedance in the fluid media and z2 is the impedance of the particle. This

term is essentially the intensity reflection coefficient for an interface between two layers.[4] Therefore, there are three regions:

1. Rayleigh region, ka << 1, where σ/πa2 is proportional to the fourth power of frequency; that is, σ/πa2 = 2.8 (ka4 ) 2. Resonance region, ka 1, where σ/πa2 oscillates 3. Large scatter region, ka > 1, where σ/πa2 → the intensity reflection coefficient; further, when ka << 1, the scatter is so large it acts like a surface When ka 1 backscattering resonates, and the angular scattering around the sphere varies and is no longer uniform or isotropic. A particle that is a gas bubble in fluid is interesting for Figure 9-7 Scattering from a sphere in three regions of size with respect to wavelength. See text for discussion.

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192

a number of medical reasons (e.g., air emboli and/or ultrasound contrast agents). The isotropic (scattering in all directions equally) scattering cross section equation for a gas bubble in water is given by σs = 4πa2 /{[(fr /f)2 − 1]2 + (f/fr )2 δ2 } where f is frequency of sound, fr is bubble resonance

frequency, and δ is the damping coefficient for the bubble in the fluid.[37] This damping coefficient is related to the thermal properties of gas and fluid, the damping owing to scattering, and the viscosity of the fluid.[38] A value of δ = 0.15 is typical for air in water at 1 MHz. A plot of σs /πa2 , the ratio of scattering to the geometric cross section of a spherical bubble, is shown in Figure 9-8 , and the bubble size needed for resonating at various frequencies is shown in Figure 9-9 . Scattering from Multiple Particles When scatters are spaced in a medium at an adequate distance from each other, then the overall scattering cross section per unit volume (i.e., scattering coefficient) is given by the sum of the scattering cross sections of all the particles in the volume. If all scatters have the same scattering cross section, the number of scatters in the volume times the scattering cross section gives the scattering coefficient. However, when the scatters are located close together, the incident intensity on each scatter may be different because of shadowing from other scatters and/or intensity scattered onto it from other scatters. Further, the scattering arriving at some distant point from each scatter may also be different because of the effect just mentioned, and the scattering pathway from each particle may be altered by other particles in the way. When the particles are close enough for this action, multiple scattering effects occur. Shung et al[39] have studied this Figure 9-8 Isotropic scattering from an air bubble in blood. The vertical axis is the normalized scattering cross section. It is normalized by dividing the scattering cross section by the geometric cross section of the air bubble. The horizontal axis (f/fr ) is the ratio of the ultrasound frequency to the frequency at which the bubble will resonate.

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Figure 9-9 Approximate air bubble size at which resonance will occur for various frequencies in blood at body temperature.

effect with respect to scattering from blood at various hematocrits (e.g., porcine blood in laminar flow). Clearly, the higher the hematocrit, the greater the density of blood cells in a unit volume, and one would expect that scattering would linearly increase with the hematocrit if there were no multiple scattering effects. Yuan and Shung[40] described the observed findings with the following equation in terms of the backscattering coefficient: ηb = [σb Wo (1 − Wo )4 ] / [V(1 + 2Wo )2 ] where Wo is the hematocrit expressed as a fraction, V is the volume being studied, and σb is the backscattering cross section from a single cell. This

equation provides an excellent fit to the data in the 1993 report of Shung et al,[39] in which σb = 2.17 × 10−2 cm2 , V = 68 cm3 , and frequency = 7.5

MHz. The results are plotted in Figure 9-10 . The backscattering coefficient increases approximately linearly with hematocrit to a value of about 8%, then the rate of increase decreases until the scattering coefficient reaches a maximum at 13%; thereafter, it decreases with higher values of the hematocrit. When scatters are located closely together, the scattering is less than expected (based on a linear increase with the number of particles). Another interesting finding with blood is that the backscattering coefficient increases as the velocity of the blood decreases. For example, scattering from venous blood is greater than that from arterial blood, which is thought to be due to red blood cells clumping together at slower flow velocities, whereas at higher velocities the fluid shear tends to separate them. Considering that the backscattering cross section in the Rayleigh region is related to the sixth power of the radius of the scatter, clumping could increase the size of each scatter considerably, thereby increasing the scattering amplitude greatly because of this sixth power effect. This may be much more dominant than the fact that the number of individual scatters would 193

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Figure 9-10 The calculated backscattering coefficient for porcine blood in laminar flow for various hematocrit values. (Data calculated from an equation given by Yuan YW, Shung KK: J Acoust Soc Am 1988;84:52– 58; Data from Shung KK, Kuo IY, Cloutier G: Ultrasonic scattering properties of blood. In Roelandt H, Gussenhoven EJ, Bom N (eds): Intravascular Ultrasound. Boston, Kluwer Academic, 1993, pp 119–139.)

be reduced. In fact, reduction may also reduce some of the multiple scattering effect for normal hematocrits of 45%, thereby increasing scattering. The effect would be somewhat like moving to the left from 45% in Figure 9-10 . Because of this increased scattering, blood speckle movement can be observed with the higher-quality B-mode imaging equipment in venous blood but generally not in arterial blood. Finally, stagnant but unclotted blood becomes hyperechoic quickly after cell motion stops. However, on stirring it the blood becomes hypoechoic until the motion stops. Backscattering from Tissue Certain types of tissue, in some ways, acoustically can be considered to be a collection of scattering particles embedded in an acoustic conducting medium. A more meaningful model has been to consider the variation of the velocity of propagation through the tissue, and a term called the correlation length of the structure.[41] The average velocity variation µc is (<∆c>2 /∆c2 )1/2 , where c is the velocity of propagation and <∆c> is the time average change in the velocity as it propagates through a region of tissue. The maximal correlation length b is an expression of the spatial distance over which the acoustic properties of a region remain correlated (based on autocorrelation) with some initial starting point in the tissue. Basically, the acoustic properties are the same for a distance of about b from the starting point. For a region of tissue there is a distribution of correlation lengths. If one assumes a uniform distribution of correlation lengths in the tissue from zero to some maximal value bm , the following expression describes the backscattering coefficient for such tissue[41]

ηd = (3µ2 k/4π)[tan−1 (kbm ) + (1/9)tan−1 (3kbm ) − kbm /(1 + k2 bm 2 ) −

kbm /3(1 + 9k2 bm 2 )]

where k is the wave constant discussed earlier. The following constants

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were found to fit scattering data from dog heart muscle: the percentage root mean square of velocity variation µ = 4.94 and bm = 0.17 mm.[42] Applying

this equation and constant for various values of frequency produces the graph shown in Figure 9-11 . This has been compared over the frequency range of 3 to 7 MHz to measurements and was found to provide a good fit.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Tissue Characterization In general terms, ultrasound tissue characterization is an effort to use ultrasound to identify certain physiologic or pathologic conditions of tissue, or to try to classify various features or traits in specific regions of tissue that may be of diagnostic value. This identification has usually involved the application of some form of quantitative measurement and therefore goes beyond the usual imaging and Doppler processing and display. The general trend is to develop in vivo methods of measuring various acoustic parameters such as the velocity of propagation, acoustic impedance, acoustic attenuation, and scattering amplitude, then to apply the methods to normal and diseased tissue. This endeavor has a history starting in the 1970s and was spearheaded, in part, by a symposium titled Ultrasonic Tissue Characterization in 1976[43] the symposium has continued annually since. This annual Figure 9-11 Backscattering coefficient versus frequency for scattering from canine heart muscle using the equation given in the text. The kbm values for 30, 14.1, 5, and 2.5 MHz are, respectively, 2.1, 1, 0.35, and 0.18, and they are found to fit data from O'Donnell, Mimbs, and Miller. [42]

194

meeting has been a forum for presenting new areas of research into this broad field. The initial endeavor met with considerable enthusiasm, but when many of the approaches failed to demonstrate clinical use, the approaches lost their support. Some approaches failed because they were too complex to be implemented in a practical manner at the time; others failed because they were never taken to the point of adequate clinical testing; and some failed just because they seemed to provide no

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improvement in the "characterization" of the tissue tested. Many of the complexities are now more easily overcome with today's computing power and improvements in transducers. Nevertheless, these solutions often pose a Catch-22. To be clinically tested they need to be implemented into commercial machines, but the companies are reluctant to implement or explore such methodologies until the clinical demand or market has been demonstrated. Furthermore, the processing involves obtaining or controlling the ultrasound signals at "primitive" levels in the system, not easily performed by people who do not have the technical details of the specific ultrasound machine involved (i.e., nonmembers of the company making the machine). In spite of this problem, and because of the diligence of the investigators involved, some significant progress has been made related to echocardiography. Worthy of note is the application of various measures of myocardium ultrasound backscattering. These measures have been more readily applied to the in vivo case because they are more compatible with standard echocardiography interrogation. However, early work in the 1970s, for example, frequency and angular scattering effects,[44] backscattering coefficients versus frequency,[45] and attenuation measurement,[46] used excised tissue. In vitro work has continued to provide more basic information from which our understanding of the ultrasound tissue interaction has grown. In addition, early in vivo work involving the study of scattering from normal and ischemic hearts[47] helped fuel some of the work that has been widely reported. The term backscattering coefficient as defined earlier has continued and is continuing to be applied as a prominent measure of tissue characterization. Interested readers can find a comprehensive review of cardiac tissue characterization up to 1986 in a chapter provided by Skorton and Collins [48] in Greenleaf's book dedicated to tissue characterization using ultrasound. There are two troublesome problems in quantitative backscatter measurement. Both problems concern obtaining calibrated data related only to the region of interest. The first problem is the way the ultrasound machines are designed. They have been developed to provide the operator with numerous controls to produce the highest quality image. Adjustment of these controls may change the power transmitted, the gain of the amplifiers, the control curves in the time-varying gain, and the signal-togray level conversion (nonlinear compression). Consequently, unless all these controls are always set the same from patient to patient (which they

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rarely are), the amplitude of the echoes at the receiver are very difficult to quantify and compare from patient to patient. Finally, the frequency response and beam patterns of various transducers and instruments tend to be different, so they require calibration. A useful method of calibration has involved applying the transducer to some type of test phantom with a standard reflector (e.g., a large metal sphere) and recording echoes from it to represent reference data for comparison.[48] The more successful methods, in addition to this, have used information from a point in the imaging system where it has not been adjusted in the various manners mentioned earlier. Usually this is early in the instrument when the signals are still in the radio frequency form. Either the signal is tapped off at this point and linearly amplified, and brought out of the machine to a data acquisition system, or a special section in the instrument has been built to process these signals in a way that is needed just for tissue characterization (which is different from that used for image production). The second major problem is that the intervening tissue between the transducer and the site for measurement interferes with the signals in its passage, which poses formidable problems. This interference is in the form of attenuation, which is unknown not only in amplitude but also in its frequency dependence. The variation in the velocity of propagation through this intermediate region also can distort the beam (phase aberration) and affect measurements. Therefore, the most practical method has been comparing (when possible) adjacent regions of tissue of interest (e.g., suspected disease versus normal, blood versus wall, or changes in echoes from the proximal to the distal portion of the region) or comparing the same region at various time points (e.g., the changes during the cardiac cycle). These comparisons produce more relative measurements, but they offer more reliable approaches. Two measurements, spectral analysis and integrated backscatter, have been particularly studied, the latter extensively. Both methods involve making measurements of the radio frequency or uncontaminated rectified radio frequency signals obtained from a region in an image by setting a window of interrogation at a specific location in the tissue. Electronically, this means sampling and measuring the returning echoes during a specific time period. In spectral analysis, the signals are converted from the time domain to the frequency domain by using the Fourier transform, then the converted echoes are normalized by dividing by the amplitude of the similar frequency components acquired from signals from a calibration target. Comparison of the rate that the amplitude of the different

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frequencies changes over the spectrum has provided a relative measure of attenuation with frequency. Integrated backscatter has been more widely employed in cardiology. The method involves operating directly on the time domain signals. All the signals received during the set duration for interrogation are rectified in some way and integrated or added. This result is then normalized by dividing it by the similar measure (e.g., summation) from a reference target. Neither the spectral analysis nor the integrated backscatter approach by itself can compensate for the intervening tissue effect; therefore, these measurements need to be compared in some manner, as mentioned earlier. Comparison to scattering from blood in the cardiac chambers has been considered, and comparison of scattering from the myocardium to the pericardial interface has been successfully employed in diabetic patients.[49] Further, recording and analyzing the variation of 195

the amplitude of the integrated backscatter during the cardiac cycle have been highly useful. In fact, the cyclic variation of integrated backscatter has been found to provide useful diagnostic information. Overall backscatter has been found to be useful in depicting cardiomyopathy, [50] [51] [52] infarcts,[53] [54] [55] ischemia,[56] [57] [58] [59] [60] [61] and stunned myocardium.[62] [63] Infarcts that have become highly collagenous produce high backscatter and are more attenuative. Calcification produces even higher scattering and prominent shadowing beyond the calcification because of the high attenuation of the calcified tissue. The cyclic variation of integrated backscatter during the cardiac cycle has been found by Milunski et al[62] to be about 3.8 dB (0.65) in dogs, with the highest amplitude occurring during the cycle shortly after the QRS complex and minimum at end-systole. When ischemia was produced in these animals (15-minute occlusion),[62] the cyclic variation was reduced to 1.7 dB and wall thickening was reduced from 37% to 17%. Within 20 minutes of reperfusion, cyclic variation had recovered to baseline, whereas wall thickening only recovered to 23% in 2 hours. Based on the wall-thickening recovery rate and results of other occlusion experiments,[64] [65] the tissue was believed to be "stunned" and would have nearly recovered in 48 hours. The findings indicated that the recovery of the cyclic variation of integrated backscatter precedes the recovery of wall thickening after the myocardium has received an ischemia insult and then been reperfused. In a second report from the same group,[63] cyclic variations in integrated backscatter were studied in 21 patients within 24 hours of having symptoms, indicating acute

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myocardial infarction. Measurements from infarcted and normal regions of the heart were made. The average magnitudes of the cyclic variations were 0.8 dB in the infarct areas and 4.8 dB in normal areas. In 15 patients patency was later determined by coronary arteriography, then the patients were restudied with ultrasound within an average of 7.1 days after arteriography. In patients in which patency was documented, cyclic variation had increased from an average of 1.3 to 2.5 dB, whereas in patients without patency the cyclic variations had no recovery. Neither group had shown any significant wall-thickening recovery based on echocardiography at the time of the studies. This second study[63] tended to confirm the findings in animals.[62] In the Milunski et al studies,[62] [63] the normal variation found in the humans was about 1 dB greater than that in the dogs. Perhaps this result reflects a difference between dogs and humans, but it also may reflect the vigorous compensatory contractions that can occur in normal regions of the heart when a portion of the heart is infarcted, in contrast to when the entire heart is normal. We have observed this compensation effect using a regional ejection fraction measure when 3D imaging infarcted hearts. [66] Therefore, care should be taken when using other regions of diseased hearts for comparison. Further, numerous studies of cyclic variation by various investigators around the world have been sparked by the earlier and other findings. Not all investigations have found the same results, perhaps owing in part to differences in the study methods. Finally, considerable interest has been stimulated in trying to understand what exactly the ultrasound scattering mechanism is that is responsible for these findings; a few of these studies are discussed further later. Two related studies provide some insight into why there may be cyclic variations during the cardiac cycle. The orientation of myocardial fibers changes from the epicardium to the endocardium.[67] The scattering from the myocardium has been modeled as cylinder-shaped scatters, centered randomly, but angularly oriented and embedded in homogeneous medium. [68] The model demonstrated anisotropic backscattering, which varied with the orientation of the ultrasound impingement to the angle of alignment of the cylinders (maximal scattering when perpendicular), and their simulations could be fit to angular integrated backscattering measurements of others.[69] More recently, Rose et al[70] used ellipsoid shells with acoustic properties of collagen as elementary scatters in a homogeneous medium with the average properties of myocardium as a scattering model. The implications were that the myocytes are surrounded by collagen that forms

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the major scattering surface, whereas the rest of the tissue is fairly homogeneous. Based on the understanding of the dominant role that collagen plays in ultrasound scattering and the geometric arrangement of the collagen matrix of the myocardium,[71] this finding is reasonable. It also may explain why the myocardium is so echogenic. Again the model could be found to fit angular measurement data of others.[69] Therefore, as the myocytes shorten and expand with contraction, their orientation also may change with contraction, and this may produce a change in the backscattering. It doesn't, however, exactly explain why stunned but perfused myocardium might have cyclic variation whereas infarcted myocardium has little. Further studies of normal, stunned, and infarcted dog hearts were conducted with 5-MHz backscattering and 100-MHz scanning laser acoustic microscope measurements.[72] Ultrasound measurements were compared with myocardial water, lipid, and protein content measurements. The average attenuation at 100 MHz was significantly greater in normal (179 dB/cm) than in stunned (136 dB/cm) and infarcted (136 dB/cm) myocardium, and the velocity of propagation was significantly higher in normal and stunned myocardium (1597 and 1600 m per second, respectively) than in infarcted (1575 m per second) myocardium. The 5MHz backscatter was increased in the infarcted (-42.5 dB) compared with the normal and stunned (-47 dB) regions. These changes are interesting when compared with the tissue findings of significantly increased water content (81%) in infarcted regions, whereas the water content in normal and stunned regions is 73%. The protein content is lower in the infarcted regions (18.5%) than in the normal regions (21.5%), and an increase in lipid content is found in stunned (8.5%) compared with normal (5.5%) and infarcted (0.8%) regions. Perhaps most interesting is the increase in water content in the infarct areas. The reduction in attenuation and speed is consistent with the increase in water, based on the earlier discussions. Loss of intermyocyte collagen struts has been found with infarction, and this loss correlated with infarct expansion. [73] If backscattering from the myocardium is operating in the region of multiple scattering, an increase in spacing 196

between scatters may decrease the canceling effect of multiple scattering and thus increase the backscattered signal, but this is only speculation. The presence of fluid can increase the echogenicity in other muscle tissue, but it

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depends on the way the fluid collects.[74] Once again, insight has been gained into myocardium backscattering, but why cyclic variation may recover in stunned myocardium but not in infarcted myocardium remains a mystery.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Harmonic Imaging The new imaging formats referred to generally as harmonic imaging have improved the quality of images considerably. Interestingly, harmonic imaging has come about by serendipity. In trying to find methods of enhancing echo contrast images, researchers developed harmonic imaging and more recently pulse inversion imaging. It has been found by accident that these techniques improve images without the need to inject echo contrast. In seeking a reason for this improvement, we have learned that some of the former ways of thinking about ultrasound propagation imaging have not been entirely correct. The generally accepted concept was that ultrasound waves at acoustic levels used in diagnostics propagate in a completely linear manner. "Linear" in this setting implies that if one transmits at a certain frequency, the received energy returns only at the same frequency as that transmitted. One exception is Doppler shifts that might occur because of tissue or blood movement. However, Doppler frequency shifts in the human body are only fractional shifts in frequency from the fundamental, whereas harmonics involves frequencies two, three, or more times higher in frequency than the fundamental. In order to understand these frequency shifts, it is helpful to review what happens in a sound wave. An acoustic wave propagates away from an acoustic source of vibrating particles because particles adjacent to them must respond to the force by applying a countering force (Newton's third law of motion). In turn, these new stressed particles also must apply force to particles more distal but adjacent to them. Therefore, such a disturbance of vibrating particles couples through the media, particle by particle, continuing to attempt to satisfy the condition that in equilibrium the sum of all forces must be zero. This dynamic coupling action constitutes the propagation of a wave. The speed at which it propagates is related to the mass of the particles (i.e., the density of the media) and its "springlike characteristics" (i.e., bulk modulus). Further, the greater the velocity at which the particles originally

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vibrate, the greater the acoustic pressure in that region and the higher the intensity. As the wave propagates, one can consider the net velocity at which the particles move. This net velocity is the sum of both the particle velocity from the vibration and the speed at which the wave propagates. In a standard longitudinal wave, the particles vibrate along an axis that is in the same orientation as wave propagation. However, during the positive pressure (compressional part of the wave) the particles move in the same direction as the wave is propagating, but during the negative pressure (rarefactional part of the wave) they move in the opposite direction. The net effect is that the particles move slower during the rarefactional portion of the wave because the particle motion subtracts from the speed of propagation. In the compressional segment of the wave, particle velocity adds to the speed of propagation. These effects accumulate as the wave propagates along and have the tendency to distort a sine wave, with the compressional part becoming sharp at the front of the wave and the rarefactional part becoming retarded. The overall appearance tends toward a sawtooth-shaped wave rather than its original sinusoidal form. This distorted wave can be described as a wave composed of a certain amplitude of the fundamental frequency (f0 ) and various levels of higher harmonics (2f0 , 3f0 , 4f0 , and so on). The closer the distortion approaches the shape of a sawtooth wave, the higher the amplitude of the harmonics. On the other hand, if the wave remains a sine wave, there are no harmonics. A final key point is that the intensity or amplitude of the acoustic pressure is important. The higher the amplitude, the more rapid or closer to the transducer this nonlinear distortion occurs. This understanding of nonlinear propagation has principally been derived from propagation in water,[75] in which the attenuation is low. There have been no reports on experimental measurements in actual tissue (of which the author is aware); however, there have been several recent reports of nonlinear modeling, including tissue equivalent attenuation.[76] [77] [78] A major effect of tissue according to these models is that the increased attenuation with frequency tends to nullify the generation and propagation of higher harmonics to some extent. Therefore, the generation of sharp sawtooth waves appears unlikely. However, the wave can still be rich with harmonics as verified by the fact that harmonic imaging actually works. Considering earlier discussions, the reasons why images are now better are explained. First, the generation of harmonics requires the fundamental

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frequency to propagate some distance. This indicates that the various aberrations and possible reverberation effects that occur at the skin, fat, and muscle layers of the chest wall do not affect the harmonic waves because they develop deeper in the tissue. Therefore, the detrimental effects on the conventional image that occur as the result of aberration to the beam[79] owing to the chest wall is avoided, at least for the transmission portion of a transceiving process. Second, the higher the amplitude, the greater the tendency to produce these harmonics more rapidly and more extensively. Therefore, the generation of harmonics occurs more rapidly in the center of the beam of the wave at the fundamental frequency because the intensity there is higher. This action causes the harmonic beam to be narrower. As mentioned earlier in the chapter, for the same size aperture a higher frequency also produces a narrower beam pattern. The net result of these effects is that higher harmonics produces a beam pattern that is narrower than the beam formed at the fundamental frequency. This narrower beam leads to a higher resolution image. Finally, as indicated in Figure 9-7 , if the scatters fall in the Rayleigh region, the backscattering increases for the higher harmonics. Therefore, one anticipates increased backscattering from cardiac muscle (see Fig. 9-11) for 197

the higher harmonics. Similarly, backscattering from a nonperpendicular angle of encounter of the acoustic beam with a semirough scattering boundary may produce higher backscatter at the higher frequencies. These two effects also are most likely contributing factors to the improved images of the endocardium obtained by harmonic imaging. Having described the mechanisms for image improvement that harmonic imaging provides, there are still some design aspects of a conventional ultrasound imaging system that have to be overcome to obtain these advantages. These aspects include features that are needed for high range resolution. A wide bandwidth system is required to ensure the transmission and reception of very-short-duration excitation bursts. The shorter the duration, the wider the frequency spectral content of the excitation signal and the wider the bandwidth needed to transceive it. A wide bandwidth excitation signal also produces wide bandwidth harmonics. The difficulty arises because the lower frequency components of the harmonics tend to overlap into the frequency range needed for the higher frequency components of the fundamental excitation signal. This action degrades the advantage of the harmonic signals. Therefore, to receive only harmonics,

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special designs are needed. Careful shaping of the excitation signal and filtering of the received signal have been successfully employed.[80] An alternative is the use of pulse inversion methods,[76] which appear to automatically suppress the fundamental excitation signal and tend to allow recovery of only the harmonic. Although the advantages of harmonic imaging are becoming well recognized in echocardiography laboratories, there are limited formal studies of the advantages of harmonic imaging. Reports from symposia have provided some documentation. Improvements were found in visualization of the aortic valve in 70% of 40 patients with harmonic imaging, whereas visualization was possible in only 35% of the patients with normal imaging.[81] Left ventricular thrombi was looked for in 93 patients with myocardial infarction and only 7 were found with use of normal imaging, but two additional ones were found with use of harmonic imaging. [82] Harmonic imaging is now routinely used in the echocardiography laboratory at the University of Washington Medical Center because of the advantageous experience with its use. The only shortcoming our cardiac sonographers report is that valve leaflets tend to appear thicker with harmonic imaging than with normal imaging. This effect most likely arises from an artifact produced in the processing system, which is caused by the rapid movement of the valve leaflets. However, a more in-depth study is needed to clarify this observation and what the artifact mechanism actually is. Of final note, harmonic imaging is being found to provide better images in numerous other areas beyond echocardiography. This method is indeed an advancement in ultrasound imaging.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary The physics of ultrasound in terms of beam patterns, propagation, attenuation, and scattering is important in echocardiography. Some of the important aspects of these factors have been discussed in this chapter. This is by no means an exhaustive review, but it may stimulate the reader to more reading in this area and may provide some assistance in understanding this sometimes nonclinical literature. The spatial resolution, which consists of range resolution (related to the pulse duration), lateral resolution (related to the lateral beam width), and elevation resolution (related to the elevation beam width), is very important in the accuracy of length, area, and volume measurements. These factors are particularly important when the ultrasound beam impinges on boundaries obliquely. Evolving technical improvements in imaging, which improve resolution and reduce aberration effects of tissue (e.g., harmonic imaging), will provide more accuracy in quantitative measurement by reducing the effects that have been discussed. Continued technical improvement and discovery is certainly a hope for the future.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Measurement Errors Numerous errors can result when quantitative measurements are made using ultrasound. One area of difficulty is the variation in the speed of sound. Generally, most instruments use a value of 1540 m per second for the average speed of sound in tissue at 37°C. The calibration markings on the screen for distance are based on this value. Further, for phase arrays the delays used in the instrument to steer the beam to produce the scanning sector also use this value. As discussed earlier, the speed in different tissues varies to some extent. For example, if the distance across the aorta is measured as 2 cm based on the calibration on the screen using 1540 cm per second whereas the actual speed of sound in blood is 1579 cm per second, there would be an error of -2.5%. This is an error in making a onedimensional measure along the direction the ultrasound propagates. If the speed of sound is different from 1540 m per second, the angle of the phased array may be different, so lateral measurements in the image also can suffer some error because of speed-of-sound differences. Circular structures can become elliptic if there is a great difference in the speed of sound. Perhaps bigger mistakes can be made when investigators are performing in vitro studies using water or excised tissue at room temperature. The problem with water can be avoided by using a salinity of 4.62% (see Table 9-1) , in which the speed of sound is 1540 m per second. The speed of sound in excised, fixed tissue at room temperature also varies from body temperature speeds. Although the speed-of-sound errors can be quite important in many situations, the larger errors often may occur because the beam patterns are not ideal (i.e., infinitely narrow and pencil-like) and the duration of the interrogation pulse is not infinitely short. The earlier discussion explains imperfections of beam patterns, and later I discuss how these imperfections can cause errors in area and volume measurements. First, some of the errors that can occur from a finite duration of the interrogation pulse are illustrated in Figure 9-12 . The beam width is assumed to be very narrow.

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Two situations (a short and a long pulse) are shown in which the beam passes from a hypoechoic Figure 9-12 Diagram illustrating how the range resolution (related to the length of the interrogating pulse) can increase thickness of the ultrasound appearance of a hyperechoic layer. See text for explanation.

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to a hyperechoic layer, then back to a hypoechoic layer, again through a hyperechoic layer, and back to a hypoechoic layer. The two types of pulse are shown at different positions along the structure. They are shown just as they are entering the hyperechoic layers and just after the trailing edge of the pulse exits the hyperechoic layers. The resulting A-mode lines are illustrated. The key points here are that the beginning of the echo starts at the leading edge of the pulse, passing from a hypoechoic to a hyperechoic region, but the end of the echoes from the hyperechoic to hypoechoic passage do not end until the trailing edge clears the hyperechoic layer. The two pulse durations, when used for linear scanning of the two layers, then produce images as illustrated. With the long-duration pulse, the hyperechoic layers appear much thicker than they really are and the distance between the layers appears shorter than it really is (compare d2 on the figure with d1). Therefore, the pulse duration (which is of course related to the range resolution) if excessive may result in quite an error in layer thickness measurements. This has been a concern in measuring the layers of intestinal walls in gastroenterology,[83] measuring blood vessel walls, and measuring cardiac wall thickness. This consideration has brought up the topic of leading to leading boundary edge outlining and trailing to leading edge with correction methods.[84] [85] The next consideration is the effects of lateral beam width, which are illustrated in Figure 9-13 for narrow pulses and in Figure 9-14 for long pulses. The transducer is on the left with a beam pattern diverging to the right. Two situations are shown: (1) when the beam encounters boundaries fairly perpendicularly ( see Fig. 9-13A and Fig. 9-14A ) and (2) when the beam encounters boundaries obliquely ( see Fig. 9-13B and Fig. 9-14B ). In Figure 9-13A , the A-line echoes from a tubular structure (perhaps a shortaxis left ventricular view) are illustrated. Echo 1 arises from the proximal wall and echo 2 from the distal wall. Even with a short-duration pulse, echo

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4 is of longer Figure 9-13 Diagram illustrating how a short-duration pulse with a lateral beam pattern that is diverging and has a finite width can affect the measurement of wall thickness. The lateral beam width is related to the lateral resolution of the system. A, Beam tends to encounter the wall fairly perpendicularly. B, Beam encounters the wall at an oblique angle. See text for discussion. Figure 9-14 Diagram illustrating how a long-duration pulse with a lateral beam pattern that is diverging and has a finite width can affect the measurement of wall thickness. The lateral beam width is related to the lateral resolution of the system. A, Beam tends to encounter the wall fairly perpendicularly. B, Beam encounters the wall at an oblique angle. Note the increase in the wall echoes compared with those of Figure 9-13 . See text for a detailed discussion.

duration than echo 2 because a portion of the beam encounters the distal wall earlier than in Figure 9-13A (normal encounter). The effects of the longer pulse are shown in Figure 9-14 . Echoes 1 and 2 are of longer duration than those of echoes 1 and 2 in Figure 9-13A because of the effect illustrated in Figure 9-12 . In addition, echoes 3 and 4 are of longer duration than 3 and 4 in Figure 9-13B . If one is measuring the inside dimension or inside area of a chamber, the oblique encounter with a wide beam reduces the inside dimensions of the structure (compare d2 with d1 in Figure 9-13 ). This effect is even further aggravated by the long pulse (compare d2 in Figure 9-14 with d2 in Figure 9-13 ). This phenomenon can contribute to the underestimation of chamber or vessel area measurements with ultrasound. The final consideration is the effect of the beam width on the elevation direction. In Figure 9-15A a tubular structure is imaged so that the ultrasound imaging plane encounters the wall of the tubular structure perpendicularly. If the lateral beam width is extremely narrow and the pulse is very short, the image that is generated is similar to that illustrated in Figure 9-15C . The geometry of the imaged structure is faithfully reproduced. However, if the imaging plane encounters the wall at an oblique angle, because it has a certain beam width, it in essence images a thick oblique slice through the wall, like the slice illustrated in Figure 915B . Considering that echoes are generated as long as a portion of the beam is cutting tissue, the imaging of the structure shown in Figure 9-15B

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results in an ultrasound image as in Figure 9-15D (i.e., essentially an image with a reduced cross-sectional area of the inner chamber and increased area of the outer contour). In the real imaging situation, the lateral beam width and pulse duration also contaminate the image; therefore, the cross section of the inner cavity is reduced even more and the outer border area increased more than shown in Figure 9-15D . These effects may play important 199

Figure 9-15 Diagram illustrating how the elevation resolution (i.e., a finite beam width in the elevation direction) can affect the ultrasound image obtained from a tubular structure. A, Beam pattern encounters the wall in the elevation direction (direction out of the paper) at a fairly perpendicular angle. B, Beam encounters the wall in the elevation direction at an oblique angle. C, Type of image of the wall structure that is produced with perpendicular encounter as in A. D, Type of image of the wall structure that is produced with an oblique encounter as in B. Note the reduced inside area and enlarged outer area.

roles in causing underestimation of the inner area or volume (such as the volume of the left ventricle) of chambers or vessels. Much of the underestimation reported in the literature when measuring volumes (e.g., with 3D ultrasound) may arise from the oblique encounter with nonperfect beam patterns and pulses. Therefore, by orientating the imaging beam of the probe so that it encounters the organ walls as perpendicularly as possible, the best accuracy can be obtained. The method reported by Gopal et al[86] [87] in making 3D measurements of left ventricular volume is favorable from this viewpoint. It is also possible to correct for some of these artifacts by the way the contours are outlined. Perhaps, in some of the measurements in which underestimation was not reported, the outlining was performed in a manner that placed the border well into the echo boundary of the image. It is therefore very important to understand the various measurement artifacts that can arise and try to design measurement methods to minimize these effects.

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202

Chapter 10 - Three-Dimensional Echocardiography Approaches and Applications Florence H. Sheehan MD

Two-dimensional echocardiography provides visualization of many structures in the beating heart; however, interpretive skills are needed for the observer to mentally formulate the heart's complex three-dimensional anatomy. In three-dimensional echocardiography, the spatial location and orientation of each two-dimensional image plane is recorded with the image so that information from multiple images can be analyzed jointly. This permits multiplanar image data to be assembled into three-dimensional displays that facilitate the assessment and communication of anatomic relations. The three-dimensional format also enables the quantification of the size, shape, and function of cardiac structures with minimal geometric assumptions, a particular advantage when dealing with disease-distorted anatomy or complex shapes such as the right ventricle. Although threedimensional echocardiography was conceptualized in 1961, most of the advances were made during the past decade after fast and inexpensive computers became more readily available; Belohlavek et al[1] have reviewed the earlier work.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Modes of Three-Dimensional Echocardiography Three-dimensional echocardiography is often equated with volumetric imaging to obtain spatial visualization of cardiac anatomy[2] [3] (Fig. 10-1) . In this mode of three-dimensional echocardiography, spatially dense image data sets are acquired and processed to permit the shape of the structures to be appreciated visually using three-dimensional display formats such as surface rendering, which employs shading to indicate topology. The image data set can be opened at any cut-plane to provide a surgeon's eye view of the heart's interior. The third dimension can also be appreciated using stereoscopy or holography.[4] [5] In the surface modeling mode of three-dimensional echocardiography, the three-dimensional surface of the targeted structure is reconstructed based on tracings of its border from multiple image planes (Fig. 10-2) . All chambers and valves can be reconstructed, as well as intracardiac structures such as the papillary muscles and chordae tendineae for quantitative analysis of size, shape, function, and spatial relationships between structures. Surface modeling is the mode of three-dimensional echocardiography that provides superior accuracy in measuring ventricular volume and mass, and for accurate, reproducible measurement of a variety of cardiac descriptors. Volumetric imaging is primarily used to search visually for structural abnormalities such as congenital defects or deformed valves, although volumetric data sets can also be analyzed to measure volume or a defect's size. In both modes of three-dimensional echocardiography, quantification currently requires manual image analysis. Because both modes of three-dimensional imaging involve 203

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Figure 10-1 Volumetric imaging provides a realistic, "surgeon's eye" view of the heart. This study is of an in vitro heart imaged in a water bath. AML, anterior mitral leaflet; AoV, aortic valve; LV, left ventricle; LVOT, left ventricular outflow tract; PML, posterior mitral leaflet; RVOT, right ventricular outflow tract. (From Sheehan FH, Wilson DC, Shavelle D, Geiser EA: Echocardiography. In Sonka M, Fitzpatrick JM [eds]: Medical Image Processing and Analysis. Bellingham, Wash., SPIE Press, 2000, pp 609–674.)

the acquisition of image data continuously through the cardiac cycle, it is possible to prepare the data in time-varying format for visual review of the heart's dynamic function or for quantitative analysis of asynchronous events. As for visualization at end-diastole and end-systole, dynamic presentation is easily automated in volumetric mode.[6] For quantitation, however, the border tracing must be repeated at every time point, a daunting prospect until the accuracy and reliability of automated border detection suffices to be used clinically. Figure 10-2 Left ventricular endocardial surface of a normal subject at end-diastole, reconstructed using the piecewise smooth subdivision surface method from freehand transthoracic scanning.

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Image Acquisition The intended approach to data analysis determines the method for image acquisition. In general, imaging for surface reconstruction uses free hand scanning. In contrast, the tight format required for volumetric imaging has until recently mandated the acquisition of these data sets using a mechanical device at fixed spatial intervals. Because certain methods for surface reconstruction incorporate assumptions concerning the position and orientation of the image planes, the requirements for a particular analysis need to be met during acquisition. Violation of the assumptions introduces error into the analysis.[7] Tracking Systems Knowledge of the position (x, y, z) and orientation (ρ, phi, theta) of the ultrasound transducer permits assembly of the images and their derived data in three-dimensional space. There are a number of methods for tracking the transducer during scanning. These methods can be classified into mechanical, line of sight, and magnetic. Each technology has its own advantages and limitations. The oldest type of mechanical system employs a series of articulated arms with encoders at the joints (Fig. 10-3) . The scanhead is placed at one end of the system and the other end (the base) is rigidly mounted to a reference frame. Reading the encoders provides rotational information about the articulated arms attached to that joint. Knowing the length of the arms and the rotations yields the position and orientation of the transducer with respect to the base. The major limitations to using mechanical arms are bulk and intrusion into the measurement space. It is awkward for the sonographer to manipulate the arms to reach all required positions and orientations. Each degree of freedom in the arm's motion presents a potential source of error.[8]

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204

Figure 10-3 Schematic representation of an articulated arm for mechanical tracking of the ultrasound transducer. This arm has 6 degrees of freedom. (From Nikravesh PE, Skorton DJ, Chandran KB, et al: Ultrasonic Imaging 1984;6:48–59.) Figure 10-4 Mechanical tracking permits acquisition of images in parallel planes (A), angulated scans (B and C), or rotational scans (D) from the transesophageal window. (From Flachskampf FA, Franke A, Job FP, et al: Am J Cardiac Imaging 1995;9:141–147.)

205

Another mechanical approach is to rotate or angulate the transducer within a constant location while recording the angle (Fig. 10-4) . Rotational scans are generally performed at the apex around the long axis of the left ventricle but can also be acquired at parasternal, subcostal, suprasternal, or transesophageal windows for volumetric imaging, such as to assess congenital defects.[3] [9] [10] By acquiring a full 180-degree rotation and checking that the first and last images are mirror images, one can be assured that transducer position was maintained during image acquisition. Rotational scanning is the most common acquisition mode for volumetric imaging. Angulating the transducer from a fixed position produces a fanlike are of images and has been successfully performed in the transthoracic parasternal window for the left and right ventricles [11] and in the transesophageal approach.[12] [13] One major disadvantage of rotational and angulated scanning is that not all hearts fit within the image volume circumscribed by the rotated or angulated sector, so that the margins of dilated hearts even in children may be incompletely imaged.[14] If the left ventricle can be visualized completely within a parasternal rotation, experimental studies indicate that the accuracy of volume measurement is greater than with an apical scan, presumably because of the low incidence angle of the ultrasound beam to most of the myocardial wall.[15] A second disadvantage is that poorly visualized structures cannot be recovered by scanning elsewhere, because imaging is limited to one acoustic window. Third, the quality of the images often varies when the transducer is rotated mechanically about a fixed axis; in contrast, freehand scanning permits adjustment of the image plane to obtain optimal image quality.[16] A fourth disadvantage of rotational and angulated scans is the relatively limited

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spatial resolution in the far field where the image planes are more widely separated. For visualization of congenital defects, this problem is handled by centering the axis of rotation over the region of interest. Linear scanning, also called bread-loafing, parallel slicing, or pullback scanning when referring to transesophageal acquisition, generates images in parallel planes (see Fig. 10-4) . The narrow intercostal space limits a transthoracic interrogation of the entire ventricle.[2] However, partial scans still permit specific localized defects to be studied, for example, to examine congenital atrioventricular valve defects or to examine the success of a surgical correction.[17] Complete data sets can occasionally be obtained from the subcostal window.[17] A transesophageal echocardiography system was developed to obtain parallel image planes by straightening the esophagus[18] (Fig. 10-5) . Unfortunately, this maneuver displaces the transducer posteriorly away from the apex.[6] Owing to these acoustic window restrictions, linear scanning is more commonly used in abdominal imaging. Line of sight systems include ultrasonic and optical tracking systems. Ultrasonic tracking systems typically utilize a single sound wave source and three fixed, known sensors[19] [20] (Fig. 10-6) . The speed of sound through air allows the range between the source and sensors to be determined. Triangulation determines position. Multiple sound sources are required to determine orientation. Ultrasonic systems suffer from shadowing, ambient noise, Figure 10-5 Diagram of system for parallel tomographic image acquisition. After the transesophageal echocardiographic probe is positioned posterior to the heart, the carriage is straightened and the transducer is retracted with the use of a stepper motor to obtain closely spaced (1 mm) images. (From Wollschlaeger H, Zeiher AM, Geibel A, et al: Transesophageal echo computer tomography of the heart. In Roelandt JRTC, Sutherland GR, Iliceto S, Linker DT [eds]: Cardiac Ultrasound. London, Churchill Livingstone, 1993, pp 181– 185.)

and interference due to acoustic reflections. The accuracy depends on maintaining constant air temperature, which affects the velocity of sound by about 2% per 10°C. [21] Furthermore, the need to maintain a clear path between transmitter and sensor restricts the sonographer's movement, the device produces unpleasant sounds, and the size of the sensor impedes imaging. Optical systems are not temperature sensitive but do suffer not only from shadowing but also from high cost and inflexibility, the latter due to the need to keep the cameras in a known alignment. Therefore, they have

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not been applied to three-dimensional echocardiography. The magnetic field system generates three orthogonal fields whose strength and direction are detected by a small, light receiver mounted on the transducer [21] [22] [23] (Fig. 10-7) . Only magnetic field systems combine the following: (1) 206

Figure 10-6 Ultrasonographic transducer with three spark gaps (arrowhead) mounted. This configuration provides direct transmission of audible sound toward the localizing array of four microphones. (From Handschumacher MD, Lethor JP, Siu SC, et al: J Am Coll Cardiol 1993;21:743–753. Reprinted with permission from the American College of Cardiology.)

They are able to track the position and orientation of the scanhead during freehand scanning; (2) they allow acquisition of images from randomly oriented image planes; (3) they allow acquisition of images from multiple acoustic windows; and (4) they permit imaging within the body as well as transcutaneously. The disadvantages Figure 10-7 Schematic of three-dimensional echocardiographic image acquisition using a magnetic field system to track the position and orientation of the ultrasonographic transducer. (From Nguyen TV, Bolson EL, Zeppa M, et al: Am J Cardiol 1999;84:208–213. Reprinted with permission from Excerpta Medica Inc.)

are that sources of ferromagnetic interference such as hospital beds must be distanced from the field, and the system's safety for patients with pacemakers or implanted defibrillators is unknown. A novel ultrasonography machine has been developed that is capable of acquiring a pyramidal volume of image 207

Figure 10-8 Schematic of the image set acquired using a matrix array transducer. Demonstrated are two adjustable orthogonal B-scans perpendicular to the transducer and three adjustable C-scans parallel to the face of the transducer. (From Zwas DR, Takuma S, Mullis-Jansson

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S, et al: J Am Soc Echocardiogr 1999;12:285–289.)

data using a two-dimensional array transducer[24] (Fig. 10-8) . Because it obtains the entire image set from one cardiac cycle instead of assembling images acquired over multiple cardiac cycles, this "real-time" system eliminates the assumption, inherent in multiple beat analysis, that all of the component two-dimensional images fall on the same phase of the cardiac cycle and that the function, position, filling, and rhythm of the heart remain constant throughout imaging. The disadvantages are that images are acquired in a single acoustic window, enlarged hearts will not fit within the pyramid, a specialized ultrasonography machine must be purchased, and image quality is poorer than for three-dimensional echocardiography acquired using conventional ultrasonography machines.[25] In addition, the C-scan images, which are short-axis cross-sectional views parallel to the transducer face, have relatively poor lateral resolution. Consequently, volume and mass are underestimated and less accurate than measurements made from the B-scan images.[26] The speed of the three-dimensional acquisition enables scans to be obtained without sedation, even in infants.[27] One system provides real-time tracking of image plane position and orientation in addition to recording these parameters. The current image's location is indicated by a line of intersection with a previously acquired reference or "scout" image[20] (Fig. 10-9) . This technology helps to verify that the short-axis images are being acquired in nonintersecting image planes, a requirement of the polyhedral surface reconstruction method.[28] Use of a tracking system assumes that the patient will remain in the same position throughout imaging. To avoid inadvertent patient movement during image acquisition, it is important to explain the procedure in advance, coach the patient through the phases of the study, and carefully monitor the patient's position. Mechanical tracking also assumes system stability, but probe slippage can occur during a rotation or other manipulation.[29] Therefore, it is prudent to check the image data for possible misregistration, to obtain accurate quantitative analysis. To avoid using tracking systems, some investigators succeeded in producing three-dimensional reconstructions of the left ventricle based on freehand scans within a single acoustic window, by making assumptions concerning the location of the image planes. In one method, the alignment of short-axis contours along a parasternal long-axis contour is deduced from their vertical span and distance from the transducer.[30] Another approach is to assume the spatial location of the image planes based on the

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anatomy visible in the image. Fazzalari et al[31] located two orthogonal apical views by scanning anatomically, then rotated the transducer ±45 degrees away to record two additional views, which sufficed to reconstruct the left ventricle. Aakhus et al[32] located three standard apical views anatomically and then assigned to each its theoretical angular rotation. Though ingenious in their utilization of image data to substitute for tracking, these methods' assumption that the image planes were correctly positioned anatomically may not be correct.[33] Imaging Protocol One advantage of three-dimensional compared with two-dimensional echocardiography is that the quantitative analysis does not rely on the ability of the sonographer to acquire images positioned properly in certain standard views relative to the patient's cardiac anatomy. That is, when the reconstructions and measurements are derived from five or more image planes, the locations of those planes are not tightly prescribed. This is because the volume and function measurements are made from surface reconstructions rather than from geometric assumptions. There remain certain minimal requirements, however. The most important are visualization of the apex to define the long-axis length of the left ventricle, and adequate coverage of the ventricle. The protocol for image acquisition is dictated first by the tracking system and then by the reconstruction method. The least flexible are the mechanical systems that acquire a rotational or angulated scan from a fixed position within a single acoustic window or a linear scan from the esophagus. In contrast, articulated arms, acoustic locators, and magnetic field tracking systems permit freehand scanning. Freehand scanning has the potential for allowing the images to be acquired from whatever combination of acoustic windows and views provides optimal image quality for a given subject. The surface reconstruction program may limit this freedom, however. For example, the polyhedral surface reconstruction method requires nonintersecting short-axis views,[34] and the bicubic spline representation was designed for multiple long-axis views.[35] In contrast, the piecewise smooth subdivision surface method and methods based on spherical templates 208

Figure 10-9 Photograph of the line of intersection display. The long-

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axis view (center) is the reference image showing the "line of intersection" display identifying the location of the short-axis images obtained for volume computation. Below and to the sides are the individual short-axis cross sections from apex to base, with endocardial borders outlined. (From Sapin PM, Schroder KM, Gopal AS, et al: J Am Coll Cardiol 1994;24:1054. Reprinted with permission from the American College of Cardiology.)

accept intersecting short- and long-axis views.[36] [37] [38] Since patients vary in the image quality available at the parasternal versus apical windows, having the flexibility to acquire images at either or a combination of windows increases study yield and interpretability. Electrocardiographic and Respiratory Gating Because a three-dimensional image or surface reconstruction is assembled from the data of multiple cardiac cycles, it is necessary to segregate the acquired two-dimensional images according to phase in the cardiac cycle. This may be done manually, by selecting the image frames occurring at end-diastole and end-systole with the aid of the electrocardiogram (ECG), visually assessed chamber area, and closure of the mitral and aortic valves. Technology is available for triggering the acquisition of a cycle of images beginning at the R wave on the ECG in each plane; a volumetric set of image data can thus be accumulated at fractional or temporal intervals through the cardiac cycle. More sophisticated systems also filter out ectopic and premature beats. One should be aware that each ultrasonographic image requires a finite time interval for inscription. Thus, for example, the images showing the peak of the R wave on the ECG trace will cover variably overlapping time intervals around end-diastole, unless triggering is employed. This is unlikely to cause significant error, however, because end-diastole and end-systole are the periods of minimum change in chamber dimension. Analysis of contrast ventriculograms has shown that reducing the frame-rate from 30 to 15 frames per second did not increase error in measuring left ventricular volume or function.[39] On the other hand, reconstructions based on multiple cardiac cycles will be affected by the variable timing if the structure is moving rapidly, for example, a valve leaflet during opening. For fetal imaging in which no ECG is available for gating, retrospective cardiac gating can be performed using Fourier analysis of pixel intensity to reconstruct dynamic volumetric data sets.[40] Patient respiration alters the position of the heart within the chest. In freehand scanning, the patient is coached to breath-hold at end expiration without a Valsalva maneuver. Even heart failure patients are able to

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perform multiple 6-second breath-holds with brief rests in between.[41] In device-driven systems, the image acquisition may be gated to the respiratory cycle, such as by impedance measurement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Ventricles For quantitative analysis of ventricular size, shape, and function from threedimensional echocardiographic scans, it is necessary to extract the borders of the structure of interest from the images that have been acquired in multiple planes, reconstruct the structure from the borders, and make the desired measurements from the reconstructed surface. The advantage of this approach is that highly accurate representation of structures such as the left or right ventricle can be achieved from which its 209

Figure 10-10 (color plate.) System for image analysis. The twodimensional images are reviewed (right), and the borders of the target organ and associated anatomic landmarks are traced. Using position and orientation information from the tracking system, the x and y coordinates of each border are transformed into x, y, and z coordinates for display in a three-dimensional window (left) in which image and border registration can be verified. Here the red and green borders are traced from the left ventricular endocardium and epicardium, the blue and violet from the right ventricle, and the spheres from valve orifices, ventricular apices, and other anatomic landmarks. (From Sheehan FH, Bolson EL, McDonald JA, et al: Comput Cardiol 1998;25:649– 652. Copyright © 1998 IEEE.)

dimensions, shape, and function can be measured directly without geometric assumptions. The disadvantage is the labor required to trace the borders. Methods are being devised to alleviate the labor of tracing by automatically detecting heart borders from the images (see Chapter 7) . Also, a rapid analysis can be made from a small number of images by sacrificing some of the accuracy or information content (see "Measurement of Volume"). Border Tracing

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Human variability in border tracing has a greater impact on the accuracy and variability of quantitative analysis than error in image plane tracking or image timing relative to the ECG.[7] However, the multiplanar nature of three-dimensional echocardiography makes it possible to review tracings in their spatial as well as their temporal context. That is, border definition can be assisted not only by playing a cardiac cycle of images to track motion but also by using image information from adjacent or intersecting planes, or both, to compensate for poor image quality.[36] Another advantage of threedimensional imaging is the ability of some surfacing algorithms to handle partial borders rather than requiring a complete contour in each image plane.[36] [42] The missing information in one plane is provided in an intersecting plane or interpolated by the surfacing algorithm from nearby border data. A recommended design feature in the tracing software is handling the border as an overlay rather than replacing pixels in the image. [42] This allows the border display to be turned off while the original image is reviewed and then on again to verify that the tracer still agrees with the border location. A three-dimensional display format for reviewing traced borders facilitates the identification of discrepant borders (Fig. 10-10) . Based on their frequency and location, it is then easy to determine whether a single image was misinterpreted or a set of images was misregistered, such as due to patient movement.[42] The technological tool that will have the greatest impact on bringing threedimensional echocardiography into clinical practice is, of course, automated border detection. Numerous studies have already been performed to solve this problem, but none has yet succeeded. Current automation algorithms are reproducible but not accurate. For example, performing three-dimensional echocardiography with acoustic quantification by online integrated backscatter analysis produces smaller endocardial contours and volumes than by manual tracing.[43] Identification of the endocardial and epicardial contours can be aided using myocardial contrast enhancement.[44] Greater accuracy as well as reproducibility in measuring myocardial mass has been obtained in animal studies. It is important to employ a long-lasting contrast agent that persists into the myocardial phase to avoid attenuation from the chamber opacification and to obtain a time window long enough for the threedimensional echocardiographic scan. Doppler myocardial imaging can increase the yield and accuracy of three-

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dimensional echocardiography by using the frequency shift of the returning ultrasound signal in addition to its amplitude. Because the frequency shift is relatively independent of attenuation by chest wall structures, 210

Doppler myocardial imaging provides more complete endocardial boundary detection (80% to 85%) than gray scale images (67% to 71%; P < .05).[45] Surface Reconstruction Many methods have been developed for reconstructing the ventricular endocardial and epicardial surface from traced borders (Table 10-1) . The methods vary in (1) the assumptions or constraints placed on the input data, (2) geometric manipulations inherent in the reconstruction model, and (3) fidelity to cardiac anatomy. Given a series of ventricular contours in parallel planes, it is easy to extrapolate between the contours to produce an enclosed surface if desired for visualization. Such surfaces take a simple form with a single opening at the valve plane if produced from short-axis images alone, since long-axis views are needed to define both valves. Another approach for images acquired in an apical rotational scan is to intersect the traced borders with a series of parallel planes perpendicular to the long axis. The points where each plane intersects the traced borders are connected into a polygon or fitted to produce a curved contour[35] [46] [47] (Fig. 10-11) . Similar surfacing can be performed even if the images are not apical; for example, parallel planes can be intersected with borders from randomly oriented views.[48] The advantage here is the ability to utilize whatever combination of views provided optimal interrogation in a given patient. Instead of intersecting a set of traced borders with parallel planes, the borders can be intersected with a set of rotationally related planes to define the ventricular surface.[19] Borders traced from an angulated scan lend themselves to reconstruction using a cylindrical coordinate system.[11] The contour's area in each pair of adjacent image planes and the plane's angle of tilt are used to compute a wedge volume; the sum over all wedges is the chamber volume. It is computationally simpler to connect the points of intersection in each plane to form a polygon instead of fitting a curve to them,[49] but one risks underestimation of slice area and ventricular volume because, for example,

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the area of a dodecahedron is 4.5% less than the area of the circle circumscribing it.[7] A comparison of 12-, 24-, 48-, and 96-sided polygons revealed that 48 sides provides accurate representation of the shape and area of borders traced from photographs of short-axis slices of excised hearts.[50] The polyhedral surface reconstruction method operates on borders traced from short-axis images. Each traced border is divided into 180 points, and corresponding points on adjacent borders are connected to form a triangular tiled surface (Fig. 10-12) .[51] To enable the connections, the input image planes need not be parallel but must not intersect each other within the body of the ventricle. To check the short-axis images being acquired, Gopal et al initially record one or two parasternal long-axis images on which they display the locations of the short-axis images as lines of intersection. [20] The left ventricle is reconstructed from about eight or nine contours; the outflow tract is not delineated. This method has been Figure 10-11 Bicubic spine surface reconstruction. A, Left ventricular borders are traced from apical views. The algorithm compensates for skewed scan planes by stretching their borders lengthwise to match the longest long axis. The borders are then intersected with planes parallel to the mitral plane. B, Wire-frame representation of the reconstructed endocardial surface. (From Maehle J, Bjoernstad K, Aakhus S, et al: Echocardiography 1994;11:397–408.)

extensively validated in vitro and in vivo for left ventricular volume and mass[52] [53] [54] and can also be applied to the atria. Reconstruction can also be done based on a spherical coordinate system. In the method by Martin et al,[38] the x, y, and z coordinates of the manually traced borders are mapped into spherical coordinates before being fitted into a surface. These authors had developed a transesophageal echocardiography probe capable of recording images from both angulated and rotational sweeps.[55] Their approach was therefore designed to facilitate the handling of borders obtained from image planes with nontraditional orientations. An advantage of this method is that irregularly spaced and partial borders can be utilized. The method tends to round off all aspects of the ventricle, however, making it difficult to create sharp edges or orifices at the valves. A similar tendency to smooth out the valve planes is seen in a method based on deforming an initially spherical

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TABLE 10-1 -- Accuracy in Measuring Ventricular Volume and Fun Reconstruction Chamber Standard Subject Method Studies in Phantoms and Heart Models Phantom True Balloons Connect borders Phantom True Balloons Polyhedral surface Phantom True Balloons Polyhedral surface

Patient, Parameter N r

Phantom True Phantom True Phantom True

Phantom True

Phantom True

Phantom True Phantom True

Balloons Spheric template Balloons Spheric template LV Volumetric models scan; sum of slices Balloons Piecewise smooth subdivision surface Balloon Volumetric + pump scan; sum of slices

Balloon Polyhedral + pump surface Balloons Bicubic spline

Volume

8 0.

Volume

17 0.

Volume

30 0.

Volume

11 0.

Volume

10 0.

Volume

23 0.

Volume

6 1.

EDV

29 0.

ESV

0.

EF

0.

Volume

—

Volume

8

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Studies in in vitro Left Ventricles LV True Heart casts LV True Excised hearts LV True Excised hearts LV True Excised hearts LV

True

Heart casts Excised hearts Excised hearts Excised hearts Excised hearts

LV

True

LV

True

LV

True

LV

True

LV

True

Excised hearts

LV

True

Excised hearts

LV

True

Connect borders Connect borders Connect borders Connect borders; polar coordinates Polyhedral surface Spheric template Spheric template Spheric template Volumetric scan; sum of slices Piecewise smooth Subdivision surface Bicubic spline

Volume

5 0.

Volume

10 0.

Volume

11 0.

Volume

7 0.

Volume

15 0.

Volume

11 0.

Volume

28 0.

Volume

10 0.

Volume

14 0.

Volume

5 1.

Volume

Excised Volumetric Volume hearts scan; sum of slices LV True Excised Pyramidal scan; Volume hearts sum of slices Studies in Experimental Animals

11

7 0.

12 0.

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LV

Thermo

LV

Balloon in heart

LV

LV

LV

Balloon in heart

balloon in heart

Balloon in heart

Exptl Spherical animals coordinate system Exptl Spheric animals template

Exptl Spheric animals template

Exptl Spheric animals template

Exptl Spheric animals template

SV

57 0.

EDV

46 0.

ESV

38 0.

SV

38 0.

EF

38 0.

Volume

69 0.

SV

32 0.

EF

32 0.

EDV

19 0.

ESV

0.

SV

0.

EF

0.

Volume

84 0.

EDV

46 0.

ESV

38 0.

SV

38 0.

EF

38 0.

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LV LV

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Flow

Exptl animals Conductance Exptl catheter animals

Pyramidal scan; SV sum of slices Volumetric EDV scan; sum of slices ESV EF

LV LV

LV

LV

Balloon in heart Angio

Angio

Angio

Studies in Humans LV Doppler LV

Doppler

LV

MRI

Exptl Cylindrical animals Patients Sum of slices

Patients Connect borders; polar coordinates

Children Connect borders

Normal subjects Normal subjects Normal subjects

Spheric template Spheric template Polyhedral surface

Volume

14 0. 15 0.

0. 0. 11 0.

EDV

9 0.

ESV

7 0.

Volume

8 0.

SV

0.

EF

0.

Volume

26 0.

SV

0.

SV

19 0.

SV

14 0.

EDV

15 0.

ESV

0.

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LV

LV

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Angio

RNA

Normal Polyhedral subjects surface

Patients Polyhedral surface

EDV

39 0.

ESV

0.

EF

0.

EF

51 0.

0. LV

MRI

LV

Doppler

LV

MRI

Patients Polyhedral surface Patients Piecewise smooth subdivision surface Children Polyhedral surface

LV

Angio

Patients Polyhedral surface

LV

RNA

LV

MRI

Patients Volumetric scan; sum of slices Patients Volumetric and scan; sum of normal slices subjects

EDV

26 0.

ESV SV

0. 5 0.

EDV

12 0.

ESV EF EDV, ESV

0. 16 0.

EF

41 0.

EDV

46 0.

ESV

0.

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LV

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EF EDV

0. 24 0.

"

ESV

24 0.

"

EF

24 0.

SV

20 0.

EDV

50 0.

RNA,

ESV

0.

MRI

EF

0.

Angio

Patients Volumetric scan; sum of slices

Thermo LV

Angio,

Patients Bicubic spline

Right Ventricular Validation Studies RV True Heart Volumetric casts scan; sum of slices RV True Excised Volumetric hearts scan; sum of slices RV True Heart Replication and casts interpolation of three borders RV True Heart Piecewise casts smooth subdivision surface RV MRI Patients Volumetric scan; sum of slices

Volume

15 0.

Volume

14 0.

Volume

24 0.

Volume

10 0.

EDV

16 0.

ESV

0.

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RV

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MRI

Children Volumetric scan; sum of slices

EDV

13 0.

ESV

0.

EF

0.

2D, two-dimensional; Angio, ventricular angiography; EDV, end-diastoli volume; Exptl, experimental; LOA, limit of agreement (95%); LV, left vent subjects; R, Pearson correlation coefficient; RNA, radionuclide angiography standard error of the estimate; SV, stroke volume; Thermo, thermodilution.

214

Figure 10-12 Wire-frame reconstruction of a left ventricle using eight unequally spaced, nonintersecting short-axis image planes positioned with the line of intersection. (From Gopal AS, King DL: Threedimensional echocardiography. In Otto CM [ed]: Clinical Echocardiography. Philadelphia, WB Saunders, 1996, p 140.)

template along rays originating from the sphere's center to fit the traced data[36] (Fig. 10-13) . Nevertheless, this method has been flexible enough to reconstruct a variety of shapes, including excised ventricles and phantoms with localized protuberances, papillary muscle indentations, and aneurysms, and it accepts partial borders from images providing only limited visualization of the target chamber. It has yielded good accuracy in both left and right ventricular volume and mass measurement.[56] [57] [58] A method that measures ventricular volume accurately may not accurately represent the ventricle's three-dimensional shape, because there is an infinite number of shapes that contain a given volume. Most methods have been validated only for volume because no clinical applications Figure 10-13 Reconstruction using an initially spheric template. Left, Traced borders of human right ventricular cast with inflow region at upper left, apex below, and outflow at upper right. Right, Surface fitted to traced borders. (From Jiang L, Handschumacher MD, Hibberd MG, et al: J Am Soc Echocardiogr 1994;7:151–158.)

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beyond volume, ejection fraction, and mass were foreseen. However, regional ventricular function, stress, and shape can only be analyzed using methods that reconstruct the ventricle with spatial accuracy. Only one method has been shown to faithfully reproduce the threedimensional shape of the ventricle: the piecewise smooth subdivision surface reconstruction method.[37] [37] This method was developed to avoid the inherent limitations of other methods, which restricted their anatomical accuracy or application to different three-dimensional image acquisition techniques. A triangulated abstract mesh is designed as a model for each ventricle. Because it embodies knowledge about the expected shape of the targeted structure, the abstract mesh allows diversely shaped structures to be reconstructed, such as the left and right ventricles, atria, and papillary muscles. For example, parts of the mesh can be marked as sharp to handle valve and venous orifices and the junction of the right ventricular septal and free walls (Fig. 10-14) . Additional facets can be added to produce complex shapes. In fitting the abstract mesh to the manually traced borders, the locations of anatomic landmarks such as the apex, borders of the interventricular septum, or papillary muscle insertions can be retained for future reference (Fig. 10-15) . All four chambers of the heart can be reconstructed (Fig. 10-16) . Two methods have been developed to evaluate a three-dimensional surface's spatial fidelity to an anatomic specimen. Pirolo et al[59] made a solid biventricular model from photographs of a canine heart cut into parallel short-axis slices and showed that measurements of slice volume, slice area, slice perimeter, and other dimensions were similar in the photographs and model. Since the images were made after the heart had been sliced, this approach avoided the difficult problem of aligning the model to the specimen to ensure that the measurements were made at anatomically corresponding locations. To validate the piecewise smooth subdivision method, surface reconstructions 215

Figure 10-14 (color plate.) The piecewise smooth subdivision surface reconstruction method begins with a control mesh that embodies knowledge concerning the expected shape of the target organ. A, For the right ventricle, the control mesh indicates that there are sharp edges (indicated by yellow line segments) around the orifices of the pulmonary and tricuspid valves (filled with pink) and between the septal (blue) and free (green) walls. B, Final surface

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reconstruction of the same patient at end-diastole (wire mesh) and end-systole (blue). (From Sheehan FH, Bolson EL, McDonald AL: Comput Cardiol 2000;27:119–122. Copyright © 2000 IEEE.) Figure 10-15 (color plate.) In the piecewise smooth subdivision method, borders of anatomic landmarks can be carried through to the final surface reconstruction. A, Wire mesh display of borders traced of the left ventricular endocardium (black), mitral annulus (blue filled circles), aortic valve (green filled circles), and papillary muscles (red). B, On the fitted surface, the locations of the papillary muscle insertions are displayed in red.

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Figure 10-16 All four chambers can be reconstructed using the piecewise smooth subdivision method. The atrioventricular valves are fitted using a Fourier series approximation,[98] and the aortic and pulmonary valve orifices are fitted to a planar ellipse.

of animal hearts generated by three-dimensional echocardiography were aligned using anatomic landmarks to laser scans of plaster casts of those hearts; the small orthogonal distance between the two three-dimensional data sets proved this method's spatial fidelity[37] [37] (Fig. 10-17) . Measurement of Volume The advantage of three-dimensional echocardiography is its avoidance of geometric assumptions concerning the shape of the ventricle that are required to estimate volume from one or two two-dimensional views. This is the reason for the superior accuracy of three-dimensional echocardiography in volume determination, since the suitability of geometric assumptions is less for diseased hearts than for normally shaped hearts. The advantage is greater Figure 10-17 The piecewise smooth subdivision method produces reconstructions that accurately represent the three-dimensional surface of the target organ.[37] Left, laser scan of a plaster cast of a left ventricular endocardium; right, surface reconstruction.

for the right ventricle. One reason is that its complex shape is more difficult to model geometrically than that of the left ventricle. In addition, the

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paucity of clear anatomic landmarks makes it difficult to obtain reproducible views; the resulting ambiguity in image plane position increases the variability of volume measurements by two-dimensional echocardiographic methods. It is actually not necessary to reconstruct the endocardial surface to measure ventricular volume. Simpson's method is a computationally simplistic approach that can avoid assumptions regarding the ventricle's shape if the heart has been imaged in closely spaced parallel image planes. Then the area enclosed by the endocardial border traced in each plane is multiplied by the distance between the planes to obtain the volume of its corresponding "slice" of the ventricle. The volume of the ventricular chamber is then computed as the sum of the slice volumes. As in integral calculus, the accuracy of the volume measurement and of the threedimensional shape representation increases with the number of slices or image planes. Once the ventricular endocardium has been reconstructed, volume is measured directly from that surface without further assumptions. For example, to determine volume from a triangulated mesh surface, the volumes of tetrahedra defined by each surface triangle and a common origin are summed. Validation of the accuracy of ventricular volume measurement by threedimensional echocardiography is performed both in vitro and in vivo. The robustness of a reconstruction method can be assessed from its ability to handle not only a range of ventricular sizes but also a variety of shapes, as might be observed in diseased hearts. In vitro testing permits validation against the true value rather than against the modality that threedimensional echocardiography is supposedly replacing. In vitro models include phantoms such as balloons or fixed heart specimens. Experimental in vivo validation has been performed by positioning a balloon within the left ventricle for measuring volume over the cardiac cycle.[60] Clinical validation is by comparison with other imaging modalities such as magnetic resonance imaging, radionuclide ventriculography, contrast ventriculography, or computed tomography, or with flow measurements by Doppler or thermodilution. All clinical imaging modalities have their respective sources of error and variability, however. For example, magnetic resonance images smooth out trabeculae on the ventricular endocardium, thus shortening the border and diminishing the computed volume.[61] Therefore, it can be argued that comparing the novel—in this case three-

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dimensional echocardiography—with a more established imaging modality is actually an assessment of intermodality variability.[58] Because of the labor required to manually trace ventricular borders, it is advantageous to determine the minimum number of image planes that need to be analyzed and the effect of further data reduction on volume accuracy. Some investigators have found that volume or its derived parameters can be accurately determined from just three or four image planes.[15] [31] [32] [62] [63] [64] However, the standard error of the estimate when volume is measured from so few views is substantially larger than the 4 to 11 mL reported using borders from at least eight views.[30] , [51] [53] Buckey 217

et al[11] recommended at least six to eight planes, depending on the size of the ventricle. Their analysis was performed in vitro, however; a larger number of image planes may be needed clinically to compensate for poorer image quality. Tanabe et al[65] were able to obtain accurate volumes with only four to six axial images. Since this study was performed in small in vitro canine hearts, the results are comparable to a report that a 1 cm distance between serial parallel image planes suffices for the left ventricle. [66] In patients, left ventricular volumes measured from a three-dimensional image set acquired by rotational scanning and cut into 8-mm thick shortaxis paraplanes was comparable to volumes measured from 2.9-mm thick paraplanes, leading the authors to recommend the sparser data set for its speedier analysis.[67] However, because endocardial definition on paraplane images is poorer than on the original images used to synthesize them, the more complete volumetric data afforded by a dense rotational scan fails to provide superior accuracy over a simpler and faster freehand scan.[68] A theoretical analysis found that variability in left ventricular volume and mass determination by three-dimensional echocardiography decreases in proportion to the reciprocal square root of the number of slices.[69] In general, there is an inverse relationship between the knowledge inherent in the reconstruction method and the number of borders that must be traced. The spherical template method requires at least 8 to 12 images for accurate left ventricular volume determination but does not constrain the position or orientation of the images.[70] The polyhedral surface method utilizes fewer borders, eight or nine, but the reconstruction algorithm assumes nonintersecting short-axis image planes.[51] The piecewise smooth subdivision surface reconstruction method incorporates knowledge of the

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expected shape of the left ventricle via its abstract mesh.[37] It is thus able to provide accurate volume measurement and shape representation with as few as five randomly oriented left ventricular borders once the valve orifices have been defined.[71] Even this method cannot reconstruct the left ventricle from two borders, however. To proceed from such sparse data requires further shape assumptions such as relating the ventricle to an ellipsoid and produces only moderate accuracy (see Table 10-1) .[51] [53] Relatively little research has been performed to define the minimum amount of border data required to measure right ventricular volume accurately. Buckey et al[11] recommended at least six to eight planes for the right as well as the left ventricle, depending on the size of the ventricle. Janicki et al[66] recommend that more image data be acquired for the right ventricle because of its shorter longitudinal length and continually changing cross-sectional area. The smallest number of borders required uses just three standard, mutually orthogonal views (coronal, sagittal, and shortaxis), which are replicated and then interpolated.[72] Good accuracy is achieved by assuming that the shape of the coronal outline is constant over the anteroposterior extent of the ventricle. Measurement of Ventricular Mass The volume of a ventricle's myocardium is computed as the difference between its endocardial and epicardial volumes (Table 10-2) . Ventricular mass is determined by multiplying the myocardial volume by its specific gravity. Three-dimensional echocardiography has been shown in most studies to provide highly accurate and reproducible measurements of left ventricular mass; however, results for the right ventricle have been much poorer against both in vitro and in vivo standards. Reasons include incomplete visualization of the entire epicardium and greater obscurity of the myocardial-epicardial interface compared with the blood-tissue interface. The underestimation of right ventricular mass in one study was attributed to the surfacing method's tendency to round out sharp edges such as at the apex and distal outflow tract.[57] Measurement of Ventricular Function Nearly all validation studies have shown that measurement of ejection fraction by three-dimensional echocardiographic surface reconstructions more closely resembles the comparison standard than by two-dimensional techniques (see Table 10-1) . This is not unexpected, given the higher accuracy of three-dimensional echocardiography for volume measurement.

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Visual assessment of regional ventricular function can be performed from volumetric data sets using software to display each region dynamically. The image data can be cut to provide views that optimize endocardial definition and orientation. In one study, however, more segments could be visualized by standard two-dimensional echocardiography than from a real-time threedimensional echocardiographic scan. [73] Quantitative analysis of regional left ventricular function in three dimensions remains in its infancy, in part because most reconstruction algorithms fail to produce surfaces that are sufficiently faithful to the shape of the ventricular surface. Unlike volume, a measurement whose accuracy can be determined objectively, the analysis of regional function assumes knowledge of the pathway by which anatomic points on the left ventricular contour at end-diastole can be tracked to the same anatomic location at endsystole. For two-dimensional image analysis, attempts have been made to track endocardial "landmarks" or surgically implanted midwall markers. The wide discrepancy (90 degrees) between the trajectories for apical motion derived from these tracking studies acts to diminish confidence in their validity, however. The alternative is to use models of wall motion instead (for a wider discussion, see Chapter 5 ). The models developed to analyze wall motion from three-dimensional image sets are similar to those for two-dimensional images. An example is measuring wall motion radially toward a central origin or long axis.[7] [74] Because of the lack of objective evidence, such models are validated using empirical criteria such as sensitivity and specificity in distinguishing normal subjects from patients, just as was done for two-dimensional models. One study compared six reference systems and found greatest agreement with visual assessment when wall motion is measured toward the long axis.[75] More studies have been performed assessing regional function from the local change in wall thickness. Wall thickening more accurately reflects function 218

TABLE 10-2 -- Accuracy in Measuring Ventricular Mass by Three-Di Reconstruction Patients, Chamber Standard Subject Method N r SEE Re LV True Excised Polyhedral 11 0.995 2.91 Y =

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LV

True

LV

True

LV

True

LV

True

LV

True

LV

True

hearts surface Excised Piecewise hearts smooth subdivision surface Excised Volumetric hearts scan; sum of slices Excised Bicubic spline hearts Excised Volumetric hearts scan; sum of slices Excised Pyramidal scan; hearts sum of slices

Excised after scan LV True Excised after scan LV at risk Contrast Exptl animals LV

MRI

LV

MRI

LV

MRI

Volumetric scan; sum of slices Pyramidal scan; sum of slices

Volumetric scan; sum of slices Normal Polyhedral subjects surface Children Polyhedral surface Patients Volumetric scan; sum of slices

8.2 5 0.998 2.5 Y = +1

7 0.95 11.97 Y = - 2. 15 —

14 0.98

12 0.99

—

M diff 1.4 9.6 Y = +0 2.8 Y = +0

8 0.997 1.05 Y = 2.2 21 0.94

8.5 Y = +1

8 0.947 21

Y= +2

15 0.93

9.24 Y = +1 12 — — M diff 5.8 12 0.78 35.8 Y = 0.6

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LV

MRI

LV

MRI

RV

True

Patients Volumetric scan; sum of slices Patients Deformable shell

20 0.99

8.5 Y = 0.7

25 0.99

6.9 Y = +1

Excised Piecewise 10 0.996 4.5 Y = hearts smooth subdivision surface RV True Hearts Polyhedral 12 0.96 2.7 Y = +0 excised surface after scan RV MRI Patients Volumetric 16 0.65 — Y = scan; sum of +1 slices 1D, one-dimensional; 2D, two-dimensional; ED, end-diastolic; ES, end-sy left ventricle; MRI, magnetic resonance imaging; RMS, root mean square; S estimate. in hypertrophied hearts[76] and is independent of artifact caused by cardiac translation. The disadvantage is the need to trace and reconstruct the epicardium in addition to the endocardium. This doubling of work is not merely time consuming but also introduces additional opportunity for error. Imaging must be performed with the intent to quantify regional wall thickening, so care is needed to ensure that the epicardium is included in the scan sector throughout the cardiac cycle. Three-dimensional wall thickening analysis requires measurement of wall thickness orthogonal to the left ventricular wall. Analysis can been performed using twodimensional techniques on short-axis image planes located near the middle of the left ventricle. Accuracy is necessarily diminished in the more apical planes, however, where the oblique sectioning causes wall thickness to be overestimated. One method to measure regional wall thickness orthogonal to the left ventricular wall is to segment the myocardium into 64 elements and divide

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each element's volume by the mean distance between its endocardial and epicardial surfaces. [77] The centersurface method measures wall thickness along locally orthogonal vectors in the same way as in the centerline method for two-dimensional borders.[41] [78] [78] The vectors are normal to a three-dimensional medial surface constructed midway between the endocardial and epicardial surface reconstructions (Fig. 10-18) . Wall thickening is computed as the change in thickness normalized by the local end-diastolic wall thickness. To indicate the severity of an observed value's deviation from normal, thickening can be converted to units of standard deviations from the mean of the reference population, analogous to the approach used in two-dimensional measurement [78] [78] (Fig. 10-19) . Regional left ventricular function has also been evaluated from reconstructions of the endocardium and epicardium using finite element analysis. [79] More recently, a biomechanical model has been developed incorporating information about local fiber direction as well as material properties. The deformation of the myocardium was tracked between enddiastole and end-systole using curvature analysis.[80] The strain measurements predicted by this model have agreed well with sonomicrometer measurements in vivo.[81] Estimation of Infarct Size Infarct size is assessed from echocardiograms by measuring the amount of dysfunctional myocardium. The underlying assumption is that the extent of infarction correlates linearly with the extent of dyssynergy.[82] As in measuring ventricular volume, accuracy depends on the number of echocardiographic image planes analyzed and on the assumptions concerning the spatial location of the image planes and the geometry of left ventricular shape. Owing to limited visualization of the left ventricle, twodimensional echocardiographic approaches have quantified the proportion of infarcted myocardium, such as its 219

Figure 10-18 (color plate.) The centersurface method permits measurement of wall thickness orthogonal to the local myocardial wall. [158] Here the close and distant thirds of the left ventricle have been "cut away" to provide a tomographic view. A medial surface (green) is constructed midway between the endocardium (yellow) and the epicardium (blue). Chords are drawn perpendicular to the centersurface and extended

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to the endocardial and epicardial surfaces. The length of each chord is the local wall thickness.

circumferential extent in a short-axis view, rather than absolute infarct mass.[83] [84] [85] Such proportional measurements are unsuitable for serial studies because the fraction is affected by myocardial remodeling and thinning of the infarct region. Because of the more comprehensive assessment of the left ventricular surface, three-dimensional echocardiography yields absolute infarct size measurements that correlate closely with the true values in experimental animals.[86] [87] The principal difficulty with estimating infarct size from the extent of dyssynergy is deciding whether to include hypokinetic myocardium in the infarct region. Theoretically, including hypokinetic myocardium will overestimate infarct size because akinesis results from fibrosis of as little as 25% of the thickness of the myocardium.[88] If the infarct is transmural, then the infarct mass is truly equivalent to the mass of myocardium displaying akinesis or dyskinesis.[87] However, the transmurality of an infarction is difficult to determine ante mortem. When regional function is quantified rather than assessed visually, it is still necessary to select a threshold. In one clinical study, infarct mass by magnetic resonance imaging was associated with myocardium having absolute wall thickening greater than 2 mm.[89] The area of dysfunctional endocardium has been reported to correlate better with histopathologic infarct size than does the mass of dysfunctional myocardium, probably because of assumptions in the mass calculation.[86] Perhaps more importantly, three-dimensional measurements are also more consistent and less variable than two-dimensional.[86] The advantage here is that use of this metric as a clinical trial end point may reduce the number of patients needing to be enrolled. Following coronary occlusion, echocardiographic contrast material can be injected to define the size of the region at risk of infarction by its failure to show contrast enhancement.[90] [91] The contrast defect region corresponds to the infarct region in the absence of coronary reperfusion. Using volumerendering techniques, the size and location of the perfusion defect can be displayed within the framework of the reconstructed ventricle. Shape There has been relatively little progress in developing techniques for analyzing regional left ventricular shape from three-dimensional echocardiographic data. Most of the research has been conducted on

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magnetic resonance images despite the poor spatial resolution in the longitudinal axis. However, the methods developed for one modality are theoretically transferable to another modality. The most common approaches to shape analysis are geometry based. Regional curvature analysis has been applied for tracking endocardial displacement [80] and analyzing regional left ventricular strain. [81] The center-axis method measures distance radially from the long axis to the endocardial surface[92] (Fig. 10-20) . Its advantage is ease of computation; however, the results shift with the location of the long axis. The alignment method differs conceptually from previously described shape analysis methods because it directly compares the shape of a patient's heart with a reference heart after aligning them along regions of similar topography[93] (Fig. 10-21) . Shape differences are then Figure 10-19 (color plate.) Example of the visual presentation of regional left ventricular function in three dimensions. Here the wall thickening at each vertex has been converted into units of standard deviations from the mean of a normal reference population. Cool colors represent levels of hypokinesis; warm colors, hyperkinesis (color scale developed by S. Maza). Visualization as an overlay on the patient's three-dimensional surface facilitates appreciation of the location, extent, and severity of dysfunction.

220

Figure 10-20 A, The center axis method measures regional shape in terms of radial distance from a center axis to the endocardial surface. To normalize for heart size, the distance from the center axis to the reconstructed surface is divided by center axis length. The left ventricle is divided into 16 segments whose shape is calculated as the mean radial distance of the points lying within that segment to the center axis. B (color plate.), The severity of shape abnormality is displayed using a color scale allowing visual appreciation of the difference between a normal subject (NL74) and anterior and anterolateral dilation in a patient with idiopathic dilated cardiomyopathy (CM99). (From Munt BI, Leotta DF, Martin RW, et al: J Am Soc Echocardiogr 1998;11:761– 769.) Figure 10-21 (color plate.) The alignment method measures regional shape in terms of distance between the patient's heart and a reference such

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as normal average heart.[93] Here a normal end-diastolic left ventricular endocardial surface (mesh) has been deformed at the inferoapical wall (arrow) and aligned with its original, undeformed self (red surface) along regions of similar shape. The magnitude of shape abnormality can be quantified using the centersurface algorithm.

221

measured in terms of local orthogonal distance between them. Applications of regional shape analysis include assessing left ventricular remodeling following acute myocardial infarction,[93] [94] assessing regional stress,[95] and defining the pathophysiology of functional mitral regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Valves Three-dimensional echocardiography has contributed much more to the understanding of valvular heart disease than to the understanding of the ventricles. The ability to reconstruct the three-dimensional geometry of the valves, associated structures, and blood flow has not only provided mechanistic insight into the nature of disease processes but also totally altered our perception of normal cardiac anatomy. Owing to the dynamic nature of valvular function, which cannot be appreciated in the arrested heart, surgeons must rely on preoperative assessment based on imaging. For this reason, it has been a major focus of investigation to improve our knowledge of the structure-function relationship to better assist in surgical planning. Mitral Valve and Mitral Apparatus It was three-dimensional echocardiography that finally provided the tools for elucidating the saddle shape of the mitral annulus in humans.[96] Through three-dimensional reconstructions, this study demonstrated how the alignment of leaflet to annulus in the apical four-chamber view can give the artifactual appearance of mitral valve prolapse, resulting in false diagnosis by two-dimensional echocardiography. The underlying concept, that incomplete Figure 10-22 Schematic of the mitral annulus as reconstructed in three dimensions using Fourier series. The various dimensional parameters provide assessment of annular shape. (From Kaplan SR, Bashein B, Sheehan FH, et al: Am Heart J 2000;139:378–387.)

visualization of complex anatomical structures can lead to profound misunderstanding of their functionality, has stimulated the application of three-dimensional echocardiographic evaluation of numerous other cardiac

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pathologies to ensure that similar oversights are avoided. The most studied component of the mitral valve apparatus is the annulus. It can be visualized clearly from a rotational transesophageal scan and reconstructed by fitting a smooth spline curve or Fourier series approximation to the traced points.[97] [98] The area and eccentricity of the annular orifice are measured from its projection onto a least squares fitted plane. Annular height is measured relative to this plane. The accuracy of three-dimensional echocardiography for measuring these parameters has been validated in vitro.[98] Additional parameters of interest are its peak-topeak and valley-to-valley spans and annular motion, consisting of descent toward the left ventricular apex and tilting (Fig. 10-22) . Four-dimensional analysis of the annulus' shape change throughout the cardiac cycle is performed by reconstructing the annulus at multiple time points defined either from cardiac events or by normalization.[99] [100] [101] [102] The shape and dynamics of implanted annuloplasty rings can also be analyzed.[103] Ignoring the valve's three-dimensional shape, annular area can be estimated by planimetering its apparent orifice from short-axis paraplanes.[104] All components of the mitral apparatus can be reconstructed and analyzed quantitatively, not just the annulus. Leaflet reconstruction permitted analysis of leaflet-annular relations.[96] The left ventricle and left atrium can be reconstructed using surfacing methods.[105] The papillary muscles can be located and measured even though they are difficult to reconstruct because of their highly variable anatomy, and the chordae tendineae can be analyzed for position and orientation[105] (Fig. 10-23) . Such measurements are useful for evaluating functional mitral regurgitation.[42]

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Figure 10-23 (color plate.) Reconstructions of the left ventricular endocardium at end-diastole and the papillary muscles of a normal subject (left) and a patient with idiopathic dilated cardiomyopathy (right). The principal chordae tendineae proceeding from each papillary muscle head are displayed as pink or green line segments. The reconstructions enable visualization of the enlargement of the left ventricle, the outward displacement of the papillary muscle insertions, and the divergence of the chordae tendineae in the cardiomyopathy patient.

Aortic Valve

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There are several theoretical advantages of three-dimensional echocardiography for measurement of aortic valve area. First, direct planimetry of the valve's cross-sectional area or measurement of its radius from two-dimensional echocardiography is subject to error because of offaxis imaging of the valve, especially if shape is distorted due to congenitally bicuspid or degenerative stenosis. Second, calculation of valve area using the continuity equation method depends on proper positioning of the Doppler sample volume. Malpositioning of the image plane by as little as 10 degrees or 1.5 mm causes significant overestimation of valve area.[106] Three-dimensional echocardiography permits the orifice to be directly planimetered from a paraplane image that is correctly positioned anatomically in the true orifice, providing more consistent agreement with area determined by the Gorlin formula or the Doppler continuity equation than planimetry from two-dimensional images.[107] Regurgitant Flow The application of three-dimensional echocardiography for measurement of regurgitant flow rate using three-dimensional echocardiography promises an improved means for estimating effective orifice area and regurgitant volume, which are more reliable indicators of regurgitation severity. The increased accuracy that has been achieved can be attributed to avoidance of geometric assumptions inherent in the two-dimensional proximal isovelocity surface area (PISA) method. These assumptions are that the isovelocity surface is hemispheric in shape, the orifice is small and circular and lies on a flat surface, and the region adjacent to the flow convergence region is free of flow interference. To date, more research has been performed for assessment of mitral than aortic regurgitation. One reason is that the saddle shape of the mitral annulus and the variable leaflet topography violate the assumptions of the PISA method. There are several approaches for assessing valvular regurgitation that totally avoid using the PISA method. These methods are subject to pathophysiologic variations and imaging factors, however. One threedimensional approach is measurement of the regurgitant orifice area from a volumetric data set by direct planimetry from a cut plane providing a left atrial view of the orifice at its maximal area.[108] The authors validated it in vivo by demonstrating agreement between the three-dimensional and PISA measurements. Another approach is to analyze the dimensions of the regurgitant jet from multiplanar color Doppler images. For example, threedimensional Doppler measurement of proximal cross-sectional jet area

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correlated well with vena contracta area determined using laser flow visualization in vitro, although with 25% overestimation despite optimization of gray level threshold and color gain.[109] This error was attributed to poor lateral resolution of Doppler echocardiography, resulting in difficulty delineating the edge of the jet core from the adjacent entrainment flow. Jet volume agreed closely with mean and peak regurgitant flow, regurgitant fraction, and regurgitation stroke volume by electromagnetic flow meter in animal models of aortic regurgitation.[110] [111] Jet volume also agreed closely with angiographic grade of regurgitation in patients with eccentric as well as central jets, whereas two-dimensional jet area predicted regurgitation severity in central jets only.[112] One reason for the 223

greater accuracy of three-dimensional analysis is difficulty finding the plane displaying the maximum area of wall jets and eccentric jets from two-dimensional images. It is important to be aware that the relationship between jet volume and regurgitant flow-rate varies with Doppler angle, jet origin, jet-wall relationship (centric or eccentric), and orifice shape.[113] [114] It is possible to modify the PISA method to eliminate invalid assumptions. In vitro studies have shown that a number of factors affect the size and shape of the isovelocity surface. Its area varies with orifice shape, being larger for elongated split orifices than for circular or triangular orifices. Its shape is flattened near the orifice and eccentric for eccentric orifice shapes. One three-dimensional study described the shape of the flow convergence region as "complex and unpredictable" in its variety.[115] The varying local shape of the isovelocity surface away from hemispheric reflects the variations in leaflet and inlet geometry.[116] Simply reconstructing the actual three-dimensional isovelocity surface observed from Doppler data has been shown to enhance accuracy in measuring aortic regurgitation in an animal model.[117] The analysis of the regional shape of the three-dimensional reconstruction can be taken one step further, to compute the flow rate at each constituent of the Doppler isovelocity surface from its area and anglecorrected velocity (Fig. 10-24) . Integration over the entire surface generates a regurgitant flow measurement that correlates with true flow in vitro over a range of flow-rates and orifice shapes.[114] This is thus a Figure 10-24 (color plate.) Cut-away view of Doppler isovelocity

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surfaces in the flow convergence region (FCR), as measured at three velocity thresholds. The surfaces are flattened and elongated, reflecting the eccentric shape of the orifice (rectangular).[159]

geometry-independent method for quantifying regurgitant flow.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Processing Three-Dimensional Echocardiographic Data for Visual Assessment Visual assessment of image data has two forms. Volume rendering is a three-dimensional presentation of image data from closely positioned planes to obtain a realistic "surgeon's eye" view of the heart primarily for visual assessment. [118] For displaying the results of a quantitative analysis, three-dimensional surface reconstruction and graphics may be employed to facilitate appreciation of the anatomic location and extent of observed abnormalities. In volumetric mode, multiple images are acquired in close proximity and regular intervals and processed to create voxels, or three-dimensional image elements. Digital reformatting and image processing may be used to fill the space between image planes through interpolation to obtain a solid volume of voxel data, align the image data temporally, segment the tissue from the blood pool, and filter out noise and artifact. An algorithm assigns a binary value to each voxel to classify them as lying within versus outside the myocardium. The surface of the myocardium is generated by the computer from the boundary between voxel classes. The spatial dimension is displayed using volume rendering, a format that uses different gray levels 224

to indicate the depth of cardiac structures so that those lying "further" from the viewer are dimmer. Image processing tools are applied to give the sense of reality to the presentation, for example hiding distant regions that lie behind proximal regions. Lighting can also be arranged to illuminate "closer" features more brightly and cast shadows on surfaces behind them. The feeling of depth can be enhanced by computing pairs of images that are slightly rotated relative to each other and presenting one of these to each eye to create a stereoscopic display. Another tool allows the voxel set to be rotated and translated smoothly so that the viewer can peer into the heart

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from different perspectives. One advantage of volumetric imaging is the ability to compute twodimensional cross sections ("any-plane views") in planes that could not be acquired from standard precordial or transesophageal transducer positions. [3] [6] The quality of such synthetic images tends to be inferior, however, probably because of the interpolation required to fill in gaps between the original images. Most frequently, volumetric images are acquired using a mechanical device to obtain a closely spaced rotational scan. Techniques are being developed for interpolation between images acquired at high spatial frequencies from angulated freehand scans, however.[119] Recently, a method has been developed for spatial compounding of ultrasonographic images that combines information from multiple views while assigning higher weights to image data acquired at a near 0 incidence angle to the ultrasound beam. [120] Applied to scans of the shoulder, the method improved image quality in synthetic planes as demonstrated by reduction in the width of the border of the bone and lessened variability in intensity along the border. This kind of novel technology thus can enhance the information content of paraplane images while permitting combined volumetric analysis of multiple freehand scans. Prior to the ready availability of three-dimensional computer graphics and inexpensive computers, multiplanar image data were presented in various two-dimensional formats. One approach is to divide the left ventricle into four longitudinal quadrants that can be laid out "flat."[121] This permits assessment of endocardial surface area and area of infarcted myocardium based on regional dysfunction.[85] The left ventricle can also be presented as a bull's eye; however, regional areas are distorted, with particular exaggeration of the area of the base.[35] [47] This distortion can be avoided by mapping the multiplanar two-dimensional data onto a three-dimensional surface reconstruction of the ventricle (see Fig. 10-19) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Applications of Three-Dimensional Echocardiography Clinical Applications The avoidance of geometric assumptions in measuring ventricular volume is an important factor in the greater accuracy of three-dimensional as compared with two-dimensional echocardiographic techniques. This is even more evident when evaluating disease-distorted hearts. For example, the volume, mass, and ejection fraction of left ventricles compressed by pulmonary hypertension and in single ventricles of left ventricular morphology is more accurately determined by three-dimensional than by two-dimensional echocardiography (using magnetic resonance imaging as the standard).[122] [123] Similarly, the asymmetric crescent shape of the right ventricle poses problems for modeling from two-dimensional views but can be accurately represented using three-dimensional echocardiography, even in patients with congenitally distorted anatomy.[14] The anticipation is that three-dimensional echocardiographic techniques are useful for monitoring patients at risk of developing right ventricular dilation and heart failure. Similar methods can also be applied for measuring atrial volume.[124] Pericardial effusion volume is more accurately measured by threedimensional than by two-dimensional echocardiography. The reasons extend beyond the elimination of geometric assumptions concerning the shape of the ventricle and the spatial location and orientation of the image planes. In particular, three-dimensional echocardiography affords better visualization of all levels of the heart and is thus able to handle loculated effusions that may be asymmetrical in shape and unusual in location.[125] Another clinical application in which three-dimensional echocardiography has proven superior to two-dimensional is measurement of aneurysm volume.[126] [127] The avoidance of geometric assumptions and ability to accept and utilize nonstandard views combine to permit reconstruction of the aneurysm separate from the body of the left ventricle. This tool may be

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useful in planning surgical repair, estimating the size of the residual left ventricle, evaluating the stroke volume wasted by dyskinesis, and computing the expected functional benefit of surgery. Diagnosis The volumetric mode offers great potential for enhancing the diagnostic yield of an echocardiographic examination for several reasons. First, the possibility of cutting the image data in any plane reduces reliance on sonographer experience and skill and may even provide views that are difficult to acquire from traditional acoustic windows.[3] [6] That is, the size, shape, and motion of cardiac abnormalities can be displayed from any perspective. Even static views, when displayed from different perspectives, can assist in identifying structural abnormalities, visualizing their shape, and measuring their extent. The volume-rendered display assists experienced reviewers in diagnosing congenital, valvular, and structural pathologies, presumably by reducing the requirement for mental integration of the image data, so that sensitivity and specificity for discriminating normal from abnormal hearts is significantly enhanced compared with diagnosis from two-dimensional views.[128] Three-dimensional imaging has been estimated to provide improved spatial understanding of cardiac pathology over conventional transesophageal echocardiography in about one third of cases.[129] Transthoracic three-dimensional echocardiographic image sets provide information not seen in the two-dimensional study in the same proportion (one third) of adults with congenital heart disease. [130]

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One application is to assess the extension of abscesses into neighboring structures and to visualize mass lesions.[131] Another application is assessment of cardiac tumors to determine their shape, dimensions, origin, location, and involvement of valves prior to surgery.[132] Cutplane views provide a surgeon's eye preview of cardiac anatomy, for example, of the aortic valve from an aortotomy or of the mitral valve from above or below ("atriotomy" or "ventriculotomy" view).[133] It is speculated that such visualization may prove useful in surgical planning. For example, mitral valve abnormalities could be visualized as they would be seen intraoperatively for discussion with surgical consultants.[17] In patients with congenital anomalies, three-dimensional echocardiography provides additional diagnostic information on the mitral valve, aortoseptal

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continuity, atrial septum, and atrioventricular septal defects.[130] [134] Identifying small lesions or visualizing thin structures such as the aortic valve is beyond the resolution of the image, however.[130] To facilitate interpretation, cutting planes can be displayed dynamically to review the motion of valves or other segments of cardiac anatomy. Intrauterine sonography can provides prenatal assessment of anatomic and functional status regarding the myocardium, valves, and great vessels.[135] Therapy Planning and Assessment Volumetric imaging has been touted for therapeutic evaluation of atrial septal and other congenital defects because it can cut the image data to provide en face views that provide direct visualization of the defect in children and adults by the transesophageal or transthoracic approach.[133] , [136] These views provide information on the shape of the defect and its location relative to adjacent structures. However, measurement of its size and shape from en face views has variable accuracy.[134] [137] [138] [139] Clinical applications are presurgical planning and evaluation of the success of transcatheter closure of the defect.[138] Transesophageal three-dimensional echocardiography of ventricular septal defects can also be performed to quantify their location relative to ventricular apices and valve insertions, area, and circumference, for planning surgical or catheter repair.[140] Intraoperative transesophageal three-dimensional echocardiography of the valves provides the surgeon with information complementary to that yielded by routine two-dimensional echocardiography in the form of additional morphologic definition or interpretation of abnormalities seen on two-dimensional study.[141] In this study, the greatest contribution as well as the greatest error of three-dimensional echocardiography was in identifying leaflet fenestrations. Visualization of the valve leaflets during mitral balloon valvuloplasty can be performed from the esophageal window to monitor the process, guide and optimize commissural splitting, and minimize valvular regurgitation by arresting the procedure once minor leaflet tears appear. [142] The functionality of rigid mitral annuloplasty rings and their impact on outflow tract patency can be assessed using threedimensional imaging and reconstruction.[143] These studies were performed using magnetic resonance imaging, but three-dimensional echocardiography analytic tools are currently available and can be applied to assess the flexibility of mitral annuloplasty rings even when the absolute accuracy of annulus dimension is suboptimal.[96] [98] [144] Volumetric reconstruction has also been shown to assist in presurgical

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planning for right as well as left ventricular outflow obstruction by providing visualization of the morphology of the obstruction.[145] [146] Reconstruction of the left ventricular outflow tract by tracing its border from parallel short-axis paraplane images provides characterization of the anomalies specific to hypertrophic cardiomyopathy, identification of abnormal geometry that may prove useful in understanding the mechanism of obstruction, and assessment of the efficacy of surgery in remodeling the outflow tract.[147] Physiology and Pathophysiology Three-dimensional echocardiography has unparalleled potential for elucidating the mechanism of disease processes, owing to its high spatial and temporal resolution. For example, four-dimensional analysis of the annulus has permitted characterization of how the normal mitral valve achieves area reduction during systole through a combination of perimeter shortening and shape modulation.[101] [102] Such techniques permit measurement of the extent to which annular dynamics and static dimensions may be altered by disease processes such as ischemic heart disease or cardiomyopathy. Three-dimensional echocardiographic analysis of the components of the mitral apparatus has been instrumental in elucidating the cause of functional mitral regurgitation.[101] [148] [149] Serial Studies Measurements of ventricular volume, mass, and ejection fraction by threedimensional echocardiography are far more reproducible than by twodimensional echocardiography or by visual assessment (Table 10-3) . The clinical advantage of reproducible measures is sensitivity in detecting changes in a patient's condition. For example, patients with valvular lesions require close monitoring to select optimal timing for a surgical repair. Another important clinical application is the long-term monitoring of right ventricular volume and function following surgical repair of congenital defects such as Fallot's tetralogy in patients with residual pulmonary valve dysfunction or an intra-atrial baffle for transposition of the great arteries. With two-dimensional techniques, variability was introduced by estimating right ventricular volume from image planes whose anatomic position may have been difficult to reproduce from study to study. With threedimensional imaging, this source of error is eliminated. One analysis of interobserver variability reported that three-dimensional echocardiography has a 92% to 95% probability of detecting a change of 15

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mL in left ventricular end-diastolic volume, of 11 mL in end-systolic volume, 226

TABLE 10-3 -- Variability in Measuring Ventricular Volume and Fu Patients, Method Parameter N Interob Polyhedral Volume 17 4. Polyhedral Volume 30 2.65

Chamber Standard Subject Phantom True Balloon Phantom True Balloon; distortions Phantom True Balloon Spheric Volume template Phantom True Balloon Volumetric Volume with scan; sum pump of slices EF LV True Excised Spheric Volume hearts template LV True Excised Spheric Volume hearts template LV True Excised Bicubic Volume hearts spline LV True Excised Volumetric Volume hearts scan; sum of slices LV True Excised Pyramidal Volume hearts scan; sum of slices LV True In vivo Spheric Volume (balloon) template LV True In vivo Volumetric Volume (balloon) scan; sum of slices LV Balloon Exptl Cylindrical Volume

11

2

29

1

11

3 4

28

3

11

-1

7

13

12

0.8 ±

14

3

14

2.

11

6±

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in heart

animals

LV

Doppler

LV

MRI

Normal subjects Normal subjects

LV

Angio

Patients

LV

RNA

Patients

LV

MRI

Patients

LV

RNA

Patients

LV

MRI

Patients

LV

Angio

Patients

LV

MRI

Patients and normal subjects

Spheric SV template Polyhedral EDV

14

2

15

4.

ESV Polyhedral EDV

39

10

51

8 — 10

26

8

25

7 4 5

12

<

16

< < 1.9 ±

ESV EF Polyhedral EF surface Polyhedral EDV surface ESV EF Volumetric EF scan; sum of slices Polyhedral EDV surface ESV EF Polyhedral EDV surface ESV Volumetric EDV scan; sum of slices

46

6

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LV

LV

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Angio

Angio, RNA, MRI

Patients

Patients

ESV EF Volumetric Volume scan; sum of slices EF Bicubic EDV spline

24

3 3 3

10

3 6

ESV 3 EF 3 RV True Heart Volumetric Volume 15 4 casts scan; sum of slices RV MRI Patients Volumetric EDV 16 4 scan; sum of slices ESV RV MRI Children Volumetric EDV 13 1.4 ± scan; sum of slices Angio, ventricular angiography; EDV, end-diastolic volume; EF, ejection experimental; LV, left ventricle; MRI, magnetic resonance imaging; RNA, r standard deviation; SEE, standard error of the estimate; SEM, standard error and a change in ejection fraction of 2% when a rotational scan is performed at 16-degree increments.[150] Another observer variability study found that three-dimensional echocardiography can detect a smaller change in left ventricular volume (11 to 13 mL) with 95% confidence than twodimensional echocardiography, which can only detect change that exceeds 21 to 24 mL.[69] However, no difference in variability was found between two-dimensional and three-dimensional measurement of mass.[69] An advantage also accrues to clinical research, since fewer patients need be enrolled in a clinical trial to obtain statistical power to detect a treatment effect.[151] Aid to Clinical Image Acquisition

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227

Unlike other tomographic imaging modalities, standard ultrasonographic image acquisition is heavily dependent on the skill and experience of the sonographer. It is often difficult to obtain standard views of the right ventricle.[14] Studies have shown that even standard views of the left ventricle are difficult to acquire consistently in the prescribed location, even by experienced sonographers. [33] Consequently, referral centers frequently repeat studies rather than trusting a study from an outside hospital or clinic. The resulting worsening of medical costs and inefficiency can, however, by improved by three-dimensional technology. One approach is to assist the sonographer in locating anatomically correct image planes for the standard two-dimensional echocardiographic views. An image plane positioning error that foreshortens the long axis by 1 cm may underestimate left ventricular volume by 5%.[7] By tracking the transducer, a line of intersection can be displayed on the ultrasonographic image that indicates the current image plane's position in relation to a previously acquired scout image to provide visual guidance (Fig. 10-25) . Such a system has been shown to reduce interobserver variability to one third the level observed for unguided measurements.[152] Performing three-dimensional echocardiography, which does not require standard views, yielded more accurate and reproducible ejection fraction determinations by novice sonographers that approached the performance of experts using twodimensional echocardiography in accuracy and reproducibility of ejection fraction determination.[153] Experts were always more accurate than novices for either three-dimensional or two-dimensional measurement, but the three-dimensional technology allowed novices to acquire Figure 10-25 Visual guidance to facilitate ultrasonogram acquisition in the anatomically correct spatial planes. A and B, A line of intersection indicates the spatial location of the current image plane where it intersects with "scout" images previously acquired in orthogonal views. C and D, More guidance is provided when the spatial orientation as well as location of the current image plane (translucent image) are displayed relative to the scout images.

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data sets of diagnostic quality. It is speculated that three-dimensional

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echocardiography may permit echocardiography in regions lacking skilled sonographers, if combined with remote expert interpretation. Modeling Three-dimensional echocardiography offers the ability to reconstruct the chambers, valves, and other structures of the heart in the highest spatial and temporal resolution of any imaging modality. These data have many potential uses. For example, surgeons involved in designing a total artificial heart have sought improved annular definition for planning inflow and outflow ports of the device. [154] Reconstructions of the endocardium and epicardium are useful for finite element analysis of left ventricular stress and material properties. [155] Heart reconstructions can also be used to model the stress and fatigue of pacemaker leads in any combination of implantation configurations[105] [156] (Fig. 10-26) . Three-dimensional echocardiographic reconstructions of valve geometries seen in mitral stenosis have been used to generate models by stereolithography for analysis of the relationship between cardiac structure, pressure, and blood flow.[157]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Three-dimensional echocardiography has the potential to become a major clinical imaging modality because it Figure 10-26 Reconstruction of a normal right ventricle illustrating its use for measuring various internal dimensions, such as the distances spanning the apex and centroids of the tricuspid and pulmonary valves (white lines). (From Sheehan FH, McDonald AL, Bolson EL: Paper presented at 11th International Conference on Mechanics in Medical Biology, April 2–5, 2000, Maui, Hawaii.)

offers realistic visualization and accurate quantitation in combination with ultrasonography's traditional advantages of cost, portability, and freedom from ionizing radiation. These qualities already make three-dimensional echocardiography a valuable and productive tool for clinical research. Application of three-dimensional echocardiography to the clinical environment awaits the development of automated image analysis.

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Section 3 - Ischemic Heart Disease

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Chapter 11 - The Role of Echocardiographic Evaluation in Patients Presenting with Acute Chest Pain to the Emergency Room Diagnosis, Triage, Treatment Decisions, Outcome Samuel Wang MD Kirsten E. Fleischmann MD, MPH

Background and Principles Several million patients in the United States each year present to emergency rooms with chest pain suggestive of acute coronary syndrome. However, a minority of these patients are ultimately diagnosed with myocardial ischemia or infarction.[1] [2] Conversely, approximately 5% of those with acute myocardial infarction are mistakenly discharged from the emergency room.[3] [4] A considerable body of evidence has accumulated since the 1980s supporting the hypothesis that early treatment of myocardial infarction improves the rate of coronary arterial patency, myocardial salvage, and patient survival.[5] [6] [7] [8] [9] Thus, it is clear that

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early diagnosis and treatment of acute chest pain have significant benefits for the individual patient, and for the society that finances the health care. The diagnosis of myocardial infarction is usually made on the basis of the patient's clinical history, electrocardiogram (ECG), and serum cardiac enzyme levels. Although these three methods in combination provide a relatively effective diagnostic approach, each has its own limitations. Patients presenting with "atypical chest pain" not infrequently rule in for myocardial infarction; on the other hand, patients presenting with symptoms typically associated with acute coronary syndrome may not, in fact, have myocardial ischemia or infarction. Although ST-segment changes on ECG provide a useful diagnostic tool for acute coronary syndrome, they may be absent in the initial ECG in a significant portion of patients who subsequently 236

meet the criteria for myocardial infarction. Pericarditis or prior myocardial infarction with aneurysm formation can cause ECG changes similar to those in acute myocardial infarction; the examination of subsequent ECGs in the former case and comparison with previous ECGs in the latter may help with differential diagnosis. The presence of pre-existing left bundle branch block (LBBB) results in baseline repolarization abnormalities that limit the utility of ECG in the diagnosis of acute myocardial infarction in these patients. Although a number of criteria have been proposed to discern indicators of acute myocardial infarction within the LBBB morphology,[10] these criteria have been found to be insensitive in the diagnosis of acute myocardial infarction.[11] Determination of serum cardiac enzyme levels constitutes a more sensitive and specific test.[12] However, serum cardiac enzyme levels may not be elevated until several hours after the onset of myocardial infarction; therefore, sole reliance on this method may delay starting appropriate treatment. Echocardiography can be a useful adjunct in the assessment of patients with chest pain. By evaluating global ventricular function as well as regional wall motion, echocardiography may allow the early diagnosis of myocardial ischemia and infarction, as well as determination of the coronary vascular territory involved. It is also useful in the differential diagnosis of acute chest pain by excluding such possibilities as aortic dissection, effusive pericarditis, and aortic stenosis among other conditions (Table 11-1) ; these topics are covered in greater detail in their respective

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chapters in this book. In the remainder of this chapter, we concentrate on the current and developing applications of echocardiography to the early diagnosis of acute coronary syndromes, as well as their advantages, limitations, and potential impact on patient management and outcome.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography and the Physiology of Acute Ischemia Acute ischemia results in a cascade of biochemical and physiologic changes in myocardial tissue.[13] When coronary flow is cut off, biochemical changes are quickly followed by abnormalities in diastolic and then systolic function. Moreover, these functional changes may precede development of classic electrocardiographic changes or even development of symptoms[14] and occur well before release of detectable amounts of enzyme markers such as creatine kinase and troponin. Thus, development of systolic regional wall motion abnormalities such as those TABLE 11-1 -- Goals of Echocardiography in Evaluation of Patients with Acute Chest Pain Diagnosis of acute coronary syndrome Determination of coronary vascular territory involved Assessment of the area of myocardium at risk Evaluation of global ventricular function Exclusion of other cardiac causes of chest pain Aortic dissection Pericarditis (with effusion) Aortic stenosis Hypertrophic cardiomyopathy detected by echocardiography occurs at a relatively early stage after onset of ischemia. This has led to considerable interest in the use of echocardiography to aid in the diagnosis and prognosis of acute coronary syndromes and in defining the coronary territory involved.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Aspects of Echocardiography in the Emergency Department Image Acquisition Echocardiographic examination of patients with chest pain in the emergency room should concentrate on the evaluation of biventricular function and global and regional left ventricular wall motion to look for evidence of cardiac ischemia or infarction. It should also screen for other possible nonischemic causes of chest pain such as aortic stenosis, hypertrophic cardiomyopathy, effusive pericarditis, and aortic dissection. The standard transthoracic two-dimensional echocardiographic views should be used for evaluation of all the left ventricular wall segments, including parasternal long-and short-axis, apical long-axis, and apical twoand four-chamber views (Fig. 11-1) . If adequate image quality cannot be achieved from the apex, subcostal four-chamber and short-axis views or parasternal short-axis views with the transducer moved more apically may be acquired instead. Off-axis or oblique views make interpretation of regional wall motion abnormalities more difficult and should be avoided. A well-trained and experienced sonographer or echocardiographer is essential in such a clinical setting. The sonographer should be trained to obtain the required images in an efficient manner, avoiding spending time on aspects of the examination not needed for immediate clinical use. Attention should be paid to proper patient positioning, use of appropriate transducers, and adjustment of machine settings. High-frequency transducers may improve the visualization of apical structures. In obese patients or those with chronic obstructive pulmonary disease, lowerfrequency (2.0 to 2.5 MHz) transducers and a subcostal window may be used to optimize the images. Colorization of two-dimensional echocardiographic images and, more recently, echo contrast have also been used to enhance visualization of the endocardial border.

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Optimization of endocardial border definition is of utmost importance. In addition to the standard techniques mentioned, newer imaging modalities such as second harmonic imaging and contrast echocardiography can be used for this purpose. Commercially available echocardiographic contrast agents contain air-filled microbubbles which are small enough to pass through the pulmonary circulation after intravenous administration. They opacify both ventricular cavities, allowing the border between myocardium and blood to be more easily identified (Fig. 11-2) . This technique is especially effective when combined with second harmonic imaging, which also improves the visualization of other cardiac structures.

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Figure 11-1 Still frames from the echocardiogram of a patient with acute chest pain, showing severe hypokinesis of the anterior, septal, and apical walls, in parasternal short-axis (A, diastole; B, systole) and apical fourchamber (C, diastole; D, systole) views.

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Figure 11-2 Improvement in left ventricular endocardial border delineation with the use of intravenous echocardiographic contrast and second harmonic imaging (A, without contrast; B, with echocardiographic contrast).

In an early study by Horowitz et al[15] on the use of echocardiography in patients with acute chest pain, adequate images were obtained in 81% of the patients. A large, multicenter study performed in Denmark in the early 1990s involving 7001 patients early after an acute myocardial infarction reported assessable echocardiograms in 93% of the patients.[16] With continual advances in echocardiographic technology since that time, one can expect to obtain adequate echocardiograms in an even larger proportion of patients. Stress Echocardiography Multiple studies have demonstrated the safety of stress testing if myocardial infarction and unstable angina are ruled out after several hours

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of observation. Echocardiographic imaging may be used in conjunction with exercise or pharmacologic stress to assess for ischemia, depending on the patient's ability to perform adequate exercise. For exercise stress, one of the standard treadmill exercise protocols, such as the Bruce or modified Bruce protocol, can be used. Because wall motion abnormalities associated with exercise may be ephemeral after treadmill exercise terminates, echocardiographic examination should start within a few seconds after exercise terminates. This helps avoid significant decrease in heart rate below the maximum achieved, which may have an impact on the sensitivity of the test. An alternative exercise method is the supine bicycle protocol. A patient in a supine position exercises on a specially designed bicycle mounted on the echocardiographic examination table. The amount of energy spent increases with each 3-minute exercise stage. In this approach, echocardiographic images can be acquired during exercise, thereby eliminating the delay seen with treadmill exercise between the cessation of exercise and the start of imaging. In addition, images can be recorded at low, medium, and peak levels of exercise stress for comparison in this protocol, whereas only preand poststress images are generally recorded for treadmill protocols. The supine bicycle exercise protocol is preferred if spectral Doppler echocardiographic measurement of tricuspid regurgitation velocity is required for estimation of pulmonary artery systolic pressure. For patients unable to achieve adequate levels of exercise, pharmacologic stress testing can be performed. The intravenous dobutamine protocol is most commonly used in the United States. After acquisition of baseline resting echocardiographic images, dobutamine infusion is generally started at 5 µg/kg/minute, and increased to 10, 20, 30, and 40 µg/kg/minute at each successive stage of 3-minute duration. The test is terminated if the patient develops evidence of cardiac ischemia, hypotension as a result of vasodilation or left ventricular outflow obstruction, significant arrhythmia, or other dobutamine-related side effects or if 85% of maximum predicted heart rate is achieved. In patients who do not achieve adequate heart rate with dobutamine infusion at 40 µg/kg/minute, such as those taking beta blockers, atropine may be administered intravenously with doses of 0.1 to 0.25 mg each, up to a total of 1 mg. Second harmonic imaging has also been found to improve endocardial border definition, diagnostic accuracy,

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and interobserver agreement for dobutamine stress echocardiography in patients with impaired image quality. In a study by Franke et al,[17] second harmonic imaging without use of echocardiographic contrast increased the sensitivity for the diagnosis of coronary artery disease in patients with poor image quality from 64% to 92% (P < .001). Specificity was 75% for both imaging modalities. Improvement in endocardial border delineation was most pronounced in all lateral and anterior segments. Image Interpretation The accurate interpretation of regional wall motion abnormalities requires an experienced echocardiographer. Using various views from the study, wall thickening and systolic endocardial motion are evaluated for all left ventricular myocardial segments. Each segment is classified as hyperkinetic, normal, hypokinetic, akinetic, or dyskinetic. The American Society of Echocardiography recommends a 16-segment model for evaluation of regional wall motion (Fig. 11-3) .[18] Each segment is assigned a score on the basis of visual inspection of its contractility: normal, 1; hypokinesis, 2; akinesis, 3; dyskinesis 4; and aneurysm, 5. A semiquantitative measure of the extent of regional wall motion abnormalities, known as the wall motion score index (WMSI), can be calculated by averaging wall motion scores for all visualized segments. A normal left ventricle has a WMSI of 1, while a ventricle with more significant left ventricular dysfunction would have a higher WMSI. WMSI has been found to relate to infarct size on clinicopathologic studies[19] and to perfusion defect size on single photon emission computed tomographic (SPECT) imaging.[20] A similar wall motion index using a 14-segment model has also been found to be a predictor of long-term survival in patients with chest pain.[21] The evaluation of stress-induced regional wall motion abnormalities in stress echocardiography requires careful comparison of rest and stress images, which is facilitated by digital acquisition and display of such images. ECG-gated digital acquisition allows video clips lasting one to several cardiac cycles to be captured and stored in memory. Thus, several clips can be acquired and the most satisfactory one for each view selected for repeated comparative display. Comparison of rest and stress images from each view is facilitated by the use of side-by-side quad-screen display of synchronized cineloops. Digital image acquisition and display in stress

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echocardiography have been found to have comparable diagnostic accuracy for coronary artery disease to videotape recording, and superior interobserver and intraobserver agreement.[22] [23] Mohler et al[24] compared digital echocardiographic images with videotape images in a prospective study involving 117 patients admitted to the emergency department with chest pain and found 94% overall agreement regarding regional wall motion and good correlation in WMSI determined using these two different technologies. The authors concluded that digital echocardiographic imaging provides an accurate summary of the complete examination, as well as relevant diagnostic data for assessment of Figure 11-3 A 16-segment model for evaluation of regional wall motion as recommended by the American Society of Echocardiography. A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; PL, posterolateral; PS, posteroseptal. (Adapted from Schiller NB, Shah PM, Crawford M, et al: J Am Soc Echocardiogr 1989;2:358–367.)

patients presenting with chest pain to the emergency department.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

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Clinical Applications Triage of Patients with Chest Pain in the Emergency Department A number of studies have assessed the use of two-dimensional transthoracic echocardiography or stress echocardiography in evaluating patients presenting with chest pain and suspected acute coronary syndrome. [15] [25] [26] [27] [28] [29] [30] [31] [32]

Horowitz et al[15] studied 80 patients who presented with acute chest discomfort to the emergency department and had no previous myocardial infarction, valvular heart 240

disease, cardiomyopathy, or significant pericardial effusion. Twodimensional echocardiography was performed within 8 hours of admission. Locations of regional wall motion abnormalities were described using a five-segment model, with septal, anterior, posterolateral, posterior, and apical segments. The echocardiograms were technically inadequate in 15 patients (19%) in this study performed in the early 1980s. Of the 33 patients with clinical evidence of myocardial infarction, 31 had regional wall motion abnormalities on the initial echocardiogram (sensitivity, 94%). The other 2 patients had uncomplicated nontransmural myocardial infarctions. In comparison, the initial ECG was diagnostic of acute myocardial infarction in 45%, and the initial creatine kinase-MB level was elevated in 52%. Of the 32 patients without clinical myocardial infarction, 27 had normal regional wall motion on the initial echocardiogram (i.e., specificity, 84%). It is noteworthy that none of the patients with normal regional wall motion on the initial echocardiogram had an in-hospital clinical complication. In the late 1980s, Sabia et al performed a prospective study using two-

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dimensional echocardiography in 180 consecutive patients who presented to the emergency department with symptoms suggestive of acute myocardial infarction.[27] [33] The echocardiographic findings were not utilized in actual patient management but in assessing the diagnostic accuracy and cost of an alternate management scenario. The echocardiograms were technically inadequate in 6%. Regional wall motion was assessed using a 12-segment model. Among the 30 patients with acute myocardial infarction, 9 had ST-segment elevation on ECG (sensitivity, 30%), 3 had normal ECGs, 8 had ECGs with LBBB, paced rhythm, or other baseline repolarization abnormalities that make the diagnosis of acute myocardial infarction impossible, and 10 had nonspecific ECG findings. Twenty-nine of these 30 patients with acute myocardial infarction had technically adequate echocardiographic studies. Twenty-seven had regional wall motion abnormalities (sensitivity, 90%). Among the 13 patients with in-hospital complications, all had regional wall motion abnormalities on the initial echocardiogram, whereas only 4 had ST-segment elevation on the initial ECG. Sabia et al proposed an alternate scenario for the management of patients who present to the emergency department with possible acute myocardial infarction.[33] Those with acute ST-segment elevation on ECG would be admitted to the coronary care unit. The others would undergo twodimensional echocardiography. If the study was technically inadequate, admission to the hospital would be decided using conventional criteria. For patients with technically adequate studies, those with regional wall motion abnormalities would be admitted to the hospital, and those with normal wall motion or with global dysfunction would be discharged. If this scenario is applied to the set of study patients, hospital admissions are reduced by 32% (coronary care unit admissions by 25%, and non-coronary care unit admissions by 41%), total hospital stay for all patients is reduced by 23%, and estimated total cost is 24% lower. Under this scenario, two patients with small acute myocardial infarctions and no complications would be sent home. In comparison, two patients with larger acute myocardial infarctions were sent home using the conventional criteria and one of them had a complication after acute myocardial infarction (complete heart block requiring permanent pacemaker). The authors concluded that two-dimensional echocardiography is superior to conventional criteria in the diagnosis of patients with suspected acute myocardial infarction in the prediction of in-hospital complications and in reducing hospital admissions and total cost. This conclusion would be strengthened by further prospective validation in a different cohort of patients.

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Use in Chest Pain Centers and Clinical Algorithms Specialized chest pain centers have been established to evaluate patients presenting with acute chest pain with published studies describing clinical outcome in patients treated according to a chest pain algorithm.[34] For example, Gibler and coworkers published results from their "Heart ER Program," a diagnostic and treatment program for patients with chest pain in an urban tertiary care emergency department.[35] Their initial evaluation algorithm is summarized in a flow diagram in Figure 11-4 . A total of 1010 patients with symptoms suggestive of acute coronary syndrome were enrolled over a 32-month period. Patients with known coronary artery disease, acute ST-segment elevation or depression of greater than 1 mm, hemodynamic instability, or clinical presentation consistent with unstable angina were directly admitted to the hospital. Other patients were entered into the 9-hour evaluation program during which creatine kinase-MB levels were checked on presentation and every 3 hours afterwards for three times and 12-lead ECG or ST-segment was continuously monitored. After the 9hour evaluation period, two-dimensional echocardiography and graded exercise testing were performed in the emergency department and used to reach discharge decisions. Of the 1010 patients, 829 (82.1%) were discharged from the emergency department, and 153 (15.1%) were admitted to the hospital for further evaluation. Among the 153 admitted patients, 52 (33.9%) were found to have a cardiac cause for their symptoms; 43 (28.1%) had acute coronary syndrome (12 with acute myocardial infarction, 31 with myocardial ischemia). The authors concluded that the "Heart ER Program" provides an effective approach for evaluation of low- to moderate-risk patients with possible acute coronary syndrome in the emergency department. Trippi et al[28] reported a clinical trial using dobutamine stress echocardiography for evaluation of patients presenting with chest pain to the emergency room to determine who can be safely discharged from the emergency department. The echocardiograms were digitized for electronic transmission according to their tele-echocardiography protocol. One hundred sixty-three patients with negative results on initial ECGs and blood studies who were recommended for hospital admission to rule out myocardial infarction or ischemia were evaluated. Rest echocardiography was performed in the emergency room and transmitted to an interpreting cardiologist. If the echocardiogram

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Figure 11-4 Chest pain evaluation algorithm used in the Heart ER Program by Gibler and coworkers. ECG, electrocardiographic; CAD, coronary artery disease; CK-MB, creatine kinase-MB; 2D, twodimensional. (Data from Gibler WB, Runyon JP, Levy RC, et al: Ann Emerg Med 1995;25:1–8.)

was normal, dobutamine stress echocardiography was performed by a trained nurse, with images again transmitted to the cardiologist. The test was completed within an average of 5.4 hours after presentation to the emergency room. Using clinical follow-up data and cardiac catheterization as the gold standard, the authors determined the sensitivity of the test to be 89.5%, the specificity 88.9%, and the negative predictive value 98.5%. In a later phase of the trial, patients with normal dobutamine stress echocardiography were released from the hospital; these constituted approximately 72% of the patients. Assessment of the Need for Urgent Coronary Angiography Coronary angiography is generally regarded as the gold standard in the diagnosis of coronary artery disease. In patients with a nondiagnostic ECG and a high pretest probability of coronary artery disease, clinicians can elect to have patients proceed directly to coronary angiography, possibly followed by percutaneous coronary interventions. This modality yields accurate information of coronary anatomy and may lead to prompt revascularization, which improves myocardial salvage and survival in patients with acute coronary artery occlusion. It does not directly provide information on the functional significance of the coronary artery stenoses, which can only be inferred from the location and severity of stenosis. Echocardiography can assist in the decision concerning the need for urgent coronary angiography. Normal global and regional wall motion may persuade the clinician to take a more conservative approach, with later stress testing to rule out significant coronary artery disease. The finding of a new wall motion abnormality, however, may prompt more urgent coronary angiography and intervention. Risk Stratification and Analysis of Long-Term Clinical Outcome Various diagnostic tests have been studied for their prognostic value in the treatment of patients with acute coronary syndrome. Savonitto et al [36]

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performed a retrospective analysis of the presenting ECGs of patients enrolled in the Global Utilization of Strategies To Open 242

Occluded Arteries in Acute Coronary Syndromes (GUSTO-IIb) study and found the 30-day incidence of death or myocardial reinfarction to be 5.5% in patients with T-wave inversion, 9.4% in patients with ST-segment elevation, 10.5% in patients with ST-segment depression, and 12.4% in patients with ST-segment elevation and depression (P < .001). Compared with those who had T-wave inversion only, the odds ratios (OR) of 30-day death or reinfarction remained higher for those with ST-segment elevation (OR, 1.68; 95% confidence interval [CI], 1.36–2.08), for those with STsegment depression (OR, 1.62; 95% CI, 1.32–1.98), and for those with STsegment elevation and depression (OR, 2.27; 95% CI, 1.80–2.86) after multivariate adjustment for other risk factors. Initial elevation in creatine kinase level is also associated with greater risk of death and reinfarction, as is elevation in serum troponin levels. [37] [38] [39] A number of studies have demonstrated the incremental utility of echocardiography, beyond clinical assessment and electrocardiography, in predicting clinical outcome of patients with acute chest pain.[40] [41] In a prospective study involving 466 visits to a large urban emergency department by patients with acute chest pain, Fleischmann et al[40] examined echocardiographic predictors of serious predischarge complications in patients with chest pain. Doppler echocardiograms were performed an average of 21 hours after presentation and used to assess global biventricular function, regional wall motion, and valvular disease. Regional wall motion was assessed using a wall motion index on the basis of a 14segment model. The composite complications end point included significant recurrent myocardial ischemia, heart failure, or arrhythmia. In univariate analysis, the following variables predicted complications: left ventricular function (OR, 2.9; 95% CI, 1.6–5.1), right ventricular function (OR, 2.7; 95% CI, 1.2–6.2), left ventricular end-diastolic dimension Figure 11-5 Kaplan-Meier survival curves for patients presenting with chest pain stratified by left ventricular function. LVD, left ventricular dysfunction. (From Fleischmann KE, Lee RT, Come PC, et al: Am J Cardiol 1997;80:1266–1272, with permission from Excerpta Medica Inc.)

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(OR, 1.6/cm; 95% CI, 1.1–2.3), left ventricular end-systolic dimension (OR, 1.4/cm; 95% CI, 1.1–1.9), and wall motion index (OR, 3.0; 95% CI, 1.8–4.8). In multivariate analysis, wall motion index remained an incremental predictor of subsequent complications beyond clinical and electrocardiographic variables. In a companion study involving 448 patients, the long-term survival of these patients was examined.[21] The follow-up period was 35.0 ± 12.1 months. In univariate Cox regression analysis, left ventricular function and size, wall motion index, right ventricular function, and aortic, mitral, and tricuspid regurgitation were significant predictors of total and cardiovascular mortality. In multivariate analysis involving a model adjusted for clinical and electrocardiographic data, the following were found to be independent predictors of mortality: moderate or severe left ventricular dysfunction (mortality rate ratio, 3.2; 95% CI, 1.8–5.8), and more than mild valvular regurgitation (mortality rate ratio, 2.0; 95% CI, 1.1–3.6). These two echocardiographic findings offer incremental prognostic value over clinical and ECG information alone in patients presenting with acute chest pain syndrome. Kaplan-Meier survival curves for these patients stratified by left ventricular function and by the grade of mitral regurgitation are shown in Figure 11-5 and Figure 11-6 , respectively. Chuah et al,[42] from the Mayo Clinic, examined the incremental utility of dobutamine stress echocardiography over clinical and rest echocardiographic variables in predicting outcome in a cohort of 860 patients with known or suspected coronary artery disease. The patient population in this study was not restricted to patients presenting to the emergency room with chest pain. Semiquantitative evaluation of regional wall motion was performed using the WMSI on the basis of the 16-segment model of the American Society of Echocardiography. The patients were followed for up to 52 months. End points consisted 243

Figure 11-6 Kaplan-Meier survival curves for patients presenting with chest pain stratified by grade of mitral regurgitation (MR) (on a 4+ scale). (From Fleischmann KE, Lee RT, Come PC, et al: Am J Cardiol 1997;80:1266–1272, with permission from Excerpta Medica Inc.)

of cardiac death and myocardial infarction. Seventy-two patients underwent

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coronary artery revascularization before any cardiac event during the follow-up period and were censored. Nonfatal myocardial infarction occurred in 36 patients, and cardiac death in 50 patients. Using a stepwise Cox multivariate regression model involving clinical and rest and stress echocardiographic data, the following were found to be independent predictors of cardiac events: a history of congestive heart failure (hazard ratio, 2.51; 95% CI, 1.54–4.07), the percentage of abnormal segments at peak stress (hazard ratio, 1.14; 95% CI, 1.05–1.23), and an abnormal left ventricular end-systolic volume response to stress (Hazard ratio, 1.98; 95% CI, 1.14–3.46). The model that incorporated clinical and stress echocardiographic data was found to be the best at predicting subsequent cardiac events. Evaluation of Other Causes of Chest Pain Although determination of global systolic function and regional wall motion is of paramount importance in the evaluation of patients presenting with acute chest pain to the emergency department, rapid screening for certain other causes of chest pain should not be neglected, especially in those patients whose presentation appears atypical for ischemic chest pain. Aortic dissection is potentially life-threatening and may be seen on transthoracic echocardiogram, although sensitivity is limited, precluding its use as a first-line imaging technique to exclude dissection. Evidence of an intimal flap may be seen in the aortic root and proximal ascending aorta on the parasternal long-axis view, in the aortic arch on the suprasternal view, and in the descending abdominal aorta on the subcostal view (Fig. 11-7) . The descending thoracic aorta cannot be adequately examined on a transthoracic study, however. In a series of 67 patients from the Mayo Clinic, the sensitivity of transthoracic echocardiogram was 79%, and the positive predictive value was 91%.[43] Transesophageal echocardiography Figure 11-7 Suprasternal view from a transthoracic echocardiogram demonstrating an aortic dissection involving the aortic arch and the ascending aorta.

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(TEE; especially multiplane) is a more sensitive and specific technique for

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examination of the thoracic aorta and should be performed if there is clinical suspicion of aortic dissection. Effusive pericarditis can be easily diagnosed, and the size of the pericardial effusion can be assessed on the transthoracic echocardiogram. The subcostal window is especially useful for this purpose even in patients in whom poor image quality is achieved on parasternal or apical views. The potential hemodynamic consequences of the pericardial effusion may be evaluated with examination of right heart chambers for collapse, Doppler echocardiography of mitral and tricuspid inflow velocities, and twodimensional examination of the inferior vena cava and its variation in size with inspiration. If pericardiocentesis is desired for diagnostic or therapeutic purposes, echocardiographic guidance can facilitate safe performance of the procedure. [44] [45] [46] [47] Rapid screening for aortic stenosis can be made with Doppler measurement of transaortic valvular flow velocity and two-dimensional examination of calcification and motion of the aortic valve leaflets. Similarly, assessment for echocardiographic evidence of hypertrophic obstructive cardiomyopathy can be made with measurement of septal thickness, detection of systolic anterior motion of the mitral valve leaflet, and Doppler echocardiographic measurement of a significant gradient in the left ventricular outflow tract.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Cost-Effectiveness Analysis Rapid advances in science and technology in the past century have improved the quality of health care and have also resulted in a great increase in health care costs. This development has generated increasing interest in applying the techniques of cost-effectiveness analysis to evaluate preventive, diagnostic, and therapeutic strategies in medicine. Table 11-2 lists key terms used in cost-effectiveness analysis. In formal cost-effectiveness analysis, cost is expressed in terms of monetary units, and effectiveness is expressed in units such as the number of lives saved, the years of life saved, the days of disability avoided, and so on. [48] To analyze difficult and complex clinical problems for which no clear consensus exists among experts, a clinical decision model may be constructed to outline explicitly various diagnostic or therapeutic options, and the possible clinical events and outcomes. Probabilities for various clinical events and outcomes can be estimated on the basis of the best available current evidence from the medical literature or, if this is not available, from the physicians' clinical judgment. Each possible outcome is assigned a cost and a utility. By convention, perfect health is assigned a utility value of 1, and death is assigned a value of 0. Various schemes have been devised to assign utility values to different degrees of disease or symptom severity. Thus, cost and health benefit can be calculated for the various options under consideration. The conclusions drawn from any type of clinical decision analysis can only be as accurate as the assumptions on which the model is based. In cases in which the TABLE 11-2 -- Key Terms in Cost-Effectiveness Analysis Cost: amount of resource required, usually expressed in monetary units. Effectiveness: health benefit achieved, commonly expressed in units such as the number of lives saved, the days of disability avoided, the years of

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life saved, and so on. Clinical decision model: a model of the clinical problem, usually constructed in the form of a decision tree, in which various diagnostic or therapeutic options are outlined, and the possible clinical events and outcomes are enumerated and assigned probabilities and utilities. This can be used to analyze the cost or health benefit of various options. Utility: the benefit associated with a specific outcome. By convention, perfect health is assigned a value of 1, and death is assigned a value of 0. Sensitivity analysis: an analysis in which certain parameters in the clinical decision model are systematically varied over reasonable ranges, so as to determine whether the results of the model are significantly affected. This is especially important if there is significant uncertainty or variability in the values of certain parameters. QALY: quality-adjusted life-year. Incremental cost-effectiveness: additional cost-effectiveness of a new strategy compared with the baseline strategy. parameters in the model can vary over a certain range or in which there is uncertainty regarding their values, it is critical to determine whether variation of parameter values over reasonable ranges significantly affects the results of the analysis. This process is referred to as sensitivity analysis. Given the results of a cost-effectiveness analysis, the decision about whether it is worthwhile to spend a certain additional amount to achieve an incremental benefit will depend on the society's values and socioeconomic conditions. In many analyses of health care delivery in the United States, the cost of renal dialysis (approximately $35,000 to $40,000 per patient per year in 1995) is often used as the benchmark for the cost that the American public is willing to bear to prolong life by 1 year. Data on the cost-effectiveness of echocardiography in patients presenting to the emergency department with acute chest pain are scarce. In more general cost-effectiveness analyses of diagnostic strategies for patients with chest pain, most studies have found the preferred initial strategy to be noninvasive testing for patients with low to intermediate pretest probability of coronary artery disease, and coronary angiography for those with high pretest probability. In a study by Kuntz et al,[49] exercise echocardiography cost $41,900 per quality-adjusted life-year (QALY) saved compared with exercise electrocardiography for 55-year-old men with atypical angina.

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Exercise SPECT cost $54,800 per QALY saved compared with exercise electrocardiography for these patients. The incremental cost-effectiveness ratio of routine coronary angiography compared with exercise echocardiography was $36,400 per QALY saved for 55-year-old men with typical angina. For 55-year-old men with nonspecific chest pain, the incremental cost-effectiveness ratio of exercise electrocardiography compared with no testing was $57,700 per QALY saved. The authors concluded that exercise electrocardiography or exercise echocardiography resulted in reasonable cost-effectiveness ratios for patients 245

at mild to moderate risk for coronary artery disease in terms of age, sex, and type of chest pain. Garber and Solomon analyzed the cost-effectiveness of five test strategies for patients with a history of chest pain and intermediate pretest probability (25% to 75%) of coronary artery disease.[50] These strategies involved a noninvasive test (treadmill exercise testing, planar nuclear imaging, SPECT, stress echocardiography, or positron emission tomography) followed by coronary angiography if the noninvasive test was positive. Using information from published literature on the sensitivity and specificity of each test, disease prevalence, and treatment efficacy, and basing cost calculations on Medicare payments, the authors developed a decision analytic model to assess the health outcomes and costs of the different strategies. They found that stress echocardiography improved health outcomes and reduced costs relative to exercise stress testing and planar nuclear imaging. The incremental cost-effectiveness ratio was $75,000 per QALY for SPECT relative to echocardiography, more than $640,000 per QALY for positron emission tomography relative to SPECT, and $94,000 per QALY for immediate coronary angiography relative to SPECT. The authors concluded that stress echocardiography, stress SPECT, and immediate coronary angiography are cost-effective alternatives to positron emission tomography and other strategies. Exercise treadmill testing for assessment of chest pain or risk stratification has been found to be cost-efficient even if greater expense is incurred when such tests are performed outside of regular laboratory hours. Krasuski et al [51] studied 195 patients scheduled for exercise stress testing during weekends or holidays for assessment of chest pain (75%) and other indications; the study population was not limited to chest pain patients from

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the emergency department. The authors found the approach to be safe and effective for risk stratification and to shorten hospital stay. Although a formal cost-effectiveness analysis was not performed in this study, this approach was found to result in cost savings even when the greater expenses associated with testing during weekends or holidays were taken into consideration. For a general discussion of cost-effectiveness analysis for noninvasive diagnostic testing for coronary artery disease, refer to the paper by Hunink et al.[52]

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Limitations Limitations in the Use of Regional Contractile Function to Evaluate Ischemia Evaluation of acute coronary syndrome with echocardiography has several limitations. Between episodes of cardiac ischemia, the patient's wall motion may be completely normal. Therefore, a normal resting echocardiogram performed in such a patient cannot rule out cardiac ischemia as the cause of the patient's symptoms. Stress testing should be considered after myocardial infarction is ruled out. The presence of pre-existing left ventricular dysfunction secondary to nonischemic cardiomyopathy or valvular heart disease makes the evaluation of new regional wall motion abnormalities more difficult and may cause the specificity of this technique to be lower for this population of patients. Image Quality The detection of regional wall motion abnormalities requires adequate visualization of endocardial borders. In patients with morbid obesity, chest wall deformity, chest trauma, or recent thoracic surgery, views with good image quality may be difficult to acquire, especially given the time constraints imposed by the need for rapid diagnosis and institution of therapy. The use of newer echocardiographic modalities, such as second harmonic imaging with echocardiographic contrast administration, may improve endocardial border delineation in such patients and make echocardiographic evaluation in the emergency department more practical. Personnel Availability Ready availability of sonographers to perform echocardiographic examinations and echocardiographers to interpret them is essential if

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echocardiography is to enjoy more widespread use in the evaluation of patients with chest pain in the emergency department. This is not a problem during usual working hours in most hospitals. However, it may not be economically practical to have the personnel physically "on call" in the hospital 24 hours a day for most community hospitals or even tertiary medical centers. Contacting sonographers and echocardiographers on call outside of the hospital inevitably causes a delay in the management of such patients. One approach to deal with this problem is to train emergency department personnel to perform echocardiograms. An obstacle to successful implementation of this approach is the difficulty in gaining and maintaining sufficient experience in performing echocardiographic studies in the context of the rotating shift system in most emergency departments. This logistical problem may be at least partially solved with the advent of digital tele-echocardiography systems. Acquired images can be transmitted over a high-speed network to an experienced echocardiographer outside the hospital for immediate interpretation. Future systems may incorporate the capability for greater real-time interaction between the off-site interpreting physician and the on-site sonographer to ensure the acquisition of all requisite images for any particular clinical situation.

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Future Developments Tele-echocardiography The accurate interpretation of stress echocardiographic images requires experienced echocardiographers, who may not be immediately available in the hospital during off-hours. Having an experienced echocardiographer available in the hospital 24 hours a day or to come into 246

the hospital when such cases occur may not be practical in many hospitals. In addition, the latter option may further delay definitive treatment. Electronic transmission of echocardiographic images has been used as part of telemedicine projects in a number of centers. In nonemergency settings, successful use has been reported in the difficult diagnostic cases requiring expert interpretation, such as patients with congenital heart disease.[53] [54] [55] In the clinical trial by Trippi et al[28] using dobutamine stress echocardiography to determine which patients presenting with chest pain to the emergency room may be safely discharged, the echocardiograms were digitized into a quad-screen systolic eight-frame cineloop format with resolution of 320 by 240 pixels, and transmitted to the interpreting physician over the standard telephone line using a proprietary "lossless" format developed before DICOM standards.[56] [57] The test was completed within an average of 5.4 hours after presentation to the emergency room. It was found to have very good sensitivity and specificity and could potentially result in significant cost savings, as discussed previously in the section on Clinical Applications. Rapid technologic developments since that time, including faster processor speed, availability of higher capacity random access memory, and faster network connections via the Internet or dedicated lines may result in more

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widespread use of this technology. Of course, the transmission of patientspecific data over publicly accessible networks will require proper encryption to ensure patient privacy. Myocardial Contrast Echocardiography The use of echocardiographic contrast with second harmonic imaging to evaluate myocardial perfusion is one of the most exciting developing areas of echocardiography. Ultrasonographic imaging for this purpose needs to be intermittent so as to minimize the destruction of micro-bubbles in the contrast agent. This technique, when perfected, has potential uses in the diagnosis of acute myocardial infarction, determination of ischemic and infarcted areas in conjunction with stress testing, evaluation of reperfusion status, detection of no reflow in the microvascular coronary circulation after restoration of flow in the epicardial coronary arteries, and evaluation of myocardial viability. Although promising, this echocardiographic technique needs to be further refined before its utility in the examination of patients with acute chest pain syndrome can be evaluated. Other Modalities Doppler tissue imaging[58] [59] [60] and color kinesis[61] [62] (Fig. 11-8) are two of the promising new imaging modalities, although further studies are needed to determine their utility in routine assessment of regional wall motion.

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Chest Pain Centers Centers dedicated to diagnostic evaluation of patients presenting with chest pain suggestive of acute coronary syndrome have been set up in a number of medical centers in the United States, with the goal of improving the efficiency of evaluation while preserving or improving outcomes.[2] [34] [63] Most chest pain centers are based within the emergency department or in an adjacent observation unit. Others are located in a part of an inpatient telemetry unit. Patients presenting to the emergency department with chest pain are first stratified into several risk groups on the basis of their history, physical examination, and initial 12-lead ECG. High-risk patients, including those with significant acute ST-segment changes, hemodynamic instability, and known history of coronary artery disease, are admitted directly, usually to the coronary care unit. Those with acute ST-segment elevation or new LBBB will receive reperfusion therapy with thrombolytic agents or cardiac catheterization. Patients with low to moderate pretest probability of acute coronary syndrome, who have no contraindications to diagnostic testing according to the chest pain center protocol and no serious comorbid conditions that may interfere with discharge from the emergency department, are evaluated further in the chest pain center. Other low- to moderate-risk patients may be admitted to a step-down telemetry unit for further evaluation. Patients with noncardiac chest pain are treated and triaged according to their diagnosis. Although individual protocols vary, patients in the chest pain center often undergo serial cardiac enzyme marker determinations (e.g., at 0, 3, and 6 hours after presentation). Serial 12-lead ECGs or continuous ST-segment monitoring is also performed. The monitoring period generally ranges from 6 to 12 hours, although an experience with immediate stress testing in lowrisk patients has also been reported. [64] [65] Patients who develop evidence of acute coronary syndrome during the period of monitoring are admitted. The

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rest will undergo further diagnostic testing after the monitoring period for diagnosis of coronary artery disease and for risk stratification. A number of studies address possible choices for diagnostic testing in emergency department patients presenting with chest pain.[27] [28] [35] , [41] [66] [67] [68] [69] Graded exercise ECG testing is often obtained for those patients who can exercise to an adequate level, have no contraindications to exercise testing, and have no baseline ECG abnormalities that may interfere with the interpretation of stress ECGs. Exercise or pharmacologic stress imaging can be utilized in other patients. The incremental value and costeffectiveness of imaging for patients being evaluated in chest pain centers who can exercise requires further study, as suggested by the American Heart Association.[70] Stress testing is usually supervised by an appropriately trained physician and performed in a dedicated area with resuscitative equipment available and should conform to American Heart Association guidelines for exercise ECG laboratories.[70] [71] As mentioned in an earlier section, accurate acquisition and interpretation of stress echocardiograms requires an experienced sonographer and echocardiographer. Thus, the chest pain center performing stress echocardiography will need a physician experienced in echocardiography to be available on call in or near the hospital, unless tele-echocardiography equipment is available to transmit images to the interpreting physician. Patients 247

Figure 11-8 (color plate.) Tissue Doppler imaging (TDI; top) and myocardial velocity gradient (MVG; bottom) images of the left ventricle in the parasternal short-axis view from a patient with left anterior descending coronary artery obstruction: at baseline (left), with low-dose (10 µg/kg/min) dobutamine (middle), and with high-dose (30 µg/kg/min) dobutamine (right). In the TDI images, the anteroseptal wall is color-coded blue because it is moving away from the transducer during systole. Similarly, the posterior wall is color-coded red because it is moving toward the transducer. MVG is derived from TDI, and it is defined as the slope of the regression line of the intramyocardial velocity profile across the myocardium. It reflects regional wall thickening and has been shown to be independent of the translational motion of the heart. In the MVG images, thickening of the myocardium is color-coded red, and thinning of the myocardium is color-coded blue. Calculated segmental MVGs are shown beside the corresponding segments. In this patient, MVG undergoes a dose-responsive increase in the posterior segment and no significant change in the anteroseptal segment supplied by the diseased coronary artery. (From Tsutsui H, Uematsu M, Shimizu H, et

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al: J Am Coll Cardiol 1998;31:89–93. Reprinted with permission from the American College of Cardiology.)

with positive stress tests will usually be admitted for further evaluation; those with negative evaluations will generally be discharged from the chest pain center with careful attention to adequate outpatient follow-up. An important part of the work of a successful chest pain center involves community outreach to increase public awareness of the importance of seeking prompt medical attention for chest pain. This will further improve the clinical outcome of patients presenting to the emergency department with acute coronary syndrome.

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Summary Transthoracic, transesophageal, and stress echocardiography may all be useful in the evaluation of patients with acute chest pain presenting to the emergency department. Echocardiography can aid in the diagnosis of cardiac ischemia and myocardial infarction, help assess for other important causes of chest pain, and provide incremental prognostic information on both short- and long-term outcomes. New developments to enhance imaging and endocardial border definition, digital acquisition of images, tele-echocardiography, and the possibility of perfusion-based imaging using echocardiographic contrast promise to increase its utility even further in the future.

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251

Chapter 12 - Echocardiography in the Coronary Care Unit Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Elyse Foster MD Zian H. Tseng MD

The earliest experimental models of myocardial infarction demonstrated that regional wall motion abnormalities ensue shortly after cessation of coronary flow.[1] When a coronary artery is ligated, the first abnormality is an impairment in relaxation of the affected wall. The diastolic abnormalities are followed within seconds by the development of systolic contraction abnormalities. These systolic abnormalities can be readily detected by conventional echocardiographic methods and form much of the basis for the echocardiographic evaluation of ischemia. Although segmental abnormalities in diastolic function are not readily measured by conventional echocardiography, the available information regarding global diastolic dysfunction has recently been found to have important prognostic significance.

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Historical Perspective The use of echocardiography in patients with myocardial infarction occurred with the introduction of the first echocardiographic imaging techniques. [2] [3] [4] [5] M-mode echocardiography, with its high frame rate, permitted precise assessment of the reduction in wall thickening, but it was limited by its narrow view of the left ventricle. For example, fractional shortening, measured from the ventricular dimensions at the level of the basal septum and posterior wall, inaccurately represented global left ventricular function in patients with mid and apical wall motion abnormalities. Two-dimensional (2D) sector scanning, developed in the late 1970s, provided the necessary tomographic views for a complete evaluation of regional ventricular function. This bedside imaging method was soon employed widely for the early identification of apical aneurysms and thrombus formation[6] , [7] in patients with anterior myocardial infarction. Two-dimensional quantitative techniques also were developed that could accurately measure left ventricular ejection fraction in the presence of regional wall motion abnormalities. The role of right ventricular infarction in low output syndromes was appreciated,[8] [9] [10] and the high prevalence of post-myocardial infarction pericardial effusions was recognized.

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The introduction of spectral and color Doppler echocardiography in the mid-1980s further enhanced the role of echocardiography by providing essential hemodynamic information. In addition, timely noninvasive diagnosis of complications of acute myocardial infarction, such as mitral regurgitation and ventricular septal defects, was possible. Newer methods, such as tissue Doppler imaging and mitral flow propagation velocities,[11] have enhanced our capacity to define left ventricular diastolic function

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Transesophageal echocardiography allows better definition of the anatomic alterations responsible for the complications of acute myocardial infarction (e.g., papillary muscle rupture). Finally, the advances in digital imaging techniques since the 1980s have enabled the dissemination of stress echocardiography, which has assumed a major role in evaluation of patients with ischemic heart disease, as discussed in Chapter 13 and Chapter 14 . The portability of echocardiography and the extent of hemodynamic and anatomic information it provides ensure its place in the coronary care unit (CCU). Although its ability to provide direct information regarding coronary anatomy and myocardial perfusion have been limited to date, there is continued progress in these areas.

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Applicable Modes of Echocardiography Transthoracic echocardiography (TTE) provides a rapid bedside assessment of wall motion and global left ventricular function, and it excludes the presence of complications.[12] [13] In the patient presenting with chest pain who has a nondiagnostic electrocardiogram, identification of a segmental wall motion abnormality assists in the determination of definitive therapy. In the patient with an established myocardial infarction, early noninvasive evaluation of ejection fraction indicates therapy with beta blockers, angiotensin converting enzyme inhibitors, or both. When recurrent pain complicates reperfusion therapy, electrocardiographic changes may be nonspecific. In this situation, echocardiography helps differentiate between recurrent ischemia and pericarditis. Importantly, the cause of hemodynamic instability in patients with myocardial infarction often can be established without invasive monitoring. In patients with severe hemodynamic compromise, TTE may be limited by mechanical ventilation and an inability to adequately position the patient. In this group, transesophageal echocardiography (TEE) has proven to be efficacious, especially in ruling out complications related to cardiac rupture.[14] [15] [16] [17] [18] [19] [20] [21] [22] Although large numbers of patients with acute myocardial infarction have not been studied, with careful sedation and close monitoring, TEE can be performed safely.[23] [24] [25] Stress echocardiography has assumed an increasingly important role in assessing the postinfarction patient for evidence of myocardial viability and for assessing the risk for recurrent ischemia. Dobutamine echocardiography, using low doses that do not significantly alter hemodynamics, has been shown to improve function in viable myocardial segments. Higher doses of dobutamine as well as exercise echocardiography can be used to detect residual ischemia, but they should be used with caution early after myocardial infarction.[26] Although one study showed no increase in cardiac enzymes after dobutamine stress, [27]

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there are isolated case reports of free wall rupture in association with highdose dobutamine stress testing within the first week following myocardial infarction.[28] [29] Contrast echocardiography remains investigational for the evaluation of myocardial perfusion. Only one intravenous left-sided contrast agent is commercially available in the United States. Although this agent crosses the pulmonary circulation and opacifies the left ventricular cavity, in the approved dose ranges it does not routinely offer adequate assessment of myocardial perfusion. In a study using an investigational agent, a comparison between single photon emission computed tomography (SPECT) and myocardial contrast echocardiography (MCE) revealed limited sensitivity and high specificity for MCE detection of moderate or severe perfusion defects. MCE also underestimated the extent of SPECT defects. [30] The accuracy of MCE was enhanced by the combination of MCE and wall motion assessment.[30] [31] Rapid technologic developments in this field are under way. Saline contrast may be indicated for enhancement of tricuspid regurgitant jets in order to estimate pulmonary artery pressures and to exclude a patent foramen ovale in patients with cerebral embolization or hypoxemia in the setting of right ventricular infarction.[32] [33]

Although three-dimensional (3D) echocardiography has proved to be an important research tool, it has not yet been widely adopted in the clinical setting. Studies in canine models suggest that accurate quantitation of infarct size with and without the use of myocardial contrast may be possible in the future.[34] [35]

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Advantages and Limitations of Echocardiography in the Coronary Care Unit The major advantages to echocardiography in the CCU include its portability, noninvasive nature, and the wealth of anatomic and hemodynamic information provided. TEE, a semi-invasive technique, has an extremely low complication rate even among the most seriously ill.[36] [37] The limitations of echocardiographic evaluation include the limited transthoracic windows often encountered in the acutely ill coronary care patient, frustrating identification of important complications. Newer technologies such as tissue harmonics have enhanced endocardial border definition even in the most difficult patients. Another limitation is the largely qualitative analysis of regional wall motion abnormalities; quantitative techniques are cumbersome, require manual tracing, and, for the most part, have not been widely employed in the clinical setting.[38] [39] Nevertheless, surface echocardiography remains a mainstay of noninvasive diagnosis in the CCU.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Pathophysiology and Echocardiographic Correlations Timing and Evolution of Infarction The effects of acute coronary ligation in animal models of experimental myocardial infarction have been studied by echocardiography, leading to several observations: 253

1. Acute coronary ligation results in diminished systolic wall thickening and outward motion of the affected myocardial segment (dyskinesis) with close correlation between echocardiography and sonomicrometry. [40] [41] [42] [43]

2. The degree of dyskinesis produced was directly related to the severity of the perfusion deficit.[40] 3. Interventions during ischemia that increase afterload worsen wall motion, whereas afterload-reducing and inotropic agents improve wall motion.[40] [44] 4. The extent of wall motion abnormalities correlates with infarct size to a variable degree. In one study the wall motion abnormalities present at 2 hours following coronary ligation tended to overestimate infarct size because function had improved over the subsequent 48 hours. Although in this dog model echocardiographic infarct size even as predicted by late (48 hours) wall motion abnormalities correlated poorly with pathologic infarct size,[45] subsequent studies demonstrated that the extent of regional contraction abnormalities on 2D echocardiography with early (20 minutes) or late (2 days) echocardiography after permanent coronary occlusion correlated well with infarct size.[46] Despite these seemingly disparate results, these early studies provided a

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basis for clinical studies using echocardiography to measure the beneficial effects of pharmacologic interventions on infarct size.[47] [48] [49] [50] [51] Reperfusion Therapy, Myocardial Stunning, and Infarct Size Experimental studies have demonstrated that approximately 30 minutes following an acute coronary occlusion, a wavefront of myocardial necrosis begins to proceed from endocardium to epicardium, resulting in a transmural myocardial infarction over a period of 4 to 6 hours.[52] This observation, coupled with the work of DeWood et al,[53] who demonstrated that an acute coronary thrombosis was responsible for most acute myocardial infarctions, led to what is probably the major therapeutic advance in cardiology: the use of thrombolytic therapy or primary angioplasty for acute myocardial infarction. The theoretical basis for the use of early reperfusion is grounded in the work of early investigators in this field who showed that timely restoration of coronary flow (i.e., coronary reperfusion) salvages myocardium. However, improvement in flow had variable immediate effects on wall motion abnormalities, with most animals showing improvement but others showing no improvement or even worsening.[40] After reperfusion there is no significant correlation between infarct size and extent of regional dyskinesis or area of systolic wall thinning by 2D echocardiography after reperfusion performed up to 10 days after reperfusion.[46] [54] Thus, echocardiographic wall motion abnormalities as a predictor of infarct extent appeared to be more accurate following permanent occlusion than after occlusion with reperfusion. There are several plausible explanations for the lack of correlation between infarct size and regional wall motion abnormalities in reperfused myocardium. Most often echocardiographic assessment results in an overestimation of infarct size. After restoration of flow, there may be persistent postischemic dysfunction in viable myocardial segments, known as myocardial stunning. The pathophysiologic basis for this phenomenon is covered in several excellent reviews.[55] [56] [57] Wall motion abnormalities 2 weeks after reperfusion correlate better with infarct size, [54] which suggests that return of function of stunned myocardium may be significantly delayed. The rate at which reperfusion occurs also affects function, and it may be relevant in terms of the type of therapy chosen in the acute postinfarction period. In a canine model of infarction, sudden complete reperfusion resulted in increased wall thickness and slow return of function over a 7-day period, which is consistent with cell swelling and reperfusion injury (albeit reversible). In contrast, staged partial reperfusion (followed

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by complete reperfusion) did not lead to an immediate increase in wall thickness, with functional recovery being seen as early as 30 minutes.[58] Thus, echocardiography early after a reperfused myocardial infarction (i.e., within 2 weeks) may overestimate the eventual area of necrosis because of stunning, reperfusion injury, or both. Infarct size also may be overestimated if the abnormal motion of infarcted myocardium impairs endocardial motion of adjacent normal myocardium owing to a "tethering" effect. [59] Alternately, the area of necrosis may be underestimated in the presence of a nontransmural infarction that subtends less than 25% of the wall thickness, with the salvaged normal subepicardial region resulting in overall normal segmental function.[60] In patients with old infarctions (>6 months), echocardiographic infarct size tends to underestimate the volume of necrosis when measured at autopsy.[61] In some cases, the ventricular remodeling process may be responsible for the change in the tendency from early (<2 weeks) overestimation to late (>6 months) underestimation of infarct size.[62] To identify postischemic ventricular dysfunction or "stunned myocardium," investigators have examined the effect of inotropic stimulation on the function of reperfused, noninfarcted myocardium and compared it with the effect on infarcted tissue. Serial 2D echocardiography during dopamine infusion demonstrates an increase in the contractility of the reperfused myocardium, with improvements in systolic wall thickening and fractional area change. This improvement in regional function is associated with an improvement in regional myocardial blood flow.[63] This study and others provided the experimental basis for the clinical use of dobutamine in detecting myocardial viability.[64] [65] [66] [67] [68] [69] Another echocardiographic method under investigation for determining myocardial viability is ultrasonic tissue characterization.[70] [71] [72] Nonischemic myocardium shows cyclic variation in the integrated backscatter, whereas in ischemic myocardium this variation is diminished or lost. MCE using sonicated iodinated contrast media identifies segments with persistent flow deficits despite reperfusion of the epicardial vessel. The areas of no reflow are believed to be due to microvascular damage and correspond to nonviable segments as identified by positron emission tomography and thallium scintigraphy.[73] MCE also can measure the extent of microvascular occlusion,

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which occurs after prolonged ischemia and prevents adequate reperfusion. [74]

Infarct Localization Infarcts are localized both with respect to the transmural extent of the infarction (i.e., subendocardial versus transmural) and to the anatomic location as related to the coronary distribution of the infarct related artery. Small nontransmural (i.e., subendocardial) myocardial infarctions may not be detected as an abnormality in contractile function. The transmural extent of infarction and regional systolic function is inversely related to fractional radial shortening in both acute (6 hours after occlusion) and subacute (72 hours after occlusion) infarctions.[60] [75] [76] Fractional shortening continues to deteriorate as the percent of total wall (transmurally) involved increases from 75% to 100%, contradicting the work of others who suggested the subepicardial third of the myocardium contributed little to systolic wall thickening.[77] The circumferential extent of the infarction and, to a lesser extent, its longitudinal extent (i.e., base to apex) correlate with the distribution of the affected coronary artery.[78] [79] The anterior, anterolateral, anteroseptal, and apical (anterior and septal) segments correspond roughly to the left anterior descending artery (LAD) distribution. The lateral wall and lateral apex are in the distribution of the left circumflex. The inferolateral wall is supplied by the posterior descending artery. In 80% of the population, the posterior descending artery arises from the right coronary artery (RCA) and supplies the inferolateral wall as well as the inferior free wall and inferior septum (right dominant). In the other 20% of patients, the posterior descending artery arises from the circumflex artery (left dominant system). The right ventricle is supplied by the RCA via its acute marginal branches. In general, infarctions in the LAD distribution tend to be more apically situated, whereas those in the RCA and the circumflex distribution are more basal in their location. Moreover, the extent of apical involvement and its distribution depends, to a degree, on the relative supply from the left anterior and posterior descending arteries. Of course, the presence of collaterals and previous bypass surgery alters the distribution of ischemia and infarction relative to the involved arterial supply. The most commonly accepted method for analyzing wall motion uses the 16-segment model recommended by the American Society of Echocardiography[38] (Fig. 12-

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1) , with the approximate and most common native coronary arterial distribution in relation to these segments depicted in Figure 12-2 . Experimental Models of Mitral Regurgitation Mitral regurgitation is common in the setting of acute myocardial infarction. Only recently have experimental studies elucidated the mechanism. These studies have demonstrated incomplete coaptation of the mitral valve leaflets owing to alteration of systolic left ventricular geometry Figure 12-1 The 16-segment model for segmental wall motion analysis recommended by the American Society of Echocardiography.[29] A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; L, lateral; PSAX, parasternal short axis; S, septal; SAX, short axis.

during ischemia.[80] [81] Infarction of a papillary muscle and the underlying ventricular myocardium results in incomplete leaflet coaptation owing to an increase in the distance from the point of mitral leaflet coaptation to the mitral annulus.[81] [82] Although the extent of the underlying wall motion abnormality may be small and left ventricular function may be globally preserved, papillary muscle ischemia alone is insufficient to cause mitral regurgitation. These studies are supported by the clinical observation that mitral regurgitation occurs in patients with ischemia or infarction of the inferolateral or posteromedial papillary muscle and a small area of underlying myocardium with otherwise well-preserved left ventricular function.[15] Incomplete leaflet coaptation also may occur as a result of severe global left ventricular dysfunction rather than localized papillary muscle dysfunction. [80] The proposed mechanisms contributing to malcoaptation of the leaflets in the setting of global ventricular dysfunction include a prolonged rate of rise of left ventricular pressure (i.e., Figure 12-2 Arterial distribution of blood flow superimposed on a parasternal short-axis view. LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery.

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decreased dP/dt), with less force exerted on the mitral leaflets; poor systolic approximation of the left ventricular walls; mitral annular dilation; and malalignment of the papillary muscles owing to increased left ventricular end-diastolic volume. More recent data from a canine model using 3D echo-cardiography suggest that functional mitral regurgitation associated with left ventricular systolic dysfunction occurs only in the presence of left ventricular dilation.[83] Hemodynamically significant mitral regurgitation relates strongly to the 3D geometry of the mitral valve attachments at the papillary muscle and annular in the presence of left ventricular dilation (i.e., postpericardiectomy). Likewise, in vitro modeling studies demonstrated an integrated mechanism of regurgitation in which an altered balance between abnormal leaflet tethering and decreased coapting forces results in mitral incompetence.[84] Thus, hemodynamically significant mitral regurgitation is seen both in patients with small inferior myocardial infarctions and posteromedial papillary muscle involvement and in patients with large anterior infarctions, left ventricular dilation, and globally reduced systolic function. Infarct Healing and Remodeling Echocardiographic studies have contributed significantly to the understanding of infarct healing and the ventricular remodeling that takes place in the hours and days following an acute myocardial infarction. The importance of these phenomena are recognized in relation to the beneficial effects of delayed reperfusion and afterload reduction with angiotensin converting enzyme inhibitors that reduce infarct expansion and ventricular dilation. The concept of infarct expansion originated with the observation that the infarcted segment of myocardium thins and stretches with an increase in the circumferential extent of the necrotic zone (Fig. 12-3) (Figure Not Available) . The clinical observation that infarct expansion is associated with higher mortality, both early (in-hospital) and late after myocardial infarction, [85] [86] , [72] led to the postulate that the change in the topography of the infarcted zone increases the hemodynamic burden on the remaining normal walls, Figure 12-3 (Figure Not Available) Concept of infarct expansion. In the initial phase of the infarction (left), there is regional dilation and thinning limited to the infarcted region. Over time, in addition to further expansion of the area of infarct, there may be

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compensatory dilation of the remaining ventricle (right). (Redrawn from Eaton LW, Weiss JL, Bulkley BH, et al: N Engl J Med 1979;300:57–62. Copyright 1979 Massachusetts Medical Society. All rights reserved.)

resulting in ventricular dilation and hypertrophy.[85] [87] [88] Both clinical and experimental data suggest the following: 1. Expansion of the endocardial segment occurs as early as 10 minutes after occlusion.[89] 2. Infarct thinning and expansion are progressive over a period of 7 days. [88]

3. A critical mass of infarction (approximately 20% of total left ventricular mass) was required for expansion.[90] 4. Infarct expansion in the dog is more likely after LAD than after left circumflex occlusion.[89] 5. Infarct expansion led to aneurysm formation.[88] 6. The segment lengths of normal myocardium increase in the presence of infarct expansion, leading to ventricular dilation.[91] 7. Microvascular obstruction in infarcted tissue plays a role in remodeling by reducing local myocardial function, which contributes to the dysfunction of adjacent noninfarcted myocardium.[92] The clinical significance of infarct expansion is further emphasized by the demonstration of the beneficial effects of a patent infarct-related artery. [87] Histologic studies in a rat model of infarction demonstrated that reperfusion too late to salvage myocardium (no reduction in infarct size or transmurality) inhibits infarct expansion[93] and was associated with increased scar thickness.[94] Echocardiographic studies in dogs showed that delayed reperfusion of an infarct (as late as 5 to 6 hours after occlusion) acutely decreases the degree of infarct thinning and ventricular dilation.[95] [96] Although delayed reperfusion may convert a bland infarct into a hemorrhagic infarct and may increase the risk of myocardial rupture slightly, many clinical studies support the concept that an open artery provides substantial benefit, possibly through decreased left ventricular dilation and aneurysm formation and, as a corollary, a decreased incidence of arrhythmias and a lower mortality.[87] [97] The time course of left ventricular remodeling following successful reperfusion in acute myocardial infarction is suggested by a 2D echocardiographic study that showed progressive infarct thinning for up to 1 month and left ventricular dilation for up to 14 days. The degree of remodeling as reflected in left ventricular volume was greatest in the patients with the largest infarcts (peak creatine kinase > 8000 U/L). Despite the progressive remodeling,

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wall motion score improved rapidly by 14 days, and it continued to improve gradually to 1 year. [98] Vasodilator therapy, theoretically through a reduction of left ventricular wall stress, influences post–myocardial infarction remodeling and improves prognosis. The salutary effects of treatment with angiotensin converting enzyme inhibitors, first shown in a rat model by Pfeffer et al,[99] [100] include attenuation of left ventricular dilation, improved left ventricular performance with a downward shift of the pressure-volume curve and higher ejection fraction, and improved long-term survival. These findings were subsequently confirmed in post–myocardial infarction patients with left ventricular dysfunction in the Survival and Ventricular Enlargement (SAVE) trial. Two canine studies using echocardiographic measurements have shown that nitrates and enalapril had similar beneficial effects on the remodeling process.[101] [102] The Carvedilol Heart Attack Pilot Study (CHAPS) demonstrated 256

attenuation of left ventricular remodeling with postinfarction administration of carvedilol. Echocardiography at baseline and after 3 months of treatment showed reduced left ventricular volumes and sphericity (long-axis–to– short-axis ratio).[103]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography in the Diagnosis and Early Risk Stratification of Acute Myocardial Infarction Transferring the experience from the animal laboratory into the CCU, clinical investigators have confirmed the usefulness of echocardiography in diagnosis, localization, prognostic staging, and detecting of complications of myocardial infarction. Diagnostic Role of Echocardiography For an imaging modality to be useful in the diagnosis of myocardial infarction, it must be feasible in the majority of patients. Images of the left ventricle adequate for segmental analysis of wall motion can be obtained in greater than 90% of patients by skilled sonographers.[104] [105] [106] Tissue harmonic imaging and left-sided contrast agents have increased the percentage of patients in whom technically adequate images can be obtained.[107] [108] [109] In one study of segmental and global function in 70 critically ill patients, the number of uninterpretable segments fell from 5.4 with fundamental (standard) imaging to 4.4 with harmonic imaging and finally to 1.1 with a left-sided contrast agent. In addition, the usefulness of the modality is directly related to its sensitivity and specificity and to the prevalence of the disease in the population studied. The accuracy of an echocardiographic diagnosis of a myocardial infarction is dependent on echocardiography's ability to detect wall motion abnormalities in the involved segment. As shown in the animal laboratory, the severity of the wall motion abnormality depends on the transmural extent of the infarction and the circumferential limits depend on the arterial distribution and collateral blood supply. In considering the specificity of wall motion abnormalities for diagnosis of acute myocardial infarction, other causes of segmental dysfunction must be recognized. A false-positive diagnosis can often be avoided if wall

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thickening is examined in addition to endocardial motion. The inward motion of the endocardial surface may be delayed or paradoxical owing to abnormal conduction in the presence of Wolff-Parkinson-White syndrome, [110] a left bundle branch block,[111] or right ventricular pacing. [112] Paradoxical septal motion also is present in right ventricular volume overload and following open heart surgery.[113] [114] In these conditions, the systolic thickening of the septum or other involved segment (e.g., posterolateral wall in Wolff-Parkinson-White syndrome, type A) should be preserved.[115] Nonischemic causes of segmental dysfunction that result in reduced systolic thickening and endocardial motion include focal myocarditis[116] and idiopathic cardiomyopathy. Several studies that have examined the specificity of echocardiographic wall motion abnormalities for diagnosis of acute myocardial infarction are worth noting. Among 65 patients presenting to the emergency room with chest pain, there were 5 false-positive echocardiograms, demonstrating regional asynergy in patients without infarction for a specificity of 85%.[117] In a more recent study by Peels et al[118] of 43 patients with chest pain and normal or nondiagnostic electrocardiogram, the specificity of echocardiographic wall motion abnormalities was 78% for ischemia and only 53% for infarction. The apparent discrepancy between the two studies is probably due to differences in prevalence of disease in the population studied. Sabia et al[105] used echocardiography to study 202 patients presenting to the emergency room with acute shortness of breath or chest pain. Of the 140 patients who were ruled out for myocardial infarction, 60 had regional wall motion abnormalities detected by echocardiography. Of those patients, 52% (31 of 60) had had a prior infarction and 53% (32 of 60) were found to have evidence of coronary artery disease on subsequent testing. Although the development of electrocardiographic Q waves is usually associated with a transmural infarction, the absence of Q waves does not always signify a nontransmural or subendocardial infarction.[119] Non–Qwave infarctions are usually smaller, are associated with smaller enzyme leaks,[120] and more often are in the distribution of the left circumflex artery. [121] Two-dimensional echocardiographic evidence of a wall motion abnormality is present in 90% to 100% of patients with Q-wave infarctions [117] [122] [123] [124] compared with 75% to 85% in patients with non–Q-wave [104] [114] [117] [123] [124] [125] infarctions. , The most widely used scoring system for grading the severity of a wall

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motion abnormality is that recommended by the American Society of Echocardiography, in which normal = 1, hypokinesis = 2, akinesis = 3, dyskinesis = 4, and aneurysm = 5[38] (Table 12-1) . Unlike other published scales,[106] hyperkinesis is not distinguished from normal contraction. Weiss et al[124] demonstrated that the finding of akinesis or dyskinesis is most common in the setting of transmural infarction, with milder degrees of wall motion abnormalities (i.e., hypokinesis) most likely representing nontransmural infarction or ischemia. Localization of Infarction Clinical studies have documented the accuracy of echocardiography in identifying the site of coronary occlusion. Echocardiographic localization has significant advantages TABLE 12-1 -- Scoring System for Grading Wall Motion[38] Score 1 2 3 4 5

Wall Motion Normal Hypokinesis Akinesis Dyskinesis Aneurysmal

Endocardial Motion * Normal Reduced Absent Outward Diastolic deformity

Wall Thickening * Normal (>30%) Reduced (<30%) Absent Thinning Absent or thinning

*In systole.

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over electrocardiographic localization, particularly for apical and lateral wall myocardial infarctions. Pierard et al[126] correlated echocardiographic infarct location with the site of coronary obstruction by coronary angiography in 45 patients and by necropsy in 4 patients. They assigned specific segments to the major coronary branches and found the following sensitivities: basal anterior = first diagonal (LAD, 71%) basal anteroseptal = first septal perforator (LAD, 83 middle anterior = second diagonal (LAD, 100%)

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middle anteroseptal = second septal (LAD, 89%) basal posteroseptal = dominant RCA (89%) right ventricular anterolateral segment = right ventr ular marginal branch (83%)

Ogawa et al[127] analyzed the location of echocardiographic wall motion abnormalities, electrocardiographic Q wave, and angiographic site of coronary artery occlusion in 26 patients with single-vessel disease. Inferior Q waves (II, III, and aVF) were associated with mid-inferior wall motion abnormalities. Furthermore, extension to the inferior septum correlated with RCA disease, whereas extension to the inferolateral wall correlated with circumflex coronary disease. A tall R wave in V1 was associated with

posterolateral wall motion abnormalities and a coronary lesion of the proximal circumflex artery. Electrocardiographic evidence of lateral infarction (Q in lead I or aVL) correlated with wall motion abnormalities of the inferolateral and anterolateral walls and disease in the circumflex system involving a large obtuse marginal branch. Circumflex disease also was associated with the presence of a Q wave in V6 and dyssynergy of the lateral and inferior apical walls.[127]

These studies did not compare echocardiographic to electrocardiographic localization of infarction. However, a study by Otto et al[106] suggested that imaging may be more precise, with an 81% concordance between echocardiography and angiography compared with 76% for electrocardiography.[106] Thus, the use of echocardiography to identify the region of segmental dyssynergy in the patient presenting with a myocardial infarction is clinically accurate in determining the site of coronary occlusion (Table 12-2) . One caveat is that the presence of pre-existing wall motion abnormalities and surgical grafts or collateral circulation altering the distribution of flow must be taken into account. Right Ventricular Infarction Right ventricular infarction (Table 12-3) occurs in up to one third of patients with inferior wall infarction and is seen rarely in patients with anterior infarction. The right ventricle is predominantly supplied by acute marginal branches of the RCA that arise in the middle third of its anatomic course. Occlusion of the RCA proximal to the origin of these branches results in ischemia and usually infarction of the right ventricle. Much less frequently, the right ventricle receives blood supply from a dominant left circumflex artery. In addition, the anterior apex of the right ventricle may

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be supplied by the LAD "wrapping" around the apex of the heart. TABLE 12-2 -- Coronary Distribution Associated with Echocardiographic Segments Echocardiographic Segment Coronary Artery Supply * Base Anterior septum Proximal LAD Anterior Proximal LAD Anterolateral Proximal LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Mid Anterior septum Mid LAD Anterior Mid LAD Anterolateral Mid LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Apex Anterior Distal LAD Lateral Distal LAD Septum Distal LAD Inferior PDA (LAD) LAD, left anterior descending artery; LCx, left circumflex artery; PDA, posterior descending artery; RCA, right coronary artery. *Coronary distribution is variable in the presence of revascularization.

The hemodynamic consequences of right ventricular infarction were first recognized in the mid-1970s with several descriptions of the associated

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clinical syndrome appearing simultaneously in the literature.[128] [129] Using gated scintigraphy, detectable right ventricular dyssynergy was reported by other investigators shortly thereafter.[130] [131] In one of these reports, Sharpe et al[112] also described the M-mode echocardiographic finding of right ventricular infarction. In 6 patients, they found evidence of right ventricular enlargement and paradoxical septal motion correlating with the scintigraphic and hemodynamic findings. Isner and Roberts[132] reported the incidence of right ventricular infarction in 236 necropsy specimens of acute and chronic infarctions. In their series, none of the 97 patients with pathologic evidence of an isolated anterior wall myocardial infarction had right ventricular involvement. In contrast, the incidence of right ventricular involvement in patients with infarction involving the posterior wall was 24% (33 of 139). Specifically, all of the right ventricular infarcts, which were confined to the posterior portion of the right ventricular free wall, TABLE 12-3 -- Echocardiographic Signs of Right Ventricular Infarction PRIMARY Right ventricular dilation Segmental wall motion abnormality of the right ventricular free wall Decreased descent of the right ventricular base SECONDARY Paradoxical septal motion Tricuspid regurgitation Tricuspid papillary muscle rupture Pulmonary regurgitant jet pressure half-time ≤150 msec Dilated inferior vena cava Right-to-left interatrial septal bowing Right-to-left shunting across patent foramen ovale

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occurred in the 65 specimens with transmural infarction involving the posterior septum (33 of 65, or 50%). A subsequent pathologic study described that infarction of the right ventricular anterior free wall occasionally can be contiguous with an extensive anteroseptal infarction.[133] The diagnosis of right ventricular infarction should be suspected in a

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patient with evidence of jugular venous distention and clear lung fields in the setting of an inferior myocardial infarction. Although the electrocardiographic sign of ST segment elevation in V4R is both sensitive

and specific for the diagnosis,[134] it does not provide information as to the extent of involvement. The 2D echocardiographic signs of right ventricular infarction include right ventricular dilation, decreased right ventricular function, segmental wall motion abnormalities, and paradoxical septal motion (Fig. 12-4) .[135] Quantitative measurement of right ventricular ejection fraction by echocardiography is difficult because of the lack of an adequate geometric model for calculation of volumes; instead, fractional area change and descent of the right ventricular base are commonly used measures of right ventricular function. Right ventricular failure with high right atrial pressures results in bowing of the interatrial septum into the left atrium and dilation of the inferior vena cava with lack of inspiratory collapse.[136] Echocardiographic indicators of right ventricular function correlate with clinical status and prognosis. Goldberger et al[136] compared the echocardiographic characteristics in patients with hemodynamically significant infarction (jugular venous pressure [JVP] > 13 mm Hg; n = 9) with those without (JVP < 13; n = 15). There was no difference in the frequency of detectable wall motion abnormalities between the two groups (77% versus 66%). However, the group with higher estimated JVP had less descent of the base (.7 cm versus 1.3 cm); less inspiratory collapse of the inferior vena cava (22% versus 45%) and a greater right-to-left ventricular size ratio (1.1 versus 0.6). The pressure half-time of the pulmonary regurgitant jet reflects the compliance of the right ventricular Figure 12-4 Four-chamber view of an echocardiogram from a patient after an inferior infarction with right ventricular involvement. There is enlargement of the right ventricle (RV) and right atrium (RA). The left ventricle (LV) appears small and the interatrial septum is deviated from right to left, suggesting elevated right atrial and right ventricular enddiastolic pressures.

chamber. In a recent study, a short pressure half-time of the pulmonary regurgitant jet (<150 msec) in patients with right ventricular infarction was the only predictor of in-hospital events.[137] Thrombolytic therapy has been proved efficacious in right ventricular infarction, and echocardiographic features correlate with effective revascularization. In a recent study of 108 consecutive patients with a right ventricular infarction, there was a 78%

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correlation between Thrombolysis in Myocardial Infarction (TIMI) grade III perfusion in and normalization or improvement of right ventricular function by echocardiography.[138] Interatrial septal motion and interventricular septal motion normalized in all reperfused patients. The major complication rate and mortality were higher in patients with echocardiographic findings of right ventricular dysfunction persisting after thrombolytic therapy.[138] Two other complications associated with right ventricular infarction deserve mention. First, papillary muscle dysfunction associated with ischemia and right ventricular dilation may result in functional tricuspid regurgitation. Rarely, papillary muscle rupture may involve the tricuspid valve. Second, severe hypoxemia owing to right-to-left shunting across a patent foramen ovale has been reported with large right ventricular infarctions in association with elevated right atrial pressures. [139] Echocardiography for Prediction of Early Mortality Using echocardiography in the setting of acute myocardial infarction, clinical investigators have identified several important prognostic indices: (1) the extent of the wall motion abnormalities within the infarct zone; (2) the degree of infarct expansion and ventricular dilation; and (3) the presence of wall motion abnormalities outside the infarct zone (i.e., infarct extension). The importance of diastolic function as a prognostic indicator is discussed later. An echocardiographic wall motion score has been the most widely used measure of functional infarct size in clinical practice. The total score is derived by assigning a grade of 1 through 5 (see Table 12-1) to each myocardial segment that is adequately visualized. For a segment to be scored, the majority of the endocardium within that segment must be apparent, and wall thickening and endocardial motion should be examined. The scores for each segment are added and then divided by the number of segments graded for a total wall motion score. Several studies have demonstrated that a higher wall motion score index (12 to 24 hours after admission) is associated with a higher rate of in-hospital complications, including malignant arrhythmias, pump failure, and death.[104] [140] A higher wall motion score index also predicts a higher rate of complications, including free wall rupture, ventricular septal defect or papillary muscle rupture, and death from cardiogenic shock.[140] A higher wall motion score, signifying a more extensive infarction, also is predictive of late mortality. [140] [141] In reviewing the literature on this subject, it is important to

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recognize that many different scoring systems have been described, with consequent variability 259

in the absolute number of the wall motion score index associated with a poor prognosis. Infarct expansion is defined as an increase in the endocardial surface area of the infarcted zone owing to thinning and stretching secondary to necrosis and scar tissue formation. A landmark study in 1979 used serial 2D echocardiography to study 28 patients in the first 2 weeks after myocardial infarction. In eight patients, all with anterior infarctions, there was a progressive increase in the endocardial length of the infarcted segment and progressive ventricular dilation. In the group without infarct expansion (9 inferior myocardial infarction patients, 11 anterior myocardial infarction patients), there was little or no dilation. Although the number of patients in each group was too small from which to draw firm conclusions, the group with infarct expansion had a higher mortality rate (50%) compared with the group without expansion (0%). Other clinical studies have suggested that this mechanism contributes to congestive heart failure and poor functional status after infarction.[142] Later studies in the era of reperfusion confirm that infarct expansion is more common in anterior infarctions, but they suggest that most of the dilation is present by 3 hours.[143] Wall motion abnormalities remote from the infarction site may be present early in the course of the infarction or may develop in the presence of postinfarction angina, suggesting de novo ischemia. The echocardiographic finding of remote asynergy at or soon after clinical presentation is strong evidence of multivessel disease. Abnormal wall motion in a second (or even third) coronary distribution is possibly due to (1) previous infarction, (2) increased myocardial oxygen demands placed on the noninfarcted segment as a result of increased wall stress outstripping its oxygen supply, (3) a cessation in its collateral blood supply that originated from the newly occluded vessel, or (4) simultaneous infarctions in multiple coronary beds, the least likely cause.[144] Infarct extension results from the development of ischemia and infarction in a region remote from the original site after the initial event. Postinfarction angina with electrocardiographic changes distant from the acute infarct (i.e., "ischemia at a distance") is associated with a worse

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prognosis than ischemia within the infarct zone.[145] Although early observations were based on electrocardiographic evidence alone, more recent echocardiographic investigations show similar results.[125] [145] [146] Isaacsohn et al[146] performed echocardiography during 19 episodes of postinfarction ischemia. Echocardiographic extension was detected in seven of nine episodes with clinical evidence of extension (recurrent chest pain, new increase in creatinine kinase level, or new electrocardiographic changes). The in-hospital mortality rate was significantly greater in those with echocardiographic evidence of infarct extension (50% versus 12%) and was poorest in those with a high wall motion score.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Detecting Complications of Acute Myocardial Infarction The prognosis of myocardial infarction is directly related to the extent of necrosis (Table 12-4) . A large TABLE 12-4 -- Echocardiography in Complications of Myocardial Infarction HEMODYNAMIC STATES Hypovolemia Right ventricular infarction Globally reduced left ventricular contractility MECHANICAL COMPLICATIONS Papillary muscle rupture Ventricular septal rupture Free wall rupture and tamponade OTHER Left ventricular aneurysm Mural thrombus infarction encompassing greater than 40% of the heart is likely to result in severe pump failure. Transmural infarction is more likely to result in complications related to rupture, occurring in up to 3% of patients. Thus, in the hemodynamically unstable patient, it is critical to exclude rupture, a situation that is potentially amenable to surgery, before concluding that cardiogenic shock is on the basis of pump failure. In most cases, TTE (supplemented when necessary by TEE) is sufficient to exclude papillary muscle, free wall, and ventricular septal ruptures. Hemodynamic Classification of Myocardial Infarction Using Doppler Echocardiography

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A carefully performed Doppler echocardiographic study can provide sufficient information to determine a patient's hemodynamic category after infarction. A hemodynamic classification on the basis of these well-studied parameters is given in Table 12-5 . A simple method of estimating stroke volume is to measure the stroke distance, that is, the velocity time integral (VTI) of aortic flow by pulsed wave or continuous wave Doppler. Although continuous wave Doppler measurements are more reproducible, they can be used only in patients with normal semilunar valves; even a mild degree of stenosis increases the VTI. At a heart rate of 70 to 80 beats per minute, the normal stroke distance is 13 to 15 cm for the pulmonary artery and 18 to 20 cm for the aorta.[147] [148] Stroke distance varies inversely with heart rate, but it holds constant over a wide range of body surface areas.[149] This method eliminates the error in cardiac output measurements introduced by estimating the cross-sectional area of the orifice. Moreover, stroke distance measurements are simple to measure online. Recently, automated cardiac output measurements, based on the digital velocities from color flow mapping, have become available on some systems.[150] A more detailed discussion of Doppler measurements of cardiac output is found in Chapter 26 . Mitral inflow, measured at the tips of the leaflets in the four-chamber view, is informative with regard to diastolic function and left ventricular filling pressures.[151] Derived parameters of the time velocity curve include the ratio of peak early filling velocity to atrial filling velocity (E/A 260

TABLE 12-5 -- Hemodynamic Classification of Myocardial Infarction * by Echocardiography Hemodynamic Category LVEF Normal Nl Hyperdynamic Nl to incr Hypovolemia

Pulmonary LVOT Mitral Venous RVEF VTI E/A Flow Nl 20 A wave S > D † cm dom † Nl >20 A wave S > D † cm dom †

Variable Nl

<20

A wave S > D †

PASP (TR velocity) IV Nl N Nl to slight incr Nl to

N

Sm

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LV Failure Mild

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Mild decr Mod decr Severe decr Variable

Nl to decr Nl to decr Nl to decr Decr

cm

dom †

Mild decr Mod decr Sev decr Decr

E wave dom E wave dom E wave dom A wave dom †

decr

S>D

sp co

Mild incr Mod incr Mod incr Decr

N pl Severe S< D Incr N incr decr pl decr, decreased; D, diastolic; dom, dominant; E/A, ratio of early to late (a ventricular diastolic inflow velocity; incr, increased; IVC, inferior vena cava left ventricular ejection fraction; LVOT, left ventricular outflow tract; Mod, MR, mitral regurgitation; Nl, normal; PASP, pulmonary artery systolic pres right ventricular; RVEF, right ventricular ejection fraction; S, systolic; SFR flow reversal; TR, tricuspid regurgitation; VSD, ventricular septal defect; V velocity time integral; w/o, without. *As described by Pasternak, Braunwald, and Sobol.[162] †In the infarction age group. ‡Dependent on extent of LV infarction.

ratio), the deceleration time of early filling curve and the isovolemic relaxation time. Two distinct patterns of inflow reflect the two categories of diastolic dysfunction: impaired left ventricular relaxation and decreased left ventricular compliance. Impaired relaxation is characterized by a decreased E/A ratio and prolonged deceleration and isovolumic relaxation times; this pattern is encountered in chronic ischemic heart disease and hypertension and as a result of normal aging. The restrictive flow pattern noted under

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conditions of diminished left ventricular compliance demonstrates an increased E/A ratio and shortened isovolumic relaxation and deceleration times. This inflow pattern occurs in restrictive cardiomyopathies and in association with elevated filling pressures. An intermediate stage of diastolic function is present with "pseudonormalization" of the mitral filling pattern, usually associated with a moderate elevation of filling pressures. In a recent study of postinfarction patients with left ventricular ejection fraction less than 35%, a mitral deceleration time of less than 120 msec was highly predictive of a pulmonary capillary wedge pressure of greater than 20 mm Hg[152] (Fig. 12-5) . In a second study of patients with systolic dysfunction after infarction (ejection fraction >40%), there was an increased rate of adverse events in two years of follow-up in patients with higher mitral E/A ratios and shorter deceleration times.[153] This finding has been confirmed in subsequent studies[11] [154] [155] (Table 12-6) . Several new parameters of diastolic function have been studied in postinfarction patients. The deceleration time of the diastolic component of pulmonary venous flow has a better correlation with wedge pressure in post patients with myocardial infarction than does the mitral deceleration time. The sensitivity and specificity of a pulmonary venous deceleration time less than 160 msec in predicting greater than or equal to 18 mm Hg in pulmonary capillary Figure 12-5 Mitral inflow signal from a patient with a large anterior myocardial infarction. There is an increased E wave velocity and a shortened deceleration time. The deceleration time was measured between the two arrows as 80 msec. This measurement is evidence of elevated filling pressures and is a poor prognostic sign (see text).

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TABLE 12-6 -- The Role of Diastolic Functional Parameters in Prognosis After Myocardial Infarction Reference n Comment Pozzoli et 107 Patients with cardiac events had significantly higher E/A ratios and shorter mitral deceleration time al[153] Sakata et 206 Decreased A wave was associated with high in-hospital mortality and congestive heart failure al[154]

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Nijland et 95 1-yr survival rate: restrictive filling, 50%; nonrestrictive al[155] filling, 100% Moller et 110 Deceleration time < 140 msec was the most powerful predictor of cardiac death al[11] Total 518 wedge pressure were 97% and 96%, respectively, compared with 86% and 59%, respectively, for a mitral deceleration time of less than 130 msec.[156] The propagation velocity of mitral inflow measured on M-mode color Doppler echocardiography also has prognostic significance.[11] Technically adequate pulmonary venous flow tracings can be obtained in the majority of patients with surface echocardiography. The predominant pulmonary venous flow pattern is triphasic, with the initial systolic (S) forward flow in pulmonary veins occurring during atrial relaxation (xdescent), a second systolic phase coinciding with basal descent of the left ventricle, and forward flow during diastole (D) occurring in the conduit phase of ventricular filling while the mitral valve is open (y-descent). During atrial systole there is a low-velocity retrograde flow signal (A wave). In subjects older than 40 years of age with normal filling pressures, the peak velocities and VTIs are higher during systole than during diastole, and the duration of the pulmonary venous A wave is less than that of the mitral A wave. With high filling pressures, diastolic filling predominates and the A wave duration exceeds that of the mitral A wave.[110] [157] [158] In patients with acute myocardial infarction, a systolic fraction of pulmonary venous flow less than 45% was highly associated with a pulmonary capillary wedge pressure greater than 18 mm Hg.[150] Additionally, systolic flow reversal in the pulmonary veins is an important sign of hemodynamically significant mitral regurgitation.[159] Measurements of pulmonary artery systolic pressure using tricuspid regurgitant jets with or without contrast enhancement have been well validated in the literature,[160] and the size and respiratory dynamics of the inferior vena cava can be used to estimate right atrial pressure. [161] Combining these parameters with measurements (quantitative or qualitative) of left and right ventricular function and color flow Doppler interrogation for valvular abnormalities results in a comprehensive evaluation of the hemodynamic state after infarction as defined by

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Pasternak, Braunwald, and Sobel[162] using invasive data. A recent study found that a combination of automated Doppler cardiac output and pulmonary venous flow measurements was highly accurate in predicting the hemodynamic subset as measured invasively.[150] When the data are incomplete from a transthoracic examination, one should not hesitate to employ TEE given its established safety even in the critically ill patient. Of course, the hemodynamic information available from an echocardiographic examination is available only at a single point in time, and continued invasive monitoring may be necessary in patients with ongoing instability. Recurrent Ischemia After Infarction Although there have been few studies evaluating the usefulness of echocardiography in patients with recurrent ischemia after myocardial infarction, many clinicians rely on echocardiographic evaluation in this setting, given the sensitivity of this technique for detection of wall motion abnormalities. Worsening of wall motion after initial improvement suggests reocclusion of the infarct-related vessel. Wall motion abnormalities in regions remote from the area of infarction suggest multivessel disease.[146] In addition, alternative causes for chest pain after myocardial infarction (e.g., pericarditis) may be evident on echocardiographic examination. Postinfarction Pericarditis and Pericardial Effusion Postinfarction pericarditis most often occurs after a Q-wave infarction between 3 and 10 days following the myocardial infarction. Onset after 10 days is usually considered Dressler's syndrome. Chest pain caused by pericarditis typically is pleuritic and is accompanied by the auscultatory finding of a pericardial friction rub. Although a pericardial effusion is very common after infarction, it is not pathognomonic of pericarditis. Several investigators have reported on the incidence of pericardial effusion following infarction,[163] [164] [165] [166] [167] as summarized in Table 12-7 . In all the studies reviewed, pericardial effusion was associated with larger infarctions as measured by wall motion scores[163] [166] or degree of creatine kinase elevation.[164] [166] The TABLE 12-7 -- Incidence of Pericardial Effusion After Infarction Study Pierard et al[166] Galve et al[165]

No. of Patients 66 138

No. with Effusion (%) Comments 17 (26) Anterior > inferior 39 (28) Anterior > inferior

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Charlap et al

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172 30 (17)

Peaked on 3rd day Echo at 72 hr

[164]

Sugiura et al

185 44 (24)

Inferior MIs only; higher incidence with RV infarct Widimsky and 192 82 (43) Peaked 5th day; CHF or [167] Gregor death more common; no increase with thrombolysis or heparin CHF, congestive heart failure; MI, myocardial infarction; RV, right ventricular. [163]

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incidence of congestive heart failure and mortality is higher in those patients with effusions apparent on echocardiography.[167] In almost all cases the effusions are small and hemodynamically insignificant. Thus, the effusion did not cause the increase in morbidity and mortality but serves as yet another marker of a large infarction. Mitral Regurgitation Ischemic mitral regurgitation can be defined as valvular incompetence associated with myocardial ischemia or infarction in the absence of primary leaflet or chordal pathology (Fig. 12-6) . Acute mitral valve incompetence may occur in the setting of myocardial infarction owing to necrosis and rupture of papillary muscle tissue or incomplete coaptation of the mitral valve leaflets owing to distortion of ventricular architecture. Mitral regurgitation is common in the setting of acute myocardial infarction, with a reported incidence rate between 10% and 50%. Of almost 12,000 postinfarction patients catheterized at Duke University, 19% had evidence of mitral regurgitation by angiography.[168] [169] Hemodynamically significant mitral regurgitation occurs equally in anterior and inferior infarcts. Risk factors for significant postinfarction mitral regurgitation include advanced age, female gender, diabetes, and prior infarction.[170] [171] In patients with myocardial infarction, moderate to severe mitral regurgitation is associated with substantially reduced short- and long-term survival, with up to a 24% early and 54% 1-year mortality rate.[171] [142]

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Severe postinfarction mitral regurgitation also is an independent risk factor for coronary artery bypass surgery operative mortality. [168] Moreover, in patients presenting to the emergency room with chest pain, moderate or severe Figure 12-6 (color plate.) Mitral regurgitation in a patient with an inferior myocardial infarction and resultant inferobasal aneurysm. A, Diastolic deformity in this apical two-chamber view (arrow). B, Lack of thickening in this region during systole (arrow). C, Moderately severe mitral regurgitation (double arrow).

mitral regurgitation by echocardiography was associated with high risk for overall and cardiovascular mortality (risk ratio = 2.0).[172] Among these patients, only 60% had audible murmurs. The clinical recognition of mitral regurgitation in the setting of myocardial infarction may be confounded by several variables. Up to 50% of patients with hemodynamically significant mitral regurgitation do not have an audible murmur owing to rapid equalization of left ventricular and left atrial pressures (especially in a low output state) or because the murmur is obscured by lung sounds in a patient with pulmonary edema or mechanical ventilation.[171] In view of the adverse prognosis, early diagnosis is desirable to institute medical or surgical interventions that potentially improve outcome. Although some authors have advocated TTE in all patients admitted with myocardial infarction, this approach is probably not costeffective. However, echocardiography is mandatory in the postinfarction patient with a new systolic murmur, pulmonary edema, or sudden cardiac decompensation. In this situation, TTE is 100% sensitive in detecting mitral regurgitation and in distinguishing mitral regurgitation from ventricular septal defect.[173] Detection and grading of mitral regurgitation is accomplished with 2D, Mmode, color, and spectral Doppler techniques. Two-dimensional imaging detects abnormalities in the mitral valve apparatus, including flail leaflets or ruptured chordae. Although color flow parameters are those most often used, accurate grading of mitral regurgitation severity should encompass other echo-Doppler signs as well.[174] [175] In the patient with pulmonary edema, the unexpected findings of a small infarction, a hyperdynamic left ventricle, increased early mitral inflow velocity, or all three [176] should prompt a careful search for mitral regurgitation even when color flow Doppler mapping is unrevealing.

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263

Papillary muscle necrosis with rupture and a flail leaflet is a life-threatening complication of myocardial infarction that requires surgical intervention. The more frequent involvement of the posteromedial papillary muscle is thought to be due to its blood supply from a single coronary artery. Chordae to both leaflets arise from each of the papillary muscles so that in cases of "complete" rupture of the entire trunk of a papillary muscle, both leaflets are affected. In less severe cases, the rupture is "incomplete" and only a single head is torn. The 2D echocardiographic findings include prolapse of one or both leaflets, a flail leaflet, and liberation of a portion of the papillary muscle.[177] In some patients, the ruptured muscle may remain tethered to the chordae and chaotic motion is not present. Spectral and color flow Doppler imaging of the jet is usually easily accomplished with surface imaging, but an eccentric path of flow may complicate its identification. In our experience, TEE is superior in this regard,[36] supported by multiple case reports in the literature[16] [19] [21] (Fig. 12-7) . When only a single head of the papillary muscle is affected (incomplete rupture), medical stabilization often is possible. Initial treatment should include afterload reduction with diuretics, angiotensin converting inhibitors, nitroprusside, and (in cases of severe cardiac decompensation) inotropic support and intra-aortic balloon pump. When rupture is complete, involving the main trunk of the papillary muscle, the complication is uniformly fatal without immediate recognition and prompt repair.[177] [178] In the other forms of ischemic mitral regurgitation, reperfusion therapy with thrombolytics or angioplasty should be considered first-line therapy because reperfusion may improve regurgitant severity and patient prognosis. Coronary bypass in conjunction with mitral valve surgery should be considered in patients who show benefit from medical therapy or nonsurgical revascularization. Coronary bypass with mitral valve surgery is necessary in patients who develop circulatory collapse as a result of mitral regurgitation, despite the relatively high operative mortality in this patient group. In those patients who receive surgery for severe ischemic mitral regurgitation, there is evidence that early surgery, concomitant revascularization, and repair, rather than replacement, improve survival.[179] [180] In the recent SHOCK trial (SHould we use emergently revascularized Occluded Coronaries in cardiogenic shocK?), the survival rate in patients with

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Figure 12-7 (color plate.) Transesophageal echocardiogram of a patient with papillary muscle rupture after an acute inferior myocardial infarction. The papillary muscle rupture was incomplete and the head of the papillary muscle remained tethered to the mitral chordae. A, The triangular density representing the head of the papillary muscle (arrow) can be seen within the body of the left ventricle during systole. B, Associated severe mitral regurgitation with a prominent area of proximal isovelocity surface acceleration (double arrow).

acute severe mitral regurgitation who underwent surgery (40%) was higher than in those treated medically (71%, P < .003).[181] Ventricular Septal Rupture Ventricular septal defect owing to myocardial rupture complicates 1% to 3% of all acute myocardial infarctions and up to 5% of all fatal infarctions. In the GUSTO-1 trial (Global Utilization of Streptokinase and TPA for Occluded coronary arteries), the incidence of ventricular septal rupture was only 0.2% (84 of 41,021 enrolled patients), suggesting that thrombolytic therapy has reduced the incidence of rupture.[182] Ruptures occur only in the presence of transmural infarction and result from hemorrhage within the necrotic zone. Independent risk factors for the development of a ventricular septal defect are similar to those for papillary muscle rupture and include first infarction, advanced age (>65), hypertension, and female gender.[183] [184] There appears to be a higher incidence in patients without a history of prior angina and with infarcts in the distribution of a single vessel.[183] [184] [185] Thus, septal rupture appears to be more likely following abrupt occlusion of a single artery that vascularizes a territory for which there is little collateral flow.[184] Unlike papillary muscle rupture, ventricular septal rupture occurs with equal frequency among patients with anterior (LAD) and inferior (RCA) infarctions but less frequently in those with lateral (left circumflex artery) infarctions.[186] Conflicting evidence exists as to the effect of thrombolytic therapy on the development and outcome of postinfarction ventricular septal defect. Thrombolytic administration that is delayed more than 12 hours following the onset of chest pain may increase the incidence of ventricular septal rupture.[97] However, in most cases the slight increase in the risk of rupture is outweighed by the overall benefit of reperfusion therapy. In the GUSTO1 study, the onset of rupture was earlier on average (1 day) than that reported previously, suggesting that although thrombolytic therapy reduced the rate of rupture, it tended to occur earlier after thrombolysis.

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Ventricular septal defects usually present 3 to 6 days after infarction with recurrent chest pain, dyspnea, and sudden hypotension or shock. A new harsh pansystolic murmur is present in approximately 50% of patients. Bedside 264

echocardiography has been demonstrated to be highly sensitive and specific in the diagnosis of ventricular septal defect. The defect can be visualized by transthoracic 2D imaging in 40% to 70% of patients.[177] [187] The use of contrast and color flow Doppler imaging improves the sensitivity to 86% and 95%, respectively.[21] [97] [173] [177] When TTE is suboptimal, TEE is highly accurate with a reported 100% sensitivity and specificity, [188] [189] with improved delineation of the site of defect, the morphology, and presence of multiple defects[190] (Fig. 12-8) . The most common site for a ventricular septal rupture is the posteroapical septum. Visualization of the area of myocardial dropout is most often accomplished in the parasternal short-axis view just below the level of the papillary muscles or in the apical four-chamber view with slight posterior angulation of the probe. Anterior septal defects most often occur in the distal one third of the septum and are visualized in the apical four-chamber view with anterior angulation or in an apical short-axis view. Postmyocardial infarction ventricular septal defects may be multiple and often have a serpiginous course through the myocardium.[191] Associated echocardiographic findings include evidence of elevated right ventricular pressure including right ventricular dilation, decreased right ventricular systolic function, and paradoxical septal motion. Signs of increased right atrial pressure include right atrial dilation, bowing of the interatrial septum toward the left throughout the cardiac cycle, and plethora of the inferior vena cava. Color flow Doppler imaging is particularly useful in demonstrating the exact position of the defect; the width of the jet correlates with the size of the defect as measured at surgery.[191] Although the peak gradient across the ventricular septal defect measured with continuous wave Doppler allows an estimate of right ventricular systolic pressure, the measurement should be used with caution in patients with complex defects involving indirect tracts through the myocardium. [191] A recent study demonstrated a fair correlation between this Doppler estimate of right ventricular systolic pressure and that measured at catheterization (r = 0.71); the values were similar to those estimated from the tricuspid

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regurgitant jet. Echocardiography provides prognostic and diagnostic information in patients with ventricular septal rupture. Rupture Figure 12-8 (color plate.) Transesophageal echocardiogram showing a large ventricular septal defect (VSD) involving the posterior septum in a patient with a large inferior myocardial infarction and right ventricular extension. Left, The area of discontinuity can be visualized as a large, irregularly shaped area of myocardial dropout. Right, Color flow demonstrates left-to-right shunting across this ventricular septal defect. LV, left ventricle; RV, right ventricle.

of the posterior septum after inferior myocardial infarction is associated with a higher mortality rate, apparently related to the degree of associated right ventricular dysfunction.[186] [192] Moreover, posterior septal ruptures tend to be more complex and associated with remote myocardial involvement. In contrast, anterior septal defects more often have a direct course and involve a discrete myocardial region. Overall mortality is 95% to 100% without surgical intervention.[193] The strongest indicator of poor prognosis is the development of cardiogenic shock associated with as much as a 90% mortality rate.[192] Although early surgery appears to improve survival when cardiogenic shock is present, results in the recent SHOCK trial were disappointing. In the surgically treated group, the survival rate (19%) was only slightly better than that of the medically treated group (5%).[186] Right ventricular systolic pressure tended to be higher and right atrial pressure lower, among the survivors. When the patient can be stabilized medically, operative mortality may be improved when surgical repair is delayed until 6 weeks following the event.[184] In summary, the value of echocardiography in patients with suspected ventricular septal rupture is its ability to provide an accurate, timely diagnosis and important prognostic information that may assist in therapeutic decision making. Rupture of the Ventricular Free Wall and Pseudoaneurysm Free wall rupture occurs in approximately 3% of all acute myocardial infarctions,[194] and it is one of the leading causes of fatality (8% to 20%).[195] [196] [197] [198] [199] Risk factors for free wall rupture are similar to those for papillary muscle and ventricular septal rupture; however, this complication is more likely to occur in patients with a transmural myocardial infarction involving the posterolateral wall associated with a left circumflex occlusion

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or with a LAD occlusion.[201] Early successful reperfusion appears to decrease the risk of rupture. In one study of approximately 1300 patients, the overall incidence of cardiac rupture was lower in those receiving thrombolytic therapy (1.7%) than in those in the conventional therapy group (2.7%). Among

[200]

265

patients who receive thrombolytic therapy, patients older than 70 years of age and women had higher rates of rupture.[202] Moreover, patients in whom reperfusion was unsuccessful had a significantly higher rate of rupture than those who were successfully reperfused (5.9% versus 0.5%).[203] Conversely, late reperfusion appears to increase the risk of myocardial rupture though decreasing overall mortality.[97] [204] The use of nitrates in acute myocardial infarction may decrease the risk of rupture by as much as 30%.[205] The intensity of post-thrombolytic anticoagulation with heparin or hirudin does not appear to affect the rate of rupture. [202] Although ventricular free wall rupture usually presents clinically as an acute catastrophic event leading to rapid demise, several recent pathologic and clinical studies have suggested that many cases may involve subacute dissection and tearing of the myocardium before hemodynamic collapse.[194] [196] [200] [205] , Intramural hematoma or hemorrhage at the junction of the necrotic and the normal myocardium results in a small endocardial rent. The tear usually takes a circuitous pathway through the myocardium, ending in a small epicardial opening. Clinically, a prodrome of ongoing or recurrent chest pain (in the absence of an elevation in creatinine kinase), repetitive large volume emesis, unexplained agitation, hypotension or syncope may be associated with the initial small tear.[194] [196] [200] A small amount of hemorrhage into the pericardial space of blood may precede the final catastrophic event. Patients diagnosed during this subacute phase and taken promptly to surgery have a greater chance of survival. A second mechanism of rupture through the wall of an aneurysm has been described. [206]

Echocardiography has a high sensitivity for rupture[194] when the diagnosis is sought and all the echocardiographic findings are considered. The most frequent finding is pericardial effusion; the absence of pericardial effusion virtually excludes rupture. Increasing size of effusion and the presence of thrombus in the pericardial space significantly increases the specificity for rupture (>98%). [194] [204] , [207] An intrapericardial thrombus appears as an

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echo-dense mass; it may be mobile, undulating within the pericardial space or immobile, impinging on the cardiac chambers.[208] Direct visualization of the myocardial tear is possible with TTE in as many as 40% of patients.[201] Other echocardiographic findings include evidence of Figure 12-9 The difference between a true aneurysm (A) and a false aneurysm (B). Note that in the true aneurysm there is continuity of myocardium in the region of dilation, in contrast to the loss of this continuity in the pseudoaneurysm. (Modified from MacKenzie JW, Lemole GM: Tex Heart Inst J 1994;21:296–301.)

tamponade with right atrial and right ventricular diastolic collapse (40%), [201] respiratory variation of the tricuspid and mitral inflow pattern, and plethora of the inferior vena cava. Echocardiographic guidance of pericardiocentesis of the hemopericardium may be life saving in the patient with hemodynamic collapse before the patient can be transported to surgery. Patients at risk for rupture may be identified by evidence of infarct expansion with significant wall thinning at the infarct site. The mortality rate of free wall rupture in the absence of surgical intervention approaches 100%,[199] although recent series report as much as a 50% survival rate in patients who underwent pericardiocentesis and conservative medical management.[201] [209] The in-hospital mortality rate for those who undergo surgical repair is in the range of 40%.[193] [201] [204] Those who survive until hospital discharge appear to have a good long-term prognosis. Thus, early echocardiographic diagnosis with prompt surgical or percutaneous drainage is mandatory in patients who develop postinfarction myocardial rupture. A pseudoaneurysm is a myocardial rupture contained by pericardial adhesions resulting in a pouch that communicates with the left ventricular cavity. [177] A distinguishing echocardiographic feature is the narrow neck, compared with the broader "entrance" to the body of a true aneurysm, with a "neck" diameter-to-maximum diameter ratio less than 0.5. An echocardiographic study showed that this sign was only 60% sensitive in patients with post-myocardial infarction pseudoaneurysms.[210] The majority of post-myocardial infarction pseudoaneurysms were located in the inferoposterior or posterolateral regions (associated with right coronary or left circumflex coronary occlusions).[210] The walls of the pseudoaneurysm are composed of pericardium rather than

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the thin-walled myocardial scar of true aneurysm (Fig. 12-9A) . Occasionally a pseudoaneurysm may occur after rupture of the thin wall of a true aneurysm with the development of a "mixed" aneurysm (see Fig. 129B) . [211] Spectral and color Doppler imaging demonstrate characteristic flow in and out of the pericardial cavity at the site of the tear, as well as abnormal flow within the pseudoaneurysm. Respiratory variation of the peak systolic velocity has also been demonstrated.[212] A meta-analysis suggested that TEE has a higher diagnostic accuracy (>75%) than TTE (26%), although data 266

was available in only a small number of patients[213] (Fig. 12-10) . Surgical repair is the preferred treatment, although new reports have demonstrated that conservative medical treatment in certain high-risk patients is not associated with an increased risk of cardiac rupture.[210] [213] Infarct Expansion and Aneurysm Formation Infarct expansion is an increase in the circumferential extent of the area of infarction that results from stretching and thinning of the infarcted zone. Early clinical studies demonstrated that this phenomenon with a consequent increase in left ventricular volume and wall stress was associated with an adverse prognosis.[85] The importance of infarct expansion has been underscored by clinical trials using angiotensin converting enzyme inhibitors in patients with left ventricular dysfunction after myocardial infarction. In the SAVE trial (Survival and Ventricular Enlargement), which showed a 21% reduction in cardiovascular mortality with the use of captopril,[214] echocardiography demonstrated that ventricular enlargement and reduced fractional area change were independent risk factors for cardiac events. Patients treated with captopril had a lower incidence of ventricular enlargement, which was associated with the lower risk of events,[50] a finding that has been confirmed in subsequent studies.[141] [215] The final expression of infarct expansion is aneurysm formation. In the Coronary Artery Surgery Study (CASS) there was a 7.6% incidence of angiographically documented left ventricular aneurysms.[216] In a study by Visser et al,[218] the incidence of aneurysm was 22% (35 of 158), and most of those occurred in patients with anterior infarction. Formation of an aneurysm occurs only with transmural infarction with a full-thickness scar and, thus, is more frequent following a Q-wave than a non-Q-wave

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infarction. An aneurysm is more likely to complicate an infarct in the LAD distribution than in the right or circumflex arteries.[218] Spontaneous rupture of an acute aneurysm is rare (see "Rupture of the Ventricular Free Wall"), and late rupture virtually never occurs. Serial 2D echocardiographic studies show that aneurysmal dilation is present as early as 5 days after myocardial infarction (15 of 35, 43%, in the Visser study), and new aneurysms after 3 months are unlikely.[218] Despite the Figure 12-10 Transgastric views in transesophageal echocardiogram showing a large pseudoaneurysm involving the inferolateral wall. Left, short-axis view (horizontal plane); right, long-axis view (longitudinal plane).

beneficial clinical course attributed to delayed reperfusion with thrombolytic therapy, there has been no reduction in the frequency of ventricular aneurysms.[219] [220] The echocardiographic appearance of a ventricular aneurysm parallels the pathology. A true aneurysm is defined as a deformity of the thinned infarct segment that is apparent during diastole as well as during systole (see Fig. 12-6) and demonstrates a diastolic contour abnormality. In contrast, a dyskinetic myocardial segment deforms during systole, extending beyond the normal contour of the myocardium. The involved myocardial segment is scarred with thin walls (<7 mm) and increased echogenicity owing to the increased collagen content. [114] The wall of the aneurysm may eventually calcify. The most common location is the left ventricular apex, which is involved in approximately 90% of patients. Aneurysms may vary in size, and very small aneurysms may be difficult to visualize by echocardiography. Technically, the detection of an apical aneurysm is highly dependent on the skill of the operator. Routine employment of highfrequency transducers with a shallow focal point enhances near-field resolution and aids examination of the left ventricular apex. Left-sided contrast agents also may enable detection of small apical aneurysms. Using these methods, the sensitivity of TTE for detection of apical aneurysms should approach 100%. Occasionally, spontaneous echocardiographic contrast may be visible in large aneurysms. It should be noted that TEE may not provide adequate visualization of the left ventricular apex and, therefore, in our experience, is less sensitive than surface imaging.

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Echocardiographic recognition of a left ventricular aneurysm is clinically relevant for the following reasons: 1. The early formation of an aneurysm adversely affects early (inhospital) and late (1 year) mortality.[218] 2. Thrombi are frequently found within aneurysms. 3. Aneurysms and left ventricular thrombi are associated with systemic embolization. In patients with refractory heart failure and angina or recurrent embolic events, aneurysmectomy may be recommended occasionally. Functional measurements of the residual myocardium using quantitative 2D echocardiography is highly predictive of operative mortality and the clinical success of this procedure.[221] [222] A basal (residual) ejection fraction of greater than 40% was associated with a satisfactory result.[222] Left Ventricular Thrombus

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Studies in the early 1980s demonstrated a high sensitivity (90% to 95%) and high specificity (80% to 85%) for the echocardiographic identification of left ventricular thrombus.[223] [224] A prerequisite for thrombus formation is the presence of a segmental wall motion abnormality, most commonly in the left ventricular apex. The ultrasonic appearance of a mural thrombus is that of a mass distinct from the endocardium and protruding to a variable extent into the left ventricular cavity. Under ideal conditions, the surface of the thrombus can be distinguished clearly from the underlying endocardium and the mass can be visualized in two different imaging planes. The tissue characteristics of an acute thrombus are usually similar to that of the myocardium (Fig. 12-11) . A chronic thrombus may have increased reflectivity, demonstrate a layered appearance corresponding to the lines of Zahn, and contain areas of calcification (Fig. 12-12) . The base of attachment to the wall may be broad in the case of a sessile thrombus and narrow in a pedunculated thrombus. When multiple characteristics of the thrombus are analyzed, mobility of the thrombus is most closely associated (positive predictive value, 85%) with embolic events.[220] [225] In any given patient, the morphology may spontaneously change from sessile to pedunculated and vice versa; mobility may resolve spontaneously.[226] False-positive echocardiographic diagnoses are usually a result of

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pseudotendons (i.e., false chordae) spanning the left ventricular apex, coarse trabeculations associated with left ventricular hypertrophy, or nearfield artifacts (commonly present with low-frequency transducers). Highfrequency transducers with a short focus point can sometimes differentiate true thrombus from these other phenomena. Left-sided contrast agents may outline the contours of the thrombus, creating a filling defect[227] [228] with improved detection of thrombus. Thrombi most commonly develop in the presence of a large infarction during the hospitalization phase of a Figure 12-11 Acute thrombus in the posterior aspect of the apical septum. Note that the large mass is homogeneous in texture, without evidence of calcification.

Figure 12-12 Four-chamber view depicting a chronic thrombus within an apical aneurysm. The appearance of the thrombus is layered with areas of calcification. The layers correspond to the lines of Zahn.

myocardial infarction.[229] Like aneurysms, they are more likely following a myocardial infarction in the LAD (up to 33%) than in the RCA or left circumflex artery distribution (less than 1%).[230] [231] New data demonstrate that the best predictor of left ventricular thrombus formation after acute anterior myocardial infarction is a high initial end-systolic volume.[232] Anticoagulant therapy appears to decrease the risk of embolic events and enhances the resolution of thrombus, although spontaneous resolution also may occur.[229] [233] Patients with a left ventricular thrombus identified during the initial hospital stay have an increased long-term mortality rate (22%) compared with those without thrombi (7%). Left ventricular thrombi usually resolve during the first month after anterior myocardial infarction with routine thrombolytic and aspirin treatment, but appearance and resolution of thrombi can continue in a significant proportion of patients (12%).[234] In general, thrombolytic therapy appears to decrease the rate of mural thrombus development. In the Western Washington Randomized Trial of intracoronary streptokinase, the incidence of thrombus and emboli was similar in both treated and untreated groups,[219] but most other trials of

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intravenous thrombolytic agents have shown a reduction in the incidence of thrombi and emboli.[235] [236] [237] [238] Moreover, in the GISSI-2 trial there was no significant difference between the four treatment groups (recombinant tissue plasminogen activator ± heparin, streptokinase ± heparin), with an overall incidence of 28%.[239] The overall tendency for reperfusion therapy to decrease the size of the infarction is likely to lower the risk of thrombus formation. In addition, after thrombolysis, most patients receive an inhospital period of anticoagulation, which is known to decrease the rate of thrombosis and embolization[239] (Table 12-8) .

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TABLE 12-8 -- Effect of Thrombolytic Therapy on Incidence of Left Ventricular Thrombus in Anterior Wall Myocardial Infarction Study Eigler et al

No. of Patients Agent 22 SK

Mean Time Treated Untreated to Rx (hr) (%) (%) P <3 1/12 (8) 7/10 (70) <.005

[235]

Stratton et al

83 SK *

[219]

Natarajan et al[237] Lupi et al[236] Bhatnagar and al-Yusuf

45 SK 63 SK 118 r-TPA

4.7 7/45 6/38 (16) (16) <6 0/27 (0) 8/18 (44) ≤3 4/19 (22) <4 3/54 (5.5)

NS <.05

30/44 (54) <.05 8/44 (18) † <.05

[238]

NA 34/74 10/25 (40) NS (46) Domenicucci 222 SK, NA 26/97 71/125 <.005 [240] et al alteplase (27) (57) NA, not available; NS, not significant; r-TPA, recombinant tissue plasminogen activator; SK, streptokinase. Mooe et al

99 SK

[234]

*Intracoronary. †Received heparin.

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The decision to prescribe oral anticoagulation following hospital discharge is influenced by two additional considerations. Embolic events occur most likely in the first month after myocardial infarction and rarely occur in the absence of thrombus identified by echocardiography.[240] However, the risk of cerebral or systemic embolization after infarction is increased in patients with large apical aneurysms and poor systolic function independent of echocardiographically documented mural thrombus. Second, chronic mural thrombi, persistent for more than 3 months following a myocardial infarction, are very unlikely to embolize. Changes in the morphology of the thrombus with evidence of protrusion are most likely to predict late embolism (>3 months).[240] Thus, most physicians perform an echocardiogram during the acute phase of an anterior wall infarction to measure left ventricular function and to detect aneurysm, thrombus, or both. In the presence of a large apical aneurysm with or without a visible thrombus, oral anticoagulation is recommended in the absence of contraindications.[241]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Post-Myocardial Infarction Risk Stratification Echocardiography has an important role in the evaluation of a patient after discharge from the CCU. Echocardiography during low-dose dobutamine infusion is used to detect myocardial viability in segments that have persistent dysfunction following reperfusion.[64] Echocardiography during higher dose dobutamine infusion or with dynamic stress can be used to detect residual ischemia. Caution should be exercised in the first week after a transmural infarction because cases of myocardial rupture during highdose dobutamine infusion have been reported.[28] [29] Contrast echocardiography will have an important role with the development of reliable perfusion agents.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Early experimental models employing echocardiography for the detection and quantitation of ischemia and infarction helped investigators elucidate the pathophysiology. This work was directly transferable into the CCU and provided the basis for the clinical diagnostic and prognostic role of echocardiography. Advances in echocardiography, especially color flow Doppler imaging, increased the capabilities of echocardiography in detecting the occurrence of complications, such as ventricular septal defect and papillary muscle rupture. Future directions include the detection of flow deficits using myocardial contrast echocardiography and more accurate quantitation of infarct size using 3D techniques.

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275

Chapter 13 - Exercise Echocardiography Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Pamela A. Marcovitz MD

Stress echocardiography consists of a number of stress techniques used in conjunction with echocardiographic imaging. Exercise echocardiography is the most established of these techniques and has been increasing in popularity since the first paper was published on the use of twodimensional echocardiography with bicycle exercise in 1979.[1] Although the images were crude, they served to successfully demonstrate ischemia following cardiovascular stress and its resolution following coronary artery bypass grafting (Fig. 13-1) (Figure Not Available) . With technologic advances, including improvements in imaging and digitization, stress echocardiography has seen widespread acceptance as a first-line technique for the diagnosis of coronary disease. Recently, stress echocardiography has been increasingly used for prognostication in various patient subsets, including patients with chronic coronary disease, patients with recent revascularization, patients with recent myocardial infarction, and female patients. Despite recent advances, however, the principles of its use remain

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the same. In the presence of a significant coronary stenosis, an adequate level of physical exertion results in a transient mismatch between oxygen supply and demand, resulting in a wall motion abnormality within an area of myocardium supplied by a stenotic artery. The wall motion abnormality is detectable by echocardiography and serves as a marker of the degree and severity of ischemia. Future advancements may bring the ability to simultaneously track myocardial perfusion.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Rationale and Theoretical Basis for Ischemia Detection with Stress Echocardiography The rationale for the use of echocardiography to detect ischemia in conjunction with stress testing is that ultrasonography can visualize wall motion abnormalities that arise as the result of a transient mismatch between oxygen supply and demand, in turn resulting in ischemia.[2] [3] [4] [5] Regardless of the stress modality used to induce ischemia, the echocardiographic response to exercise will reflect the underlying state of the coronary arteries.[6] [7] [8] [9] In the absence of coronary artery disease, there will be inward motion (endocardial excursion of at least 5 mm) and increased wall thickening. These characterize the "normal hyperdynamic response" following exercise and signify normal underlying coronary arteries. Conversely, in myocardium subtended by a critical stenosis, a mismatch between oxygen supply and demand will develop during exercise, resulting in ventricular systolic dysfunction or dyssnergy, in a segment or segments of myocardium during cardiovascular stress. Dyssynergic responses may be classified by the degree of abnormality present: 1. Hypokinesia: less than normal (5 mm) degree of inward myocardial excursion and thickening 2. Akinesia: complete lack of inward motion and thickening 276

3. Dyskinesia: paradoxical outward motion and thinning of affected segment or segments. Figure 13-1 (Figure Not Available) Images from a 30-degree sector scanner demonstrating an exercise-induced apical abnormality prior to coronary artery bypass grafting (A) and normal apical wall motion after revascularization (B). (From Wann LS, Favis JV, Childress RH, et al: Circulation 1979;60:1300–1308. Reproduced with permission. Copyright 1979 American Heart Association.)

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The observation that abnormal wall motion reflects an underlying mismatch in supply and demand serves as the premise for the use of echocardiographic imaging in stress testing and occurs during a variety of states in which oxygen supply to the myocardium is reduced. Using a stylus attached directly to myocardium in an animal model, Tennant and Wiggers [10] were among the first to demonstrate that disruption of the coronary blood supply produces wall motion abnormality. Immediately after snare occlusion of a coronary artery, a reduction in wall thickening was observed, followed by normalization of wall motion along with release of the snare. This observation has since been validated with echocardiography in clinical settings in which arterial occlusion occurs, including balloon angioplasty and myocardial infarction.[11] [12] A variety of models have been studied to determine, in detail, the temporal and spatial sequence of events that occur during decreased regional blood flow of sufficient severity to create an imbalance in the myocardial oxygen supply-demand relationship. These models have included graded snare coronary occlusion in animals, balloon angioplasty, exercise, atrial pacing, and observation of spontaneous anginal episodes in humans.[13] [14] [15] [16] [17] [18] [19] In the early animal studies, a closely coupled relationship was noted between myocardial wall thickening and coronary flow, such that reductions in blood flow of 10% to 20% were found to impair regional (but not global) wall thickening within an ischemic zone. The observed reduction in wall thickening was found to be proportional to severity of flow reduction, with greater degrees of flow restriction causing greater severity in regional wall motion abnormalities.[16] , [20] Thus, whereas hypokinesis is noted following a threshold reduction in blood flow of around 10% to 20%, akinesis is observed with flow reduction of greater than 80%, and paradoxial motion, or dyskinesis, with transmural reductions in flow. These early studies also noted a tendency for decreased wall thickening to be more closely coupled with subendocardial rather than subepicardial flow and to extend into adjacent regions beyond welldemarcated zones of reduced flow, a phenomenon known as tethering.[3] [21] As the opportunities for echocardiographic monitoring grew, these observations in animals were extended to humans.[22] [23] [24] [25] Taken together, these studies form the basis for what we now regard as standard echocardiographic observations of ischemic myocardium. After acute, complete coronary occlusion, a series of predictable changes takes place in the myocardium, beginning with the development of diastolic and systolic dysfunction, followed by ST segment depression and angina. A

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wall motion abnormality is one of the initial events seen with the development of ischemia and precedes development of ST segment changes or angina by several minutes. This so-called ischemic cascade, which is known to occur after occlusion of a coronary artery, may occur in ischemic myocardium subtended by a critical stenosis whenever oxygen supply-demand mismatch occurs.[26] [27] [28] A similar temporal relationship between wall motion and electrocardiographic changes has been noted in multiple studies of patients undergoing balloon angioplasty.[12] [29] [30] [31] Hauser et al[31] noted that regional endocardial dysfunction was seen by echocardiography at 19 seconds, electrocardiographic changes occurred at 30 seconds, and chest pain occurred at 39 seconds after balloon inflation. In addition to clinical settings involving coronary occlusion, the "ischemic cascade" was found to occur in ischemic myocardium subtended by a severe stenosis subjected to cardiovascular stress. Examining changes following exercise-induced ischemia in the region of a coronary stenosis, Sugishita et al[28] noted that the average time to onset of wall motion abnormality was 30 seconds, versus 90 seconds for electrocardiographic changes. Clinically, the ability to detect exercise-induced regional wall motion abnormalities increases with the severity and number of coronary occlusions.[32] [33]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Diagnostic Approach Choosing the Optimal Form of Stress

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Exercise is one of a number of stress modalities performed in conjunction with echocardiographic imaging. An adequate level of stress is a prerequisite to performing exercise echocardiography. For the purposes of stress testing, clinically adequate exercise is usually defined as the ability to reach at least 85% of predicted heart rate, based on resting heart rate and age. For patients able to exercise maximally, exercise echocardiography provides a wealth of information regarding the overall level of fitness, functional capacity, and the clinical significance of an ischemic response, as well as the prognosis related to coronary disease. Given the additional diagnostic and prognostic information provided by exercise and hemodynamic parameters, exercise should be the stress method of choice whenever feasible. In the event that a patient cannot perform adequate exercise, other stressors are used (Table 13-1) . For patients unable to perform maximal exercise or to reach a target heart rate, pharmacologic methods of inducing stress are commonly used. These are discussed in greater detail in Chapter 14 , but briefly, currently available pharmacologic methods can be divided into one of two general categories: agents that simulate exercise and coronary vasodilators. [34] The first of these are sympathomimetic amines, are infused intravenously, and induce stress in similar fashion to exercise, that is, through increasing heart rate, blood pressure, and contractility. Of the exercise-simulating agents, dobutamine has emerged as the agent of choice in the United States, largely because of its availability and low cost. Dobutamine exerts its physiologic effects through beta agonist activity, increasing myocardial oxygen demand in a similar fashion to exercise. Unlike exercise, however, dobutamine is unable to provide information about level of fitness or electrocardiographic or

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hemodynamic response to exercise. In addition, TABLE 13-1 -- Stress Modalities Used with Echocardiographic Imaging Exercise Treadmill Supine bicycle Upright bicycle Lateral bicycle Pharmacologic stress Dobutamine Dobutamine-atropine Arbutamine (not currently available) Epinephrine Isoproterenol Dipyridamole Dipyridamole-dobutamine Adenosine Pacing Esophageal Atrial Other Hand grip Cold presser Mental stress Hyperventilation Postventricular beats dobutamine frequently does not cause an adequate rise in heart rate, and for this reason, atropine is often needed to increase myocardial oxygen demand.[35] [36] Despite these drawbacks, dobutamine can provide information about the presence or absence of coronary disease, which is valuable in patient management decisions and prognostication. Arbutamine, which is the only pharmacologic stress testing agent approved by the Food and Drug Administration, provides a more balanced heart rate and blood

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pressure response without the need for atropine.[37] [38] Because of cost, however, and because it did not provide a clear advantage over dobutamine, Arbutamine was withdrawn from the market. Isoproterenol, because it produces extreme tachycardia, is no longer used as a stress agent. Atrial pacing, sometimes employed via a transesophageal approach, is reliable but is cumbersome and uncomfortable for the patient and therefore rarely used. Vasodilators, such as dipyridamole and adenosine, create ischemia through the mechanism of coronary steal, or the selective dilation of nonstenotic coronary beds. Following administration of these agents, normal coronary beds dilate preferentially in relation to stenotic beds, in effect shunting flow away from stenotic beds and rendering them ischemic. Some experts believe, and the medical literature suggests, that echocardiography has a lesser sensitivity for the detection of coronary disease when vasodilators are used, as compared with exercise and dobutamine.[39] [40] [41] Nonetheless, dipyridamole continues to be used for the detection of coronary disease, chiefly outside the United States, where the cost of this agent is lower. The type of stress one chooses to apply in conjunction with echocardiography should be based on the patient's ability to exercise and the diagnostic information one wishes to gain from testing. For example, for the initial diagnosis of coronary artery disease in a patient whose chest pain is provoked by physical exertion, exercise would be preferred. For patients unable to exercise maximally because of arthritis, peripheral vascular disease, or general deconditioning, pharmacologic stressors are more appropriate. Rarely, chest pain may be believed to be provoked by vasospasm, and for those patients whose chest pain is suspected to be vasospastic, ergonovine or hyperventilation may be appropriate.[42] [43] The choice of stress should also be governed by the patient's familiarity with types of activities. In the United States, the most popular form of applied physical stress for the purposes of diagnostic testing for coronary disease remains treadmill exercise. Familiarity with walking may lead to achievement of higher cardiovascular workloads. In European countries, upright bicycle exercise is a more familiar activity and has assumed a prominent role. More recently, the supine bike, sometimes with lateral angling, is emerging in the United States as a popular technique for assessment of coronary artery disease. Supine bicycle exercise facilitates imaging whenever a continuous record of echocardiographic images is desired. In the diagnosis of coronary disease, bicycle exercise allows one to determine more precisely the level of exercise at which ischemia develops,

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which, as discussed later, may be advantageous in the serial assessment of patients. Bicycle exercise also facilitates assessment of the clinical significance of valvular 278

Figure 13-2 Stress echocardiography laboratory equipment set-up, beginning in the lower left-hand corner and moving clockwise: crash cart, frame grabber, echocardiography machine, bed with shelf above for pulse oximeter and automated blood pressure cuff, electrocardiographic monitoring machine, blood pressure (BP) cuff (manual), treadmill, intravenous (IV) infusion pump for pharmacologic stress echocardiography, and IV equipment. The room measures 15 × 18 feet and requires no more than two steps for the patient between treadmill and bed.

heart disease and pulmonary hypertension through assessment of Doppler jets at various workloads. Equipment, Methodology, and Personnel The equipment needed for exercise echocardiography partially depends on the type of stress applied in conjunction with echocardiography. In all cases, high-quality echocardiographic instrumentation with an integrated or free-standing digital frame grabber, an offline analysis system, and either a treadmill or bicycle (supine or upright) connected to a computerized 12lead electrocardiograph are required. The ergonomics of the stress echocardiography laboratory should facilitate moving from the imaging bed to the treadmill and back to the imaging bed immediately after exercise in as few steps as possible. Following the use of any standard treadmill protocol, the patient steps off the treadmill and onto the imaging bed. Extra steps spent between equipment may result in a critical loss of imaging time during the immediate postexercise period, leading to loss of sensitivity. Thus, the most critical period of time in performing exercise echocardiography is that spent between the termination of exercise and the start of imaging. A typical floor plan for a stress echocardiography laboratory that requires a minimum number of steps for both patient and technician-sonographer is shown in Figure 13-2 . The set-up shown in Figure 13-2 rarely requires multiple steps for the patient between the treadmill and imaging bed. Imaging should take place as quickly as possible, since it has been shown that information about ischemia, particularly single-vessel disease, will be lost as the heart rate returns to

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normal. Some experts believe that special imaging beds with lateral cut-outs for apical imaging facilitate image acquisition. Images are typically captured in four views for side-by-side comparison in a digital format. The parasternal long- and short-axis and apical four- and two-chamber views have traditionally been used, with the substitution of subcostal images, if necessary, for patients with chronic obstructive pulmonary disease or postbypass surgical bandages that interfere with imaging windows.[44] Modification of chest lead placement is sometimes necessary to 279

obtain the best imaging windows and rarely interferes with the integrity of the electrocardiographic response. The question of whether to perform a complete baseline study with Doppler imaging or to simply capture the minimum number of images required for stress imaging often arises. In our laboratory, the practice is to perform a complete baseline study unless one has recently been performed and there has been no interim change in the patient's clinical status. The personnel required to perform exercise echocardiography varies in different laboratories depending on local standards of practice, hospital regulations, and level of billing. In most cases, at least two people are required to carry out exercise echocardiography: a technician-sonographer to perform the imaging and a second technician to monitor the patient's hemodynamic, electrocardiographic, and symptomatic responses to exercise. Regardless of the type of exercise used (i.e., treadmill or bicycle), a sonographer records baseline images at rest, followed by images during or immediately after peak exercise, while a monitoring technician notes and records the hemodynamic and electrocardiographic responses to exercise. At the completion of exercise, the monitoring technician assists the patient in quickly stepping off the treadmill or upright bicycle and reassuming the left lateral decubitus position for postexercise and recovery images, which take place on an imaging table or bed. Alternatively, a nurse or a physician may monitor and assist the patient. One advantage to physician monitoring is that it allows for immediate image interpretation of poststress images. Some laboratories use registered nurses trained as sonographers for both imaging and monitoring functions, eliminating the need for two staff members. Depending on local standards of practice, some hospital laboratories require physician presence in all cases, either in the stress

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echocardiography room itself, or within the immediate area. In our hospital's echocardiography laboratory, all pharmacologic stress tests and high-risk patients referred for exercise tests are supervised directly by a physician. Outpatient clinic echocardiographic laboratories are growing in number. The equipment is the same as for hospital laboratories, but often one technician performs both monitoring and imaging functions, with a physician available within a few steps of the laboratory. The need for frequent hemodynamic monitoring will be facilitated by the use of an automated blood pressure cuff. Obviously, it is best not to perform exercise echocardiography on high-risk patients in this setting. The safety of exercise echocardiography is comparable to the safety of other stress testing modalities. A reported mortality rate of 1 in 10,000 patients with adverse events ranging from 4 to 9 in 10,000 are reported for stress electrocardiography, echocardiography, and nuclear scintigraphy.[45] [46] [47] [48] As with any form of stress testing, a crash cart should be kept within the vicinity of the testing area. Outpatients referred to hospital laboratories may not be well known to the staff performing the test, and for safety reasons, heart rate–lowering medications such as beta blockers and calcium channel blockers are sometimes continued. A question occasionally arises about whether to stop a patient's beta blocker prior to testing, since rapid decay of heart rate response after discontinuing exercise is largely responsible for loss of wall motion information. This may create the problem of achieving a submaximal test because of inadequate heart rate response. One potential solution in clinically stable patients is to decrease their beta blocker dose on the evening prior to testing to one-half dose, and to hold beta blockers on the morning of the test. This simple protocol often allows patients to minimize the antichronotropic effects of beta blockade while still retaining some measure of safety with a weaning protocol. Analysis of poststress images has been greatly facilitated by online digitization of images, which allows side-by-side comparison of views.[6] [49] [50] Prior to the development of digital images, the feasibility was lower— around 70%—for successful imaging in an unselected population owing to motion and respiratory artifact. With the advent of digital techniques, feasibility has risen to well over 90% in experienced laboratories. Frame grabbers for digital display allow selection of the optimal images out of multiple cardiac cycles, after all images are obtained. Thus, the technician

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is able to select images without lung interference after all imaging is completed. Asking the patient to perform a breathing maneuver for 2 to 5 seconds during acquisition is another technique that facilitates obtaining high-quality images devoid of respiratory artifact. This maneuver, which works best when practiced during baseline imaging, involves asking the patient to exhale completely or "take in a half breath" and hold his or her breath for a few seconds during the postexercise images. Following optimal image selection, which may be performed by the physician or an experienced sonographer, images are then displayed in side-by-side format with prestress and poststress images adjacent to each other for comparison, generally in right-to-left fashion (Fig. 13-3) . Side-by-side comparison of segments in a gated format facilitates recognition of more subtle abnormalities, raising diagnostic accuracy. Most digitization systems acquire loops of eight frames for each view, with 50 msec allowed for each frame. This time period allows for systolic frames, with a limited portion of diastole, to be captured by triggering image acquisition at the beginning of the R wave of the electrocardiogram. Eight frames are then displayed in a continuous loop format for playback. Imaging acquisition time should be of sufficient duration to digitize all four views but must be performed quickly enough to visualize transient wall motion abnormalities, lest important information be lost as ischemia quickly resolves. Approximately 10 to 20 seconds are needed for digital capture of each view. Ideally, all four views can be digitally captured in approximately 1 minute. In our laboratory, postexercise apical views are captured first to facilitate recording wall motion in distal coronary territories, which are most likely to display ischemic abnormalities. A videotaped recording is made for back-up, and review of these images is recommended to ensure that the captured images are representative of the videotape. Treadmill Exercise Echocardiographic Protocol The most popular form of stress used in exercise echocardiographic testing in the United States is treadmill 280

Figure 13-3 Quad-screen format depicting parasternal long-axis and shortaxis views. Diastolic frames (DIAS) and systolic frames (SYS) at baseline (PRE) and immediately after treadmill exercise (POST) are shown. The

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ventricular response is normal after exercise, with increased endocardial excursion and increased wall thickening in all visualized segments.

exercise, partly because of the familiarity of walking as a form of exercise and partly because of improved image quality over that of bicycle protocols. Analysis of images depends on the direct comparison of preexercise and postexercise images. Parasternal long-axis, short-axis, fourchamber, and two-chamber images are obtained at rest both on videotape and, as noted previously, on an eight-cell cine loop for display in a side-byside quad-screen format at 50 msec per frame. In our laboratory, a complete baseline study with Doppler examination is usually performed simultaneously. The patient is then asked to step onto the treadmill and to begin exercise on one of various standard protocols available. The Bruce protocol is the most commonly used protocol, but the modified Bruce or the Cornell protocol are options for patients who are not in optimal cardiovascular condition or who require a longer warm-up period. Once baseline images are obtained, treadmill exercise proceeds in usual fashion, limited by symptoms, significant electrocardiographic changes, or a predetermined maximal exercise capacity. After cessation of exercise, the patient steps off the treadmill and reassumes the left lateral decubitus position for 281

Figure 13-4 Wall motion score index incorporating a 16-segment model using the scoring system depicted at the top. Numbers 5 and 7 are arbitrarily assigned a score of 4 (indicating dyskinesis), whereas 6 (akinesis with scar) defaults to 3 (akinesis) for the purposes of calculating the wall motion score index. The report shows scores for pre-exercise and postexercise wall motion and demonstrates apical akinesis after treadmill exercise. The global wall motion score index is normal before exercise (1.0) and worsens (1.3) after exercise.

posttreadmill imaging within seconds. This requires a degree of patient agility, as well as considerable operator skill. As noted, because time delays may allow the decay of heart rate, and induced wall motion abnormalities may normalize quickly after exercise, any undue delays during the critical period between cessation of exercise and start of imaging may have the effect of lowering the overall accuracy of the test, particularly in areas of collateral flow, single-vessel disease, and moderately stenotic (50–70%) lesions.[51] Conversely, at higher workloads, greater degrees of ischemia

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occasionally ensue, and prolonged myocardial stunning may take place, with wall motion abnormalities persisting for several minutes after exercise.[1] [52] [53] [54] Because of the technical difficulties involved in the acquisition of images within a limited time frame, a learning curve exists for the experienced technician-sonographer of about 50 stress echocardiographic studies. This learning curve is clearly required prior to smooth performance and acquisition of images within the required 90second time period. Bicycle Exercise Echocardiographic Protocol Two bicycle protocols are currently in use: upright and supine. Although these are more widely used in Europe in conjunction with echocardiography, both have enjoyed an increase in popularity in the United States. In each of the bicycle protocols, imaging is performed at baseline, at peak exercise, and immediately after exercise. The upright bicycle protocol is shown in Table 13-2 . In the upright bicycle protocol, two-dimensional baseline images are recorded at rest in the parasternal long- and short-axis and apical four-chamber and two-chamber views in the left lateral decubitus position. The patient moves onto the upright bicycle, and the apical views are repeated at rest in the upright position. Using the same view facilitates comparison between rest and peak images. Exercise then begins with the patient pedaling, sometimes following a brief warm-up period, and proceeds in increments of 25 to 50 watts in 2- or 3minute stages. As the patient exercises, apical views can be recorded on tape throughout the examination. End points for bicycle exercise are the same as for treadmill imaging: predetermined age-related peak heart rate, the development of significant symptoms, or significant electrocardiographic changes. Just prior to stopping at peak exercise, the apical four-chamber and two-chamber views are recorded, and the patient resumes the left lateral decubitus position on an examining bed or table for immediate postexercise parasternal views, as well as repeat apical views. Digital TABLE 13-2 -- Upright Bicycle Protocol 1. Complete baseline study performed in left lateral decubitus position 2. Parasternal long-axis, short-axis, four-chamber, and two-chamber views recorded on tape and digitized 3. Patient assumes upright position on bicycle for apical rest views 4. Pedaling begins at 60 rpm, 25 watts, and increases by 25 watts every 2

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to 3 minutes 5. Peak exercise views obtained at the end of each stage 6. At completion of exercise, patient reassumes left lateral decubitus position for immediate postexercise and recovery images

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images are captured at the end of each stage, with each subsequent stage overriding the previous peak image. In this way, if a patient suddenly stops exercising early in any stage, the last image captured will be the peak exercise image. The exercise protocol itself may vary. One popular protocol is to have the patient begin pedaling at 60 rpm at 25 watts and to increase the resistance by 25 watts every 2 minutes while the patient continues to pedal at 60 rpm. Maximal exercise is then terminated at 250 watts or at 85% of the predicted maximal heart rate. Because many patients undergoing testing are older, their ability to pedal is highly variable, and tremendous latitude may be necessary in selecting workloads. Smaller increases in resistance are usually necessary in elderly individuals and patients unaccustomed to bicycle exercise. Also, variations in the imaging protocol are sometimes needed because of technical difficulty in obtaining apical views during exercise. One alternative to apical imaging is subcostal views.[44] This approach eliminates superimposition of the air-filled lung and may be more feasible for patients with chest wall deformities or chronic obstructive lung disease. Compared with the upright bicycle, supine bicycle exercise has a simpler protocol in that all imaging takes place with the patient on the bicycle, eliminating the need for an additional imaging table or bed for parasternal views. After acquisition of all four baseline views (parasternal long-axis, parasternal short-axis, four-chamber, and two-chamber) as described earlier, the patient begins pedaling in the supine position while apical views are obtained at each stage and recorded on videotape during exercise in similar fashion to the upright bicycle. At peak exercise, the images are digitized for viewing in quad-screen side-by-side format as previously described. In our laboratory, the four quadrants consist of pre-exercise images on the left and peak exercise images on the right, a display similar to that used in posttreadmill exercise. In addition, recovery images are

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recorded on videotape after the heart rate and blood pressure have returned to pre-exercise levels. Comparison of Stress Modalities As mentioned earlier, all forms of exercise have their relative advantages and disadvantages, and selection of stress modality should be based on individual patient characteristics, the patient's ability to exercise, and the information one wishes to obtain (Table 13-3) . With treadmill exercise, imaging at peak stress is technically difficult and, although a few reports have explored the feasibility of peak treadmill imaging, posttreadmill imaging TABLE 13-3 -- Comparison of Peak Bicycle and Posttreadmill Imaging Peak Bicycle Imaging Improved sensitivity Slightly decreased specificity Lower cardiovascular workloads More leg fatigue

Posttreadmill Imaging Less cumbersome protocol Improved image quality Higher cardiovascular workloads More familiar, better tolerated by most patients

remains the most widely applied technique. Advantages of treadmill exercise include patient familiarity as well as a lack of need for additional equipment, since most laboratories and hospitals are already equipped with a treadmill for routine exercise testing. In many cases, a digital frame grabber to digitize images at baseline and at peak exercise for side-by-side comparison is the only additional equipment required. One of the main disadvantages of the treadmill is that it relies on capture of images in "allor-none" fashion after exercise, providing a post-stress "snapshot" of the heart. Unlike with bicycle stress, which provides multiple views of the heart at various intermediate stages of stress, the exact stage of onset of ischemia cannot be detected with treadmill protocols. An advantage of bicycle exercise, therefore, is the ability to image at various levels of stress, allowing the time to onset of ischemia to be recorded and compared between serial studies, possibly providing additional prognostic information. Peak images, rather than posttreadmill images, also have the theoretical advantage of higher sensitivity, since wall motion abnormalities may revert to normal within seconds after exercise.[52] This advantage of bicycle exercise over treadmill exercise may be offset,

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however, by the fact that in the United States patients are usually more accepting of treadmill exercise and less limited by leg fatigue, since walking is a familiar activity. Exercising in the supine position requires that the weight of the legs be supported against gravity and may lead to earlier stopping because of leg discomfort and fatigue. In addition, supine exercise may lead to submaximal heart rate response and lower cardiovascular workloads, with the development of angina at a lower pressure rate product. [55] [56] Thus, maximal workloads attained in the supine position may actually be lower than those obtained in the upright position on the bicycle or the treadmill. Upright bicycle exercise theoretically produces higher workloads at equivalent levels of blood pressure and heart rate but provides a more cumbersome protocol. The major potential advantage of imaging performed at peak exercise rather than postexercise is that transient ischemia and its ensuing wall motion abnormalities may resolve quickly and be missed with posttreadmill testing, leading to a lower sensitivity for the detection of coronary artery disease. As noted, however, the higher workload achieved with treadmill exercise may offset the potential benefit of imaging during peak exercise. One study has directly compared the sensitivity and specificity of peak versus postexercise imaging using the same exercise modality in the same patients. Presti et al[52] used upright bicycle echocardiography to evaluate 104 consecutive patients referred for known or suspected coronary disease. Of these, 96 patients had echocardiograms suitable for wall motion analysis at rest, during peak bicycle exercise, and immediately after bicycle exercise (feasibility, 92%). The overall sensitivity of postexercise imaging for the detection of coronary disease was 70%, compared with 100% for peak exercise images. When the parasternal views were added, three additional patients demonstrated postexercise abnormalities. When the coronary anatomy of patients with false-negative studies was examined, it was found that the development of wall motion abnormalities 283

at only peak exercise was more likely to occur in patients with stenotic areas supplied by collateral flow. There have been few direct comparisons of different types of exercise in conjunction with echocardiography in the same patient population. Three studies have compared treadmill testing and bicycle exercise testing in conjunction with echocardiography. The earliest of these, by Applegate et

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al,[57] evaluated 21 patients after myocardial infarction using low-level, symptom-limited stress testing, with similar workloads achieved in each form of exercise. This study suggested that the delay in posttreadmill imaging did not significantly affect the sensitivity for detection of exerciseinduced ischemia in this postmyocardial infarction population. Two studies have compared posttreadmill with peak supine bicycle exercise in a stable population with coronary disease.[58] [59] One of these studies noted an advantage for peak stress bicycle imaging in the identification of coronary disease. Dagianti et al,[58] examining a small series of 10 male patients with coronary disease, noted 100% sensitivity for supine bicycle with only 60% for posttreadmill imaging. In a larger series of 74 patients, Badruddin et al [59] noted a sensitivity of 83% and specificity of 70% for supine bicycle and 75% and 90% for treadmill echocardiography, a difference that did not reach statistical significance. Taken together, these data may indicate a relatively small advantage in the detection of ischemia for selected patients who are able to perform bicycle exercise, particularly patients with singlevessel disease or collateral flow. Interpretation of Stress Echocardiograms Echocardiograms can be interpreted qualitatively, with a descriptive summary of the myocardial response to exercise, or quantitatively, providing a numeric description of wall motion (see Fig. 13-4) . For clinical purposes, a descriptive summary of wall motion response often provides enough information to aid the referring clinician in patient management. Regardless of the chosen scheme, a normal echocardiogram is one in which there is normal resting wall motion and a hyperdynamic response to exercise with symmetric wall thickening and equal excursion in all segments. The development of a wall motion abnormality either at peak exercise or immediately after exercise is sensitive and specific for ischemia and is evidence of underlying coronary disease. Using a qualitative approach, wall motion is often described as "normal," "ischemic," or "fixed," depending on the response to exercise (Table 13-4) . Ischemic segments are labeled as such if they appear normal or mildly hypokinetic at rest and worsen with exercise, whereas fixed areas are akinetic at rest and are unchanged or become dyskinetic with exercise, implying scarred myocardium due to transmural infarction. In most studies, new wall motion abnormalities may be detected when a coronary stenosis of greater than 50% exists, with increased likelihood for detection with stenoses of greater than 70%. Accordingly, using a visual estimate of 50%

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as a cut-off point would result in a lower sensitivity for detection of coronary disease than using 70%. Hypokinetic TABLE 13-4 -- Categorization of Exercise Echocardiographic Wall Motion Responses Wall Motion at Rest Normal Normal Abnormal excursion (thinned) Abnormal excursion (preserved thickness)

Wall Motion During Exercise Normal Abnormal: Worsening Fixed: No significant change New or worsening abnormality

Category Normal Ischemic Scar: Transmural infarction Hibernating

areas with full-thickness myocardium that worsen after exercise are likely to represent areas that are both viable and ischemic, the resting abnormality representing stunned or hibernating myocardium. Using qualitative terms such as these, one generally reports a description of wall motion and a diagnosis such as "inferior hypokinesis following exercise, consistent with inferior ischemia." Occasionally, lack of hyperdynamic response or frank hypokinesis will be noted in myocardium that is not supplied by a significant stenosis. This situation has been noted in aortic valve disease, in extreme elevations in blood pressure, and, in our experience, occasionally with occult myopathy. The most widely accepted quantitative approach is the wall motion score index recommended by the American Society of Echocardiography, which uses a scoring system from 1 to 4 depending on the degree of abnormality. [60] A grade of 1 is assigned to normal segments and 2 through 4 for hypokinetic, akinetic, or dyskinetic segments, respectively. Some laboratories also grade the lack of development of a hyperdynamic response as abnormal, assigning a grade of 0 to hyperkinetic regions. Grading lack of hyperdynamic response as abnormal results in higher sensitivity for the detection of coronary disease but may result in poorer specificity.[61] Using this wall motion scoring system, one then assigns a number to each of 16 segments and divides by the total number of segments for the calculation of a global wall motion score index (Fig. 13-5) . Alternatively, individual coronary territories can be assigned a "regional" wall motion score index. Either a global score or a regional score can then be used to assess responses to specific medical therapy or to cardiac

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interventions over time. With use of a regional wall motion score index, it is possible to predict the specific location of a coronary artery stenosis from the area of the wall motion abnormality and thus to provide important prognostic information regarding the nature of the underlying disease. A schematic representation of coronary blood supply in each segment using a 16-segment model is shown in Figure 13-5 . With this scheme, accurate distinction of anterior from posterior circulation is possible. Within the posterior circulation, separating left circumflex from right coronary artery territory is much more difficult because of individual variation in anatomy. In most situations, however, important diagnostic information is provided simply by separating the left anterior descending territory from the posterior circulation. Obviously, segments with normal resting ventricular 284

Figure 13-5 Diagram depicting how coronary artery territory is incorporated into the 16-segment model. Although some overlap is commonly seen, separation of anterior from posterior circulation is 80% to 90% accurate. Individual variation in coronary anatomy usually precludes accurate separation of right coronary from left circumflex territories. (Modified from Segar DS, Brown SE, Sawada SG, et al: J Am Coll Cardiol 1992;19:1199, with permission from the American College of Cardiology.)

function that augment during exercise indicate a patent coronary blood supply. Figure 13-3 depicts a normal hyperdynamic ventricular response after exercise, implying normal coronary arteries. As noted, normal resting ventricular function in a segment or segments that worsen during exercise indicates the presence of significant underlying coronary disease and ischemia. Figure 13-6 depicts an ischemic response following treadmill exercise. In this case, a 52-year-old woman with new-onset exertional discomfort demonstrated normal resting systolic function. After 6 minutes of exercise, a wall motion abnormality developed in the anterior septum, signifying left anterior descending artery ischemia (as seen in the postexercise systolic image). This patient was found to have a 75% stenosis of the left anterior descending artery. Abnormal resting ventricular function that worsens during or after exercise is sometimes a confusing picture and may represent one of a number of

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potential clinical possibilities. Areas of full-thickness myocardium that are hypokinetic at rest may represent areas of chronic repetitive stunning, chronically ischemic (hibernating) myocardium, or previous nontransmural myocardial infarction supplied by a critically stenosed artery. Regardless of the cause of resting hypokinesis, worsening after exercise is likely to represent an ischemic response. Segments that are bright, thin, and akinetic at rest and become dyskinetic after exercise are more likely to represent transmural infarction without significant ischemia. The patient depicted in Figure 13-7 is a 54-year-old man with chest discomfort who was able to exercise for 8 minutes on a Bruce protocol. The wall motion is normal at rest. Following treadmill exercise, an abnormality developed in the basal inferior segments (seen in the lower right-hand frame), and at catheterization the patient was found to have an 80% stenosis of the right coronary artery. One sees a break point in the myocardium (arrow) at the junction of the right coronary and left anterior descending artery territories, signifying left anterior descending artery patency juxtaposed against a stenosed right coronary artery. The patient in Figure 13-8 demonstrates abnormalities in the same myocardial segments of the basal inferior wall; however, in this case the myocardium is thinned and aneurysmal at rest, consistent with prior transmural infarction of the interior wall. Worsening 285

Figure 13-6 Exercise echocardiogram demonstrating anterior ischemia with dyskinesis of the anterior septum in parasternal long-axis view after exercise. The response suggests hemodynamically significant disease in the left anterior descending artery. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic.

in this case from akinesis to dyskinesis represents a fixed abnormality consistent with scar rather than ischemia. At catheterization, a total occlusion of the right coronary artery was found. As noted, myocardium that is hypokinetic at rest may represent stunning, hibernating, or a mixture of normal and infarcted myocardium. Accurately sorting out and interpreting the responses to exercise in these complex cases often requires integration of angiographic data derived from cardiac catheterization as well as the clinical

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Figure 13-7 Exercise echocardiogram demonstrating inferior ischemia. Diastolic (DIAS) and systolic (SYS) frames at baseline (PRE) and after exercise (POST) demonstrate normal resting wall motion with outward systolic motion (dyskinesis) of basal inferior segments after exercise. This patient had a critical stenosis of the right coronary artery. (See text for further explanation.)

history. Some of these complex responses and the possible relationship to the underlying clinical significance are shown in Table 13-5 . Advantages and Disadvantages of Exercise Echocardiography When compared with routine treadmill exercise, there are a number of advantages to performing exercise echocardiography, 286

Figure 13-8 Exercise echocardiogram demonstrating prior inferior wall myocardial infarction due to right coronary artery occlusion. The basal inferior segments are echogenic and akinetic at rest, suggesting scar. After exercise, the scarred region becomes dyskinetic, indicating "fixed" disease. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic.

as shown in Table 13-6 . Although routine treadmill testing remains the most prominent form of diagnostic testing for patients with known or suspected coronary disease in the United States, its sensitivity and specificity are limited in many patients in whom the ST segment response is unreliable or uninterpretable.[62] [63] [64] [65] Patients who have a high likelihood of false-positive, false-negative, or nondiagnostic electrocardiographic responses demonstrate improved accuracy for the detection of coronary TABLE 13-5 -- Clinical Interpretation of Complex Responses * Interpretation Normal Excursion Wall thickness CAD/No MI Excursion

At Rest

After Exercise

Normal Normal

Hyperdynamic

Normal

Hypokinetic, akinetic, or dyskinetic

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Wall thickness Normal CAD/Nontransmural MI Excursion Hypokinetic or akinetic

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Augmented, hypokinetic, akinetic, or dyskinetic (dependent on infarct artery patency)

Wall thickness Partial or full CAD/Transmural MI Excursion Akinetic Akinetic or dyskinetic Wall thickness Thinned CAD/Hibernating/Stunned Excursion Hypokinetic or Incompletely investigated May akinetic augment with mild exercise Wall thickness Partial or full CAD, coronary artery disease; MI, myocardial infarction. * Response depends on extent of residual stenosis.

disease with the addition of echocardiography.[6] These include women; patients with left bundle branch block; patients taking digoxin; patients with prior nontransmural myocardial infarction, Wolff-Parkinson-White syndrome, or mitral valve prolapse; patients with hyperventilation ST segment changes; and a large group of patients with nonspecific ST-T wave changes at rest. Echocardiographic imaging in conjunction with exercise stress testing has been shown to increase the diagnostic accuracy in patients such as these with resting electrocardiographic abnormalities, which some experts believe make up as much as 30% to 40% of patients presenting for exercise testing. A major advantage of exercise echocardiography is its versatility in the diagnosis of structural heart disease not related to coronary disease. Echocardiography has the ability to diagnose any and all forms of structural heart disease as a cause of angina or other cardiac symptoms. Thus, if exertional symptoms are due to valvular heart disease, pulmonary hypertension, diastolic dysfunction, or pericardial disease, the diagnosis can be made with exercise echocardiography. Figure 13-9 provides an example in which shortness of breath was suspected to be an anginal equivalent in a

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patient with multiple risk factors TABLE 13-6 -- Relative Advantages and Disadvantages of Stress Echocardiography Advantages Versatile (evaluates all structural abnormalities) Portable

Disadvantages Analyzed qualitatively Requires additional trained personnel Requires additional equipment Adds time to routine treadmill test

Minimal space requirements Increases sensitivity and specificity Evaluates wall thickening Low risk

287

Figure 13-9 Parasternal long-axis and short-axis views depicting a normal hyperdynamic response to exercise in a patient with severe left ventricular hypertrophy and resting repolarization changes on electrocardiogram. Systolic frames (SYS) are compared before (PRE) and after (POST) treadmill exercise. DIAS, diastolic.

for coronary disease. In this case, a patient with chronic renal disease, hypertension, and obvious left ventricular hypertrophy demonstrated baseline secondary ST segment changes and a positive electrocardiographic response to exercise, while the echocardiographic response clearly demonstrates a normal hyperdynamic response, with increased endocardial excursion and symmetric wall thickening in all segments. In some cases, the baseline study may provide clues to diagnosis and reveal a contraindication to stress testing, such as the finding of critical aortic stenosis or significant pericardial effusion. In our laboratory, a previously unsuspected but important cardiac diagnosis occasionally emerges from the resting echocardiographic study and engenders a reason to cancel the stress test. In this respect, exercise echocardiography provides a measure of safety unattainable by routine electrocardiographic monitoring or radionuclide imaging. Another advantage is that echocardiographic equipment can be transported to any area equipped with a treadmill or stationary bicycle, such

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as the hospital emergency department. Echocardiography is also the only bedside imaging technique that evaluates systolic wall thickening. There are some potential disadvantages to the addition of echocardiography to routine treadmill testing. First, it requires additional personnel and training. In most laboratories this requires two technicians, but one experienced technician may perform both the imaging and monitoring tasks, provided there is a physician in the immediate area (see Equipment, Methodology, and Personnel and also Fig. 13-2) . Another potential disadvantage to exercise echocardiography is the need for additional equipment, which in some cases is only a device for frame-grabbing digital images, since many outpatient clinics and hospitals are already equipped with echocardiographic instrumentation and a treadmill. Echocardiographic imaging also adds approximately 30 minutes to the time of the routine treadmill test. Also, although the results are reproducible, to date no highly quantifiable methods exist to evaluate wall motion or systolic thickening in the clinical setting.[64] Until an easily quantifiable system for wall motion evaluation exists, interpretation of stress echocardiograms remains largely qualitative. Given the overall accuracy reported, this has not proved a major disadvantage. Obviously, these potential disadvantages are a trade-off for increased diagnostic accuracy compared with treadmill testing. It is important to remember, however, that as with any form of imaging in conjunction with exercise testing, the sensitivity of stress echocardiography will be poor in patients who cannot reach an adequate level of cardiovascular stress. For those patients, pharmacologic stress echocardiography is a desirable alternative (see Chapter 14) . Patients who should undergo pharmacologic stress because of high rates of false-negative results due to inadequate exercise levels include patients with peripheral vascular disease, patients with orthopedic problems, elderly persons, and individuals who are deconditioned. For these and other unselected patient populations, the reported accuracy of dobutamine echocardiography for the diagnosis of known or suspected coronary disease has been excellent, around 85% to 95%. This is well within the range of competing nuclear imaging techniques.[7] [8]

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Clinical Applications of Exercise Echocardiography Accuracy in the Identification of Coronary Artery Disease Several studies have been published reflecting the overall accuracy of exercise echocardiography in the diagnosis 288

of coronary artery disease.[44] [51] [52] [55] , [61] [66] [67] [68] [69] [70] [71] [72] [73] [74] [75] [76] [77] [78] [79] In the first of these studies, published by Wann et al[1] [6] in 1979 at Indiana University, patients were studied with a 30-degree sector scanner during peak supine bicycle exercise. Despite primitive equipment, the overall sensitivity was 87% and the specificity was 100%, not unlike the sensitivities and specificities currently reported with state-of-the-art imaging equipment and digital acquisition techniques. The accuracy of various exercise stress echocardiographic techniques has been verified in numerous laboratories. Many early studies reported sensitivities in the range of 60% to 90%, whereas more recently, particularly with the advent of digital imaging methodologies, sensitivities have more consistently been in the higher end of this range. Table 13-7 compares the sensitivities and specificities of some of the larger reported studies. Many of the early studies focused on the ability of stress echocardiography to detect changes in global function, sometimes using radionuclide ventriculography as the gold standard.[69] [80] [81] [82] These studies demonstrated an increase in indices of global systolic function (such as ejection fraction or pressure/volume ratio) for normal subjects and depressed indices for patients with previous myocardial infarction. One of the first large studies demonstrating increased sensitivity and specificity with the addition of echocardiography to routine treadmill testing using arteriography as the gold standard was that of Armstrong et al,

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[6]

in which 95 patients underwent both posttreadmill exercise and cardiac catherization. Of the 59 patients in whom there was no evidence of prior infarction, 44 were found to have coronary disease at subsequent coronary arteriography. Exercise echocardiography was abnormal in 35 of these 44 patients, for an overall sensitivity of 80%. In contrast, the exercise electrocardiogram demonstrated ischemia in only 19 of these patients (sensitivity, 43%) and was normal in 13 patients (30%) and nondiagnostic in 12 patients (27%), demonstrating the ability of exercise echocardiography to identify coronary disease in patients with an ambiguous or inaccurate treadmill response. Conversely, exercise echocardiographic results were normal in 13 of 15 patients without coronary disease, for a specificity of 87%. In 36 patients with prior infarction, 35 had rest or exercise-induced wall motion abnormalities, or both, for a sensitivity of 97%. TABLE 13-7 -- Accuracy of Exercise Echocardiography

Study Limacher et al[69] Armstrong et al[6] Armstrong et al[32] Ryan et al

Patients, n Modality 73 Treadmill

Single Stenosis Vessel * Grade, Sensitivity, Disease, Sp % % % 50 91 64

95 Treadmill

50

88

—

123 Treadmill

50

88

81

64 Treadmill

50

78

76

[72]

Sawada et al[124] Crouse et al[61] Marwick et al[76] Hecht et al

57 Treadmill/upright bicycle 228 Treadmill

50

86

88

50

97

92

150 Treadmill

50

84

77

180 Supine bicycle

50

93

84

[50]

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Ryan et al

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309 Upright bicycle

50

91

86

150 Treadmill

50

91

—

80 Treadmill

50

89

76

[51]

Roger et al [67]

Marangelli et al[143]

* Definition of significant coronary artery disease.

Because the inclusion of patients with left ventricular wall motion abnormalities at rest falsely elevates the sensitivity of echocardiography for the detection of coronary disease (a fact that is also true for radionuclide imaging), a later study from the same laboratory examined the use of exercise echocardiography in 64 patients with normal wall motion at rest.[72] Twenty-four patients had no angiographic evidence of coronary artery disease, and all 24 had a negative exercise echocardiogram, for a specificity of 100%. Of 40 patients with coronary disease, 31 had a positive exercise echocardiogram (sensitivity, 78%). In a more current era, Marwick et al[76] reported an overall sensitivity of 84% and a specificity of 86% in 150 patients who underwent exercise echocardiography and coronary arteriography, with slightly higher sensitivity and slightly lower specificity when patients with nondiagnostic test results were excluded. Nondiagnostic test results stemming from an inability to reach a target heart rate in the setting of beta blocker use is a common problem in a clinical setting and appears to affect sensitivity more than specificity.[83] Sensitivities and specificities may vary between studies depending on the prevalence of disease in the population under study, the definition of significant disease, and the criteria used for a positive test. Clinical factors such as age, cardiac risk factors, and prior history of angina, all of which affect pretest likelihood of coronary disease, influence sensitivity and specificity, with sensitivities tending to be higher in populations with a higher pretest likelihood of disease. Sensitivity and specificity are also affected by the criteria used to define a positive test. Crouse et al[61] reported a high sensitivity of 97% and a relatively low specificity of 64% in a series of 228 patients undergoing treadmill echocardiography as a screening test. In this study, a normal test was defined as the presence of hypercontractility in addition to the absence of inducible wall motion abnormalities, adding to

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the sensitivity but detracting from the specificity of the results. Probably the biggest influence on specificity is that of posttest referral bias, which alludes to the fact that as a test becomes more accepted by the medical community, more patients with positive tests, and fewer of those with normal studies, are referred for coronary arteriography. Since only a small proportion of those with normal studies are given the opportunity to verify their test results, this 289

tends to lower specificity dramatically. Concomitantly, sensitivity is raised, since more patients with positive tests are referred for angiography. This point was illustrated in a study of 244 men and 96 women by Roger et al[80] that noted that bias in referral patterns for angiography may have a dramatic effect in lowering specificity. Accuracy of all types of stress testing is equally affected by biased referral for cardiac catherization or "verification bias," with lower sensitivities and higher specificities likely compared with those reported. To overcome posttest referral bias, in some studies a "normalcy" rate is calculated for subgroups thought to be at low risk for coronary artery disease within a population. This can then be used as a reasonable substitute for specificity. Thus, through clinical characteristics and demographic factors, subgroups likely to have a less than 5% pretest likelihood of significant coronary disease are identified, and these patients are then assumed to be free of significant coronary artery disease. The number of patients with a normal stress test within this group are identified. Normalcy is then calculated as the number of patients with a normal exercise test divided by the number of those at very low clinical risk for the disease. A few studies have reported normalcy rates when the catheterized population was skewed in the direction of patients with coronary disease. In a published series of 180 patients studied with supine bicycle and coronary arteriography, Hecht[50] reported an overall sensitivity of 93%, a specificity of 86%, and an overall accuracy of 92%. The normalcy rate for 42 patients who had a less than 5% pretest likelihood of significant coronary disease was 100%. Similarly, Marwick et al[36] have reported a normalcy rate of over 90% in 29 of 150 patients with normal results on an exercise echocardiogram and low pretest likelihood. Another influence on the accuracy of exercise echocardiography is the definition of significant disease, which is in part determined by the physiologic significance of a stenosis. This was illustrated in a study by

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Sheikh et al[33] who found that stenoses of greater than 75% diameter were more frequently associated with wall motion abnormalities during exercise echocardiography than stenoses of less than 25%. Stenoses in the range of 50% appeared to be evenly divided between positive and negative results when assessed by visual estimates of stenosis. Using quantitative angiographic methods, however, the authors were able to further stratify the ventricular responses into two subgroups. Those patients with wall motion abnormalities were associated with luminal stenoses of greater than 50%, whereas normal wall motion was associated with stenoses of less than 50%, suggesting that visual estimates may be unable to determine which stenoses in the moderate range are significant. This and other studies highlight the limitations inherent in using a diameter stenosis as visually determined to define significant disease.[73] [85] [86] Factors such as proximal location, presence of collateral flows, and plaque morphology have been shown to influence coronary flow, particularly in the setting of submaximal effort. Some recent studies have used intravascular ultrasonography rather than arteriography to define significant stenoses, and these studies further emphasize the limitations of "luminography" as a gold standard. An arteriogram being a two-dimensional representation of a three-dimensional artery may under- or overrepresent the degree of stenosis depending on the views selected. Factors such as bends or kinks in the vessel may cause some areas to falsely appear stenotic, whereas plaque irregularity may lead to underassessment of the functional significance of stenoses.[87] In clinical practice, functional assessment of a stenosis in relation to results of stress testing should always be undertaken along with integration of clinical factors with angiographic results. Currently, the overall accuracy of exercise echocardiography is in the range of 80% to 90%. A recent meta-analysis of 2637 patients reported in 24 articles noted an overall sensitivity of 85% and specificity of 77% for exercise echocardiography, examining only studies in a current era that reported results for all patients such that the calculation of sensitivity and specificity was possible with numbers of patients reported, along with coronary angiography used as the reference test.[88] Taken together, these studies illustrate the ability of exercise echocardiography to identify patients with angiographically significant disease and to provide an assessment of the physiologic significance of stenoses comparable to other stress imaging tests. Exercise Echocardiography After Angioplasty

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Because of its ability to target separate coronary artery distributions, exercise echocardiography may be an ideal tool for surveillance of patients after coronary interventions. Studies suggest that echocardiographic imaging can assess the initial outcome of angioplasty, atherectomy, and stenting, as well as provide valuable information regarding the presence of restenosis.[89] [90] [91] [92] [93] [94] [95] [96] [97] [98] [99] [100] One of the early studies demonstrating the ability of exercise echocardiography to provide a functional assessment in patients before and after angioplasty was that of Broderick et al[91] in which 36 patients were studied before and after coronary angioplasty. Thirty-one patients demonstrated ischemia with either an abnormal exercise test result (exercise-induced ST depression or angina) or an abnormal exercise echocardiogram (exercise-induced wall motion abnormalities). After successful angioplasty, 17 patients continued to demonstrate exerciseinduced ischemia by either electrocardiographic or echocardiographic criteria. Although 12 of these 17 patients continued to demonstrate exercise-induced wall motion abnormalities, most were improved compared with the studies prior to angioplasty. Exercise duration, workload, and METS (metabolic equivalents) increased after angioplasty, suggesting that some of the wall motion abnormalities after angioplasty might be explained by a greater ischemic burden. Since follow-up studies were performed 2 weeks or more after angioplasty and no patient had undergone repeat angiography, it is possible that some of these failures to demonstrate improvement represented early restenosis. A few other studies from high-volume laboratories have reported success in the use of exercise echocardiography to evaluate patients before and after angioplasty. Labovitz et al[94] noted new exercise-induced echocardiographic abnormalities in 12 of 17 patients prior to angioplasty and 290

in none of these patients after angioplasty. When 1 mm of ST segment depression was added to the criteria for ischemia, 16 of 17 patients demonstrated ischemia prior to angioplasty. Thus, using a combination of electrocardiographic and echocardiographic criteria increased the sensitivity for the detection of coronary artery disease from 71% to 94%. Both of these studies demonstrate improved accuracy with the addition of two-dimensional echocardiography to exercise testing in postprocedure

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assessment of the functional significance of coronary artery disease. In the study by Labovitz et al,[94] exercise ejection fraction also improved after angioplasty and was similar to that noted in age-matched normal control subjects. In our laboratory, if inducible wall motion abnormalities remain or recur after angioplasty at similar workloads as those noted prior to angioplasty, coronary arteriography is generally undertaken if the patient has symptoms or if a large coronary territory is in jeopardy. Figure 13-10 demonstrates the resting and posttreadmill systolic frames from a patient who had undergone angioplasty of the left anterior descending artery 3 months previously and who had developed atypical chest pain. Postexercise systolic images of the apical four-chamber view demonstrate an apical wall motion abnormality. At catheterization, the patient was found to have restenosis with a 90% luminal narrowing of the middle left anterior descending artery. Limited data have been published on the use of exercise echocardiography in the detection of restenosis, but these have been encouraging in suggesting a role for exercise echocardiography in the long-term follow-up of patients undergoing angioplasty. Hecht et al[93] used supine bicycle echocardiography to examine 80 patients an average of 6 months after angioplasty to determine whether this Figure 13-10 Systolic frames of apical four-chamber (A) and twochamber (B) views at rest (PRE) and after exercise (POST) demonstrating an apical abnormality in a patient with prior left anterior descending artery angioplasty. This patient was found to have restenosis at the site of previous percutaneous transluminal coronary angioplasty.

technique could detect restenosis. The overall sensitivity of supine bicycle exercise echocardiography was 87%, compared with 55% for electrocardiographic sensitivity. The specificity was 95% for exercise echocardiography, compared with 79% for exercise electrocardiography. Sensitivity was highest (91%) for the left anterior descending artery. The sensitivity of supine bicycle echocardiography for the detection of restenosis was surprisingly high, despite a low percentage of patients achieving 85% of predicted maximal heart rate, suggesting that the restenosis lesion was hemodynamically significant at a low cardiovascular workload. The fact that supine bicycle stress echocardiography utilizes peak exercise imaging may account for the higher sensitivities reported with this technique. In another study, Dagianti et al[101] demonstrated the

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usefulness of supine bicycle echocardiography shortly after balloon angioplasty to detect clinical restenosis at 6 months. Sixteen of 18 patients who subsequently went on to develop symptomatic restenosis documented angiographically had an early positive bicycle echocardiogram, suggesting that visual estimates may overestimate the early procedural success and that substrate for the restenosis lesion may begin early. Supine bicycle echocardiography was not successful in predicting asymptomatic angiographic restenosis, again pointing out that when performed in an asymptomatic population, percent diameter stenosis as determined by arteriography may not be an accurate reflection of the adequacy of flow. Chest pain is more closely linked to coronary flow reserve than is absolute stenosis diameter.[102] [103] Thus, patients who are asymptomatic despite angiographic evidence of restenosis may be better treated conservatively, particularly if they are able to engage in exercise without limitation. Few studies have compared radionuclide methods with 291

stress echocardiography for assessment of angioplasty results. One study compared single photon emission computed tomography (SPECT) thallium and exercise echocardiography before and after angioplasty. Fioretti et al[92] compared the results of exercise echocardiography with thallium-201 SPECT before and after angioplasty in 23 patients. Prior to angioplasty, the concordance rate between the two techniques was 78%. Nineteen patients were restudied with both techniques within 4 weeks after angioplasty. Echocardiography and SPECT were concordant in 17 of these 19 patients (89%), suggesting that exercise echocardiography is a feasible alternative to thallium-201 SPECT techniques for assessing patients who are undergoing angioplasty. These studies suggest that exercise echocardiography may have a role in serial assessment of patients undergoing coronary revascularization, both in the initial detection of functionally significant stenoses and in the assessment of the results of interventions. In contrast to these, an earlier study by Aboul-Enein et al[104] reported a sensitivity of only 67% using posttreadmill echocardiography to detect restenosis 6 months after successful coronary angioplasty. Looking at maximal predicted heart rate, pressure rate product, and exercise duration, the authors could find no significant differences between the 32 patients in whom exercise echocardiography correctly predicted restenosis and 16

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patients with false-negative results, suggesting a lack of functional significance of the angiographically determined stenosis. Differences in populations between this study and others with better sensitivity for restenosis detection may explain the lower sensitivity noted by these authors. Whereas the patients in the latter study underwent exercise echocardiography and coronary arteriography 6 months after angioplasty as part of a study protocol, regardless of symptoms, the patients in the study by Hecht et al,[93] for example, were evaluated because of recurrent chest pain, suggesting a higher pretest probability. Also, 38 of 48 (80%) of those found to have angiographic restenosis in the study by Aboul-Enein et al[104] had single-vessel disease, which is less likely to produce a positive test result. More recently, Mertes et al[95] examined the role of bicycle stress echocardiography utilizing peak exercise imaging in 86 patients approximately 6 months after nonsurgical revascularization, including angioplasty, stenting, and atherectomy. The overall sensitivity for peak bicycle stress echocardiography in the detection of significant coronary artery disease was 83%, and the specificity was 85%. This is compared with a sensitivity of 42% for stress electrocardiographic detection of significant coronary artery stenoses. In this study, stress echocardiography was also found to be useful for detecting progression of previously existing coronary stenoses that had not undergone revascularization. Interestingly, all patients with false-negative results in this study had failed to achieve the target heart rate at peak exercise. To circumvent the problem of suboptimal exercise, Hoffman et al [105] used transesophageal pacing echocardiography in the detection of restenosis in 60 patients approximately 5 months after successful angioplasty. The sensitivity of transesophageal pacing echocardiography for the detection of restenosis or progression of coronary disease in nondilated vessels was 84% and compared favorably with the 86% sensitivity for technetium-99m sestamibi-SPECT imaging. The sensitivity of electrocardiography in this study was 50%. Many centers have gone to the use of pharmacologic stress echocardiography after revascularization in patients who are unable to perform maximal exercise. Preliminary data suggest that dobutamine stress echocardiography is able to identify patients with significant coronary stenosis prior to angioplasty and to demonstrate improvement in wall motion abnormalities after successful angioplasty (see Chapter 14) .

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Exercise Echocardiography After Coronary Artery Bypass Grafting Although exercise echocardiography has become an accepted modality as a screening test in the initial evaluation of patients with suspected coronary artery disease, limited data exist regarding the use of exercise echocardiography to predict graft patency after coronary artery bypass grafting. Treadmill exercise testing has been the accepted modality for evaluation of patients after bypass surgery, but the high prevalence of resting electrocardiographic abnormalities in this group introduces a high rate of nondiagnostic electrocardiographic responses. For this reason, thallium SPECT imaging was recognized early on as a valuable adjunct in sorting out the nondiagnostic electrocardiographic responses in such patients.[106] It seems logical that if exercise echocardiography is able to accurately detect ischemic segments in territories deprived of blood supply via native vessels, segments supplied by stenotic grafts would be similarly detected. Although few in number, published studies using exercise echocardiography to detect graft patency have been extremely encouraging; these are summarized in Table 13-8 .[107] [108] [109] Sawada et al[107] used upright bicycle exercise echocardiography to assess bypass graft patency in 41 patients at a mean of 6 years after coronary artery bypass surgery. The presence of inducible ischemia was correlated with vessel stenoses, including obstructed bypass grafts, obstructed native vessels without prior revascularization, and diseased native vessels distal to anastomotic sites. In the 35 patients with graft stenosis, exercise echocardiography demonstrated ischemia in 33 patients, a sensitivity of 94%. Exercise echocardiography also correctly identified five of six patients without significant disease, with a specificity of 83%. Through the use of segmental wall motion analysis, accurate identification of the location of significant stenoses (i.e., anterior vs. posterior circulation) was possible. The sensitivity for detection of TABLE 13-8 -- Accuracy of Exercise Echocardiography After Coronary Artery Bypass Grafting (CABG) Study Sawada et al[107] Crouse et al[108] Kafka et al[109]

Patients, n 41 125 182

Years After CABG 6 7 3.6

Sensitivity, % 94 98 79

Specificity, % 83 92 82

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292

compromised arterial supply in the left anterior descending distribution was 89%, and in the posterior circulation it was 88%. Crouse et al[108] studied 125 patients a mean of 7 years after coronary artery bypass grafting and reported a sensitivity of 98% and a specificity of 92% for the detection of graft or native vessel stenoses of 50% or greater reduction in luminal diameter. More recently, Kafka et al[109] reported that exercise echocardiography was able to successfully detect both singlevessel disease and multivessel disease, with a sensitivity of 77% and 96%, respectively, in a population of 182 patients undergoing symptom-limited treadmill exercise, electrocardiography, and exercise echocardiography for routine follow-up. Patients in this study had undergone revascularization with coronary artery bypass grafting 3½ years previously. Despite a lower prevalence of disease in this series when compared to the series of Sawada et al[107] and Crouse et al, [108] the overall sensitivity and positive predictive value were high (85%) when compared with exercise electrocardiography, which had a positive predictive value of only 62%. The negative predictive value for the corresponding techniques was 81% and 52% for exercise electrocardiography and echocardiography, respectively. In summary, the results of exercise echocardiography compare favorably to results of studies using thallium SPECT in the detection of ischemia in the region of coronary artery bypass grafts. Echocardiography performed in conjunction with exercise electrocardiography has a high feasibility rate— greater than 90% in these reported series—and provides superior sensitivity and specificity than exercise electrocardiography alone. These studies illustrate the ability of exercise echocardiography to identify graft as well as native disease stenosis in a population in whom interpretation of electrocardiographic response is less than optimal. Exercise Echocardiography After Acute Myocardial Infarction Following successful reperfusion for acute myocardial infarction, accurate prognostic assessment is critical in directing expensive and limited invasive resources to those patients who will receive the greatest benefit. Two important determinants of prognosis are left ventricular systolic function and the severity of underlying coronary artery disease. Medical centers performing primary angioplasty may use the results of cardiac catheterization to provide risk assessment, but most clinicians have traditionally performed noninvasive testing to predict prognosis and guide

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future therapy. The practitioner has a choice of tests with which to accomplish this assessment. In the past, two tests have frequently been called upon to provide assessment of systolic function and ischemia: radionuclide ventriculography or echocardiography to determine systolic function and submaximal exercise testing for the assessment of ischemic burden. More recently, stress echocardiography has been used to provide data about both left ventricular function and the presence of residual ischemia to assess future risk of cardiac events. Future ischemic events appear to involve increasingly complex interactions between an ischemic milieu and inflammation, but stress echocardiography is a relatively inexpensive test that has been shown to correctly stratify patients into highand low-risk subgroups. Submaximal exercise testing can be safely performed after myocardial infarction and has been shown to provide useful prognostic information with regard to subsequent cardiac events.[110] [111] Treadmill testing, however, while able to identify some patients who are at high risk for subsequent cardiac events, has a sensitivity of only 50% to 70% for the prediction of subsequent coronary events.[112] [113] Thallium scintigraphy has been shown to improve the sensitivity for prediction of cardiac events after myocardial infarction.[114] More recently, two-dimensional echocardiography after low-level treadmill exercise has been shown to provide useful information for the purposes of risk stratification and prediction of subsequent cardiac events.[57] [115] [116] Most of the studies examining exercise echocardiography for postmyocardial infarction assessment were performed before the widespread use of reperfusion therapy and included as events the "soft" events of revascularization. Nonetheless, these studies demonstrate the ability of exercise echocardiography to identify a high-risk group, particularly when combined with clinical risk assessment. Jaarsma et al[115] studied a group of 43 patients with exercise echocardiography within 3 weeks of acute myocardial infarction. All patients were noted to have resting wall motion abnormalities. Images obtained immediately after exercise demonstrated new wall motion abnormalities, remote from the site of myocardial infarction, in 18 patients, 17 of whom were shown to have multivessel coronary artery disease. This is compared with only 5 of 25 patients without remote wall motion abnormality who were found at catheterization to have multivessel disease. The development of a new wall motion abnormality, remote from the site of myocardial infarction, predicted multivessel coronary disease with a

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sensitivity of 77% and a specificity of 95%. It also predicted a high-risk group for reinfarction or recurrent angina within 12 weeks, demonstrating the ability of exercise echocardiography to predict a higher risk group for cardiac events based on the identification of patients with multivessel disease. Transient remote ischemia during the first several hours of acute myocardial infarction has been attributed to a supply-demand imbalance in areas perfused by a critically stenosed vessel in noninfarcted segments of myocardium. Because remote ischemia signifies multivessel disease, these patients would presumably be at high risk for the development of subsequent events. Ryan et al[116] examined the predictive value of either remote or adjacent asynergy in 40 patients shortly after myocardial infarction using posttreadmill exercise echocardiography and found it to have an excellent predictive value for subsequent cardiac events. In a 6- to 10-month follow-up period, cardiac events occurred in 20 patients, 16 of whom had a positive exercise echocardiogram (80% sensitivity). A negative exercise echocardiogram was predictive of a good clinical outcome without subsequent cardiac events in 19 of 20 patients (specificity, 95%). In this group of postmyocardial infarction patients, treadmill characteristics were unable to identify high- and low-risk groups. Likewise, Applegate 293

et al[57] found that neither electrocardiographic nor clinical characteristics could identify a high-risk group in another study of 21 patients who underwent symptom-limited treadmill exercise shortly after acute myocardial infarction. In this study, multivariate logistic regression analysis was performed on several clinical, treadmill, and electrocardiographic characteristics. Wall motion abnormalities immediately after exercise and echocardiographically determined ejection fraction had the highest predictive value (P < .001) for the prediction of future cardiac events. In patients treated with thrombolysis, the ability to exclude significant multivessel disease may help to avoid cardiac catheterization and to direct expensive resources and higher risk technologies to those patients who are at higher risk for poor outcome. Quintana et al[117] examined exercise echocardiography within a week after myocardial infarction in 70 patients, about half of whom had received thrombolytic therapy. Exercise

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echocardiography correctly identified a high-risk group for cardiac events within 2 weeks after myocardial infarction. Twenty-two percent (6 of 27) of those with a positive exercise echocardiogram, versus only 5% (2 of 43) of those with negative studies, suffered an early cardiac event. At 4-year follow-up, the cumulative event-free survival rate was significantly better in patients with a negative exercise echocardiography. While the electrocardiographic response also identified patients in whom events were more likely to occur, exercise electrocardiography was unable to identify a low-risk group. These studies demonstrate the usefulness of twodimensional exercise echocardiography in helping to stratify patients into high- and low-risk groups after myocardial infarction and to predict a highrisk group for subsequent cardiac events on the basis of ischemia. An area of current active clinical investigation is the application of pharmacologic stress echocardiography to identify stunned and hibernating myocardium after myocardial infarction. The goal of these techniques is to determine potentially viable segments of myocardium that would be expected to recover function without revascularization after myocardial infarction, as opposed to those that are more likely to benefit from revascularization. Dobutamine echocardiography, discussed in Chapter 14 , has shown promise in the area of identification of stunned segments in the immediate post-infarction period and has been widely utilized for this purpose. Recruitment of myocardial segments with low-dose dobutamine shortly after acute myocardial infarction identifies segments that are likely to recover function without further intervention.[118] [119] Subsequent deterioration of some segments with higher doses of dobutamine (the socalled "biphasic" response) signify segments that may improve only after revascularization is performed. In theory, a low level of exercise could potentially be used to identify viable myocardium in analogous fashion to low levels of dobutamine infusion. A study by Hoffer et al[120] has investigated the utility of low-level bicycle exercise shortly after myocardial infarction to identify reversible dysfunction through augmentation of stunned segments. These authors noted improvement with low-level bicycle exercise in some akinetic segments within the infarction zone of patients with recent myocardial infarction, similar to the augmented response seen in viable segments with low-dose dobutamine infusion. Segments that improved with exercise were more likely to recover function at follow-up, signifying reversible dysfunction. Since multiple graded levels of exercise were not tested, it is unknown whether some segments that improve with low levels of exercise would demonstrate a biphasic response as well, with higher cardiac workloads. Whether

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echocardiographic monitoring during multiple graded levels of exercise could detect ischemic segments suitable for revascularization has not been investigated. Exercise Echocardiography in Women Despite the fact that cardiovascular disease is the number one killer of women in the United States, accounting for approximately 500,000 deaths annually, most studies involving noninvasive techniques to identify patients with coronary artery disease focused exclusively on men, until relatively recently. Because of a variety of social, economic, and medical beliefs, women were excluded from populations with coronary disease under study. Even in the current era, there are surprisingly few studies examining diagnostic and prognostic implications of noninvasive testing of women (Table 13-9) . One reason for the paucity of published data in the noninvasive assessment of coronary disease in women is the fact that stress testing is believed to be less accurate in women. Indeed, early studies of electrocardiographic stress testing in women usually displayed poorer sensitivity and specificity for the identification of significant coronary disease.[63] [121] [122] In retrospect, however, the majority of these studies were performed in women who, according to Bayesian theory, were of low pretest likelihood with lower disease prevalence than their male cohorts, a factor that adversely affects specificity. The low disease prevalence in populations under study contributed to the belief that women are less likely to suffer from coronary disease and less likely to need referral for invasive testing. As discussed previously, verification bias, or the tendency to avoid sending those with negative test results for cardiac catheterization, is also a major contributor to lower test specificity in women. Contributing to the lower sensitivity of stress testing in women is the fact that, in many early studies, women appear to have lower exercise capacity, achieving submaximal levels of cardiovascular stress more often, thereby rendering it less likely that ischemia would be provoked. In addition, hormonal and autonomic factors, inappropriate catecholamine release, syndrome X, and the presence of more comorbid diseases at the time TABLE 13-9 -- Studies Examining the Accuracy of Exercise Echocardiography in Women Study Sawada et al[124] Williams et al[125] Marwick et al[126]

Year 1989 1994 1995

Patients, n Sensitivity, % Specificity, % 57 86 86 70 88 84 161 80 81

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Roger et al[84]

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1997

96

79

37

294

of diagnosis, may further contribute to test inaccuracies in women. In an effort to increase the overall accuracy of stress testing in women, some practitioners have advocated the use of imaging techniques as an initial test. Recent studies have focused on the addition of echocardiographic imaging as a means to increase the accuracy of stress testing as an initial diagnostic test in women.[123] Recent studies have examined the echocardiographic responses to treadmill or bicycle exercise in women also undergoing diagnostic catheterization. [84] [124] [125] [126] Sawada et al[124] examined the diagnostic value of exercise echocardiography in 57 women with chest pain syndromes using coronary arteriography as the gold standard. Sensitivity and specificity for echocardiographic detection of coronary stenosis of 50% or greater were both 86%. Exercise echocardiography was particularly useful in sorting out patients with atypical chest pain with coronary disease (sensitivity, 84%) from those with a nondiagnostic exercise electrocardiogram who were free of coronary disease (specificity, 82%). Similarly, Williams et al[125] compared the accuracy of the exercise echocardiogram to the accuracy of 12-lead electrocardiography performed during maximal treadmill exercise in 70 women with a 53% pretest probability for coronary disease. Defining significant coronary disease as greater than 50% stenosis, exercise echocardiography had a sensitivity of 88% for the detection of coronary artery disease, compared with 57% for electrocardiographic analysis using ST depression of greater than 0.1 mV. The specificity of exercise echocardiography was 84%, compared with 51% for echocardiographic analysis. In both of these studies, the accuracy of exercise echocardiography significantly exceeded that of exercise electrocardiography and paralleled larger studies of predominantly male patients. [6] [51] , [61] [76] Marwick et al[126] investigated the use of exercise echocardiography in the detection of coronary disease in women and found it to have an overall accuracy of 81%, compared with overall accuracy of 64% for exercise electrocardiography. In addition, these authors examined the cost of exercise echocardiography and noted that it compared favorably with

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several potential diagnostic strategies in the work-up of cardiac symptoms in women. These authors sought to identify a diagnostic strategy that would balance the cost of diagnostic testing (defined as local Medicare reimbursement) with the lowest number of false-negative results and the fewest inappropriate referrals for cardiac catheterization. Compared with electrocardiography or echocardiography as an initial test (with and without Bayesian analysis) or angiography alone as the only diagnostic work-up, exercise echocardiography provided the best overall accuracy at the least cost. Data continue to accumulate that exercise echocardiography, because of preserved accuracy in patients with low to intermediate pretest likelihood of disease and because Medicare reimbursement rates are roughly half of those for radionuclide methods, may be the initial stress test of choice for women. The ultimate test of any noninvasive strategy may not be its ability to detect disease but its ability to predict future events. Recent studies have examined the ability of exercise echocardiography to predict prognosis in patients with known or suspected coronary artery disease.[127] [128] [129] Some of these studies focus on outcomes of women or include women as a major proportion of patients. One of the first of these studies was that of Sawada et al,[127] which encompassed 71 women among 148 patients who were followed for 28 ± 8 months after having a normal exercise echocardiogram. Cardiac events occurred in 2.8% (2 women) at 28 months without evidence of abnormality on exercise echocardiogram, demonstrating the ability of exercise echocardiography to identify a low-risk group for future events. Likewise, McCully et al[128] reported, in a large group of patients of whom about half were women, an excellent event-free survival rate for patients with normal treadmill echocardiograms who achieved an adequate level of cardiovascular stress (>5 METs for women). Another study examining prognosis in women reported that exercise-induced ischemia predicted cardiac events. In a multivariate analysis, Heupler et al[129] demonstrated incremental predictive value for exercise echocardiography in addition to clinical factors and exercise electrocardiography. Many of these studies have been performed in academic centers where referral of higher risk patients may falsely elevate the sensitivity of diagnostic testing and its ability to prognosticate. Exercise echocardiography has also been shown to correctly stratify women as to risk in a community setting. In a study of 1188 women with known or suspected coronary disease who underwent treadmill exercise echocardiography, the degree of ischemic wall motion abnormality was an

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important factor in identifying a very high risk group.[130] Patients with resting wall motion abnormalities in addition to exercise-induced ischemic abnormalities had the highest rate of cardiac death and myocardial infarction. These studies highlight the ability of echocardiography to risk-stratify patients into high-, intermediate-, and low-risk subsets based on echocardiographic response to exercise and to select patients who will most benefit from further invasive procedures. Further studies will need to be performed. Exercise Echocardiography in the Determination of Prognosis The acceptance of stress echocardiography as a diagnostic tool able to guide decision making for medical and interventional procedures has allowed for follow-up of patients with coronary disease. Published event rates for patients with myocardial infarction undergoing exercise echocardiography were discussed earlier and demonstrate a higher rate of cardiac events in patients with significant degrees of inducible ischemia after infarction. As with acute myocardial infarction, the major determinants of prognosis in chronic coronary artery disease are overall left ventricular function and the presence and severity of ischemia. Echocardiography, in its ability to evaluate both of these factors, makes an ideal tool for the determination of prognosis. Event rates for patients with chronic coronary disease with normal or abnormal test results have been examined with regard to "hard" cardiac events such as myocardial infarction and cardiac death as well as "soft" cardiac events such as revascularization. These findings demonstrate a more benign prognosis for patients with normal exercise echocardiograms, with higher event rates noted for those with inducible ischemia (Table 13-10) 295

TABLE 13-10 -- Exercise Echocardiography for Prognostic Assessment of Patients with Known or Suspected Coronary Artery Disease

Study Sawada et al[127]

Patients, n Follow-up, mos 148 28

Event Rates * Abnormal Normal SE SE — 1.7/.85 *

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Marwick et al[132] Krivokapich et al

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463 360

44 12

9/6.5 34/9

7/2 9/2

1325

23

—

2.5/<1

[131]

McCully et al[128]

* Percentage of events at 12 months, total/spontaneous. SE, stress echocardiography.

Two studies have noted low event rates of less than 1% per year in patients with normal resting function and no exercise-induced wall motion abnormality.[127] [128] Importantly, in both of these studies, a normal study finding is defined as one that is normal both at rest and with exercise. In some cases, higher event rates have been noted for patients with negative test results, and often these higher event rates were reported in studies that allowed patients with resting wall motion abnormalities to be included within the "negative" group. Krivokapich et al,[131] defining a negative test result as lack of ischemia with exercise, noted a higher event rate of 9% in patients with a negative exercise echocardiogram. In this study, soft events such as revascularization were also included as events, obviously having had an adverse affect on total event rate. When only myocardial infarction is examined, the event rate dropped to only 2%. Likewise, Marwick et al[132] noted in a group of 463 patients an event rate of 7% for patients with a negative exercise echocardiogram but when 15 of 20 patients with revascularization as the only event were excluded, the event rate was reduced to less than 2% per year for spontaneous events. These studies demonstrate that exercise echocardiography in patients undergoing stress testing for known or suspected coronary disease is able to effectively stratify patients as to future risk and to guide therapy for patients at higher risk. The presence of electrocardiographic ST depression appears to add prognostic information to the value of the echocardiographic response. For example, in the study of Marwick et al[132] , the rate of events including revascularization was highest in patients with both echocardiographic and electrocardiographic evidence of ischemia (event rate, 45%), with a lower event rate of 38% in patients without exercise-induced electrocardiographic changes. Likewise, Krivokapich et al[131] noted highest event rates for patients with both electrocardiographic and echocardiographic evidence of ischemia. In patients without echocardiographic evidence of ischemia,

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however, event rates were still higher in patients with a positive exercise electrocardiogram compared with a negative electrocardiogram. In both of these studies, although echocardiographic wall motion response appears to provide the greatest prognostic information, the electrocardiographic response appears to add prognostic value. Dobutamine echocardiography, discussed elsewhere, has provided the largest group of data for prognostication in patients referred for known or suspected coronary disease.[133] [134] In particular, dobutamine echocardiography appears to be able to accurately stratify risk in patients scheduled for vascular surgery, with published data encompassing more than 1500 patients.[135] Together, exercise and pharmacologic stress echocardiography is quickly gaining momentum as a test that can accurately and effectively stratify patient risk and guide therapeutic decisions. Cost-Effectiveness Issues The rising tide of health care costs, along with recent government budget cuts for reimbursement for many inpatient procedures, mandates that physicians be aware of the relative costs of procedures they order or perform on their patients. The cost of any procedure can be examined from a variety of viewpoints, including the cost to the patient—that is, insurance or Medicare reimbursement—the actual cost to the hospital or physician performing the test, and the cost of further diagnostic testing that the test result initiates. Cost-effectiveness examines cost versus healthcare outcome, usually expressed as a unit of effect on health care, such as survival or quality-assisted life-years. This is not meant to be a comprehensive discussion of cost analysis but a simple comparison of stress echocardiography with other testing strategies that provide similar information at similar risk to the patient. Several authors have addressed the issue of cost-effectiveness of stress testing as an initial strategy as compared with proceeding directly to invasive tests, and many of these assessments highlight the importance of determining pretest likelihood of disease prior to testing.[136] [137] [138] [139] If a high degree of likelihood exists that a patient has coronary disease, (greater than 75%), then the best initial strategy is likely to be proceeding directly to angiography, as suggested by Bayes' theorem. On the other hand, in case of very low pretest likelihood (i.e., less than 20%), perhaps no further testing is recommended. For patients with intermediate pretest likelihood of disease, the best initial strategy has been shown to be noninvasive testing

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followed by catheterization in patients with high likelihood of significant coronary disease based on results of noninvasive testing. In contrast, Shaw et al[136] examined the use of radionuclide imaging as an initial strategy in women and found that noninvasive testing was approximately $1000 less over a 2.5-year period as compared with proceeding directly to catheterization for patients with intermediate pretest likelihood of disease. Similarly, Marwick et al[126] examined multiple different strategies involving stress electrocardiography or echocardiography versus catheterization as an initial strategy, noting that exercise echocardiography led to the least number of false results, providing the greatest sensitivity and specificity for detection of coronary disease. False-positive test results were presumed 296

to lead to inappropriate angiography. Thus, although exercise electrocardiography was a less costly test from the standpoint of reimbursement, it was assumed to lead to a higher number of inappropriate catheterizations. Medicare fees and volumes for various stress testing techniques, which were published in 1996, compared professional and technical fees as well as relative value units (RVUs), which provide an estimate of relative cost.[140] Within the published guidelines of the American College of Cardiology and the American Heart Association for exercise testing, while treadmill testing alone was noted to be least costly (3.30 RVUs), performing this test in all cases would not necessarily result in lower cost of patient care, since test inaccuracies can be expected to lead to further unnecessary testing. Imaging adds considerably to the cost of reimbursement (5.3 times that of treadmill), as does echocardiography (2.3 times higher). However, as discussed previously, given the improved accuracy of exercise echocardiography, its relatively lower expense as an imaging modality when compared with radionuclide technology makes it an attractive alternative. In comparison with radionuclide techniques, echocardiography is likely to be reimbursed at roughly half the relative cost, based on Medicare reimbursement. In this light, few studies have examined nuclear techniques with echocardiography as a screening test. Garber et al[137] compared an initial strategy of arteriography with one of five noninvasive strategies, initially including echocardiography, nuclear techniques with SPECT, positron emission tomography, or treadmill electrocardiography. There were no significant differences in life expectancy based on the initial diagnostic test. The total cost of a strategy

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that used echocardiography was less than one that began with radionuclide based on a cost-effectiveness ratio. Because of improved sensitivity compared with treadmill testing, exercise echocardiography resulted in better outcome. Thus, echocardiography was a highly cost-effective alternative to treadmill or radionuclide imaging. Kuntz et al[138] examined the cost-effectiveness of noninvasive strategies with exercise treadmill electrocardiography, exercise echocardiography, or SPECT nuclear imaging versus arteriography in the initial diagnosis of coronary disease. These authors found that either exercise electrocardiography or exercise echocardiography resulted in "reasonable" cost-effectiveness ratios for patients with mild to moderate risk for coronary artery disease. Proceeding directly to arteriography was costeffective for patients with high pretest probability of coronary artery disease. Further studies of both cost and outcome will need to be performed in randomized fashion with longer term follow-up to determine whether exercise echocardiography will continue to assume a greater role in settings where HMO-driven decisions mandate the most information at the least cost.

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Exercise Echocardiography Compared with Other Imaging Modalities A number of studies have compared exercise echocardiography with the more well established radionuclide techniques for the diagnosis of coronary disease. An early study compared two-dimensional echocardiography with radionuclide angiography during left lateral decubitus bicycle ergometry.[44] This study noted a higher sensitivity, 91%, for radionuclide angiography versus 76% for exercise echocardiography using a bicycle protocol. The problem with this and many subsequent studies is that such comparisons take place in centers where one or the other of the techniques being compared is more widely utilized, and different levels of expertise exist for the competing technologies. An exception to this is the large study of 292 patients reported by Quinones et al[141] that analyzed all patients with both exercise echocardiography and SPECT thallium for the diagnosis of coronary disease. Sensitivity for single-vessel disease was quite low with both techniques (58% for echocardiography and 61% for thallium SPECT), and both techniques correctly identified three-vessel disease with a 94% sensitivity. Specificity was similar in both groups (88% for echocardiography and 81% for thallium SPECT). In a comparison of exercise echocardiography with technetium-99m MIBI-SPECT, Pozzoli et al[142] found a good correlation between perfusion and wall motion in 103 consecutive patients, with concordance in 84% of segments overall. Concordance was especially high (91%) in patients with previous myocardial infarction. These studies, while limited, demonstrate the ability of both techniques to detect patients with significant disease, providing similar clinical information about the functional significance of underlying coronary disease. The advantage of echocardiography lies in its ability to provide additional information about left ventricular function and underlying valvular disease without adding significantly to the time of the echocardiographic study. The accuracy of exercise echocardiography has also been compared to that

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of echocardiography with different forms of cardiovascular stress. Beleslin et al[40] compared exercise, dobutamine, and dipyridamole echocardiography in 136 consecutive patients with a high prevalence of coronary artery disease. The sensitivity of exercise echocardiography was 88%, compared with 82% for dobutamine echocardiography and 74% for dipyridamole echocardiography. Specificity for exercise, dobutamine, and dipyridamole echocardiography was 82%, 77%, and 94%, respectively. All three tests were noted to have acceptable diagnostic value, with a higher diagnostic accuracy for stress echocardiography in patients with singlevessel disease. Similarly, Marangelli et al[143] compared exercise, dipyridamole, and transesophageal atrial pacing in conjunction with echocardiography in 104 consecutive patients with normal resting wall motion who underwent coronary arteriography. The sensitivities for exercise, transesophageal atrial pacing, and dipyridamole were 89%, 83%, and 43%, respectively, suggesting that exercise and atrial pacing have similar sensitivities and may exceed the sensitivity of pharmacologic stress with vasodilators. In comparison with nonexercise forms of cardiovascular stress, the additional information gleaned from analysis of the hemodynamic response to exercise proves to be an invaluable adjunct in the clinical assessment of patients. If the patient is able to exercise, the additional clinical value gained in analyzing the physiologic exercise data adds 297

incrementally to the information learned from wall motion analysis alone.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary Exercise echocardiography is an accurate technique for initial diagnosis of coronary disease and can provide prognostic information in many subgroups with known disease. Over the past decade, its acceptance by the medical community has grown and current applications have expanded to include diagnosis and prognosis in a wide range of patients, including women, for whom accuracy and cost appear better than other comparable techniques. Current clinical applications of exercise echocardiography include diagnosis of suspected coronary disease, guiding percutaneous intervention, surveillance of patients following coronary bypass surgery, and prediction of prognosis in chronic coronary disease as well as acute myocardial infarction. Accuracy of exercise echocardiography is now considered to be at parity with other noninvasive imaging techniques with a cost roughly half that of competing nuclear techniques. Its lower cost makes exercise echocardiography an attractive alternative as an initial diagnostic test and in follow-up of patients with coronary disease.

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301

Chapter 14 - Stress Echocardiography with Nonexercise Techniques Principles, Protocols, Interpretation, and Clinical Applications Thomas H. Marwick MD, PhD

302

TABLE 14-1 -- Indications for Nonexercise Stressors Unable to Exercise Inability to exercise maximally Diagnosis of coronary artery disease, decision making

Able to Exercise Specific indications Coronary spasm

Myocardial viability Risk stratification Developing indications Situations preventing exercise Onset of ischemia Angiography laboratory, operating room New technologies (TDI, CK, contrast) CK, color kinesis; TDI, tissue Doppler imaging.

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Background Indications for Nonexercise Stress Testing The performance of a maximal level of exercise is a critical determinant of the sensitivity of all stress modalities for the detection of coronary artery disease. Unfortunately, many patients—fully 30% to 40% at some tertiary centers (Fig. 14-1) (Figure Not Available) —either cannot exercise at all or cannot exercise maximally,[1] but these patients may still need to undergo stress testing for diagnostic, decision making, or prognostic purposes. The most common causes of limited exercise capacity are vascular disease (either peripheral or cerebrovascular) and orthopedic problems. Other situations warranting nonexercise stress testing include severe cardiopulmonary disease and general debility, especially among the elderly, in whom pharmacologic testing with both dobutamine and vasodilators has been shown to be well tolerated and reliable.[2] [3] [4] [5] Although the inability of a patient to exercise maximally constitutes the main indication for the use of nonexercise stressors, such stressors are less commonly indicated in other situations (Table 14-1) . The most important of these situations include circumstances in which the use of a pharmacologic agent may offer diagnostic dimensions that are not available from exercise stress, for example, the diagnosis of coronary spasm using ergonovine stress testing.[6] [7] A similar scenario involves patients early or late after myocardial infarction, after which left ventricular dysfunction may not be permanent. The diagnostic challenge in this situation is that whereas stunned myocardium improves spontaneously, the revascularization of hibernating Figure 14-1 (Figure Not Available) Proportion of patients undergoing exercise testing who are unable to exercise maximally. (From Marwick T: Acta Clin Belg 1992;47:1– 51.)

myocardium has implications for functional capacity and prognosis. As discussed later in the chapter, echocardiography can be used with dobutamine[8] or dipyridamole[9] [10] stress, or both,[11] for the identification of viable myocardium. Pharmacologic agents are more appropriate than exercise for stress testing in some environments, such as the cardiac catheterization laboratory or operating rooms. Finally, nonexercise methods have been used in

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preference to exercise echocardiography even in patients who are able to exercise because of their relative technical ease. The incremental nature of these stressors means that the time-course of ischemia can be identified; these data are not available using posttreadmill stress and are more difficult to obtain with bicycle exercise testing. Although the decision to use a nonexercise stress may not be justifiable with routine echocardiographic imaging at present, the facilitation of adjunctive techniques discussed subsequently—such as tissue Doppler, color kinesis, and contrast echocardiography (which may be less feasible during exercise than nonexercise stress)—could in the future justify the use of nonexercise techniques in patients who are able to exercise. Choice and Mechanism of Action of Nonexercise Stressors There are two general groups of nonexercise stress agents: those that induce ischemia by increasing myocardial work and oxygen consumption (exercise-simulating agents), and those that induce ischemia by influencing coronary perfusion and therefore myocardial oxygen supply (vasoactive agents). The latter include the coronary vasodilators dipyridamole and adenosine, which cause ischemia by provoking coronary steal, and ergonovine, which can be used to provoke coronary spasm. In addition to these stressors, nonpharmacologic approaches including hand-grip and the cold pressor test[12] [13] have been used. Hand-grip testing is often combined with dobutamine-atropine testing,[14] but the cold pressor test has not been widely adopted clinically because of limited efficacy and patient discomfort. Exercise-Simulating Agents

The exercise simulators include dobutamine and other sympathomimetic agents, pacing stress, and atropine 303

(usually used as an adjunct to the other approaches), all of which increase cardiac work and myocardial oxygen requirement. Thus, the induction of ischemia and regional dysfunction reflects the inability of the diseased coronary circulation to respond to this increased oxygen demand, a process that parallels the response to exercise. However, processes additional to classic "demand" ischemia may be active, and sympathomimetic agents may place an additional stress on the heart through effects on cardiac metabolism—an "oxygen-wasting" effect. In a group of patients with

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ischemic responses to both dobutamine and exercise, ischemia appeared at a significantly lower rate-pressure product during dobutamine than during exercise stress, consistent with the presence of a factor additive to that of cardiac work suggested experimentally.[15] [16] [17] Another contributor to this process might include concurrent "supply" ischemia due to reduction of coronary flow; certainly, sympathomimetic agents cause a dose-dependent reduction of subendocardial perfusion and maldistribution of coronary flow, in the face of mild coronary stenoses.[18] The latter component, together with regional flow heterogeneity based on tachycardia-induced coronary vasodilation, [19] is responsible for perfusion defects detected at myocardial perfusion imaging. Because increased cardiac workload and oxygen demand is the usual mechanism underlying ischemia in most ambulatory situations, the exercise-simulating agents are often considered to be a more physiologic means of stressing the heart, although "demand" ischemia may be combined with reduction in coronary supply due to vasospasm or coronary steal. Vasoactive Agents

The use of dipyridamole in combination with myocardial perfusion imaging is based on the induction of maximal coronary vasodilation in all territories. Flow heterogeneities (and therefore apparent perfusion defects) develop if a coronary stenosis limits the regional hyperemic response.[20] Of note, this process does not involve the provocation of ischemia in a functional or metabolic sense. In contrast, the development of regional wall motion abnormalities at stress echocardiography necessitates the induction of ischemia. The chief mechanism of vasodilator-induced ischemia is coronary steal,[20] which may be either "vertical" or "horizontal" through the left ventricular wall. The best known mechanism is horizontal steal, in which blood flows to nonstenosed from stenosed territory, owing to reduced collateral flow into the stenosed territory because of depressurization of vessels supplying the collaterals due to increased runoff. Vertical steal also occurs because of vasodilator-induced depressurization of the microcirculation, causing subendocardial vessels to collapse under the greater extravascular pressure in this region and "stealing" flow to the subepicardium from the subendocardium. Other mechanisms of vasodilator-induced ischemia, unrelated to coronary steal, include reduced coronary supply because of coronary spasm (which is the major effect of ergotamine), systemic hypotension, or collapse of the stenosis. Under conditions of maximal coronary hyperemia, driving pressure is the main determinant of

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myocardial perfusion because vasodilator reserve is exhausted. Hence, systemic hypotension may accentuate hypoperfusion due to coronary steal. Stenosis "collapse" may be provoked if profound microcirculatory vasodilation causes a reduction of lateral pressure induced by increased flow. Finally, myocardial oxygen demand may be increased in response to increased cardiac workload because of increased sympathetic activity secondary to angina. Agents Used to Identify Myocardial Viability

In the presence of dysfunctional but viable myocardium, regional function is enhanced by the inotropic effect of low-dose dobutamine, although this appears to require both recruitable perfusion and an increment in metabolism.[21] The mechanism of this is ill-defined but most likely pertains to enhanced calcium cycling. Viable myocardium supplied by a patent infarct-related vessel (generally corresponding to stunned myocardium) demonstrates a sustained improvement during the infusion, which then reverses after the test. Viable tissue supplied by a stenosed infarct-related artery (which may involve stunned or chronically ischemic— "hibernating"—tissue) is characterized by an initial improvement, occurring at low doses (<20 µg/kg/minute), or low heart rates, or both, followed by deterioration of regional function as the chronotropic effect becomes more prominent and myocardial work increases.[8] If the region is supplied by a critically stenosed artery, however, it may be possible for the territory to become ischemic before there is a noticeable enhancement of contractility. Moreover, the ability of the myocardium to thicken is determined by the amount of infarcted tissue within the segment.[22] Myocardial viability may also be inferred from the contractile response to dipyridamole. The mechanism of this is also putative but probably relates to myocardial congestion with interstitial fluid due to vasodilation. A socalled mini-Starling effect may be caused by this congestive process, producing additional tension on the myofibrils.[23]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Principles of Nonexercise Stress Techniques Pharmacology and Physiopathology of Nonexercise Stress Techniques Exercise-Simulating Agents

The exercise-simulating agents include dobutamine, dopamine, epinephrine, and isoproterenol. Of these, dobutamine has become the most commonly administered exercise-simulating agent, and the majority of published data on pharmacologic stress echocardiography have involved this agent. Arbutamine, a dobutamine isomer, was developed in the last decade but showed no substantial clinical merits compared with its parent compound, and distribution of the agent has been discontinued.[24] [25] Dopamine 304

stimulates alpha receptors and, if it extravasates, may cause localized limb ischemia due to vasoconstriction. Dopamine may also be a less effective precipitant of myocardial ischemia than is dobutamine.[26] Although other sympathomimetic agents have been used for stress testing,[27] epinephrine and isoproterenol are probably the more arrhythmogenic. This side effect is dose dependent, but its avoidance by conservative dosing may compromise the sensitivity of the test by limiting the amount of stress on the heart. Dobutamine is predominantly a beta-1 agonist, and normal areas become hyperkinetic in response to its inotropic effect. Myocardial segments supplied by a stenosed coronary artery may become akinetic or dyskinetic but more commonly are unable to augment their thickening and excursion, and the contrast between this response and the hyperkinetic function of normal segments facilitates the detection of zones with abnormal function. Vasodilation and chronotropy appear at higher doses, [26] usually at the 20 µg/kg/minute level of the routine dobutamine stress protocols, reflecting

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the stimulation of other receptors to a lesser degree. This chronotropic response appears to be the most important factor in terms of precipitating ischemia; most dobutamine stress protocols cause a mean heart rate increment of 40 to 50 beats per minute and mean peak heart rates of 110 to 120 beats per minute.[28] [29] [30] [31] [32] [33] [34] However, reflex bradycardia may occur in response to hypertension. The vasodilator effects of dobutamine may cause blood pressure to fall at peak doses, although blood pressure normally rises in response to the inotropic effect of the drug. Increases in myocardial oxygen demand due to increased cardiac work, as well as a weak vasodilator effect, lead to the development of coronary hyperemia in territories supplied by normal coronary arteries. Although this response is probably less than that induced by coronary vasodilators, the coronary hyperemic response to dobutamine stress permits its combination with perfusion scintigraphy.[34] [35] [36] [37] The detection of myocardial perfusion defects in the presence of coronary disease may be augmented by partial volume effects due to thinning of the ischemic wall. Vasoactive Agents

Most of the experience with pharmacologic stress echocardiography using vasoactive agents has been obtained with the coronary vasodilators dipyridamole and adenosine. The coronary vasodilators differ with respect to the onset and duration of their effects. Dipyridamole increases endogenous adenosine levels by reducing cellular reuptake and metabolism, and thereby acts indirectly.[20] This indirect mechanism causes some delay between the administration of this agent and the timing of peak vasodilation, the half-life of this effect being 6 hours. The indirect action of dipyridamole may account for interindividual variations in the magnitude of its effects. Adenosine acts directly on the vasculature, its vasodilator efficacy being equivalent to that of papaverine.[38] The potency and speed of onset of adenosine cause its side effects to be more intense but also more short-lived than those of dipyridamole. An increasing amount of literature describes the combination of ergonovine with echocardiography. This agent has a direct effect on the vessel; responsiveness to acetylcholine may be related to loss of nitric oxide production at the site of disease. Exercise Simulation Using Pacing Stress

Several nonpharmacologic approaches have been used for stress echocardiography, including "physiologic" stresses such as the cold pressor

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test, which are poorly tolerated. Pacing is an alternative means of increasing cardiac work without resorting to pharmacologic techniques. Pacing-induced tachycardia increases myocardial oxygen consumption and thereby causes myocardial ischemia in the setting of significant coronary stenoses.[39] [40] The reduction of subendocardial perfusion with pacing[40] may also contribute to the development of ischemia. Ventricular pacing is not favored, as it causes both abnormal regional contractility and abnormal perfusion, so that pacing stress techniques generally involve atrial stimulation, either transvenously or via the esophagus (only the latter having gained acceptance as a routine stress modality). Of these, direct atrial pacing has been used for other stress imaging tests, but it is invasive and therefore has not achieved acceptance. Of the transesophageal pacing approaches, the "pill" electrode has formerly been studied, but although this technique is effective, it has the disadvantage of causing significant discomfort. Attachment of pacing electrodes to transesophageal echocardiography probes has been reported in trials[41] [42] but has not moved into commercial production; perhaps miniaturized transnasal probes could make this feasible. The development of a small esophageal pacing catheter offers enhanced contact between the electrodes and the esophagus, which facilitates the test. In particular, the technique causes less discomfort than other pacing techniques because of the presence of smaller pacing thresholds.[43] Atrial pacing stress is more invasive than pharmacologic stress echocardiography but may be useful in patients in whom the pharmacologic approaches are contraindicated or associated with side effects. Moreover, this technique has additional attractions that might justify its use in preference to pharmacologic testing. These include the capacity to achieve a target heart rate in virtually all patients, the potential to immediately terminate the tachycardia if the patient develops complications (in contrast to pharmacologic methods, which require a period of time for the effects to dissipate), and the ability to perform measurements in the ischemic ventricle at a low heart rate (after cessation of pacing). The latter may be of particular value if Doppler indices of diastolic function are being assessed, as these are difficult to measure in the presence of tachycardia (which with dobutamine takes some time to resolve, by which time the ischemia may also have dissipated). Using atrial pacing stress, ischemic myocardium has been shown to have reduced ventricular compliance.[44] Sudden termination of stress during ischemia may also be of value in the combination of stress testing with color flow Doppler echocardiography, as the use of low frame-

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rates may pose a problem at high heart 305

rates. However, despite the benefits of transesophageal atrial pacing, its availability for many years,[45] and recent data showing correlation with dobutamine echocardiography despite a shorter test duration and better patient tolerance,[43] this technique has not become widely used because it remains somewhat invasive. Combined Approaches

Atropine reduces the depressant effect of vagal stimulation on heart rate and may be particularly useful when reflex reduction of the heart rate occurs in response to blood pressure elevation. The combination of atropine with dobutamine has been found to be useful in patients who fail to develop an adequate degree of tachycardia in response to dobutamine, the most common situation involving patients taking beta receptor antagonists.[46] [47] [48] An additional component of tachycardia (and therefore ischemia due to increased oxygen demand) can also be obtained by combining atropine with dipyridamole.[49] [50] [51] In both circumstances, the addition of atropine to other stressors has been associated with an increment in sensitivity. Indeed, there is a trend toward earlier use of atropine during the dobutamine protocol,[52] [53] especially in beta-blocked patients. However, although nondiagnostic results of a submaximal heart-rate response can be avoided by the use of atropine, this adjunct does not help the results of submaximal tests that reflect premature termination of pharmacologic stress due to side effects. The rationale for combining dobutamine and dipyridamole Figure 14-2 End-diastolic apical four-chamber image in fundamental (A) and harmonic (B) modes. The use of harmonic imaging substantially improves visibility of the lateral wall and distal structures.

reflects their action through different mechanisms. The sequence of drug administration can be used to produce a stepwise stress on the heart. The initial administration of dipyridamole permits detection of the most severe coronary stenoses due to the development of coronary steal. The subsequent incremental administration of dobutamine progressively increases oxygen demand, permitting the identification of progressively

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more moderate stenoses.[54] The combination has also been used to enhance the accuracy of detection of myocardial viability.[11] Although the combination of these techniques has afforded higher levels of sensitivity than the individual tests can provide, using the current methodology, this is obtained at the cost of an unacceptably long stress protocol.[54] Echocardiographic Approach to Nonexercise Stress Techniques Image Acquisition

The technical challenges of pharmacologic and pacing stress, although less extreme than those posed by exercise echocardiography (as the patient is neither moving nor hyperventilating), mandate the use of the best available echocardiography equipment. The development of harmonic imaging has made a substantial impact on endocardial visualization[55] [56] [57] (Fig. 14-2) and therefore the feasibility of stress echocardiography.[58] Although very few patients (<2%) have completely uninterpretable images, 306

failure to detect the endocardium in every myocardial segment is very common, and contrast is indicated if two to four segments are completely or partially obscured (Fig. 14-3) . Typically, transthoracic images are obtained in the four standard views (parasternal long- and short-axis and apical four- and two-chamber). Transesophageal echocardiography has been employed in combination with both pharmacologic[59] [60] [61] and pacing stress,[41] [42] [62] usually for patients with inadequate transthoracic images. During transesophageal imaging with pharmacologic stress, we approximate the standard imaging planes as closely as possible by recording transverse and longitudinal esophageal and transgastric short- and long-axis views. During pacing with electrodes attached to the transesophageal echocardiography probe, the need to stimulate the esophagus inhibits the ability to move the transducer, so that imaging is performed in the transgastric planes only. Although the constraints of a busy stress echocardiography schedule may preclude the performance of a detailed examination in every patient, a "screening" M-mode, pulsed wave (especially for left ventricular inflow), and color Doppler echocardiographic examination should be performed at the beginning of every study. Time should also be taken to optimize twodimensional echocardiographic images, gain settings (for endocardial

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detection), and image size (to obtain the best spatial resolution and framerate). During the stress, the patient is imaged continuously, and the images are stored on videotape. When the study is performed for the diagnosis of coronary disease, the digital quad-screen display is filled with a resting image, a low-dose image (10 µg/kg/minute dobutamine, 0.56 mg/kg dipyridamole, or a small heart rate increment with pacing), and two highdose images (40 µg/kg/minute dobutamine or 0.84 mg/kg dipyridamole with or without atropine), or a peak and early poststress image. When a resting wall motion abnormality is present, and the clinical question pertains to the possibility Figure 14-3 Use of myocardial contrast for left ventricular opacification during stress echocardiography. Compared with harmonic imaging (A), the post-contrast end-diastolic apical four-chamber image (B) shows significant improvement of lateral wall resolution.

of viable myocardium, we obtain two low-dose images (5 and 10 µg/kg/minute dobutamine) and one high-dose image. Image Processing

Both videotape and digital techniques are used for interpretation and archiving of stress echocardiograms. Because modern echocardiography systems are fully digital, digital image capture is an easy process that permits rapid acquisition. Moreover, digital image processing facilitates image display and interpretation by allowing a side-by-side display of resting, low-dose, and high-dose images, as well as the ability to review individual frames (the latter permitting an effective evaluation of the temporal sequence of contraction). Although the use of digital echocardiography enhances the accuracy of nonexercise echocardiography, however, all studies should be recorded on videotape as well as in digital format. This provides a back-up in case technical problems with the digital capture (especially triggering) or corruption of the archived data threaten loss of the study. Indeed, routine review of videotape has a significant impact on diagnosis, probably by permitting review of off-axis images and regions that are not adequately represented by saving a single cardiac cycle. [63]

Qualitative Interpretation

The interpretation of stress echocardiograms for clinical purposes is based on a qualitative evaluation of regional function at rest and stress.[64] Some

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standardization is obtained by scoring regional wall motion and thickening in a number of segments, the most widely used being a model based on that of the American Society of Echocardiography,[65] wherein the left ventricle is divided into 16 307

Figure 14-4 (Figure Not Available) Effect of a training period on the accuracy of interpretation of dipyridamole stress echocardiograms by learning and experienced groups of observers (shown at initial [Before] and follow-up [After] periods). (From Marwick T: Stress Echocardiography. Amsterdam, Kluwer Academic Publishers, 1994.)

segments (anterior, septal, lateral, and inferior at the apex, with these segments as well as anteroseptal and posterior segments at the base and midpapillary muscle level). Despite this standardization, however, the expertise of the physician interpreting the test is critical, and even accomplished echocardiographers require a significant learning period. In a study of echocardiographers learning dipyridamole stress echocardiography, Picano et al[66] reported that 100 supervised studies were required to bring the accuracy of "novices" to the level of "experts" (Fig. 14-4) (Figure Not Available) . The standard qualitative algorithm for interpretation of pharmacologic stress echocardiography is summarized in Table 14-2 . With the exception of the low-dose responses to dobutamine and dipyridamole, which denote myocardial viability (see later discussion), it may also be applied to pacing or other stressors. Regional wall motion at rest may be classified as normal, hypokinetic, akinetic, or dyskinetic. Severe hypokinesia may be difficult to distinguish from akinesia; a useful guide is based on endocardial excursion, with less than 2 mm identifying akinesia and less than 5 mm indicating hypokinesia. Regions that fail to thicken or that move only in late systole (after movement of the adjacent myocardium) may be moving passively and should be considered akinetic, irrespective of endocardial excursion. Segments with resting akinesis or dyskinesis are most likely composed of infarcted myocardium if the wall is TABLE 14-2 -- Interpretation of Myocardial Viability and Ischemia Using Dobutamine Echocardiography Resting

Peak/Poststress

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Function Normal Normal

Low-Dose Normal Normal (unless severe CAD)

Function Hyperkinetic Reduction vs. rest

Reduction vs. other segments Delayed contraction Viable, patent Hypo/akinetic Improvement Sustained IRA improvement Viable, Hypo/akinetic Improvement Reduction (c/w lowstenosed IRA dose) Infarction A/dyskinetic No change No change CAD, coronary artery disease; c/w, compared with; IRA, infarct-related artery. thinned and dense,[67] but in the absence of thinning are quite likely to consist of viable tissue. Indeed, hypokinetic segments are not identified as being infarcted, on the basis that residual contraction implies the presence of residual viability. Because the process of thinning and fibrosis takes some time after infarction, myocardium of normal thickness is commonly seen after recent or non-transmural infarction. Improvement of abnormal function in response to low doses of dobutamine (5 or 10 µg/kg/minute) or dipyridamole (0.28 or 0.56 mg/kg) suggests the presence of viable myocardium (Fig. 14-5) , although this finding is more reliable if the segment subsequently deteriorates, which indicates ischemia. The global left ventricular responses to dobutamine stress include an increase in cardiac output and reduction of left ventricular cavity size, although neither is as prominent with vasodilator stress. Left ventricular dilation implies multivessel or left main coronary artery disease, but this is less commonly seen with pharmacologic than exercise stress,[68] probably because of reduction of left ventricular loading. Together with an extreme inotropic response, this afterload reduction may produce cavity obliteration, and although this response is favorable prognostically (presumably reflecting a low probability of multivessel disease), it may impair sensitivity because endocardial excursion is reduced and small areas of wall motion are unrecognized.[69]

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The normal regional response of segments to maximal 308

Figure 14-5 End-diastolic and end-systolic freeze-frame images illustrating left ventricular enlargement at dobutamine echocardiography in a patient with left ventricular dysfunction and multivessel coronary artery disease. There is a resting wall motion abnormality in the apex, which is unchanged with stress. At peak stress, there is left ventricular enlargement with reduction of systolic motion and thickening of the lateral (and to a lesser degree the septal) wall.

inotropic stress is to increase endocardial excursion, speed of contraction, and degree of myocardial thickening. A deterioration of function from rest, or after an initial enhancement of function, indicates the development of ischemia with either dipyridamole or dobutamine (Fig. 14-6) . Variants of an overt deterioration include delayed contraction ("tardokinesis") and a reduction of myocardial thickening. Caution should be applied in the assessment of areas adjacent to zones of myocardial infarction, which may be tethered by the infarcted zone and hence fail to improve function with stress, or even appear dyskinetic if the infarct bulges during stress. Careful examination of wall thickening may assist in distinguishing peri-infarct ischemia and tethering. The diagnosis of ischemia in segments with abnormal resting function depends on the stress agent and is more difficult. At dobutamine echocardiography, if a segment shows akinesia or dyskinesia at rest, a further deterioration of function probably reflects increased loading rather than ischemia.[70] The most challenging interpretation is the diagnosis of ischemia in segments with resting hypokinesis. Segments demonstrating a stress-induced improvement are classified as normal, and those showing a deterioration (compared with either rest or low-dose) are identified as ischemic. However, differentiation between degrees of hypokinesia may be difficult, even with side-by-side cine-loop analysis. Some caution needs to be applied in the interpretation of regional variations in the degree of hyperkinesis, as these may occur in normal patients.[71] The diagnosis in hypokinetic regions that fail to improve function in response to stress is debated; if adjacent segments mount a hyperkinetic response, we characterize these as ischemic. The greatest limitations of the current application of stress

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echocardiography are concerns related to subjectivity and reproducibility. Although single-center studies 309

Figure 14-6 Apical two-chamber views illustrating the development of myocardial ischemia (reduced wall thickening) of the apex during dobutamine stress echocardiography. End-diastolic images are given on the left and systolic images on the right, with resting images above and peak dose below.

have suggested that the interobserver variation in interpretation is small,[72] interinstitution variability (although similar to that of other imaging techniques) is significant.[73] Interinstitution variability is particularly a problem in studies of poor image quality and in patients with mild ischemia. This discordance has been progressively reduced by definition of standard reading criteria[74] and more recently by the adoption of harmonic imaging.[75] The following reading guidelines are useful for controlling variation: minor degrees of hypokinesia are not identified as ischemia (especially if only apparent at peak and not at poststress readings); focal abnormalities that do not follow angiographic territories are ignored; abnormalities are corroborated whenever possible with another view; basal inferior and septal segments are not identified as abnormal in the absence of a neighboring abnormal segment; studies are read by multiple observers whenever possible; and reading is blinded to all other data. Finally, we find a standard sequence to be of value in the interpretation of stress echocardiograms (both exercise and nonexercise). We first review the video images of the resting examination, including M-mode and Doppler components. On beginning the review of the digital images, we first check that images are triggered correctly and the prestress, peak stress, and poststress views are comparable. We then briefly review the side-byside display to see if there are new wall motion abnormalities or obvious changes in cavity size (suggesting multivessel disease) or cavity shape. Segmental analysis is carried out by careful comparison of regional function in each of the 16 segments, comparing the same site at rest and at stress. Both wall motion and thickening are compared, using both cine-loop and frame-by-frame review of the digital images. If image quality is not good enough to permit the use of thickening criteria, the reader should focus on the first part of systole to minimize the contribution of rotational or translational movement. Finally, videotaped stress images are examined,

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to review nonstandard views 310

and to check on conclusions based on the digitized images. From review of digital and video data, the site, extent (number of abnormal segments), severity (segmental wall motion score), time of onset and offset of ischemia, and the effect of ischemia on global left ventricular function can be derived.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Aspects of Nonexercise Stress Techniques General Considerations The preparation for nonexercise stress testing does not deviate substantially from preparation for exercise stress testing. These tests should be performed in the fasting state, partly because nausea is a side effect with some agents (especially transesophageal pacing, dipyridamole, and adenosine), and also in case complications ensue, with attending risks of aspiration. For dipyridamole stress testing, coffee, tea, and cola drinks should be avoided for 12 hours before the examination, as xanthines antagonize the effects of dipyridamole on adenosine metabolism, as well as by direct competitive inhibition of adenosine activity. For diagnostic testing, patients should be instructed to stop anti-ischemic drugs on the day of the procedure, but medications may be continued if testing is being performed to assess the adequacy of therapy. During the preparatory stage of the test, intravenous access is secured, and electrocardiographic monitoring may be modified to remove electrodes from the echocardiographic windows. A minimum of two personnel (sonographer and physician) is mandatory for performance of these protocols, and many centers involve a nurse as well. Clinical and electrocardiographic monitoring during the tests parallels the monitoring undertaken during exercise stress testing. In addition to the usual resuscitation equipment, intravenous beta-adrenoreceptor blocking agents and nitrates should be available to treat severe ischemia, and for dipyridamole testing, aminophylline should be available for the treatment of severe ischemia, which occurs occasionally. Exercise-Simulating Agents Protocols for Administration of Sympathomimetic Agents

Dobutamine has been administered using various empirical dose regimens,

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but the relative plasma levels with these have not been studied, and none is clearly superior to the others. The most widely used is an incremental administration (Fig. 14-7) from 5 µg/kg/minute to 40 µg/kg/minute in 2- or 3-minute stages.[28] [29] [30] [31] [32] [33] [34] Variants include maximal doses of up to 50 µg/kg/minute and down to 20 µg/kg/minute; lower dose-rates administered over longer periods are able to attain hemodynamic effects similar to those obtained by the high-dose protocols.[33] New accelerated dobutamine protocols are currently being used to reduce the duration of the test, but whichever regimen is applied, a reasonable (i.e., 2- to 3-minute) period at peak heart rate is desirable, as ischemic wall motion abnormalities may take a short time to become apparent. If atropine is added to induce an increase in heart rate, the usual dose is 1 to 2 mg total in 0.25-mg increments. Arbutamine is no longer marketed, but other agents might be applied using a similar closed-loop computerized delivery system. The age and weight of the patient, target heart rate, and rate of heart rate augmentation (heart rate slope) were entered into the device. Based on the response to an initial dose, the microprocessor automatically increased the infusion rate to achieve the required rate of augmentation and eventually the desired peak. As the target rate was approached, the infusion was reduced and stopped. The device had a number of alarms to alert the supervising physician to responses that require attention, as well as safety features that permitted automatic shut-off of the system. Such a system could reduce the need for a nurse to increase the drug and monitor the hemodynamics. Hemodynamic Responses to Sympathomimetics

Dobutamine enhances left ventricular contractility at low doses, usually without the development of tachycardia. At doses greater than 20 µg/kg/minute, systolic blood pressure increases, and the heart rate augments to more than 100 beats per minute. Using a standard protocol without atropine, heart rate can be expected to increase to about 120 beats per minute in most patients, reflecting a heart rate increment of 40 to 50 beats per minute. In normotensive patients, the systolic blood pressure usually increases to about 170 mm Hg (an increment of 30 to 40 mm Hg), without a significant change of diastolic blood pressure. The systolic pressure response may be marked in hypertensive patients and blunted in patients with left ventricular dysfunction or multivessel coronary disease. The peak rate-pressure product increases to the range of 16,500 to 20,000. Although the development of ischemia at lower dobutamine doses and cardiac workloads indicates the presence of more extensive coronary

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disease, there is too much overlap for the hemodynamic response to be a reliable predictor of one-, two-, or three-vessel disease. The hemodynamic response to dobutamine shows significant variability between patients. Beta-adrenergic blockade may attenuate the physiologic responses to dobutamine through a process of competitive antagonism at the receptor level. Patients taking beta blockers have a significantly lower heart rate response (to a peak of 90 to 100 beats per minute), and a lower double-product (to levels of around 14,000), although this may be attenuated by use of atropine. The peak systolic blood pressure is less during dobutamine than exercise, although this difference is less than with heart rate.[29] Indeed, the cardiac stress imposed by dobutamine (even at maximal dobutamine dosage) is less than that obtainable with maximal exercise testing. In several head-to-head comparisons between 311

Figure 14-7 Standard incremental dobutamine protocol, starting at 5 µg/kg/min and going to 40 µg/kg/min with incremental atropine. Images and hemodynamics are obtained at the end of each stage.

dobutamine and exercise stress in the same patients, systolic blood pressure levels were comparable, but peak heart rate and double product were significantly greater during exercise than dobutamine stress.[33] [76] [77] [78] [79] [80] [81] These disparities have important implications for the relative sensitivity of dobutamine and exercise echocardiography (see later discussion). Side Effects of Stress Testing with Sympathomimetic Agents

Other than the development of myocardial ischemia, dose-limiting side effects experienced during dobutamine protocols generally reflect intense adrenergic stimulation. Consequently, dobutamine stress is contraindicated in patients with severe hypertension and serious arrhythmias. Serious side effects are rare during dobutamine stress testing. In more than 1000 dobutamine studies reported by Mertes et al,[82] no patients died or suffered myocardial infarction or sustained tachyarrhythmias. Similarly, in 650 studies with dobutamine and atropine reported by Poldermans et al,[83] no patients died or suffered myocardial infarction, and cardiac arrhythmias were most likely in patients with left ventricular dysfunction or pre-existing

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ventricular arrhythmias. In a multicenter study reported by Picano et al,[50] nine major cardiac events occurred in nearly 3000 studies (three due to ventricular tachycardia, two from ventricular fibrillation, two from myocardial infarction, one with severe ischemia, and one with hypotension). In this study, atropine psychosis was observed in five patients, but this finding has not been reported from other studies and this author has yet to see this complication in a personal experience of over 5000 studies, many of which have involved atropine usage. In our experience, serious side effects of dobutamine stress occurred in 3 per 1000 patients,[84] a similar result to that of a large German study.[85] Nonetheless, in case reports, fatalities have been reported from ventricular fibrillation and cardiac rupture.[86] Moreover, the safety of the test in patients at highest risk—those with severe left ventricular dysfunction—has been described only in small populations.[87] Nonetheless, considering that the sickest patients (those unable to exercise and those with questions of myocardial viability) undergo the test, this safety profile can be considered to be quite favorable and may in part reflect the detection of the extent and severity of ischemia by online echocardiographic imaging, permitting termination of the stress before serious problems arise. The most frequent serious but nonfatal complications are myocardial infarction and arrhythmias, although atrial fibrillation and sustained ventricular tachycardia are rare, and more common rhythm problems include atrial and ventricular extra systoles and nonsustained atrial and (less often) ventricular tachycardias. Other problems include palpitations (due to increased contractility), hypertension, anxiety (sometimes manifested as dyspnea or vagal reactions), tremor, and urinary urgency. Hypotension may arise from the vasodilator effect of high-dose dobutamine, the development of outflow tract obstruction, or the development of severe ischemia. [88] [89] [90] [91] Unlike hypotension during exercise testing, it does not denote the presence of serious coronary disease or left ventricular dysfunction. [92] All of the studies documenting the sensitivity and specificity of dobutamine stress echocardiography have documented these complications, but the recorded frequency of these side effects has varied from 5% if only serious, dose-limiting side effects are considered[28] to 82% if all side effects are included.[33] One source of variability relates to the definitions used to identify side effects. For example, in the initial experience with dobutamine stress testing, hypotension (which is usually asymptomatic) provoked termination of the test if the systolic blood pressure decreased by more than

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20 to 30 mm Hg or a greater than 15 mm Hg fall from baseline, whereas most centers now continue the infusion unless the systolic blood pressure falls to less than 100 mm Hg or the patient becomes symptomatic. Another source of variability relates to the type of stress protocol, the incidence being lower if the test is terminated for attainment of a target heart rate or when echocardiographic evidence of ischemia is seen[28] or if submaximal test responses are excluded.[29] Vasodilator Stress Protocols Stress Protocols

For dipyridamole stress, an intravenous line is inserted into a large proximal arm vein to minimize local discomfort from this strongly alkaline compound. Various dipyridamole administration regimens have been used, both intravenous and oral, although the absorption of the latter is variable and the approval of the intravenous form of 312

this agent by the Food and Drug Administration has removed the main reason for using this route. For myocardial perfusion imaging, the most commonly administered dose is 0.56 mg/kg IV,[93] but this infusion protocol has unsatisfactory levels of sensitivity when combined with stress echocardiography. The sensitivity of dipyridamole echocardiography can be significantly enhanced[94] [95] by an additional 2 minutes of infusion if the initial response is negative and no major side effects have appeared. Because the time of onset of ischemia correlates with the severity of coronary disease and prognosis (see later discussion), we record images every 2 minutes from the conclusion of the first dose until 18 minutes from the start of the study. Digitized images are saved at rest, before the start of the second dose (8 minutes), after the second dose (12 minutes, which is the most common time for the onset of ischemia), and at 16 minutes. Aminophylline (in aliquots of 50 to 75 mg IV) can be used to counteract the effects of dipyridamole if severe ischemia or side effects arise; the threshold for using this agent is influenced by the overall left ventricular function and the clinical state of the patient. Because dipyridamole acts via endogenous adenosine release, there is some delay between the time of its administration and the development of its effects. In contrast, because exogenous adenosine is able to act directly, it rapidly achieves steady state, and its biologic effects are of rapid onset.[38] It

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is therefore suitable for injection using an incremental dose schedule, with echocardiographic imaging at the end of each stage. Various dosing regimens have been used for echocardiographic studies, including a fixed dose of 0.14 or 0.17 mg/kg/minute and incremental protocols (3-minute stages starting at 0.10 mg/kg/minute, increasing to 0.14 and 0.18 mg/kg/minute).[96] [97] [98] [99] The use of aminophylline is rarely required for side effects, as these resolve within a minute of stopping the infusion. Hemodynamic Responses to Vasodilators

The mechanism of action of vasodilator agents is chiefly through the phenomenon of coronary steal. There is a small contribution of increasing oxygen demand from tachycardia,[23] which may be a response to angina and side effects rather than arising from the agents themselves. Similarly, blood pressure is usually little changed by these stressors, which may cause hypotension. The addition of atropine leads to an augmentation of heart rate and cardiac work, [49] [51] effectively combining reduced coronary supply with increased oxygen demand. Side Effects of Dipyridamole and Adenosine

The development of side effects during dipyridamole stress usually follows completion of the infusion and rarely precludes completion of the study. Side effects usually resolve spontaneously, but, if necessary, aminophylline can be used to reverse the effects of dipyridamole. Minor side effects, including flushing and headache (which reflect the systemic vasodilator effects of the compound), occur in about two thirds of patients studied with high-dose dipyridamole.[100] Severe or prolonged myocardial ischemia is infrequent but can be treated with nitrates or aminophylline. Serious side effects are very rare[50] [101] severe myocardial ischemia and infarction, bronchospasm, and complete heart block and even death have been reported. The frequency of these serious complications is probably less than with dobutamine, although ensuring that the comparison groups are matched for baseline risk is always difficult. Dipyridamole stress is contraindicated in patients with untreated atrioventricular block and bronchospastic disorders, although patients with chronic obstructive airway disease with no or minimal airway reactivity may undergo the test. Adenosine differs from dipyridamole stress only to the extent that the adenosine causing the physiologic effects is exogenous rather than endogenous. The side effect profile is therefore similar, and although the intensity and frequency of side effects with adenosine exceed those of

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dipyridamole, they are of shorter duration. Some form of side effect occurs in most patients undergoing adenosine stress.[102] In response to a high-dose protocol, [99] side effects prevented about one third of patients from achieving peak dose, a comparable frequency to that found with dobutamine. As the effect of adenosine is very transient, cessation of the infusion is usually the only treatment required for side effects. Vasoconstrictor Protocols An increasing amount of literature has developed regarding the use of ergonovine for the diagnosis of coronary spasm, especially in regions where this diagnosis is made in the absence of fixed coronary stenoses. In the West, however, this finding is considered unusual, with spasm being recorded in 4% of patients in whom it is suspected clinically, although the return may be increased significantly by focusing on smokers and patients with some coronary disease.[103] Although most practitioners feel more comfortable with the use of this agent in the angiography laboratory,[103] because spasm can be visualized directly and intracoronary nitrates infused to treat severe spasm, a significant evidence base attests to its safety when applied noninvasively in patients without significant stenoses.[104] [105] [106] Although most of the evidence base relates to patients in whom significant stenoses have been excluded, the test has been applied to some patient groups without previous angiography.[6] [7] The standard protocol involves repeated bolus doses of ergonovine maleate at 5-minute intervals up to a total cumulative dose of 0.35 mg, unless echocardiographic evidence of abnormal left ventricular wall motion is detected. Pacing Stress Stress Protocols

The use of transesophageal pacing requires topical pharyngeal anesthesia and mild sedation. The end points of the test are the same as those for other nonexercise stressors; 313

in the absence of these end points, pacing at peak heart rate is continued for 3 minutes. No protocol has been uniformly accepted. Although formerly we used an incremental protocol commencing at 100 beats per minute, with increases in 2-minute stages, we now take the heart rate to 85% of predicted maximum immediately, followed by 100% of predicted

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maximum. The benefit of a short protocol is that electrode movement and loss of capture are less likely. Atropine is often required to overcome Wenckebach's atrioventricular block. In our practice, we digitize resting, 100 beats per minute, peak, and post-pacing images and apply the usual guidelines for interpretation. Hemodynamic Responses

The hemodynamic response to pacing stress is more controllable than the response to pharmacologic agents. The heart rate is usually increased to 150 or 160 beats per minute, and systolic blood pressure is increased by only a small amount, giving a rate-pressure product of 15,000 to 20,000. In the case of atrial pacing using transesophageal imaging, the insertion of the transesophageal probe in an awake patient may itself provoke hemodynamic TABLE 14-3 -- Sensitivity and Specificity of Echocardiography with Dob 50 Patients)

Study Sawada et al

Significant Multivessel Myocard Dobutamine Stenosis Disease, n Infarctio n (% Al Patients, Protocol, Diameter, (% All N µ/kg/min % CAD) CAD) 103 30 >50 14 (40) 35 (43)

[28]

Cohen et al[29] Salustri et al

70 52

40 40

>70 >50

35 (69) 17 (46)

19 (37) 14 (38)

Marcovitz & 141 Armstrong[32] Mazeika et al 50

30

>50

47 (43)

—

20

>70

24 (67)

13 (36)

40 + atropine 40

>50

15 (32)

28 (60)

>50

74 (52)

0 (0)

66

40

>70

21 (42)

0 (0)

80

40

>50

33 (58)

15 (26)

[31]

[33]

McNeill et al

80

[46]

Marwick et al 217 [34]

Hoffmann et al[81] Previtali et al [78]

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Takeuchi et al 120

30

>50

37 (50)

62 (84)

40 + TEE 40 + TEE 40

>70 >70 >50

16 (76) 37 (60) 11 (9)

7 (33) 23 (37) 41 (34)

40 40 40 + dipyridamole 30 40 40

>50 >50 >50

21 (49) 16 (12) 16 (12)

9 (21) 38 (29) 38 (29)

>50 >50 >70

36 (55) 27 (67) 15 (60)

24 (37) 18 (41) 41 (39)

40 + atropine 40 + atropine 40 + atropine 40 + atropine 40 + atropine 40 + atropine

>50

42 (46)

25 (27)

>70

109 (74)

105 (71)

>50

34 (54)

0 (0)

>50

48 (40)

38 (30)

>50

122 (58)

>50

142 (61)

214 (70)

>50

113 (66)

55 (24)

>50 >50

— 15 (60)

>50

70 (64)

[214]

Prince et al[215] 81 Panza et al[59] 76 Beleslin et al 136 [79]

Senior et al[216] 61 Ostojic et al[54] 150 Ostojic et al[54] 55 Daoud et al[217] 76 54 Ho et al[218] Dagianti et al 60 [219]

Pingitore et al 110 [51]

Ling et al[220]

183

San Roman et al[221] Anthopoulos et al[222] Dionisopoulos et al[223] Elhendy et al

102 120 288 96 f

[224]

210 m Hennessy et al 219 [225]

Huang et al[226] 93 Lewis et al[227] 93 Nagel et al[228] 208

40 + atropine 40 Modified protocol 40 + atropine

—

— — 0 (0)

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Beleslin et al 168

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40

>50

0 (0)

40 (24)

[117]

SVD = single vessel disease, TEE = transesophageal echocardiography. changes and hence ischemia, so that "resting" transesophageal echocardiographic images may not be truly acquired at rest. Side Effects

Fewer side effects occur during transesophageal pacing than with pharmacologic stressors. The frequency of esophageal discomfort, gagging, or nausea is much lower with modern pacing electrodes. Angina may be provoked by stress but is usually self-limiting after cessation of pacing. Atrial flutter or fibrillation may also be precipitated. Esophageal injury is theoretically possible in response to high levels of stimulation over a prolonged period, but this has not been reported clinically.

MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/120.html/top

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Accuracy of Nonexercise Stress Echocardiography for Diagnosis of Coronary Artery Disease Dobutamine Stress Echocardiography The sensitivity and specificity of dobutamine echocardiography for the detection of coronary artery disease and results of recent studies are summarized in Table 14-3 . The 314

sensitivity for significant disease (defined as visually assessed stenoses of greater than 50% or greater than 70%) is variable between studies, with an interquartile range of 75% to 92%. The addition of atropine appears to enhance the sensitivity of the test, as does transesophageal imaging. The interquartile range for specificity ranged from 77% to 93%, which is comparable to that of exercise echocardiography. No single feature accounts for these false-positive results, although the most frequent site of false-positive results[107] is the basal inferior wall. Patients with apparent abnormalities in this segment should be identified as having coronary disease only if an adjacent segment (basal septal, mid-inferior, posterior) is also involved. One problem with assessments of sensitivity and specificity is that a 50% or 70% stenosis cutoff is arbitrary and does not take into account stenosis location or vessel size, both of which clearly influence the likelihood of an abnormal response. This concern has been addressed in several studies that have compared the results of dobutamine echocardiography with stenosis diameter at quantitative coronary angiography.[108] [109] [110] The angiographic cut-off value with the best predictive value for a positive dobutamine test was a luminal diameter of 1.07 mm, percent diameter stenosis of 52%, and percent area stenosis of 75%, of which minimal lumen diameter was found to have the best predictive value for a positive dobutamine stress test (odds

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ratio, 51; sensitivity, 94%; specificity, 75%).[108] Stenoses smaller than 1 mm in diameter can be identified with a sensitivity of 86%. [109] [110] The previous analyses were limited by comparison with the anatomic severity of stenosis, whereas a more physiologic comparison would be more meaningful. Myocardial fractional flow reserve is a functional index of coronary stenosis severity that takes into account collateral flow and is calculated as the ratio of mean hyperemic distal coronary to aortic pressure. The degree of dobutamine-induced dyssynergy correlates significantly better with myocardial fractional flow reserve than percent stenosis or minimal lumen diameter, and the sensitivity of dobutamine echocardiography is significantly lower for lesions in vessels smaller than 2.6 mm than for larger vessels.[109] Because the existence of a regional wall motion abnormality identifies the presence of coronary disease, dobutamine echocardiography demonstrates higher sensitivities in patients with myocardial infarction. In patients with single-vessel coronary disease, the sensitivity of dobutamine echocardiography (ranging from 40% to 70%) is lower than in patients with multivessel disease. As dobutamine produces a less potent stress on the heart than exercise (see earlier discussion), the results of dobutamine stress are probably more susceptible to external influences than are those of exercise echocardiography or myocardial perfusion scintigraphy. This may be pertinent to the extrapolation of results from clinical trials (in which patients were carefully supervised and tested under optimal conditions, off therapy), to routine clinical practice, in which patients are often tested on therapy and are more likely to have a "suboptimal" test result because of inability to complete the protocol or interference by beta-blocker therapy.[34] Stress Echocardiography Using Other Sympathomimetic Agents Combination of echocardiography with other agents, such as epinephrine and isoproterenol, offers moderate sensitivity in the diagnosis of coronary artery disease.[111] Failure to attain higher levels of sensitivity with these compounds has in part reflected limitations in the administered dose brought about by concerns about side effects. The sensitivity of arbutamine echocardiography for the identification of ischemia was 76%, and the sensitivity for identification of coronary disease was 84%. No specificity data were obtained, but in a group at low probability of coronary disease, the normalcy was 96%.[112] As in the case of dobutamine and exercise echocardiography, the sensitivity was lower in

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patients with less extensive disease and also in patients who were stressed submaximally. However, arbutamine stress echocardiography seems unlikely to be developed further for commercial reasons. Dipyridamole Stress Echocardiography Studies of more than 50 patients that address the accuracy of vasodilator stress echocardiography for the identification of coronary artery disease are summarized in Table 14-4 . The use of the low-dose (0.56 mg/kg) protocol is associated with lower sensitivities than those generally reported with the high-dose regimen, which range from 58% to 94%. The addition of atropine to dipyridamole appears to enhance the sensitivity of the test.[49] [113] In patients with single-vessel coronary disease, the sensitivity of dipyridamole echocardiography is in the range of 50%, and this has an important influence on the sensitivity of this test in comparison with dobutamine. Most studies show the specificity of the technique to be excellent. As in the case of dobutamine, the use of transesophageal imaging has enhanced the accuracy of dipyridamole stress echocardiography.[114] There appears to be more variation in the sensitivity of vasodilator stress echocardiography than for dobutamine and exercise echocardiography. The main variables that account for this heterogeneity are patient selection and the definition of "significant" disease. The use of greater than 70% diameter stenosis as a criterion of significant coronary disease has tended to enhance the sensitivity, as patients with milder stenoses (who would be more difficult to detect) are not included. Of more importance, however, are clinical factors, such as the prevalence of myocardial infarction and multivessel disease and the cessation of antianginal therapy[115] many of the more favorable results pertain to populations with a high percentage of patients with more severe coronary disease. As in the case of dobutamine stress, investigators have sought to address the accuracy of dipyridamole stress with physiologic rather than anatomic criteria of significant stenosis.[116] In 30 patients with isolated stenoses of the left anterior descending coronary artery, predictors of an abnormal dipyridamole echocardiogram were a stenotic flow reserve of less than 2.8, stenosis diameter greater than 59%, lumen diameter less than 1.35 mm, and coronary flow reserve less than 2.0, of which stenotic flow reserve was the only independent predictor of ischemia. This 315

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TABLE 14-4 -- Accuracy of Vasodilator (Dipyridamole and Exercise) Ech of More Than 50 Patients)

Patients, Study N Picano et al 66 [94]

Picano et al

93

[100]

Masini et al

83

[229]

Massa et al

52

[156]

Cohen et al

50

[230]

Picano et al

445

[231]

Simonetti et al[232] Zoghbi et al

51 73

[97]

Severi et al

429

[126]

Mazeika et al[233] Picano et al

55 130

[49]

Previtali et al[78] Marwick et al[99]

80 97

Multivessel Myocardia Definition Disease, n Infarction n (% All of CAD, (% ALL CAD) Agent Dose % CAD) Dipyridamole, >70 20 (40) 9 (18) 0.56 mg/kg 48 (67) 17 (24) Dipyridamole, >70 * 0.84 mg/kg Dipyridamole, >70 24 (62) 15 (38) * 0.84 mg/kg Dipyridamole, >70 12 (23) 9 (17) * 0.84 mg/kg Dipyridamole, >70 28 (78) 16 (44) 400 mg PO 119 (46) 0 (0) Dipyridamole, >50 * 0.84 mg/kg Dipyridamole, >70 0.84 mg/kg * >75 24 (44) 38 (70) Adenosine, 0.14 µg/kg/min * 114 (46) 0 Dipyridamole, >75 * 0.84 mg/kg 30 (75) 18 (45) Dipyridamole, >70 * 1.00 mg/kg Dipyridamole, >50 — — 0.84 mg/kg + atropine 33 (58) 15 (26) Dipyridamole, >50 * 0.84 mg/kg Adenosine, >50 28 (47) 0 (0) 0.18 µg/kg/min *

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Ostojic et al [54]

Marangelli et al[123] Beleslin et al[79] Dagianti et al[219] Tawa et al[98]

Djordevic et al[234] San Roman et al[221] Pingitore et al[51] Anthopoulos et al[222] Beleslin et al[117] HG, hand grip.

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150 Dipyridamole, 0.84 mg/kg * 60 Dipyridamole, 0.84 mg/kg * 136 Dipyridamole, 0.84 mg/kg * 60 Dipyridamole, 0.84 mg/kg * 67 Adenosine, 0.17 µg/kg/min + HG 58 Adenosine, 200 µg/kg/min * 102 Dipyridamole, 0.84 mg/kg * 110 Dipyridamole, 0.84 mg/kg + atropine 120 Adenosine, 0.14 µg/kg/min * 168 Dipyridamole, 0.84 mg/kg *

>50

16 (12)

38 (29)

>75

19 (54)

>50

11 (9)

41 (34)

>50

15 (60)

41 (39)

>50

7 (18)

22 (55)

>50

34 (54)

0 (0)

>50

48 (40)

38 (30)

>50

0 (0)

40 (24)

—

>50

* Low-dose positivity permits conclusion of study before stated "peak" dose.

study was interesting on two grounds: First, it implies that dipyridamole identifies fewer mild stenoses than dobutamine echocardiography, and second, it identified angiographic variables of stenosis severity to relate to dipyridamole echocardiographic results better than intracoronary Doppler variables. Other studies have confirmed that the optimal angiographic cutoff point for dipyridamole stress echocardiography is 60%, as compared with 58% for dobutamine and 54% for exercise echocardiography.[117]

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Vasodilator Stress with Adenosine Echocardiography The accuracy of adenosine stress echocardiography is also detailed in Table 14-4 . There is less of an evidence base for this test than for other pharmacologic approaches, and the published data show significant variations in accuracy. The most favorable results may be influenced by a high prevalence of multivessel coronary disease or prior infarction, the sensitivity being only 60% in patients with a normal electrocardiogram.[97] In patients without prior infarction, the sensitivity of this test was less than 60%.[99] The dose and duration of adenosine have an important influence on sensitivity, as does the coadministration of atropine. The accuracy of adenosine echocardiography has recently become the source of considerable interest because of the possibility of combining standard stress echocardiography and assessment of myocardial perfusion, either using contrast echocardiography or coronary flow reserve. Several studies have now shown that the intense coronary vasodilation induced by adenosine permits the comparison 316

of rest and hyperemic images using contrast echocardiography.[118] , [119] Although this comparison is certainly also feasible with dipyridamole,[120] adenosine may be superior. Similarly, coronary flow reserve may be measured at transthoracic or transesophageal echocardiography, using adenosine[121] as a vasodilator. The longer time course and less predictable peak flow with dipyridamole make this a less attractive agent, and if this is selected, high dose is certainly required. [122] Pacing Stress Echocardiography Table 14-5 details the accuracy of studies that have combined atrial pacing with echocardiography. Generally, very favorable results have been obtained with this stress, although the number of studies and patients within studies is still limited. The accuracy of both transesophageal imaging and pacing probably reflects the benefits of high-quality images as much as the role of pacing stress, as similar favorable findings have been obtained using transesophageal echocardiography with dobutamine and dipyridamole, as discussed earlier. The discrepancy between the reported accuracy in contrast with the limited application of the test is striking. Indeed, this became more prominent after

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a recent landmark study[43] found that transesophageal atrial pacing had a high level of feasibility, and safety, duration, and patient acceptance were more favorable than with dobutamine stress echocardiography. Moreover, the tests showed a high level of concordance in inducing regional wall motion abnormalities. Although the lack of clinical uptake for this modality may not appear to be readily understood, the following are important issues that influence our continued use of pharmacologic stress. First, the evidence base for diagnostic, management, and prognostic information using pharmacologic agents is substantially greater than with pacing stress. Second, the pacing test is unlikely to be useful for the detection of viable myocardium, and even when this is not needed from a clinical standpoint (e.g., the patient is not being evaluated for possible revascularization), the biphasic response has been shown to facilitate the distinction of ischemia in the setting of resting wall motion abnormalities. Third, although advances in pacing catheter technology have improved patient tolerance, as documented earlier, most patients and some TABLE 14-5 -- Sensitivity and Specificity of Atrial Pacing Stress Ech Definition Sensitivity: Patients, Feasibility, of CAD, Overall, % Sensi Study N Method % % (n) SVD, Iliceto et al 85 TTE 95 >75 91 (56) 80 (2 [45]

Lambertz 50 et al[42] Zabalgoitia 36 et al[235] Kamp et al 71

TEE

100

>50 93 (41)

85 (2

TEE

90

>70 90 (21)

100 (1

TEE

99

>50 83 (52)

69 (1

TEE

94

>70 86 (20)

—

31

TTE

—

75 92 (26)

—

80

TTE

77

>75 83 (35)

75 (1

65

TTE

69

TTE

[41]

Norris et al 32 [236]

Anselmi et al[237] Marangelli et al[123] Michael et al[238] Schroder

>50 87 52

>50 82 (69)

— 82 (6

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et al[239] SVD, single vessel disease; TEE, transesophageal echocardiography; TTE echocardiography. clinicians look upon the test as being excessively invasive. We believe the test will have several "niche" applications for situations in which dobutamine is unattractive: patients with hypertension or rhythm contraindications to dobutamine, potentially unstable patients (because the stress can be stopped suddenly), or patients with chronotropic incompetence of various causes. Comparison Between Nonexercise Stressors for the Diagnosis of Coronary Artery Disease Selection of the Optimal Pharmacologic Stress

It is clear from Table 14-3 and Table 14-4 that both dobutamine and vasodilator stress echocardiography are effective for the diagnosis of coronary artery disease. However, the relative efficacy of the stressors cannot be assessed by merely comparing the results of individual studies in the literature, because of variations in the study groups. The optimal study design should be based on a head-to-head comparison of the tests in the same patients, under the same conditions, as summarized in Table 14-6 . Such studies have generally demonstrated similar levels of feasibility with dobutamine and vasodilator stress. The sensitivity of dobutamine stress echocardiography has been shown to exceed that of vasodilator stress almost exclusively, although the two are close enough to be considered comparable in several studies. The main source of discrepancy appears to be patients with single-vessel coronary disease, among whom dobutamine appears to be superior to dipyridamole echocardiography. This difference parallels a significantly greater cardiac workload with dobutamine compared with vasodilator stress. As the contraindications to inotropes and vasodilators vary, the selection between them may be individualized; patients with hypertension or arrhythmias should undergo a vasodilator stress, and patients with bronchospasm or conduction disorders should be submitted to inotropic stress. However, in the majority of patients who do not have these contraindications, dobutamine appears to be the most sensitive agent for pharmacologic stress echocardiography, at least for diagnostic purposes.

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317

TABLE 14-6 -- Studies Comparing Sensitivity and Specificity of D Echocardiography Multivessel Myocardial Disease, n Infarction, Sensitivity: S (% All n (% All Dobutamine, Dip CAD) CAD) % 18 (72) — 76 56

CAD, Patients, n Study N (%) Martin et al 40 25 [240] (63) Salustri et al 46 18 18 (64) [152] (39) Marwick et 97 59 28 (47) [99] * al (61) 80 57 33 (58) Previtali et [78] (71) al Beleslin et 136 119 11 (9) [79] al (88) Ostojic et al 150 131 16 (12) [54] (87) Dagianti et 60 25 15 (60) [219] al (42) Anthopoulos 120 89 48 (40) [222] * et al (74) 102 63 34 (54) San Roman [221] (62) et al Loimaala et 60 44 18 (41) [205] al (73) Fragasso et 101 56 37 (65) [241] al (56) CAD, coronary artery disease.

15 (83)

79

82

0 (0)

85

58

15 (26)

79

60

41 (34)

82

74

38 (29)

75

71

41 (39)

72

52

38 (30)

87

66

0 (0)

77

77

0 (0)

93

95

0 (0)

88

61

* Adenosine used instead of dipyridamole.

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Selection of Pacing Rather than Other Nonexercise Stress

Few data are available to evaluate the relative status of pacing in relation to pharmacologic approaches to nonexercise stress testing. A recent comparison of pacing to dipyridamole stress echocardiography in 80 patients with suspected coronary disease and without prior infarction[123] showed the feasibility of the test was less with pacing stress than dipyridamole (77% versus 96%, P < .0001). In patients in whom pacing and dipyridamole testing were feasible, the respective sensitivities were 83% and 43% (P = .0005), and specificities were 76% and 92% (P = NS). Although these favorable results for pacing stress may reflect the inadequacies of dipyridamole echocardiography for diagnostic stress testing, a recent comparison with dobutamine stress echocardiography recently documented[43] that transesophageal atrial pacing showed safety, duration, and patient acceptance results more favorable than those achieved with dobutamine stress echocardiography, with a high level of concordance in inducing regional wall motion abnormalities.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Disease Significance Using Nonexercise Echocardiography In patients with known coronary artery disease, stress imaging procedures are often performed to facilitate clinical decision making, for example, regarding the referral of patients for coronary intervention. The location, extent, and severity of coronary disease can be important in this respect, and all can be determined using nonexercise echocardiography. The use of stress echocardiography for identification of the "culprit" coronary lesion is often constrained by the assumptions inherent in allocating territories of the heart to individual coronary vessels. The most ambiguous areas in this respect are the apex (usually assumed to be within the territory of the left anterior descending coronary artery) and the posterior wall (usually assumed to be supplied by the left circumflex artery). Because of the equivocal involvement of the right coronary or left circumflex vessels in the posterior territory, investigators have examined the ability to discern the presence of coronary disease in the anterior and posterior circulations. Although in the pre-harmonic imaging era the lateral wall was a source of false-negative results, the accuracy of dobutamine echocardiography in each territory appears to be equivalent (Fig. 14-8) . More severe disease in the vessel supplying an ischemic region generally correlates with a more severe wall motion disturbance. Likewise, multivessel disease usually corresponds to extensive areas of ischemia or the development of global ventricular dysfunction, or both, evidenced by poststress reduction of ejection fraction or increase of end-systolic volume, although these are much less common than with exercise, probably because of left ventricular unloading at peak stress. The presence of stenoses in multiple vessels is well known to be predictive of an adverse prognosis in patients with coronary artery disease. Consequently, the recognition of multivessel disease as such may be important in planning revascularization rather than medical therapy. The ability of dobutamine stress

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echocardiography to predict multivessel disease is greatest in patients with a history of previous myocardial infarction, under which circumstances its sensitivity for the correct identification of disease is 80% to 85% and its specificity is 88%.[28] [124] In contrast, the sensitivity for multivessel disease in patients without previous infarction is approximately 70%[28] and exceeds the levels reported in this situation using exercise echocardiography. A close correlation has been demonstrated between the extent of ischemia defined by dobutamine echocardiography and perfusion scintigraphy, although both underestimate the angiographic extent of disease as measured by the Gensini score,[34] a reflection of the difficulties of assessing the functional implications of disease extent on anatomic grounds. In addition to the "space coordinate" (i.e., extent of abnormal segments),[20] another physiologic indication of the extent of coronary disease is the "time coordinate" (i.e., ischemic threshold). Using dobutamine stress, multivessel disease may also be predicted if ischemia has an early onset (similar to the "ischemia-free" time at 318

Figure 14-8 Lateral wall ischemia. Freeze-frame images in the apical four-chamber view demonstrate normal thickening at rest (above), with reduced thickening at peak stress (arrows).

exercise testing), corresponding to its occurrence at a low dose or provocation at a low heart rate and rate-pressure product.[29] [125] Similarly, at dipyridamole stress, ischemia at "standard dose" (0.56 mg/kg) correlates with the presence of multivessel disease, [100] a lower ischemic threshold at exercise testing [126] as well as a worse prognosis (see later discussion). Nonetheless, patients with severe single-vessel disease may also demonstrate an early onset of ischemia, so that this relationship is only an approximate guide to lesion severity.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prognostic Evaluation Using Nonexercise Echocardiography Comparison of the results of nonexercise echocardiography with those of angiography validates the accuracy of these tests for diagnostic purposes and permits comparison with other noninvasive methodologies. The disadvantage of this approach, however, is that the angiographic criteria of stenotic significance are somewhat arbitrary and may not correlate with "physiologic" significance. A less artificial analysis is to use patient outcome to judge the efficacy of testing. Functional testing is commonly used for cardiac risk stratification in various groups of patients, such as those with chronic, stable angina or those who have had a myocardial infarction; for predicting complications at major noncardiac surgery; and in planning which patients should undergo coronary intervention. Prediction of Cardiac Events in Patients Undergoing Major Noncardiac Surgery Coronary artery disease is highly prevalent in patients with vascular disease elsewhere,[127] and cardiac events are the leading cause of perioperative complications at vascular surgery.[128] However, whereas coronary disease and 319

"soft" end points (postoperative unstable angina and heart failure) are frequent in patients with vascular disease, "hard" end points (death, myocardial infarction) occur in less than 10% of patients in the perioperative period, even in the absence of preoperative coronary intervention.[129] As the pretest probability of an event is low, Bayes' theorem would suggest that even if a noninvasive test were positive, the chance of an event would remain small. This explains the low predictive value of a positive test in many previous studies of stress testing in this setting. However, it is also important to remember that severe coronary

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disease is also the major contributor to late deaths after vascular surgery, and the screening of vascular patients for significant coronary disease is important for both perioperative and late risk stratification. The first step in preoperative risk stratification is clinical evaluation.[130] Patients with unstable coronary syndromes within the last 6 months constitute a high-risk group and, if surgery is mandatory, warrant careful functional testing to delineate the extent of jeopardized myocardium and possible intervention preoperatively. Those with previous bypass surgery (within 5 years) or coronary investigations (within 2 years) do not require reinvestigation in the absence of recurrent symptoms. The nature of the planned surgery is important; procedures carrying low cardiac risk such as ophthalmic or laparoscopic surgery should not provoke extensive risk evaluation, whereas vascular, major orthopedic, and major abdominal operations engender significant cardiac risk. Finally, the patient history has an important influence on risk, but the standard anesthetic risk scores[131] have limited applicability among vascular patients, who have greater cardiac risk than the general surgical populations from whom these risk scores were initially obtained. A simple score derived from the patient's age, presence of diabetes, angina, prior infarction, and congestive heart failure has been shown to identify low-risk patients, who do not need further investigation.[132] In a recent series of more than 4300 patients[133] undergoing high-risk surgery, history of ischemic heart disease, congestive heart failure or cerebrovascular disease, insulin treatment, and preoperative serum TABLE 14-7 -- Use of Stress Echocardiography to Predict Events in Patients Undergoing Vascular Surgery

Study Tischler et al[242] Sicari et al [243]

Rossi et al [244]

Predictive Value, % Patients, Events, POSITIVE NEGATIVE Stress N n TEST TEST Even Dipyridamole 109 8 78 99 MI, UAP, CHF Dipyridamole 121 9 25 98 Death MI, UAP Dipyridamole 110 10 100 Death MI,

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Pasquet et al Dipyridamole

129

9

30

97

Dobutamine

57

4

21

100

Dobutamine

60

13

29

93

Eichelberger Dobutamine et al[247] Langan et al Dobutamine

70

5

19

100

74

3

48

100

93

4

74

100

Poldermans Dobutamine et al[250] + atropine

131

15

43

100

Poldermans Dobutamine + atropine et al[251]

181

18

32

100

Poldermans Dobutamine + atropine et al[125]

300

27

38

100

Pellikka et al[252]

Dobutamine + atropine

80

8

29

98

Ballal et al

Dobutamine + atropine

233

8

all rvs

96

[136]

Lane et al [245]

Lalka et al [246]

[248]

DavilaDobutamine Roman et al + atropine [249]

[253]

UAP Death MI, UAP Death MI, CABG Death MI, UAP MI, UAP MI, AP, CABG MI, UAP, CABG Death MI, UAP, CHF Death MI, UAP, CHF MI, AP, LVF Death MI, UAP, CHF Death MI, UAP

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AP, angina pectoris; CABG, coronary artery bypass graft surgery; CHF, congestive heart failure; LVF, left ventricular failure; MI, myocardial infarction; UAP, unstable angina pectoris. creatinine level greater than 2.0 mg/dL were markers of risk; patients with none, one, two, or three or more of these factors had major cardiac complication rates of 0.4% to 0.5%, 0.9% to 1.3%, 4% to 7%, and 9% to 11%, respectively. It is important to keep in mind that patients with vascular disease are often inactive and are usually asymptomatic even in the presence of significant coronary disease. For patients at intermediate risk, stress imaging techniques with nonexercise stressors are required if screening is to be undertaken, as limitations of their exercise capacity render exercise testing approaches inadequate for the diagnosis of coronary artery disease, and the low sensitivity of pharmacologic stress electrocardiograms mandates the use of an imaging test. The relative availability and low cost of stress echocardiography, along with the potential for combining this approach with nonexercise stress, makes this an attractive technique for preoperative risk stratification. Table 14-7 shows that both dipyridamole and dobutamine stress echocardiography are effective for this purpose. The predictive value of a negative test is very high (usually greater than 90%), but as is the case with perfusion scintigraphy, the predictive value of a positive test is intermediate, varying from 20% to 70%. This value may be further stratified by paying attention to the ischemic threshold and the clinical risk factor status (Fig. 14-9) (Figure Not Available) . Clearly, the occurrence of cardiac events at the time of surgery does not only relate to the presence of coronary stenoses but is also modulated by medical treatment and anesthetic intervention. Only a handful of studies have compared stress echocardiography with single photon emission computed tomography (SPECT) for the prediction of perioperative cardiac events. From a meta-analysis of published work with dobutamine echocardiography and SPECT (mainly with dipyridamole stress), Shaw et al[134] concluded that the tests had comparable levels of accuracy but that cost features weighed in favor of echocardiography. A direct comparison by the group in Liege, Belgium showed the techniques to have similar prognostic value,[135] but another 320

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Figure 14-9 (Figure Not Available) Evaluation of risk in patients undergoing vascular surgery. Patients without clinical predictors of risk rarely have a positive dobutamine study (DSE), are unlikely to suffer events, and usually do not require testing. The presence of ischemia is predictive of events, especially if the patient has multiple clinical risk factors or a low ischemic threshold. MI, myocardial infarction; neg, negative; pos, positive; preop, preoperative. (From Poldermans D, et al: J Am Coll Cardiol 1995;26:648–653.)

comparison by a different Belgian group showed echocardiography to be significantly more specific than SPECT.[136] Prognostic Evaluation of Patients with Stable Coronary Disease Although the frequency of major cardiac events is low in stable chronic coronary disease (less than 1% per year), risk stratification is an important aspect of these patients because some have been shown to have a more favorable prognosis with intervention. The detection of left main or multivessel disease at coronary angiography is often used to identify subgroups likely to benefit from revascularization, but this procedure is too costly and invasive to be used for prognostic evaluation of all patients. As in the case of preoperative risk stratification, clinical data (including the severity of angina, prior infarction, heart failure, and diabetes) may identify high- and low-risk subgroups,[137] [138] and additional investigations are of most value in those at intermediate or greater risk. Exercise capacity and ST segment depression at exercise testing offer important prognostic information in patients who are able to exercise,[139] [140] and exercise SPECT [141] or exercise echocardiography have been shown to provide incremental data in some patients.[142] In those patients who are unable to exercise, pharmacologic stress echocardiography is a useful prognostic tool (Table 14-8) . The detection of ischemia at pharmacologic stress echocardiography has been shown to be an independent predictor of adverse outcomes, incremental to clinical and resting echocardiographic data. During dipyridamole stress, cardiac events occurred in 41% of patients with wall motion abnormalities occurring at low dose and 26% of those with high-dose responses (a reflection of the prognostic importance of ischemic threshold). Even in patients with known exercise electrocardiographic and coronary angiographic data,[143] ischemia at dipyridamole echocardiography was a better predictor of cardiac events (relative risk, 1.9) than either coronary stenoses or age (relative risks, 1.3 and 1.0, respectively). Similar data have been gathered during dobutamine stress testing (see Table 14-8) . The prognostic value of pharmacologic stress appears to be preserved within various subgroups, including

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hypertensive patients.[144] Few data have been gathered regarding comparisons between the stressors. Dobutamine and dipyridamole have been shown to offer effective and comparable efficacy of risk stratification in patients at low to moderate risk of cardiac events.[145] The prognostic content of stress echocardiography seems to be similar to that of SPECT.[146] The prognostic components of both tests include the presence, severity, and extent of induced ischemia. Perhaps the most important aspect of the prognostic literature is that a negative test portends extremely low risk, evidenced by an event rate of 1% or less per year. Prognostic Evaluation of Patients after Myocardial Infarction The frequency of cardiac events in the first year after myocardial infarction exceeds that in patients with chronic stable angina. Although clinical features such as age and the presence of heart failure should be used in the initial stratification of patients, the amount of infarcted and 321

TABLE 14-8 -- Use of Stress Echocardiography to Predict Events in Patie with Chronic Stable Coronary Disease Predictive Value, % Mean Patients, Follow- POSITIVE NEGATIVE TEST Comm Study Stress N up, mo TEST 51 24 68 77 High ri Mazeika et Dobutamine [254] al 77 10 50 87 Afridi et al Dobutamine [255]

Poldermans et al[256] Kamaran et al[257] Marcovitz et al[258] Schroder et

Dobutamine

430

17

26

87

Dobutamine

210

16

43

92

Dobutamine

291

15

10–17

99

Dobutamine

134

19

31

94

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al[259] Steinberg et al[260]

Pagina 7 di 8

Dobutamine

Senior et al Dobutamine

120

60

67

67 All eve

13 121

15

45

95 Hard events 88

860

52

14

96

13

—

1659

36

8–20

539

36

26

539

36

41

94

134

19

27

92

[261]

Chuah et al Dobutamine [262]

Davar et al Dobutamine

72 F

[263]

Poldermans Dobutamine et al[264] Picano et al Dipyridamole [144] (high dose) Dipyridamole (low dose) Schroder et Dipyridamole al[259]

100 Norma studies 96 Hard events 94

residual ischemic myocardium are major determinants of outcome that cannot be quantified clinically. Previously, the techniques used for this purpose included the exercise electrocardiogram, resting echocardiography, nuclear ventriculography, and thallium imaging. In a comparison of these alternatives,[147] the optimal approach for prediction of postinfarction complications was shown to be thallium imaging and nuclear ventriculography. Stress echocardiography, however, offers a means of replacing these two tests with one. Ischemia may be assessed as homozonal dyssynergy (peri-infarct ischemia) or heterozonal dyssynergy (multivessel disease), and infarction may be estimated from the resting wall motion score index. Exercise testing offers prognostically important adjunctive data on functional capacity. However, the majority of the postinfarction stress echocardiography literature (Table 14-9) concerns pharmacologic stress studies for three reasons: first, nonexercise studies are useful in patients who cannot exercise; second, they are useful for assessment of myocardial viability (see later discussion); finally, they provide an opportunity for

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obtaining a near-maximal stress reading early in the patient's admission, before many patients and physicians feel comfortable about performing maximal exercise stress testing. The last aspect is perhaps the most important, as early risk evaluation may identify at-risk patients before the occurrence of an event, permitting a reduction in hospital length of stay for low-risk patients and justifying angiography and possible intervention in those at higher risk. Both pharmacologic and atrial pacing stress tests have been used for risk assessment after myocardial infarction. All have proven to be effective for the detection of multivessel disease[124] [148] [149] and predictive for the subsequent development of cardiac events. Although atrial pacing is very safe (as the stress may be terminated instantly), it remains invasive and uncomfortable, and the pharmacologic techniques are best validated for this purpose. Moreover, the use of pharmacologic stress permits evaluation of myocardial viability, the detection of which has important implications for revascularization decisions. Table 14-9 summarizes the prognostic implications of positive and negative nonexercise stress echocardiography in patients after infarction. With dipyridamole stress echocardiography, the presence of ischemia and its time of onset are important predictors of cardiac events[150] in elderly patients, ischemia was an independent predictor of mortality.[151] An equivalent evidence base has been reported with dobutamine in the postinfarct period.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Therapy Using Nonexercise Echocardiography Medical Therapy In contrast to myocardial perfusion scintigraphy, the identification of ischemia with stress echocardiography is dependent on the development of ischemia. This is a disadvantage to the extent that antianginal therapy reduces the sensitivity of stress echocardiography, particularly when dipyridamole stress is used.[115] Patients on beta blockers account for most patients who fail to attain a heart rate greater than 85% of age-predicted maximum. With dobutamine echocardiography, the interaction between dobutamine and beta blockers involves competitive inhibition, and if enough dobutamine is administered, this effect may be overcome, leading several studies to suggest that concurrent drug therapy has no effect.[152] Atropine can be used to enhance the sensitivity of dobutamine stress testing, without reducing specificity or inducing serious side effects. The interaction between medical therapy and the development of ischemia may be of use in evaluating the adequacy of therapy.[153] [154] Although some data are being gathered with exercise echocardiography, the role of nonexercise stress remains largely unexplored. [155] In large part, this lack of data reflects the subjectivity of wall motion scoring, and use of stress echocardiography should become more feasible with a truly quantifiable approach. Follow-up after Coronary Interventions After angioplasty and bypass surgery, recurrent symptoms of chest discomfort may result because of restenosis 322

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TABLE 14-9 -- Application of Nonexercise Stressors to Post

Patients, FollowStudy Year N Timing Stress up, mo Outcomes Iliceto[44] 90 83 <3 wks Atrial Pacing 14 Reinfarction, angina Res * 95 69 3–5 Atrial Pacing 12.6 Cardiac death, days reinfarction, revascularizatio 217 Dipyridamole 24 Cardiac death Bolognese 92 [202]

Sclavo †

92

103 5–8 days

Dipyridamole 14.5

Picano[49] 93 Chiarella ‡ 94

925 10 days Dipyridamole 251 70 hrs Dipyridamole

Picano § 95 Neskovic 95

1080 10 days Dipyridamole 93 2–3 Dipyridamole wks

Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death

Cardiac death, reinfarction Cardiac death, reinfarction, angina 14 Cardiac death 13 days Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina 14 Reinfarction 16 Cardiac death Cardiac death,

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Sclavo ¶

Pagina 3 di 4

97

Lanzarini 96

60 3–4 days

Dipyridamole 15

41 8 days Dobutamine

7.5

[129]

Carlos £

97

214 2–7 days

Sicari[166]

97

778 12 days Dobutamine

9

Greco

97

178 12 days Dobutamine

17

Previtali

98

152 9 days Dobutamine

15

Dobutamine

>12

reinfarction Cardiac death, reinfarction, angina Cardiac death, reinfarction, angina, revascularizatio Reinfarction, angina, revascularizatio Cardiac death, reinfarction, angina, ventricular tachycardia, congestive hea failure Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Cardiac death

[30]

Cardiac death, reinfarction Cardiac death, reinfarction,

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Picano[237] 98

Pagina 4 di 4

314 12 days Dobutamine

9

angina Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina

* Res et al: Am J Cardiol 1995;76:1112–1114 † Sclavo et al: Eur Heart J 1992;13:1348–1355 ‡ Chiarella et al: Eur Heart J 1994;15:842–850 § Picano et al: J Am Coll Cardiol 1995;26:908–913 Neskovic et al: Am Heart J 1995;129:31–39 ¶ Sclavo et al: G Ital Cardiol 1997;27:1000–1007 £ Carlos et al: Circulation 1997;95:1402–1410 Greco et al: J Am Coll Cardiol 1997;29:261–267

and graft closure, respectively. Because angioplasty is most often performed for single-vessel disease, routine exercise testing is usually considered to be insensitive for the diagnosis of restenosis, and exercise echocardiography or exercise myocardial perfusion imaging are often performed. Pharmacologic stress echocardiography performed before and after angioplasty has been shown to predict resolution of ischemia using dipyridamole[156] [157] and dobutamine stress.[158] [159] If the patient cannot exercise, pharmacologic stress echocardiography can be used effectively for the diagnosis of restenosis,[160] [161] the sensitivity being significantly greater than that of the stress electrocardiogram.[162] Similarly, after bypass surgery, stress imaging tests are usually obtained for diagnostic purposes (because the resting eletrocardiogram is often nondiagnostic). Exercise echocardiography has been shown to be accurate in this context, and if the patient cannot exercise, pacing or pharmacologic stresses can reasonably be used.[163] [164] The major application of echocardiography and perhaps stress echocardiography after revascularization, however, is to assess the improvement of dysfunctional but viable myocardium.[165]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Myocardial Viability Using Nonexercise Echocardiography Clinical Significance Left ventricular dysfunction after myocardial infarction is due not only to loss of myocardium but also to stunned and hibernating myocardium. Stunned myocardium shows spontaneous resolution of dysfunction,[166] but hibernating tissue requires myocardial revascularization to 323

resume normal function.[167] [168] Myocardial revascularization in patients with viable myocardium may be indicated to improve cardiac function or overall functional capacity, as well as to avoid subsequent cardiac events from this inherently unstable tissue. Thus, clinical decisions about whether to revascularize, which vessel to revascularize, and how to do it may be influenced by the detection of viable myocardium. In the following section, evaluation of the accuracy of various tests for the identification of viable myocardium is based on recovery of function after myocardial revascularization. This criterion is an imperfect gold standard, being influenced by the adequacy of revascularization, bypass graft closure, and restenosis, but it has the attraction of having direct clinical relevance. By this criterion, conventional techniques used for the detection of myocardial scar and viability (Q waves on the electrocardiogram, regional left ventricular dysfunction at ventriculography, and "fixed" perfusion defects at conventional scintigraphic procedures) have been found to be inaccurate. More accurate alternatives include position emission tomography and thallium scintigraphy using rest-redistribution or stressredistribution-reinjection protocols, both of which have a high negative predictive value.[169] A positive test result is less predictive of functional recovery, however, probably manifesting the sensitivity of these tests for

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small regions of viable myocardium that may not be able to contribute to regional function when revascularized. The use of dobutamine and dipyridamole stress echocardiography to detect viable myocardium has a large evidence base and is now part of standard practice. Use of Dobutamine Echocardiography for the Diagnosis of Viable Myocardium Administration of sympathomimetic agents (such as isoproterenol, dopamine, and dobutamine) has been shown to reverse postischemic left ventricular dysfunction.[170] [171] [172] [173] The typical response of viable myocardium is to increase thickening in response to low doses of dobutamine; in the presence of a stenosed infarct-related artery, function subsequently deteriorates as the tissue becomes ischemic. Indeed, there is a balance between the recovery of function and the development of ischemia, and, at least in theory, the development of ischemia may compromise the functional recovery of areas that are marginally perfused at rest. The highdose response (>20 µg/kg/minute) has been shown to be a less reliable predictor of recovery.[8] Although some investigators start at lower doses, or use only a low-dose protocol for the assessment of viability, and others use 5-minute rather than 3-minute increments, [174] there does not appear to be a clear benefit in favor of any of these alternatives. Dipyridamole has been shown to enhance both segmental shortening and load-independent indices of ventricular function in stunned myocardium.[175] The mechanism of this phenomenon is unclear, but a "local Frank-Starling response" (whereby augmentation of myocardial blood volume leads to increased sarcomere separation) appears to be the most likely explanation. Additionally, an indirect sympathomimetic response to dipyridamoleinduced ischemia may contribute to improvement of regional function, as may resolution of ischemia secondary to improvement of coronary perfusion. Dipyridamole appears to be an effective alternative in low-dose and "infra-low-dose" protocols[176] the choice of agent is dependent on local expertise and preference. The interpretive criteria are similar, irrespective of the stressor. Viable segments are characterized by reduced resting function, which augments in response to low-dose dobutamine (usually 7.5 to 10 µg/kg/minute). There is continued augmentation if there is a patent infarct-related artery or the tissue is well collateralized. In the presence of a stenosed infarct-related artery, an increasing proportion of segments become ischemic at dobutamine doses greater than 10 µg/kg/minute.[177] This initial

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improvement followed by deterioration in function constitutes the "biphasic response," which is strongly predictive of eventual functional recovery of the tissue.[177] A uniphasic response is less predictive of recovery, and a classic ischemic response is not very predictive of the recovery of resting function. Because the biphasic response is the most reliable finding (Fig. 14-10) , our preference is to induce ischemia whenever possible by proceeding to maximal stress (i.e., 40 µg/kg/minute dobutamine with or without atropine), rather than using a discreet "viability" or low-dose protocol. In patients with severe left ventricular dysfunction, this approach warrants caution, and early termination may be needed if ischemia is progressive or if other responses might induce instability. Finally, viability studies are the most difficult to interpret, and we commonly use both digital display, including doses of both 5 and 10 µg/kg/minute, and videotape for review of the study. The response of regional function to dobutamine is influenced by the extent of viable tissue, the degree of residual stenosis, the extent and magnitude of collateral vessels, the size of the risk area (which influences tethering), and the presence of drug therapy,[178] of which the extent of viable tissue and perfusion warrant further attention. The uniphasic response is an ambiguous signal that may be caused by part of the wall mounting a dobutamine response (i.e., admixture of scar and normal tissue) or all of the wall mounting a partial response (i.e., viable myocardium). The ability to discriminate the extent of subendocardial damage, with its implications for the likelihood of subsequent functional recovery, is poor. With respect to perfusion, augmentation of function is dependent on delivery of more substrate; thus, tissue supplied by more severe stenosis may become ischemic before it augments function. This may compromise the recognition of viability. The accuracy of dobutamine for prediction of regional functional recovery is summarized in Table 14-10 , although there is a large evidence base, most studies are relatively small and derive from expert centers. The overall sensitivity of dobutamine (approximately 80%) appears greater than that of dipyridamole stress (approximately 60%), although the specificity of the former is less (78% vs. 87%). Moreover, the nuclear approaches are more sensitive but less specific than these echocardiographic techniques.

324

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Figure 14-10 Apical four-chamber diastolic (right) and systolic (left) views at rest (top), with low-dose dobutamine (middle), and with peakdose dobutamine (below), illustrating a "biphasic" response to dobutamine stress (reduced systolic thickening at rest, increment with low dose, and deterioration at peak dose) in the lateral wall.

Prediction of Recovery of Global Function and Outcome Improvement of left ventricular function within individual segments is not usually the goal of revascularization, whereas improvements in ejection fraction, exercise capacity, and outcome are therapeutic goals. Recent work has sought to address the ability to predict these parameters. Stress echocardiography can be used to predict improvement of global left ventricular function after revascularization. Cornel et al[179] has reported an 89% sensitivity and 81% specificity for prediction of a significant (5%) improvement in ejection fraction, using a cut-off point of 4 of 16 viable (biphasic) segments at dobutamine echocardiography. Similarly, the global ventricular response to low-dose dobutamine is a strong predictor of global functional recovery.[180] Other factors clearly influence the likelihood of recovery, including an inverse relationship with the number of thinned and akinetic segments or ventricular volumes. [181] The revascularization of patients with adequate amounts of viable myocardium (usually >25% of left ventricular mass) is associated with improved functional class. The presence of viable myocardium may influence outcome in two ways. First, revascularized viable tissue may lead to improved function and thereby improved outcome.[182] Second, non-revascularized viable tissue may be unstable and act as a substrate for recurrent events,[183] including mortality.[184] These outcomes have not been reported in all series,[185] probably because of heterogeneity in populations studied and responses; for example, a uniphasic response early after infarction may be a benign finding.

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New Technologies that May Solve Limitations of Stress Echocardiography Image Quality Although perfect image quality is certainly not essential for a stress echocardiographic study to be interpretable, 325

TABLE 14-10 -- Sensitivity and Specificity of Dobutamine Echocardiogra for Identification of Myocardial Viability (Segmental Analysis) * Study Pierard †

Stress Dobutamine

Smart * [8]

Dobutamine

Previtali[30]

Dobutamine

Cigarroa ‡ Marzullo[275] Alfieri § Watada

Dobutamine Dobutamine Dobutamine Dobutamine

La Canna ¶ Dobutamine Dobutamine Charney[276] Perrone-Filardi Dobutamine

Patients, Sensitivity, Specificity, N % (n) % (n) Comm 17 83 (6) 73 (8/11) Early p MI 51 86 (22) 90 (26/29) Early p MI 42 79 (63) 70 Early p (109/158) MI 25 82 (11) 86 (12/14) 14 82 (49) 92 (24/26) 14 91 (93) 78 (25/32) 21 83 (66) 86 (43/50) Early p MI 33 87 (205) 82 (89/109) 17 71 (31) 93 (27) 18 88 (48) 87 (27/31)

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£

Afridi Arnese[70]

Dobutamine Dobutamine

20 74 (38) 38 74 (33)

Senior[110] Bolognese[202]

Dobutamine Dobutamine

45 87 (45) 30 89 (27)

73 (55/76) 95 (130/137) 82 (123) 91 (45)

Poli #

Dobutamine

51 72 (78)

68 (176)

Dipyridamole

51 51 (78)

82 (176)

40 40 36 73

40 79 (73)

94 (133) 94 (133) 63 (65) 86 (238/277) 83 (36)

53 69 (32) 86 (50) 30 89 (62) 18 68 (46)

100 (26) 57 (46) 82 (106) 83 (63)

Varga[10]

Dipyridamole Dobutamine Dobutamine Bax[283] Vanoverschelde Dobutamine

78 (40) 76 (40) 85 (27) 76 (167)

[285]

Perrone-Filardi Dobutamine

Early p MI Early p MI Early p MI

[282]

Furukawa[67] Cornel[87] Nagueh[279]

Dobutamine Dobutamine Dobutamine Dobutamine

Total

Dobutamine Dipyridamole

Akinet Hypok Biphas respon

726 81 78 (1065/1312) (1401/1796) 91 60 (71/118) 87 (269/309)

MI, myocardial infarction. * Average ejection fraction approximately 35%. † Pierard et al: J Am Coll Cardiol 1990;15:1021–1031 ‡ Cigarroa et al: Circulation 1993;88:430–436 § Alfieri et al: Eur J Cardiothoracic Surgery 1993;7:325–330 Watada et al: J Am Coll Cardiol 1994;24:624–630 ¶ La Canna et al: J Am Coll Cardiol 1994;23:617–626 £ Perrone-Filardi et al: Circulation 1995;91:2556–2565

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Afridi et al: Circulation 1995;91:663–670 # Poli et al: Heart 1996;75:240–246

it certainly favors concordance between observers[73] and facilitates an accurate diagnosis of disease extent and distinction of ischemia and scar. Major improvements in image quality obtained from harmonic imaging have translated into improvements in the accuracy of stress echocardiography.[58] Likewise, the use of contrast echocardiography may facilitate delineation of the endocardial border; the implications of this finding are addressed in another chapter. Quantitative Approaches to Interpretation As mentioned earlier, the current qualitative algorithm for interpretation of stress echocardiograms requires a significant level of expertise on the part of the observer. A less subjective means of interpretation would be attractive on the grounds of feasibility and reproducibility. Either semiquantitative or fully quantitative strategies of examining wall motion can be used to evaluate global and regional left ventricular function. Global indices (ejection fraction or end-systolic volume) are insensitive to milder degrees of ischemia and are not an answer to the shortcomings of qualitative interpretation. Wall motion scoring offers a semiquantitative regional approach, which may improve the reproducibility of observers, but this does not constitute a major deviation from the regional approach used by most experienced readers and does not measure function independent of the observer. True quantitation of regional function may be based on following either radial or longitudinal myocardial motion (see Chapter 5) . The simplest approach involves tracing of endocardial (and for some methods, epicardial) interfaces and their superimposition using a fixed or floating reference system and measurement of endocardial excursion or myocardial thickening. Historically, this approach has been limited by three major technical limitations, but recent developments have addressed some of these limitations. First, excellent border definition of both endocardium and epicardium (especially in the apical views) was obtainable in less than 50% of images, but harmonic imaging has improved image quality substantially, and contrast echocardiography may also be of value. Second, failure to

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compensate for rotational or translational cardiac movement may be associated with false-positive results, but correction for movement of the heart may also compromise sensitivity. A postprocessing approach (using color-enhanced digitized cine-loops) may be used to correct translational movement.[186] Third, the 326

process of tracing multiple systolic and diastolic frames is tedious, timeconsuming, and unattractive for clinical practice. However, recent developments in edge-tracking have led to automated programs for measuring endocardial excursion. Along similar lines, Perez has developed an online quantification of ventricular function during dobutamine echocardiography using acoustic quantification.[187] The feasibility and accuracy of this approach has now been documented in several studies[188] [189] (Fig. 14-11) (Figure Not Available) . Myocardial tissue Doppler may provide another means of quantifying regional function. A unique aspect of this approach is that it can be used to quantify motion in the longitudinal (base-apex) direction, which corresponds to the contribution of longitudinal subendocardial muscle fibers.[190] Tissue Doppler measurements can be obtained using color or pulsed wave modalities to gather peak velocity and timing parameters. Pulsed wave Doppler, although useful for resting imaging,[191] is less feasible during stress because of the need to acquire all values online within a limited time at peak stress. Tissue velocity profiles within each segment of a color myocardial Doppler image may be obtained by postprocessing, but this requires a high frame-rate (at least 80 to 100 frames per second) to ensure that true peak systolic velocity is captured (Fig. 14-12) . The development of ischemia causes a reduction of peak velocity and transmyocardial velocity gradient and a delay in the development of peak velocity, of which the first is the most reproducible. Peak velocity has been shown to correlate with wall motion interpretation[192] [193] and ischemia with dual isotope SPECT.[194] More recently, normal ranges at peak stress have been described, and these ranges have been applied to the identification of angiographically defined coronary disease, [195] providing comparable accuracy to an expert reader. This technique presents some unresolved problems; it appears to be more amenable to dobutamine than exercise stress, and further efforts are needed to remove the contribution of translational movement.

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Another quantitative approach that is independent of edge detection is the analysis of myocardial backscatter. Cyclic variation of backscatter has been shown to change during ischemia,[196] [197] but, until recently, backscatter analysis was strictly a research technique that was dependent Figure 14-11 (Figure Not Available) (color plate.) Color kinesis images with color coding showing sequential frames in systole and diastole in short-axis and apical fourchamber views. The graphics express regional fractional area change in each segment. (From Mor-Avi V et al: Circulation 1997;95:2087–2097.)

on the ability to export and process voluminous raw data from the echocardiography machine. Recent developments in computer technology, especially storage, have made this approach more feasible,[198] although whether it can be incorporated into clinical imaging remains to be seen. Stress Doppler Echocardiography Stress Doppler echocardiography has been used to examine systolic or diastolic blood flow alterations caused by ischemia. Unfortunately, because compensatory hyperkinesis of the nonischemic wall tends to preserve overall ventricular function, changes in stroke volume occur mainly in the presence of extensive ischemia,[199] and stress-induced alterations in global cardiac function are not specific for coronary disease. The development or worsening of mitral regurgitation on color flow mapping (which may explain the occurrence of dyspnea disproportionate to the severity of coronary disease) is another systolic parameter that may be predictive of ischemia during dobutamine stress testing,[33] but the frequency of this finding is low,[200] as vasodilation at peak dobutamine dose tends to reduce left ventricular cavity size and therefore regurgitation. Left ventricular relaxation is an active process that may be altered by the development of myocardial ischemia. These changes can be examined by transmitral flow measurements of the peak E and A wave velocities, E/A ratio, E wave deceleration time, diastolic time intervals, and flow-velocity integrals of passive and active flow.[201] Unfortunately, tachycardia causes the E and A waves to merge at higher heart rates. Nonetheless, reductions in passive left ventricular filling (probably reflecting impaired relaxation secondary to ischemia) have been correlated with ischemia during dobutamine stress echocardiography.[202] The same pattern has been recorded with other stressors that provoke ischemia without tachycardia, such as dipyridamole and pacing with cessation after the development of ischemia.[203] Unfortunately, however, the effects of ischemia (delayed

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relaxation) may be pseudonormalized by ischemia-induced increases in left atrial pressure (Fig. 14-13) . Tissue Doppler assessment may be of value in 327

Figure 14-12 (color plate.) Importance of high frame-rate to tissue Doppler velocity. Doppler velocity profiles are shown in the same segment at different frame-rates. A high frame-rate (>100 frames per second [f/s]) is necessary to obtain the true peak velocity as well as timing variables.

examining regional diastolic function with less influence from left atrial pressure. [204] Changes of diastolic function in response to stress are not specific for ischemia, however, and may be induced by left ventricular hypertrophy, for example.

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Alternatives to Nonexercise Stress Echocardiography Exercise Stress Echocardiography Nonexercise stress approaches are invaluable in patients who are unable to exercise maximally. Attempts to use exercise stress in such patients are attended by suboptimal sensitivity, and this is true also of isometric exercise. [205] Pharmacologic stressors have also been used in patients who are able to exercise, among whom the results of Figure 14-13 Development of a pseudonormal pattern, probably due to ischemia-induced increment in left atrial pressure. This patient with resting left ventricular dysfunction developed extensive ischemia by wall motion assessment. However, there is an increment of E wave velocity and shortening of the deceleration time, rather than development of a delayed relaxation pattern.

exercise and pharmacologic techniques can be compared. Table 14-11 summarizes several studies that compared exercise and nonexercise stress echocardiography on a "head-to-head" basis. Most studies have shown no significant differences in sensitivity or specificity between exercise and nonexercise stress echocardiography. Some of these comparisons have suggested that the nonexercise technique has greater feasibility, although this may be colored by greater expertise in pharmacologic than in exercise echocardiography at some centers. However, several of these comparisons have involved designs that do not replicate the usual clinical scenario, such as exclusion of patients with technically difficult studies, as well as cessation of antianginal therapy before the test. The latter may have an important influence on this analysis; in one comparison of dobutamine and exercise echocardiography, the sensitivity of dobutamine stress was significantly less than that obtained with bicycle exercise in patients who

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were treated with beta receptor blockers, or who failed to complete the dobutamine protocol because of the development of side effects. Interestingly, among the patients with coronary disease in whom both tests were positive, the extent of ischemia was reliably greater with exercise than with dobutamine, reflecting the greater cardiac workload imposed by exercise. This more extensive ischemia may lead the observer to be more confident in the results of exercise than dobutamine stress testing, despite the image quality being better with dobutamine. The advantages of pharmacologic approaches are feasibility, better image quality, and ability to image the heart during stepwise increments of stress as well as at peak stress. These are balanced by a number of considerations that favor the use of exercise stress in those who can perform it. Exercise stress testing provides a greater level of stress on the heart, renders electrocardiographic data useful (the results of which are less useful with pharmacologic stressors), and gives results regarding functional capacity and data about stress that are readily extrapolated to everyday life. Exercise also offers important prognostic 328

TABLE 14-11 -- Sensitivity and Specific

Study Picano et al[265]

Myocardial CAD Multivessel, Infarction, Patients, CAD, Diameter, n (% all n (% all N n % CAD) CAD) EXERCI 55 34 >70 18 (53) 6 (18) 76

Hoffman et al[81]

66

50 >70

21 (42)

0 (0)

80

Cohen et al[76]

52

37 >70

21 (57)

11 (30)

78

136

119 >50

11 (9)

41 (34)

80

Beleslin et al[79]

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Marangelli et al[123]

60

35 >75

19 (54)

—

89

Marwick et al[77]

86

56 >50

34 (61)

0 (0)

88

Dagianti et al[219]

60

25 >70

15 (60)

0 (0)

76

Rallidis et 85 85 >70 [266] al CAD, coronary artery disease.

40 (47)

42 (49)

77

329

data. Based on these considerations, exercise echocardiography appears to offer more data than the nonexercise approaches, and we limit the use of exercise-simulating techniques to patients who are unable to perform maximal exercise. However, the new techniques that are adjunctive to stress echocardiography (for example, contrast, tissue Doppler, and acoustic quantification echocardiography) are more easily performed in the stationary patient and may lead to an increase in the number of nonexercise studies in the future. Stress Electrocardiography In the current medical-economic climate, much attention is being paid to using less expensive diagnostic and therapeutic methodologies. Because stress electrocardiography is substantially less expensive than stress imaging tests, it might be considered as an alternative to stress echocardiography. In this respect, it is important to differentiate between the stress electrocardiographic component of the pharmacologic tests and

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the exercise electrocardiogram. The latter is an option only if the patient can exercise maximally, and in this situation, both dobutamine and dipyridamole stress echocardiography are as sensitive as or more sensitive than the exercise electrocardiography. Nonetheless, the discussion suggests that if the patient can exercise, the choice should be between the exercise echocardiogram and the exercise electrocardiogram. If the use of nonexercise stress is restricted to patients who cannot exercise, there is little to recommend the use of the pharmacologic stress electrocardiogram, which has poor sensitivity for the diagnosis of coronary artery disease, even if the standard exercise electrocardiographic criteria are altered for use with nonexercise approaches. Although this test should not be performed in isolation, the presence and characteristics of ischemic electrocardiographic changes add useful information about the severity and prognostic implications of an abnormal stress echocardiogram.[206] TABLE 14-12 -- Comparison of Pharmacologic Stress Echocardiography Coronary Arte Patients, Study N Stress 25 Adenosine Nguyen et [267] al Amanullah 40 Adenosine [268] et al Marwick 97 Adenosine [99] et al Marwick 217 Dobutamine [99] et al Forster et 21 Dobutamine [269] al Gunalp et 19 Dobutamine [270] al 61 Dobutamine Senior et [216] al Ho et al[271] 54 Dobutamine Huang et 93 Dobutamine

Sensitivity, % NUC ECHOCARDIOGRAPHY IMA 60 90

Dose 0.14 mg/kg/min 0.14 74 mg/kg/min 0.18 58 mg/kg/min 40 µg 72

94 86 76

40 µg + atropine 30 µg

75

83

70

90

40 µg

93

95

40 µg 40 µg

93 93

98 90

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al[126] Santoro et al[272] San Roman et al[273] Perin et al [274]

Simonetti et al[232] Santoro et al[272] San Roman et al[273]

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60 Dobutamine 40 µg

61

91

102 Dobutamine 40 µg + atropine

78

87

25 Dipyridamole 0.56 mg/kg 35 Dipyridamole 0.84 mg/kg 60 Dipyridamole 0.84 mg/kg 102 Dipyridamole 0.84 mg/kg

58

95

86

91

55

97

81

87

Pharmacologic Stress Echocardiography versus Perfusion Scintigraphy Thallium (or technetium MIBI) imaging has the advantage of being the most widely used imaging technique for the noninvasive diagnosis of coronary artery disease and is technically easier to perform and interpret than is stress echocardiography. However, nuclear imaging has disadvantages pertaining to specificity, cost, and inconvenience to the patient. As there is a substantial variation in the reported accuracy of both stress echocardiography and nuclear imaging, based on variations in the population studied, the relative accuracies of each test can only be addressed by direct comparison in the same patient population. The relative abilities of the tests to deal with the diagnosis of coronary disease, identification of viable myocardium, and prognostic assessment are discussed separately. Bearing in mind the preceding discussion regarding the selection of patients for nonexercise stress, this discussion is confined to patients who are for some reason unable to exercise. Diagnosis of Coronary Artery Disease

Several studies focusing on the comparison of stress echocardiography and scintigraphy using dipyridamole, adenosine, dobutamine, or atrial pacing stress for the diagnosis of coronary disease have been published (Table 14-

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12) . The concordance rates between scintigraphy and echocardiography for the presence or absence of disease range from 80% to 90% in most studies. There are several pertinent points in the interpretation of this literature. First, it is important to have a reference standard (coronary angiography) to judge which test is "wrong" if the results are discordant, despite the inherent selection bias that this design produces toward studying patients with more severe disease, as well as the imperfections of using angiography as the arbiter of disease. Second, because both techniques may be technically demanding and require 330

considerable interpretive skill, studies coming from centers with expertise in one or the other are unlikely to be meaningful. The corollary of this observation is that for the choice even to be considered routine practice, high-quality nuclear and echocardiographic laboratories should be available; if a center has expertise in only one methodology, the alternative should not be considered. Simply put, good scintigraphy is always better than poor stress echocardiography and good stress echocardiography is always better than poor scintigraphy. Using dobutamine or pacing stress, the sensitivities of both tests for the identification of coronary artery disease are comparable, with most studies showing slightly greater sensitivity with scintigraphy (see Table 14-12) . This difference is most evident in patients with single-vessel disease,[207] a finding that might be expected from the identification of flow heterogeneity with perfusion imaging, which is an earlier event in the ischemic cascade than regional dysfunction, identified by echocardiography. For the same reason, antianginal therapy influences the results of echocardiography because it prevents the development of ischemia[115] but does not influence the results of perfusion scintigraphy.[208] On the other hand, the better spatial resolution of echocardiography and the ability to categorize wall motion independently in each segment (contrasting with the relative flow comparisons used in myocardial perfusion imaging) may compensate for its requirement of ischemia. Thus, the similarities in the sensitivity of echocardiography and scintigraphy reflect the balance between the underlying physiology of the tests and their imaging characteristics. In contrast, studies with adenosine and dipyridamole have shown vasodilator stress echocardiography to be significantly less sensitive than perfusion scintigraphy.[209] This

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Figure 14-14 (Figure Not Available) Prognostic content of single photon emission computed tomography (201 TI SPECT) and stress echocardiography scans. The correlation with outcome of the extent of perfusion defect (PDS) and wall motion abnormality (WMS) appears comparable in this exercise stress study. (From Olmos LI, et al: Circulation 1998;98:2679–2686.)

difference is most marked in patients with single vessel coronary disease and reflects failure to develop coronary steal in the absence of extensive coronary disease. This difference in sensitivity is less prominent in patients with multivessel disease. With either dobutamine or vasodilator stress, the specificities of stress echocardiography and perfusion scintigraphy are also comparable, with most series showing a small benefit for echocardiography. Whereas the high sensitivity of myocardial perfusion imaging with SPECT may have been gained at the cost of a sacrifice in specificity, two important sources of false-positive results are patients with left bundle branch block and patients with left ventricular hypertrophy. The influence of left bundle branch block has been investigated in a small number of patients,[210] among whom stress echocardiography produced more favorable results for specificity, although insufficient numbers of patients have been studied to reliably address sensitivity. Patients with hypertension and left ventricular hypertrophy are prone to false-positive SPECT results, probably owing to small vessel disease. Stress echocardiography, especially with dobutamine stress, appears to offer greater levels of accuracy.[211] Prognostic Assessment

Stress myocardial perfusion scintigraphy is widely used for risk stratification of patients undergoing vascular surgery, patients with chronic coronary disease, and patients who have had a myocardial infarction. Unfortunately, although a substantial amount of literature regarding the individual predictive abilities of echocardiography and 331

TABLE 14-13 -- Comparison of Nuclear and Stress Echocardiographic T (Evidenced by Improvement of Regional Left Ventric Sensitivity, % Dobutamine

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DOBUTAMINE Thallium Protocol, THALLIUM SPECT ECHOCARDIOGRA Study Technique µg/kg/min Low-dose, 86 82 Marzullo et al Rest[275] redistribution 10 Low-dose, 95 71 Charney et al Rest[276] redistribution 10 Kostopoulos et RestLow-dose, 90 87 [277] al redistribution 10 Qureshi et al[278] RestHigh-dose, 90 74 redistribution 40 Nagueh et al[279] RestHigh-dose, 91 68 redistribution 40 Low-dose, 92 87 Senior et al[280] Stress (dobutamine)- 10 rest/NTG Arnese et al[281] Stress Low-dose, 89 74 (dobutamine) 10 reinjection Low-dose, 100 79 Perrone-Filardi Stress [282] (dobutamine) 10 et al reinjection Stress Low-dose, 93 85 Bax et al[283] (dobutamine) 10 reinjection Low-dose, 100 94 Haque et al[284] Stress (exercise) 20 reinjection Vanoverschelde Stress High-dose, 72 88 [285] et al (exercise) 40 reinjection High-dose, 87 95 Elsasser et al[286] Stress (dobutamine) 40 reinjection SPECT, single photon emission computed tomography. * Average ejection fraction 38%.

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perfusion imaging is available, comparative data are sparse. In patients undergoing surgery for vascular disease, dipyridamole stress thallium imaging has been shown to have a negative predictive value of more than 90% in most studies.[130] The occurrence of unexpected cardiac events in some patients is probably due to intracoronary thrombus formation on nonsignificant stenoses (which do not cause abnormal perfusion results). The predictive value of ischemia at scintigraphy ranges from 30% to 50%, this result being attributable to positive perfusion studies in the context of mild (prognostically benign) coronary disease and falsepositive results. Overall, these results are comparable to those of pharmacologic stress echocardiography (see Table 14-7) . There are few comparative studies between stress echocardiography and SPECT. The group of Pierard[135] compared the ability of dobutamine stress echocardiography and dobutamine technetium-99m sestamibi SPECT to predict postoperative cardiac events in 156 patients, among whom the adverse event rate was 5.6%. Both tests were characterized by a high negative predictive value (96% for echocardiography; 97% for SPECT). Postoperative cardiac events were predicted by previous cardiac symptoms, a Detsky score of 15 or greater (RR, 3.0), a positive dobutamine echocardiogram (RR, 3.7), and a positive dobutamine SPECT scan (RR, 7.4). In contrast, work by Pasquet et al[212] suggests that the specificity of stress echocardiography exceeded that of SPECT for the prediction of subsequent events. In patients with chronic stable coronary disease and after myocardial infarction, the relative prognostic roles of stress echocardiography and myocardial perfusion scintigraphy appear comparable (Fig. 14-14) (Figure Not Available) . Ischemia may be difficult to identify within segments having abnormal resting function, and this is a source of discrepancy from the findings of perfusion scintigraphy. Because the territory is supplied by the infarct-related artery, the analysis of sensitivity and specificity does not permit discrimination of which test is correct. Preliminary data comparing dipyridamole stress echocardiography and MIBI-SPECT in patients after recent myocardial infarction have shown the finding of ischemia at echocardiography (and not at scintigraphy) to be predictive of subsequent hard events.[213] Diagnosis of Viable Myocardium

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Positron emission tomography, thallium reinjection techniques, and dobutamine echocardiography have all been shown to reliably identify viable myocardium. A significant evidence base has been accumulated regarding the comparison of these variables (Table 14-13) . In one of the initial studies of patients after thrombolysis, dobutamine responsiveness and spontaneous improvement at follow-up were detected in stunned myocardium (normal flow with reduced function), and no dobutamine response correlated with failure to improve at follow-up was seen in infarcted tissue (reduced flow and reduced fluorodeoxyglucose activity). Hibernating tissue (reduced flow with preserved fluorodeoxyglucose activity) was responsive to dobutamine but failed to improve at follow-up, although not all patients in this category underwent myocardial revascularization. The majority of the comparative studies show SPECT techniques to be more sensitive but of lower specificity for the prediction of functional recovery.

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Consequences of Special Characteristics In addition to the effects noted earlier, there are other differences in intravascular ultrasound owing to the use of high frequencies and size constraints. The strength of backscattered ultrasound relative to the incident ultrasound strength is called the backscattering coefficient. This coefficient is determined not only by the composition of the tissue but also by the frequency of the ultrasound. The backscattering coefficient increases with higher frequencies for virtually all tissues, but the rate of increase is different for each tissue, depending on the microscopic structure.[4] In particular, the strength of the backscattered signal from fibrous tissue increases at a rate greater than that of the other tissues in the arterial wall.[5] A fibrous plaque may have strong echogenicity compared with other tissues at 10 MHz, but it still may be less than calcified tissue. At 30 MHz, however, the strength of the signal from fibrous tissue may be equal to or even greater than that from calcified tissue (Fig. 15-7) . Strong echo alone cannot be used to identify the presence TABLE 15-2 -- Comparison of Characteristics of Systems Type of System Electronic Cable, direct Cable, mirror Motor, direct

Resolution Good Very good Very good Very good

Nonuniform Rotation No Yes Yes No

Ring Down Yes Yes No Yes

Figure 15-7 Calcified and fibrous tissue can have very similar echo intensities. This clinical intracoronary image shows an area of dense fibrosis with some calcification. The area of fibrosis extends from 10 to 4 o'clock, but the area from 11 to 1 o'clock, which has the brightest echo

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intensity, also has the least shadowing. This finding indicates that there is calcification in the plaque in all areas except 11 to 1 o'clock. Note the "halo" surrounding the catheter, owing to ring-down artifact.

of calcium in the wall of the vessel, because fibrous tissue may mimic this. Calcified tissue can be distinguished by the additional presence of "shadowing," a profound weakening of signal strength distal to the calcified tissue, owing to the intense attenuation caused by the calcification. Fibrous tissue does not cause this same degree of attenuation, regardless of the intensity of the backscattered signal. Thus, if we see a very bright echo without shadowing, we should suspect that it is fibrous tissue, whereas a bright structure with shadowing should be identified as calcification. It should be noted, however, that the actual classifications are not so clearcut. Fibrous tissue may have microscopic calcifications, which also cause shadowing. Size constraints lead to other practical issues as well. Intravascular ultrasound catheters need a guidewire for placement, and of the several different types that have been developed, the simplest and least flexible is a fixed guidewire at the tip of the catheter. This type of guidewire does not interfere with the imaging function, but it cannot be used for the exchange of catheters over it. A much more adaptable approach is a removable guidewire, but this approach poses the problem of where to place the guide in the already tight constraints of space at the tip of the catheter. For catheters with electronic beam steering, the center of the catheter is free for use by a guidewire because there is no motor or drive cable. For mechanical systems, there is a space problem, which can be solved in one of two ways. The first solution is to have a channel on the outside of the imaging portion of the catheter through which the guidewire can pass. This approach leaves the imaging portion relatively unchanged, but the guidewire is present in the imaging field, causing a bright echo. The second solution is to use the same channel for the guidewire and an imaging core consisting of the transducer and drive cable, alternately withdrawing one to 345

allow passage of the other. This approach has the advantage of a concentric design with no echo from an adjacent guidewire. Because the imaging core

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and the guidewire do not have to occupy the tip at the same time, the tip size can be much smaller. For this reason, this design enables the use of the smallest catheters now available. One final consideration is the need to prepare the catheter. All the mechanical designs must be flushed with fluid before use to provide sound transmission from the transducer to the blood; the presence of even microscopic bubbles can adversely affect image quality. The various designs also differ in how easy they are to flush, depending on the size of the catheter and the size of the flushing channel. This consideration is not applicable with electronically steered systems, because the blood itself provides the contact with the transducer.

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340

Chapter 15 - Principles of Intravascular Ultrasound David T. Linker MD

Intravascular ultrasound is a relatively new technique for imaging a vascular structure from a catheter placed within that structure.[1] The basic physical principles are the same as those for other ultrasound techniques, but the physical constraints and characteristics of a catheter-based imaging technique lead to solutions different from those normally employed in other forms of ultrasound examination. This chapter examines the ways in which the constraints and characteristics of intravascular ultrasound dictate certain forms of design solutions and their consequences on the resultant capabilities of the systems used. The practical consequences for clinical application and future development are also outlined.

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Special Ultrasound Characteristics The principles governing all types of ultrasound imaging are the same, whether the transducers are outside the body, as in transthoracic ultrasound, or within the body, as in transesophageal or intravascular ultrasound. The major differences are transducer size, the distance to the structure being imaged, and the intervening tissues (Table 15-1) . For intravascular ultrasound, these parameters are significantly different. The transducer itself must be very small so that it can be placed inside a catheter, which is inside the arteries or veins. Typical catheter sizes range from less than 1 up to 2.6 mm in diameter. The distance to the structures being imaged is very short, and there is an enveloping layer of fluid (blood) surrounding the transducer at all times. This homogeneous layer of fluid TABLE 15-1 -- Comparison of Intravascular Ultrasound with Other Ultrasound Techniques Technique Transthoracic Transesophageal Intravascular

Transducer Size (cm) >2 <1.2 <0.26

Depth (cm) ˜3–20 ˜2–20 ˜0.05–4

Intervening Tissues Skin, fat, muscle Esophagus, atrium Blood

is also the main tissue between the transducer and the structures of interest. In transthoracic echocardiography there is little constraint on the size of the transducer, other than convenience and the size of the interspace between ribs. The distance between the transducer and the structures of interest can be much larger, up to tens of centimeters. The intervening tissues are very heterogeneous, including skin, subcutaneous tissues, fat, and muscle. The connection between the transducer and the body must be improved by use of ultrasound gel.

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Transesophageal echocardiography has some of the constraints of intravascular ultrasound but not all. The transducer must be small but not as small as that for intravascular ultrasound. Typical sizes are 10 to 12 mm in diameter. The distances to the structures imaged are short, but they still range from 2 to 20 cm. The contact is through a structure with both fluid and air, and therefore variable, and the structures through which sound must pass are almost the same as for transthoracic ultrasound, except for the skin. In summary, the special characteristics of intravascular ultrasound are a very small transducer size, a very short distance from the transducer to the tissues being imaged, and a relatively homogeneous medium between the transducer and the structure being imaged. To understand the consequences of these characteristics and constraints, we must review some details of the physics of ultrasound imaging. Resolution/Attenuation Most imaging transducers are used both for transmission and for reception of the ultrasound energy. For transmission there is a spatial pattern of signal strength, and for reception there is a spatial pattern of sensitivity. These patterns are often similar in form, and taken together they are referred to as the beam pattern of the transducer. A narrow beam leads to improvement of lateral resolution of the image, whereas a wider beam yields lower resolution. This beam pattern is primarily determined by the shape of the transducer and its frequency. The 341

pattern is similar to the diffraction pattern resulting from light traveling through a single small slit. This "single-slit diffraction," which is covered in basic optics, results in a bright central band and less bright alternating bands on either side of the main band, because of interference. A similar pattern results with a single ultrasound transducer: a single main "lobe" of sensitivity and smaller side lobes, owing to interference. For a transducer of given shape and size, the width of the main lobe becomes narrower if the frequency of the transducer is increased, thereby improving lateral resolution. If the frequency is lowered, the main lobe becomes wider, degrading lateral resolution. Increasing the diameter of the transducer creates a narrower main lobe and improves resolution, whereas decreasing the diameter increases the width of the main lobe. These two

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effects of frequency and diameter are closely related. In fact, for two transducers of different size but the same shape, the product of the frequency of emitted sound and the transducer diameter determines the beam pattern (Fig. 15-1) . If we reduce the transducer size and wish to maintain the same lateral resolution, we must increase the frequency proportionately. The main constraint on increasing frequency in diagnostic ultrasound is poor tissue penetration because of attenuation (reduction of the signal strength). Attenuation is increased with higher frequencies and with higher depth. Attenuation also is a function of the tissues through which the sound passes, and it is increased by varying tissue composition, so a uniform tissue such as blood reduces attenuation significantly. Because large distances increase attenuation, the short distance in intravascular ultrasound is also an advantage. Because of these factors, higher frequencies can be used for intravascular ultrasound: up to 40 MHz in some coronary instruments used clinically today, and 20 to 30 MHz for peripheral vascular studies, without encountering prohibitive attenuation of the ultrasound signal strength. The frequency of the transmitted ultrasound can be increased to match the smaller transducer size, improving lateral resolution. Resolution in the direction Figure 15-1 Simulated beam profiles for four transducer size and frequency combinations. Each profile has a central main lobe and may have side lobes as well. Each profile represents the result obtained with a given frequency-diameter product, with the other variables held constant. Moving from A to B represents reduction of the frequency or the transducer diameter by half. Each additional step is another halving of the frequency-diameter product, so that A represents a frequency-diameter product eight times higher than D.

of the beam (axial) is also increased, because shorter pulse lengths can be used at higher frequencies. Short Imaging Distance The other effect of very short distances is that imaging is performed very close to the surface of the transducer itself. Imaging close to the transducer face can be unfavorable because of two physical effects: ring-down and near-field artifact. When the transducer is electrically excited to generate the pulse of sound, it "rings" for a short time, much like a bell. This vibration generates electric

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signals similar to, but much stronger than, the signals generated by returning ultrasound. As a result, if we use the same transducer for transmission and reception of the ultrasound signal, which is the case in most systems, the received signal is buried in the ring-down signal (Fig. 152) . This signal creates a limit on the shortest distance from the transducer within which we can generate a useful image. This period of ringing can be shortened by damping the transducer, which has an effect similar to placing a gloved hand on the ringing bell. The problem with this approach is that it reduces both the transmitted ultrasound energy and the sensitivity to received ultrasound signals. Increasing the frequency of the transducer also reduces the ringing time, but it can never completely eliminate it. The other effect is near-field distortion. If the source of the reflected ultrasound is a long distance from the transducer, each wavefront arrives at roughly the same time across the entire face of the transducer, and the resultant signal is the sum of all the received signal (Fig. 15-3) . If the source of the reflected ultrasound is a very short distance in front of the transducer, there is interference of the wavefronts across the face of the transducer, causing loss of signal and distortions in the image. The distance at which this occurs is a function of the frequency and diameter of the transducer. The range of distances that are affected is much larger than that affected by ring down. These two effects combine to make imaging close to the transducer undesirable. Beam Steering To create a two-dimensional image, ultrasonic pulses must be transmitted and received in various directions. There are two fundamental ways of doing this, and the constraints of size and the length of the catheter affect how these methods can be used. The first method is mechanical motion of the transducer element (or elements) to point it (or them) in the different directions. This method can use a rocking motion, as is used in most mechanical ultrasound systems today, or a rotary motion, which was more common in earlier transthoracic systems. Rocking motion is difficult to reproduce at the end of a long catheter, so it has not been used so far for intravascular ultrasound. Rotation of the element is a uniform motion and therefore easier to produce. All mechanical systems used for intravascular ultrasound so far use this technique.

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342

Figure 15-2 Transducer ring down is demonstrated using an actual signal from a clinical 30-MHz intravascular ultrasound probe. The region labeled Ringing shows the signal caused by excitation of the transducer to create the ultrasound pulse. The area labeled Catheter shows returning ultrasound signals, in this case very strong signals from the housing of the catheter. The areas labeled Blood and Tissue show the returning signal from blood and adventitia, respectively.

The most direct way to cause the rotary motion of the transducer would be to use a small motor at the tip of the catheter (Fig. 15-4) , but it has been difficult to develop such a small motor with sufficient power. In spite of this, one group has made such a catheter for use in larger vessels. The more common method of causing the transducer to rotate is to have the drive motor outside the body and to use a flexible cable to transmit the torque to the transducer end of the catheter. With this sort of design a significant problem is nonuniformity of rotation of the transducer end of the catheter, because the position is measured at the motor end of the catheter. If the drive cable binds, either through a manufacturing defect or because of sharp bends in the catheter, there is a hesitation of rotation of the distal, transducer end, whereas the proximal, motor end continues to turn.[2] When this Figure 15-3 The cause of near-field artifacts is the difference in timing of arrival of wavefronts across the transducer. If the echo source is far away from the transducer face (left), the wavefronts arrive roughly at the same time all across the transducer face. If the echo source is close to the transducer (right), different parts of the transducer receive different phases of the wavefronts, possibly even parts of other wavefronts. The result is decreased and variable signal strength, causing distortion.

happens, several pulses are transmitted in the same direction but are displayed as if they are in different directions, causing a blur in the image (Fig. 15-5) . When the rotation is finally resumed, the speed is much faster than Figure 15-4 Schematic examples of three different types of catheter construction. Cable mirror and motor direct are examples of mechanically steered designs, using a flexible cable or a micromotor to cause rotation. One uses a mirror to direct the beam in differing

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directions, reducing near-field and ring-down artifacts, whereas the other uses a transducer pointed directly outward. Either of these can use a micromotor or a drive cable to provide torque. The electronically steered catheter has no moving parts and a large number of smaller transducers mounted on the surface. Only a few transducers are shown here, for clarity.

343

Figure 15-5 Illustration of how nonuniform rotation causes distortion of images from a mechanical system. Beams are sent out and received in uniformly spaced directions to create an image. If the transducer is delayed in its rotation because of a mechanical problem, the motor continues to turn and pulses continue to be sent out, but they will go in the same, or almost the same, direction (beams 1 to 5, left). When the transducer starts to rotate again, it rotates much faster, skipping some regions (beams 6 to 10). The display, however, distributes the beams equally, causing distortion (right).

normal and the image is compressed. This process can occur at one part of the image or at several (Fig. 15-6) . The construction of the transducer end can also vary. There are two fundamental types of transducer orientation. The simplest to understand is the one with the transducer pointed directly out of the catheter toward the vessel wall. The actual direction of the transducer is usually slightly forward, so that internal reflections within the catheter cause less of a problem. This design has the advantage of simplicity, but there are difficulties stemming from the proximity of the transducer to the structures being imaged. Because the same transducer is used to generate and receive the signals, and there is a very short distance from the transducer to the outside of the catheter, ring down causes a bright halo near the transducer, although this is often blanked out on the screen. Near-field distortion can also be a problem close to the transducer. These two artifacts can be troublesome if the structures of interest are adjacent to the catheter, as they can be in small vessels or in tight stenoses. Figure 15-6 Clinical examples of nonuniform rotation distortion on intracoronary images. A, There is distortion due to nonuniform rotation in one region, similar to what is illustrated in Figure 15-5 . Note that the "smeared" portion from 3 to 4 o'clock represents when the transducer was not rotating fast enough, whereas the compressed region from 5 to 6 o'clock represents when the transducer was rotating too fast. A clue to this artifact is the size of the speckle, which

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becomes larger when the transducer is rotating too slowly and smaller when it is rotating too fast. B, Demonstration of what happens when the rotation of the transducer is slowed in several different directions as it rotates, at about 12, 2, 4, 7, and 10 o'clock.

The alternative transducer orientation deals with the problems of near-field artifact and ring down directly by increasing the effective distance between the transducer and the outside of the catheter. This increase in distance is achieved by directing the transducer toward an internal rotating mirror, which then directs the ultrasound outward. Although slightly more complex, this type of design results in less or no ring-down effect at the surface of the catheter and reduced near-field distortion. The other technique for steering the beam is based on electronic combination of the signals from multiple small transducers. These signals can be arranged in a linear phased array, with all the elements potentially contributing to the image formation, or a curvilinear array, in which only some of the elements are used at one time. Because an intravascular device images in all directions, a linear phased array would not be able to steer the beam in all those directions, so the curvilinear array is the one that has been applied. As a result of the constraint of size, it is difficult or 344

impossible for each of the elements of the array to be wired separately, as is the case in the usual array system. Specialized electronics at the tip of the catheter are necessary in order to switch sequentially between the individual transducer elements; therefore, elements cannot be used simultaneously, and several sequentially acquired signals from adjacent transducers must be added together electronically after they have been received in order to create the "beam" signal. This technique is called synthesized aperture, because the equivalent of a simultaneous signal from the entire transducer (aperture) is created (synthesized) by adding the individual signals together. As a result of the need to send the beams out sequentially, the frame rate of image generation is reduced. Also, because the array is curved, some of the elements at the sides of the beam direction contribute little to the imaging, resulting in a smaller effective transducer diameter, reducing effective resolution.[3] Electronic systems share some, but not all, of the problems of mechanical

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systems. The transducer elements are on the surface of the catheter, so they are even closer than in the direct, rotating transducer designs, which means that the ring-down effect and near-field distortion are even more problematic for these systems than for mechanical systems. Because there are no moving parts, however, there is no problem with nonuniform rotation, and the images are stable no matter how much the catheter is bent (Table 15-2) .

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Practical Issues Unless we understand the limitations and variations of generation of the intravascular ultrasound image, we may misinterpret what is seen. What we see is primarily generated by the differences in acoustic properties between different tissues rather than the absolute value of those properties. An example of this is the media of the artery, which we can see quite clearly as an echolucent zone if there is intimal thickening, but which disappears completely if the intima is of normal thickness. It is reasonable to ask why the intima is not always visible. The answer to this is not clear, but there are two hypotheses. The first is that the intima must exceed a certain thickness, similar to the resolution limit, before it becomes visible. Once it exceeds this resolution limit, it is clearly visible. The problem with this explanation is that a plane reflector should be visible, even if it is smaller than the resolution limit, because the latter refers to resolving two sources of reflection, not one. An alternative explanation is that the normal intima has acoustic properties that are close to those of blood and media, and therefore are not visible, whereas thickened and abnormal intima has different properties and is visible. An issue discussed previously in this chapter is that of Figure 15-8 Altered appearance of calcification using different imaging systems. The clinical intracoronary image (A) shows intense shadowing owing to calcium from 2 to 3 o'clock, imaged with a mechanical system. B, Much less intense shadowing is visualized when using an electronically steered system, from 9 to 11 o'clock.

the relative intensity of echoes from structures and their relationship to the frequency of ultrasound. Although calcium may have a much stronger echo than fibrous tissue at the frequencies of ultrasound used for transthoracic and transesophageal imaging, the relationship may be reversed at the

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frequencies used for intravascular ultrasound. Thus, the brightness of the generated echo may not be sufficient to identify calcium, and other findings, such as the presence of shadowing, should be used (see Fig. 157) . The appearance of pathologic structures can also be influenced by the type of ultrasound instrument used and the settings of the instrument. These factors influence the range of gray values that can be accurately represented, and they can in some cases completely alter the appearance. Shadowing caused by calcification can be less apparent with curvilinear array systems than with systems that use a mechanically rotating transducer (Fig. 15-8) , for reasons that are not entirely clear. If we use the same criteria to-diagnose calcification in both situations, we may misinterpret the images. Similarly, the ability to see thickened media or lipid-rich plaque may be altered by the instrument gain settings and the type of instrument. Numerous distortions in the image can occur.[6] The most obvious cause, mentioned earlier, is nonuniform rotation with a mechanical catheter system. The visual distortions may be obvious or may be mistaken for abnormalities of the vessel contour and, therefore, pathology. These distortions may also affect any measurements that can be performed, so interpretation of vessel and lesion size should be made with great caution in the presence of such artifacts. The degree of distortion is greater the more eccentric the position of the catheter, so if the catheter is concentric with the vessel and the disease is also concentric, cautious interpretation may be possible. Another source of alterations in measurement is angulation of the catheter relative to the vessel. This type of problem is more difficult than problems of angulation with other forms of ultrasonic examination in which the operator has both direct control and awareness of the orientation of the transducer. In intravascular ultrasound the transducer moves freely within the vessel. It is not possible to determine the orientation of the vessel relative to the catheter from the images themselves, nor from 346

manipulation of the catheter. Angulation of the catheter relative to the wall can introduce geometric distortion owing to the oblique plane of imaging.[7] This distortion can lead to misinterpretation of the wall pathology or the dimensions of the vessel or lesion. In general, however, the actual

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magnitude of these distortions is minimal. As an example, a 10-degree angulation can cause less than a 2% increase in luminal area; 20-degree angulation causes about a 6% change. Quantitative evaluation of lesions is also affected by the imaging medium surrounding the catheter because the distances on ultrasound examination are determined by time-of-flight of the ultrasound, which in turn is determined by the speed of ultrasound in the intervening medium.[7] The speed of ultrasound in solids and liquids is predominantly governed by the specific gravity and compressibility, the former being the main variable in liquids. In blood, the main variable determinants of specific gravity are protein content and red cell content. Both change specific gravity, and as a result the time-of-flight of the ultrasound pulse, and the calculated measurements change (see Chapter 9) . This change can be as much as a 5% difference in the clinical range of proteins and red cell counts.[8]

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Future Directions The clinical application of intravascular ultrasound depends in large part on being able to identify clinical situations in which the information obtainable with the technique would lead to better or more specific treatment. So far, the best example of this is using intravascular ultrasound to assess the placement of vascular stents. Such observation has demonstrated that many stents that appear to be properly placed on the basis of angiographic images show poor apposition to the arterial wall on intravascular ultrasound images.[9] [10] The use of additional balloon inflations to improve the ultrasound appearance has reduced the incidence of subacute thrombosis of the stents, even though the patients received less intense anticoagulation than is otherwise customary.[11] As a result, the use of intravascular ultrasound has become routine whenever there is any question about stent placement. In addition, intravascular ultrasound is frequently used to help evaluate lesions with difficult or hard to interpret angiographic appearance. It seems likely that more specialized intravascular ultrasound probes will be developed. Smaller size is one possible direction, and there are already reports of imaging guidewires.[12] Combination with interventional devices is an obvious direction of development and combined imaging/balloon catheters[13] and imaging/atherectomy catheters [14] have already been produced. Other possibilities likely to be developed include forwardlooking devices, which have already been reported by two groups.[15] [16] [17] [18] Also, the advantages of ultrasound guidance of lasers[18] [19] [20] [21] [22] have spurred interest in combined laser/imaging catheters. Another general trend is toward increasing transducer frequencies, which result in improved resolution, both in the lateral and in the axial directions. In addition to the formidable technologic difficulties of dealing with higher frequencies, there is the physical difficulty of increased backscatter from

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blood. Increased backscatter results from the marked increase in relative backscatter from blood at higher frequencies compared with all other tissues, which translates into decreased contrast between blood and arterial tissues. Because of this, there have been studies using signal processing techniques to reduce the relative intensity of the blood signal relative to tissue, thereby improving contrast at higher frequencies.[23] [24] Although it is possible to correlate the visual appearance of plaque on the intercoronary ultrasound image with histology,[25] [26] there have been numerous attempts to improve discrimination and reproducibility by automating this process of discrimination. The two general approaches have been to base the processing on the images as they are presented to the viewer, or to use the raw ultrasound signal before it is processed into an image. The former example has the advantage of being easier to implement, requiring only a video digitizer, which is currently easily available. Analyzing the raw signal is much more complicated, requiring modification of the ultrasound instrument as well as specialized digitization hardware to sample the signal at the high frequencies observed. Nonetheless, reasonable results have been achieved using both techniques. An automated analysis of digitized images correlated well with both histology and visual analysis.[27] In another study, the normalized backscatter power and slope were examined in a limited number of samples, and they showed some discrimination of different tissue types.[28] A limiting factor of all of these studies is the need for a standard, because the characteristics of different instruments as well as different catheters can vary, requiring some measurement to normalize the results. For studies based on video digitization, this measurement is normally based on something that is easily visible in the image, and most frequently this has been the adventitia. Because the only parameter being measured is brightness of the ultrasound image, the results are normalized to the brightness of adventitia. For raw ultrasound signal studies, the benchmark has been the reflection from a perfect reflector, which is either a steel or plastic block. This method is clearly impractical in the clinical setting because it requires very careful measurements with micromanipulators to position the reflector. A recently proposed alternative is to use backscatter from the flowing blood within the artery as a standard.[29] In addition to being readily available, the results are less variable than the backscatter from adventitia. Overall, although there have been some intriguing results to date regarding automated analysis for tissue identification, as well as improved tissue identification, the ultimate limits of discrimination of

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intravascular ultrasound are still unclear, and unambiguous identification may be possible only in very limited situations.

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349

Chapter 16 - Intravascular Ultrasound Histologic Correlation and Clinical Applications Katsuhiro Kitamura MD Paul G. Yock MD Peter J. Fitzgerald MD, PhD

More than 10 years have passed since intravascular ultrasound (IVUS) was introduced into the clinical setting, bringing about a new era for the assessment and treatment of vascular pathology. Moreover, it has provided a method to directly examine atherosclerosis and other vascular disease processes. The ability to image the vascular wall as well as its lumen has changed the focus of the assessment of vascular disease by clinicians. Although pathologists have long recognized that measurement of lumen dimensions often poorly reflects the extent and importance of arterial disease,[1] [2] [3] IVUS has the ability in vivo to measure both lumen and vessel size.[4] [5] This information brought forth by IVUS has also brought new insights into coronary interventions by direct examination of their effects on atherosclerotic plaque and the vascular wall. With increasing experience and continuing advances in image quality and catheter design, IVUS has become the standard for the assessment of vascular disease.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Background Angiography: A Shadow of the Truth The introduction of coronary angiography to assess coronary atherosclerosis by Sones in 1958[6] focused attention on the vascular lumen; however, several investigators[7] [8] [9] [10] [11] have subsequently demonstrated that a particular coronary lesion involved in an acute coronary syndrome is not related to its angiographic severity. Pathologic reports have shown that the underlying mechanism of coronary occlusion is thrombus formation precipitated by the rupture of a lipid-laden atherosclerotic plaque, rather than the progression of a previously severe coronary stenosis.[12] [13] [14] [15] [16] [17] [18] Furthermore, it has become apparent that narrowing of vascular lumen is a late event in the development of atherosclerosis. Glagov et al[19] demonstrated that vessels compensate for the development of atherosclerosis by increasing their cross-sectional area to accommodate the plaque burden. Luminal narrowing does not occur until this compensatory mechanism fails. On average, angiographically apparent atherosclerosis occurs only when greater than 40% of the vessel area is occupied by plaque.[20] Thus, angiography, which generates a silhouette of the vessel lumen and no direct information about the vascular wall composition, underestimates the severity[21] and extent[22] of atherosclerosis and offers little information about the characteristics of obstructive plaque. Although angiography provides a road map, IVUS may provide a clinically applicable means to augment the road map by imaging the arterial wall as well as its lumen in vivo. The History of Intravascular Ultrasound The development of IVUS has been made possible by the advances in computerization and electronics and, in particular, the miniaturization of ultrasound transducers. Although catheter-based ultrasound was shown to be feasible in 1956 by Ciezynski, these initial attempts to

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350

develop IVUS systems were aimed at measuring the dimensions of cardiac chambers. [23] The first real-time, two-dimensional intracardiac images were produced by Bom et al[24] using a 5.6-MHz, 32-element phased array transducer mounted on a 3.2-mm catheter, but the development and widespread clinical application of transcutaneous echocardiography overshadowed the progress in intravascular cardiac imaging. It was not until catheters were further miniaturized that the assessment of atherosclerotic plaque became practical.[25] [26] [27] [28] [29] The first real-time, two-dimensional images from human peripheral vessels were recorded in 1988,[30] followed by the first in vivo imaging of human coronary vessels in 1989.[31] [32] Since that time, advances in catheter design and image quality have allowed the introduction of ultrasound catheters less than 1 mm in diameter that are capable of accurately assessing lumen and vessel dimensions as well as plaque morphology. In 1990, three-dimensional IVUS reconstruction was first described by Burrell et al,[33] and it has dramatically progressed by advances of catheters, pullback devices, and sophisticated computer algorithms.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Basic Principles Catheter Design Two basic approaches to catheter design have been developed. The first approach involves the use of a single piezoelectric crystal with mechanical rotation of the ultrasound beam to achieve circumferential imaging. The second approach involves a solid-state, multielement transducer (Fig. 161) . These catheters are delivered into the vascular lumen over a guidewire to enable their safe delivery to the region of interest. Both systems are fundamentally different and have their own unique strengths and weaknesses. A mechanical catheter has a flexible drive cable, traveling the whole length of the catheter, which rotates its single transducer on the distal tip at a speed of 1600 to 1800 rpm. Because the maximum delivery of acoustic power is larger than a solid-state system, the penetration Figure 16-1 Diagram of the two basic IVUS imaging catheter configurations.

and resolution of the surrounding tissue becomes larger, resulting in better image quality. One problem associated with this type of catheter is nonuniform rotational distortion, which is characterized by portions of stretched or compacted images and is caused by kinking or compression of the ultrasound catheter. This artifact is problematic in vessel curvature of greater than 40 degrees and may cause absolute errors for diameter and area measurement by more than 20%.[35] Solid type catheters have 64 multiple imaging elements, arranged cylindrically at the distal tip, which visualize cross-sectional images perpendicular to catheter axis. This type of catheter does not experience

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nonuniform rotational distortion, which is an important advantage In addition, the over-the-wire design makes the catheter relatively easy to use and manipulate in the coronary arteries. The multielement design, however, produces ring down. This artifact, seen as a bright ring surrounding the catheter, is generated by continued vibration of the piezoelectric crystals after cessation of the activating electrical impulse. Although this artifact can be electronically subtracted out by eliminating all early signals detected by the catheter, this masking may prevent the detection of structures close to the catheter surface. With respect to image quality, transducers, made from small parts of elements have relatively weak acoustic power, leading to an ambiguous image. The size of both types of catheters has continually decreased to diameters less than 1 mm, which allows for compatibility with 6-F guiding catheter platforms. Imaging frequencies have also increased, now greater than 40 MHz, providing substantially higher resolution for delineating subtle plaque variations in the vessel. Typical ultrasound images are shown in Figure 16-2 . It can be easily recognized that a higher frequency catheter can provide higher resolution at the expense of increased signal strength in blood and decreased signal penetration in tissue.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Image Interpretation The Normal Artery The ultrasound appearance of an organ or tissue depends on the acoustic properties of its components, specifically the degree of acoustic impedance difference between its layers. From the ultrasound point of view, normal arteries are mainly composed of collagen and elastin, which are highly echo reflective, and smooth muscle cells, which are relatively sonolucent. The arterial adventitia, which is mainly composed of collagen and elastin, is highly echo reflective, producing bright signals on IVUS. The media of arteries varies according to the respective anatomic location. Large central arteries, such as the aorta and iliac arteries, have an elastic media, which is also highly echo reflective, making the differentiation of media, adventitia, and intima indistinct, especially when the adventitial collagen is densely packed.[36] [37] [38] Typically in elastic arteries, the media is as bright as the surrounding tissue.[28] However, medium size arteries, such as the coronary 351

Figure 16-2 Ultrasound images obtained by 30-MHz (A), 40-MHz (B), and 50-MHz (C) catheters. Higher frequency catheters can provide improved resolution, but signal strength of blood increases as signal penetration decreases.

and femoral arteries, have a muscular, echolucent media. The detection of arterial intima depends on its thickness.[39] [40] In normal peripheral muscular arteries, reflections from the intima produce a bright inner layer, which helps to produce a distinctive three-layered appearance[41] [42] (Fig. 16-3) . Siegel et al[43] studied the precise origin of this three-layered

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appearance. These researchers confirmed that the innermost bright layer is produced by the intima and internal elastic lamina, the echolucent middle layer is produced by the media, and the bright outermost layer arises from the adventitia and external elastic membrane. However, in coronary arteries, the intimal thickness may not be sufficient to generate a distinct reflective layer. Fitzgerald et al[39] demonstrated that vessels with a threelayered appearance have a significantly thicker intimal layer than those without ultrasound layering. An intimal thickness of at least 178 µm was required before layering was seen with a 30-MHz transducer. Thus, Figure 16-3 Ultrasound image of mild coronary disease, illustrating the typical three-layered appearance. This appearance is a result of the acoustic difference between the layers of the artery: intima, media, and adventitia.

in truly normal coronary arteries without intimal thickening, a layered appearance is not seen. Because the "normal" appearance of coronary arteries was first described in patients with diffuse intimal thickening, a three-layered appearance was considered to be normal. Assessment of Atherosclerosis Atherosclerosis is a diffuse vascular disease process initially characterized by intimal thickening. In the early phases, lipid and macrophages accumulate within the intima, then, as the disease progresses, collagen is added by vascular smooth muscle cells.[44] [45] [46] As the production of collagen and accumulation of lipid continues, calcium may also be deposited and the media may thin.[47] The amount of lipid, collagen, and calcium within individual plaques varies widely. Plaque composition is related to the clinical course of coronary atherosclerosis. Fibrous 352

plaques tend to be stable and slowly progressive, with a clinical presentation of stable angina. Lipid rich plaques are less stable and may rupture, producing an acute, unstable ischemic syndrome.[12] [13] [14] [48] , [49] IVUS allows the quantification of the extent of atherosclerosis and an assessment of the composition of the plaque. In muscular arteries the echolucent media provides a separation between the thickened intima and the adventitia, which allows the cross-sectional area of the plaque to be

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clearly delineated. The plaque area should be measured using a leading edge technique, outlining the blood-intima and media-adventitia boundaries. The media-adventitia border is selected because this boundary corresponds to a true anatomic boundary compared with the outline of the plaque, which does not always correspond to the plaque-media boundary. Signal attenuation at the outline of a plaque may produce dropout in the image, masking the true plaque-media boundary. A large plaque burden may also be associated with thinning of the media, making the separation of plaque from adventitia difficult. [28] [47] , [50] However, this boundary is usually apparent in adjacent proximal or distal cross sections. Regions of calcification within the plaque are highly echo reflective. Calcification generates bright echoes (more intense than the surrounding adventitia) associated with acoustic shadowing and reverberations (Fig. 164) .[29] , [51] [52] This acoustic shadowing obscures the media-adventitia border and makes the assessment of the plaque burden difficult, especially when the calcification is extensive and superficial.[28] The reliability of ultrasound in detecting plaque calcification is pretty high. In a histologic comparison study, Di Mario et al[51] reported that calcium deposits were detected by IVUS with 97% accuracy. In vivo studies have also confirmed that IVUS often detects calcification not visible by angiography.[53] [54] Mintz et al[55] reported that calcification was present in 48% of target lesions by fluoroscopy and 76% of lesions by IVUS (P < .001) in patients with coronary interventions. Calcification was more likely to be visible by ultrasound only if it occupied less than 90 degrees of the vessel circumference and/or was less than 5 mm in length. These researchers also reported that calcium was detected in 72% of target lesions in 1442 patients and lesions with an ultrasound plaque burden greater than 0.75 or an angiographic Figure 16-4 Examples of calcified plaques. Deep and superficial calcium with acoustic shadows (A and B) and circumferential calcification with reverberations ("napkin-ring" appearance, C) are shown.

diameter stenosis greater than 0.25 had a prevalence of calcium of at least 65%. [56] Fibrous plaque is also echo reflective, although less so than calcium. It produces relatively bright echoes, often of a similar intensity to the adventitia.[28] [29] [42] [51] However, the intensity of echoes from fibrous plaque is variable. This variation may, in part, reflect machine gain settings, but it

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is also likely to be related to the collagen content of the plaque. Dense fibrous plaque can produce echoes that are brighter than the adventitia and can even cause acoustic shadowing, but they cannot produce the reverberations typical of calcification. Lipid is a poor reflector of ultrasound. Therefore, predominantly lipid-rich plaques, fibrofatty or fatty plaques, are often echolucent and less intense than the surrounding adventitia. Lipid pools can also be detected within plaques as echolucent regions without internal structure.[28] [29] The accuracy of IVUS in detecting lipid plaque has been reported to be as high as 78%.[29] In practice, however, echolucent regions must be cautiously interpreted. Artificial echolucency can be produced by ultrasound systems with limited dynamic range. When the dynamic range of the system is low, weak signals are not displayed, creating an image that mimics "lipid lakes" within plaque. The detection of thrombus is also difficult by IVUS because of the acoustic properties of thrombus, which are weakly echo reflective, variable, and often similar to blood or soft atherosclerotic plaque. At 20 to 30 MHz, blood has a fine, variably speckled appearance. This backscatter from blood is often valuable in the interpretation of IVUS images, allowing the discrimination of the inner plaque margin. The echogenicity of blood in vivo is mainly determined by the flow rate. At low flow rates, red blood cells aggregate, increasing the strength of the backscatter. Regions of slow blood flow, such as around dissections or within aneurysms, produce a brighter ultrasound image. The ultrasound appearance of thrombus varies with its composition. Platelet-rich thrombi have a very low echogenicity (similar to saline in vitro), whereas thrombi rich in red blood cells have a much greater echogenicity and demonstrate a uniformly speckled appearance.[57] [58] The echolucency of platelet-rich thrombi may explain the frequent failure of IVUS to detect thrombus in patients 353

Figure 16-5 An example of in-stent thrombus. A large amount of homogeneous echo patterns is observed inside stent struts (arrows).

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with unstable angina.[59] [60] In vivo, thrombus often has a diffuse, illdefined, homogeneous appearance (Fig. 16-5) . The sensitivity for detecting thrombus by IVUS has been reported between 36% and 80%.[60] [61] [62] Validation of Intravascular Ultrasound Measurements Numerous in vitro studies have validated IVUS measurements using histology as the gold standard.[25] [27] [28] [29] , [63] [64] Nishimura et al[65] reported an excellent (r = 0.98) correlation between lumen area measured by IVUS and histologic measurements in 130 fresh arterial segments. In vitro measurement of atherosclerotic plaque thickness has also been shown to be accurate (r = 0.91), [27] although in some studies plaque thickness was consistently smaller by histology, possibly owing to tissue shrinkage during processing. [28] IVUS measurements have been compared with angiographic measurements in a variety of studies. Nissen et al[66] reported, using normal human arteries, high correlation of diameter measurements between ultrasound and angiography (r = 0.98). The correlation between angiography and IVUS in diseased vessels, however, is not as close, especially when the lesion is eccentric.[67] [68] Following balloon angioplasty, the correlation between ultrasound lumen area and histology is good (r = 0.88),[69] but the correlation between angiography and IVUS is poor (r = 0.26),[5] [54] [70] , [71] These differences reflect the limitations of angiography in quantifying the complex, irregular lumen, which is typical following balloon angioplasty.[72] Many studies have also compared ultrasound assessment of lesion severity by cross-sectional area with traditional quantitative angiography.[54] [66] [73] [74] [75] [76] Nissen et al[67] reported that the cross-sectional lumen area by ultrasound has only a moderate correlation (r = 0.63) with the angiographic lumen area, which was supported by Tobis et al.[54] The reason for lack of correlation is because lesion severity by IVUS is calculated as a ratio of lumen area to vessel area, whereas for quantitative angiography it is based on the minimal lumen diameter within the lesion and the reference segment. Angiographically normal segments are often diagnosed as diseased by ultrasound. [22] Typically, reference segment plaque occupies 35% to 40% of the vessel cross-sectional area. The ultrasound assessment of lesion severity is affected by the remodeling phenomenon[77] [78] [79] therefore, the vessel size at the lesion may not be representative of the nondiseased vessel size. Lesion Morphology

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In addition to these issues of quantification, IVUS and angiography also provide different views of plaque morphology. Fitzgerald et al[76] compared lesion eccentricity by ultrasound with that by angiography. They found 77% of plaques were judged to be eccentric by ultrasound, but only 33% were eccentric by angiography. Additionally, many of the angiographically eccentric plaques were found to be concentric by ultrasound. The accuracy of the detection of morphologic features of plaque remains less certain. Histologic studies have demonstrated that IVUS can detect endothelial tears. Van der Lugt et al[80] reported that the sensitivity of IVUS in detecting morphologic features for each vascular specimen was high for dissection and media rupture (79% and 76%, respectively), but it was low for plaque rupture (37%). The ability of ultrasound to detect spontaneous plaque ruptures, which are often microscopic, is poor.[81] Ge et al[82] performed IVUS on patients with angina and compared groups with disrupted and nondisrupted plaques by IVUS findings. They found that disrupted plaque was related to unstable angina and concluded that IVUS can identify plaque rupture and vulnerable plaques. Yamagishi et al[11] reported that large eccentric plaques, containing an echolucent zone by IVUS, can be at increased risk for instability even though the lumen area is preserved at the time of initial study. They also showed that among 12 coronary sites with an acute occlusion at follow-up, 10 sites contained the echolucent zones. Inter- and Intraobserver Variability of Intravascular Ultrasound Measurements The limited image quality of early IVUS systems often made the interpretation of in vivo images difficult. Despite these limitations, early reports indicated that the inter- and intraobserver correlation of measurements was greater than 95%.[29] [64] [83] In one study, Blessing et al[84] assessed the inter- and intraobserver variability in 100 Palmaz-Schatz stent cases. The result showed that interobserver correlation ranged from 0.92 to 0.97 and intraobserver correlation ranged from 0.94 to 0.97 for measuring reference and minimal stent areas. These studies have clearly shown that the IVUS analysis of selected frames is highly reproducible. However, the variability introduced by selection of frames to be analyzed 354

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is another problem. Pathology reports indicated that lesion morphologic characteristics were typically constant only over a region 100 to 200 µm in length.[81] The characterization of a plaque may depend on which section is analyzed, and it is common practice to assess a lesion at the minimal lumen area, which may not be representative of the plaque as a whole within the target segment.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Applications of Intravascular Ultrasound Safety Clinical use of IVUS has been emphasized as a safe procedure, [54] [64] , [67] [85] [86] [87] but the studies cited involved only a small number of patients. Coronary artery spasm was reported to occur, but only rarely was it found to be severe.[88] Hausmann et al[89] reported safety information from 2207 patients undergoing IVUS, including 505 cardiac transplant recipients. In 3.9% of patients, complications occurred that might have been related to the performance of the ultrasound. Sixty-three patients (2.9%) had coronary artery spasm during performance of the ultrasound, which did not lead to further complications. Major procedural complications were more frequent in patients with unstable angina or acute myocardial infarction (2.1%) compared with stable patients (0.8%, P < .01) and more frequently in association with coronary interventions (1.9%) than for other indications (0%, P < .001). Bocksch et al[90] reported that IVUS imaging was done in 103 patients with acute myocardial infarction and showed a remarkable abrupt closure rate of 3.9%. These studies are not comparable because patient characteristics were so different from those of Hausmann's report, but Bocksch emphasized that IVUS should be performed by experienced investigators. Batkoff and Linker[86] reported safety data from 718 IVUS cases. Eight (1.1%) complications occurred, including spasm, vessel dissections, and guidewire entrapment, but no cases resulted in critical outcomes. No differences in frequency of complications among participating institutions were reported (P = .232). In order to perform IVUS safely, it is important to ensure adequate anticoagulation during the procedure. It is our practice to administer 5000 to 10,000 U of IV heparin before performing an IVUS interrogation as well as nitroglycerin before IVUS to standardize measurements.

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Detection of Angiographically Silent Disease One of the most basic insights derived from IVUS is the ubiquitous nature of coronary atherosclerosis. Patients with angiographic "discrete" stenoses were found to have significant plaque burden throughout the coronary tree by IVUS. In fact, Mintz et al[22] reported that reference segment crosssectional narrowing was 51% ± 13%, and only 6.8% of angiographically "normal" reference segments were normal by IVUS. Hausmann et al[91] found that patients with familial hypercholesterolemia had extensive coronary plaques by IVUS, even if angiography showed only minimal narrowing (Fig. 16-6) . This undetected plaque is not visible by angiography because the lumen size is preserved by arterial remodeling, despite significant intimal thickening. [19] [77] [78] [79] [92] , [93] However, such plaques may be of clinical significance. Vasospastic angina and acute coronary syndromes can occur in patients with coronary arteries that are normal by angiography.[11] [94] IVUS also aids in the assessment of lesions that are not well displayed by angiography and may change therapeutic strategy.[95] [96] Angiographic interpretation of lesions may be difficult because of overlapping branches or extreme vessel tortuosity. Bruchhauser et al[96] reviewed cases with ambiguous angiographic appearances using IVUS and, as a result, changed therapy in 21 of 31 patients, thereby eliminating interventions in 19 patients, with excellent clinical results. The accurate assessment of ostial lesions may also be difficult by angiography. Ge et al[97] reported finding plaques in 31 of 92 angiographically "normal" left main coronary arteries. In this study, the average diameter stenosis was 19.3%, with an area stenosis greater than 50% detected in four patients. Assessing the severity of ostial right and ostial left anterior descending lesions is often difficult by angiography; however, IVUS can offer another venue for interrogation and may assist in more careful assessment of these clinical situations. Guidance of Coronary Interventions One of the most widely investigated and applied uses of IVUS is to guide percutaneous coronary interventions. In addition to balloon angioplasty, a variety of new interventional devices, including stents and directional and rotational coronary atherectomy, are currently available to treat coronary stenoses. IVUS has provided new insights into the mechanisms of action of these devices. These insights have led to more appropriate device selection based on the ultrasound appearance of lesions. Additionally, IVUS has

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influenced the way in which operators gauge procedural success. Balloon Angioplasty

Andreas Gruentzig[98] speculated that balloon angioplasty compresses atherosclerotic plaque, thus increasing lumen diameter. Early pathologic reports from fatalities following percutaneous transluminal coronary angioplasty (PTCA) reported extensive plaque dissection.[99] It was not until the introduction of IVUS, however, that the mechanism of successful balloon angioplasty could be investigated directly in living patients. Ultrasound studies have demonstrated that lumen area doubled after angioplasty. Three basic mechanisms of this lumen enlargement have been described, including tearing of the plaque, stretching of the vessel wall, and a redistribution of plaque at the treatment site.[69] [100] [101] [102] [103] [104] [105] [106] [107] [108]

The efficiency of PTCA seems to depend on a controlled 355

Figure 16-6 Typical example of angiographically silent disease. The angiogram shows no evidence of disease, but at A, B, and C, corresponding IVUS images show mild intimal thickness.

disruption of the plaque. Dissections typically occur at the thinnest region of the plaque, at the junction of the plaque and normal vessel wall, or between the media and adventitia.[106] [109] [110] The GUIDE I study[76] found that plaque fracture or dissection was detected by ultrasound in 49% of lesions imaged following PTCA. The study by van der Lugt et al[110] showed that dissections were detected in 63% of whole cases and were generally seen at the thinnest region of the plaque on both histologic sections (92%) and IVUS cross sections (93%). Angiography clearly underestimates the frequency of dissection following PTCA.[111] [112] Typical IVUS images after balloon angioplasty are presented in Figure 16-7 . Dissections appear to be of therapeutic importance. Botas et al[104] demonstrated that vessel distensibility and compliance were returned to normal by balloon angioplasty. Schroeder et al[111] suggested that substantial coronary dissections after PTCA, which do not diminish antegrade blood flow, do not lead to an increase in acute or long-term events. A significant portion of luminal gain may be within these plaque fractures.[113]

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Dissections after PTCA vary in severity from limited intimal surface tears to full-thickness dissections, extending into the adventitia. The site of these dissections can often be predicted by ultrasound. In an in vitro and in vivo study, van der Lugt et al [110] reported that plaque fracture after angioplasty occurred at the thinnest region of the plaque, regardless of the preinterventional plaque characteristics. Fitzgerald et al[114] showed the close association between lesion calcification and dissection in vivo. Additionally, in this study, calcified lesions had larger dissection flaps. Direct ultrasound data also suggest that stretching and compression or displacement of plaque are important mechanisms of balloon angioplasty. Vessel area has been reported to increase following balloon angioplasty. [101] [102] [115] , Marsico et al[115] reported that a 2.4-mm2 increase in lumen area of coronary arteries following balloon angioplasty was associated with a 1.6-mm2 increase in total vessel area. It has been suggested that plaque area reduction is a result of plaque compression; however, atherosclerotic plaque is relatively incompressible. A possible explanation is that plaque is redistributed to each side of the lesion rather than physically compressed by balloon angioplasty. Baptista et al[108] indicated that plaque compression or redistribution accounted for 57% of the lumen enlargement following coronary balloon angioplasty. The precise mechanism of balloon angioplasty in a particular case depends on the mechanical properties of individual plaques[101] and may explain the variation in effects seen in various studies.[102] [105] [116] , [117] Stents

IVUS has made a significant contribution to the safe and effective deployment of coronary stents. Two types of stents are currently available, demonstrating distinctive ultrasound appearances. For stents with a slottedtube 356

Figure 16-7 Ultrasound images of dissection after balloon angioplasty.

design (e.g., Palmaz-Schatz, Multilink), the images show distinct points corresponding to the struts of the stent encountered in cross section by the beam (Fig. 16-8A) . Coil stents (e.g., Gianturco-Roubin, Wiktor) are

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composed of stainless steel wire arranged in a sinusoidal coil. The image of the stent shows a combination of points and short arcs, derived from the struts at any given cross section within the stent being either orthogonal or oblique to the imaging plane (see Fig. 16-8B) . The use of IVUS to guide stent deployment was pioneered by Colombo et al.[120] A major clinical problem with the use of stents was the 3% to 6% incidence of subacute stent thrombosis or hemorrhagic complications from the use of anticoagulants. Colombo's group recognized that most stentrelated complications were due to inadequate deployment despite an angiographically satisfactory appearance.[36] [118] [119] This work led to the routine use of high-pressure inflation (greater than 12 atm) for stent deployment, which has lowered the rate of subacute thrombosis to approximately 1%.[120] The Multicenter Ultrasound Stenting in Coronaries (MUSIC) study[121] demonstrated that IVUS-guided stent deployment could be safely performed with aspirin alone. In this study, the rate of subacute thrombosis at 1 month was only 1.3% and Figure 16-8 Ultrasound images of different stent echo signatures. A, A typical cross-sectional view of the slotted-tube design. B, A view from coil design stent. Variation of its echo patterns comes from the struts at any given cross section within the stent being either orthogonal (solid arrow) or oblique (open arrow) to the imaging plane.

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the 6-month restenosis rate was 9.7%. Despite the use of high-pressure deployment, ultrasound still shows, in a significant portion of cases, that the struts are not as well expanded as the angiogram suggests. In the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study,[122] 36% of the IVUS-guided group received additional PTCA because of insufficient stent expansion by IVUS, resulting in an increased minimal stent area from 6.25 to 7.14 mm.2 Figure 16-9 illustrates successful stent delivery following high-pressure deployment by angiography, but the stent is not yet well expanded by ultrasound. Several randomized trials have been published to assess whether complete expansion with IVUS guidance can produce a clinical benefit after stenting. The CRUISE study compared angiography-guided with IVUS-guided stenting.[122] There were significant differences between groups for poststent

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minimal stent area (7.78 versus 7.06 mm2 ; P < .001) and 9-month target vessel revascularization (8.5% versus 15.3%; P < .05). The RESIST (REStenosis after Ivus guided STenting) study[123] compared stent deployment with and without additional ballooning according to IVUS criteria. The group with IVUS guidance had significantly larger minimal stent area at 6-month follow-up (4.47 versus 5.36 mm2 ; P < .03), but the rate of restenosis was almost the same between the two groups (29% versus 23%). Although final results have not been published, the AVID trial [124] [125] compared angiography-guided stenting with IVUS-guided stenting. There was a significant difference between both groups regarding final minimal stent area (7.54 versus 6.94 mm2 ; P < .01) and 12-month target lesion revascularization (7.9% versus 14.6%; P < .04) for vessels less than 3.25 mm by angiography. Lower 12-month target lesion revascularization rates were seen in vessels with a distal reference diameter of 2.5 mm by angiography and in vessels with greater than 70% preprocedure stenosis by angiography, saphenous vein grafts. Directional Coronary Atherectomy

IVUS has also provided insights into the mechanism of directional coronary atherectomy (DCA). Based on Figure 16-9 Angiogram after stent deployment in the mid right coronary artery shows an acceptable result (A), but the initial IVUS image (B) reveals underexpansion. IVUS image after further dilation with bigger ballon (C) demonstrates substantial improvement in minimal stent area.

angiographic studies alone, it has been unclear how much of the beneficial effect of directional atherectomy is due to plaque removal and how much is due to lesion dilation by the atherectomy catheter (Fig. 16-10) . Ultrasound has revealed that about 40% of increased lumen area is due to vessel wall stretching and more than 60% is due to plaque removal.[115] [116] [126] , [127] Lesion morphology influences the outcome of directional atherectomy. Softer, more echolucent plaques are more effectively treated with directional atherectomy than fibrocalcific plaque.[128] Popma et al[129] found that the residual plaque area was greater in calcified than noncalcified lesions, especially in lesions with an arc of calcium that extended for more than 90 degrees of the lesion circumference. The current cutting capabilities of the DCA device depend on not only the presence of calcium in a lesion but also the location of the calcium relative to the lumen. A superficial rim of calcium at the lumen border generally prevents any tissue removal.

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Ultrasound has significant potential to optimize the performance of directional atherectomy. The angiographic appearance of a lesion reveals little about the volume or distribution of atherosclerotic plaque. Several studies have reported the retrieval of media and adventitia by atherectomy, [130] [131] which may lead to increased rates of intimal proliferation.[131] IVUS provides detailed information about the orientation of plaque and the residual plaque burden. The CAVEAT study failed to show any restenosis benefit for DCA versus PTCA,[132] but additional studies have compared IVUS-guided atherectomy and PTCA. The Optimal Atherectomy Restenosis Study (OARS) [133] was a prospective, four-center registry demonstrating that IVUS-guided DCA resulted in high rates of procedural success, with 2.5% in-hospital major complication. The rates of restenosis and target lesion revascularization at 6 months were 29% and 18%, respectively.[134] The Adjunctive Balloon Angioplasty After Coronary Arthrectomy Study (ABACAS) was another multicenter trial[135] that showed that IVUS-guided DCA followed by balloon angioplasty resulted in lower residual plaque mass compared with DCA alone (42.6% versus 45.6%; P < .001), with 358

Figure 16-10 Images of IVUS-guided directional coronary atherectomy (DCA). The lumen area is increased following serial atherectomy without dissections.

low complication rate (2.7% versus 3.6%; P = ns). Moussa et al[136] have reported that stenting after DCA (81% cases were IVUS guided) produced a lower restenosis rate (11% at 6 months) and target lesion revascularization rate (7% at 18 months). DESIRE is a multicenter randomized trial that compared stenting with or without DCA under IVUS guidance. [137] It showed that the acute lumen gain was greater in patients who underwent stenting after DCA compared with those who underwent stenting alone (7.2 versus 5.7 mm2 ; P = .02), resulting in a larger minimal luminal area after the procedure (8.6 versus 7.2 mm2 ; P = .03).[137] Followup data are forthcoming. Radiation Therapy

Recently, intracoronary radiation has emerged as a potential antiproliferative therapy to prevent restenosis after angioplasty or stenting.

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Many animal models and clinical trials have revealed that lowdose ionizing radiation reduces the incidence of neointimal formation and positive vessel remodeling.[141] [142] [138] [139] [140]

IVUS can play a valuable role to elucidate the response following intracoronary radiation therapy. Sabate et al[143] demonstrated in 21 patients, investigated by three-dimensional IVUS analysis and treated with PTCA followed by radiation therapy, that both the mean external elastic membrane volume and plaque volume increased significantly, but the luminal volume remained unchanged in the β-irradiated segments. IVUS also has clarified several important mechanisms of findings specific to radiation therapy. Edge effect, which is not specific to radiation therapy, is a phenomenon of restenosis at the stent margins. Albiero et al[144] [145] reported in a study of 32 P radioactive β-emitting stents that the incidence of edge effect was 42%, and it remained unchanged even after deployment of radioactive stents with a higher activity level (12 to 21 µCi). The mechanisms of edge effect are now hypothesized to be due to the combination of low-dose radiation and injuries in the segments adjacent to the irradiated site.[143] [144] The edge effect for catheter-based radiation therapy has been described as geographic miss,[146] causing neointimal growth of non- or poorly irradiated adjacent segments. It is the most important issue for preventing edge phenomenon. Intracoronary radiation may also prevent normal healing processes after balloon injury, called unhealed dissection, although nearly all angiographic dissections heal within 6 months after nonradiated angioplasty.[52] Kay et al [147] reported, based on the data from the BERT 1.5 study, that 16 dissections were recognized among 22 cases by IVUS after intervention, and at 6 months follow-up 8 unhealed dissections were seen by IVUS. No relationship between the existence of unhealed dissection and prescribed radiation dose was found. Meerkin et al[148] found 7 of 16 dissections partially healed but still remained at follow-up, yet there was no correlation with poor outcomes. Another important finding by IVUS is late stent malapposition. This phenomenon was first reported by Kozuma et al[149] after new stent deployment followed by 32 P β-radiation. They speculated that positive vessel remodeling and inhibition of neointimal formation by radiation were the primary mechanism. IVUS is the only method currently available to elucidate this specific phenomenon.

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Three-Dimensional Reconstruction

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Although coronary angiography provides the longitudinal information of the vessel lumen shape, conventional two-dimensional IVUS cannot provide such information, which has been a big limitation. Also, the lumen and vessel parameters are measured manually, which is very time consuming and suffers from high inter- and intraob-server variability.[150] Three-dimensional IVUS, however, combines wall and lumen characteristics of single planes with the longitudinal extension of the vessel, providing quantitative analysis of the coronary vessel morphology in an objective and reproducible manner through automated contour detection techniques. The three-dimensional reconstruction of a vessel from twodimensional images may provide a greater appreciation of the distribution of plaque and other morphologic features. In order to reconstruct a three-dimensional image from a series of twodimensional pictures, information is required about the longitudinal relationship of the images. This information is usually provided by performing a pullback at a known speed (0.5 or 1.0 mm per second) and assuming that in each time interval the transducer moves a known distance. The video image signal is digitized and each pixel is assigned a unique position in a three-dimensional grid with the x- and y-axis derived from the two-dimensional image and the z-axis derived from the timing sequence of the frame. Such three-dimensional pixels are known as voxels. To perform three-dimensional reconstruction with IVUS, several corrections must be made. For cyclic changes in vascular dimensions that create image artifacts (sawtoothed appearance), an ECG-gated threedimensional IVUS system has been developed.[151] [152] The other corrections include catheter movement during cardiac contraction and respiratory movement, curved path of the transducer, and axial IVUS image rotation. Slager et Figure 16-11 A longitudinal three-dimensional reconstruction of the left anterior descending artery (LAD) from a series of cross-sectional images during pullback at 0.5 mm per second. A fibrofatty plaque and superficial calcium are seen in the mid-LAD (arrowheads). The trajectory of the intravascular ultrasound pullback is assumed to be straight (center dark bank). IM,

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intermediate branch; LCx, left circumflex coronary artery; LM, left main coronary artery.

al[153] developed a new technique for correcting these artifacts. They investigated the feasibility of a new three-dimensional reconstruction model by fusion of angiography and IVUS (ANGUS). This system can reconstruct the three-dimensional contour of lumen and vessel along a spatial trajectory of IVUS pullback by combining the data of biplane angiography. High correlation for geometric measurements (r = 0.84 to 0.97) was observed between three-dimensional and biplane angiographic images by this system. Figure 16-11 illustrates a longitudinal view of a pullback from distal left anterior descending to left main coronary artery. The spatial relationship among plaque, calcification, and vessel wall can be easily recognized. In addition, computer-assisted automated vessel quantification is possible from these three-dimensional images. Several algorithms have been developed to trace automatically.[154] [155] Three-dimensional IVUS has been used for the creation of dose-volume histograms for interventional radiation therapy for restenosis[156] [157] [158] and to control intimal hyperplasia after PTCA followed by brachytherapy.[143] [159] In addition, it may serve as a valuable tool in the assessment of the regression and progression of arteriosclerosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions Tissue Characterization By IVUS, several in vitro and in vivo studies have tried to identify plaque components in coronary artery lesions with visual analysis of the gray scale images or quantitative videodensitometry analysis.[160] [161] [162] These gray scale IVUS images, however, cannot accurately distinguish among plaque components (fibrous tissue, fibrofatty tissue, and various stages of thrombus).

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Analysis of the unprocessed backscattered radiofrequency ultrasound signal has been conducted, which may convey more specific information relating to the intrinsic architecture of the plaque substance and permit a more reliable means for intravascular plaque characterization.[163] The internal backscatter from plaque, whether assessed by its peak amplitude or frequency, combined with time averaging methods, has been shown to distinguish plaque types.[164] Vulnerable plaque with lipid pool beneath thin fibrous cap, responsible for acute coronary syndromes and myocardial infarction, generally cannot be identified by the current level of image quality.[51] Several investigators have reported the usefulness of frequency or backscatter analysis in detecting vulnerable plaque.[165] [166] Komiyama et al[165] reported on in vitro study in which radiofrequency signal analysis could detect plaques with lipid core with higher sensitivity and specificity compared with gray scale analysis. Ultrasound frequency and backscatter analysis may be useful to detect plaques at risk of spontaneous rupture or complication with percutaneous

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interventions and also provide information for atherosclerotic plaque and thrombus characterization as well as transplant vasculopathy.[167] [168] Sonotherapy IVUS has been used for therapeutic purposes. Several investigators have reported biomechanical effects of ultrasound for prohibiting migration and adhesion of smooth muscle cells,[169] [170] which can be applied for the prevention of neointimal hyperplasia after coronary intervention. A system for intracoronary sonotherapy treatment (URX, PharmaSonics Inc.) has been developed, and favorable effects on neointimal hyperplasia in vivo have been reported using a porcine stent injury model.[171] This system is composed of ultrasonic transducers, generating a peak intensity of 100 W/cm2 at a center frequency of 700 kHz. At 7 days, smooth muscle cell proliferation assessed by bromodeoxyuridine histology preparation was significantly reduced in the sonotherapy group compared with the sham group (24.1% versus 31.2%; P < .05). The catheters have been further miniaturized for coronary use and investigated (Fig. 16-12) . Post et al[172] found, also in a porcine model, that sonotherapy significantly decreased the intimal hyperplasia after stenting compared with the control group. In this study, sonotherapy was associated with slight increase in mild vessel wall injury, but endothelialization was complete at 180 days. Intracoronary sonotherapy may be a good modality to inhibit restenosis, and it may also offer treatment advantages when compared with intracoronary brachytherapy. The sonotherapy system does not require the use of radioisotopes, thus negating the need for shielding and oncologists' support, thereby facilitating procedural "ease of use." Ultrasound has been reported to enhance drug delivery as well as gene transfection, suggesting that sonotherapy may be augmented further with a pharmacologic approach.[173] [174] [175] Therapeutic catheter-based sonotherapy Figure 16-12 (color plate.) A schematic view of a sonotherapy catheter (URX IST, PharmaSonics Inc.). This catheter is compatible with an 8F guiding catheter and peak intensity of 100 W/cm2 at a center frequency of 1 MHz with 5 minutes dwell time.

is currently under clinical investigation as a tool to prevent restenosis.

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Drug-Eluting Stent Because coronary stent use has become widespread for reducing restenosis after intervention, stents have been proposed as means for local drug delivery. Recently, several drugs with antiproliferative properties have been reported to reduce intimal hyperplasia after balloon angioplasty or stent implantation. Rapamycin, an immuno-suppressive agent with antiproliferative properties, has been reported to inhibit intimal thickening after balloon angioplasty in animal study[176] or after stent implantation in clinical study.[177] Paclitaxel, a microtubule-stabilizing compound with potent antitumor activity, has also been reported to prevent intimal hyperplasia after intervention.[178] [179] These drugs showed dramatic neointimal inhibition in long-term and short-term findings, but excessive or too-fast drug elution provoked incomplete intimal coverage over the stent struts. Although the optimal dose and the elution rate of the drug have yet to be determined, incomplete apposition (which has been observed in 6% to 30%[180] [181] ) may prevent effective tissue drug delivery and increase the risk of strut thrombosis by retarding endothelialization. IVUS can detect incomplete apposition easily and maximize drug delivery to the arterial wall.

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Summary IVUS provides a new window for viewing the vascular system. It allows the characterization and quantification 361

of the vascular wall as well as its lumen. This advantage has provided a new understanding of the pathology of atherosclerosis and provided insights into the mechanisms and outcomes of percutaneous coronary interventions. Because IVUS, unlike angiography, can detect stent underexpansion, additional PTCA to optimize stent deployment may translate into better long-term clinical results. Moreover, for brachytherapy, IVUS can provide precise information about mechanisms and appropriate dosing for therapy. IVUS is now being investigated to detect vulnerable plaques (tissue characterization), thereby contributing to "lesion-specific" therapy. In view of IVUS as a therapeutic modality, the use of sonotherapy is just beginning. The unique information provided by IVUS promises to lead to continuing advances in the understanding and treatment of vascular disease.

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Section 4 - Valvular Heart Disease

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Chapter 17 - Quantitation of Valvular Regurgitation Beyond Color Flow Mapping Sheila K. Heinle MD

Echocardiography is an essential tool in the diagnosis and management of patients with valvular regurgitation. Cardiac chamber size and function are assessed by two-dimensional echocardiography, and severity of regurgitation is semiquantitatively assessed by Doppler color flow mapping of jet area as mild, moderate, or severe. However, more precise quantitation of valvular regurgitation may be necessary for early detection of hemodynamically significant valvular regurgitation before development of left ventricular dysfunction.[1] [2] Furthermore, since valve repair is associated with low mortality rates, some investigators now suggest that minimally symptomatic patients in whom significant valvular regurgitation is identified be considered as candidates for valve repair procedures.[3]

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Limitations of Doppler Color Flow Mapping Doppler color flow mapping provides real time visualization of regurgitant flow signals. Although Doppler color flow images are derived from autocorrelation techniques that provide mathematical estimates of mean velocities along each scan line, this technique is most commonly applied qualitatively to assess the presence and spatial distribution of the flow disturbance due to valvular regurgitation. Numerous studies have demonstrated concordance in results of color flow mapping and other methods for evaluating regurgitant severity of aortic or mitral regurgitation. For mitral regurgitation, initial studies compared depth of jet penetration into the left atrium[4] 368

and maximal jet area with angiographic severity. Improved correlation was observed when mitral regurgitant jet area was corrected for left atrial area.[5] In patients with aortic insufficiency, measurement of the aortic regurgitant jet height relative to the left ventricular outflow tract height was a better predictor of angiographic grade than the maximal length and area of the regurgitant jet.[6] Criteria based on regurgitant jet size also have been proposed to assess the severity of tricuspid and pulmonic regurgitation.[7] Although maximal jet area correlates well with the semiquantitative angiographic grade of severity, however, only limited correlation is observed with quantitative measures of regurgitant volume (r = 0.55) and fraction (r = 0.62).[8] In addition, maximal jet area is not predictive of hemodynamic abnormalities such as an elevated pulmonary wedge pressure or reduced forward stroke volume. This lack of correlation is related to several factors, including jet geometry, physiologic variability, and instrument settings.[9] In any image plane, regurgitant jet area depends on the geometry and

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direction of the jet.[10] Doppler color flow mapping of free regurgitant jets that are unbounded by surrounding structures may lead to overestimation of severity due to entrainment of adjacent fluid by the high-velocity jet.[11] In contrast, the area of an eccentric jet is only 40% of the area of a free jet with the same regurgitant fraction.[10] Eccentric jets are influenced by adjacent constraining surfaces,[12] so that area measurements correlate poorly with regurgitant volume.[13] It also is important to note that the color flow map of a regurgitant jet represents the spatial distribution of velocities and is not a direct measure of volume flow rate.[14] Although color Doppler jet area increases with regurgitant volume, this relationship is not linear because it is highly influenced by driving pressure,[15] compliance of the receiving chamber,[16] and the size and shape of the regurgitant orifice.[17] Further, evaluation of regurgitant jet area depends on the echocardiographic approach, transducer frequency, and other instrument parameters. Specific factors influencing regurgitant jet size include ultrasonographic system variability, gain settings, pulse repetition frequency, transducer frequency, and tissue priority algorithm. [18] Thus, estimates of regurgitant severity often are greater when measured by transesophageal compared with transthoracic echocardiography. [9] In addition, measurements of color Doppler jet area are subject to substantial intraobserver[19] and day-to-day[20] variability. A superimposed change in loading conditions or hemodynamics between examinations further confounds evaluation of color Doppler jet area.[21] For example, acute severe mitral regurgitation may be underestimated by color Doppler imaging because of increased heart rate, decreased systemic blood pressure, and a rapid rise in pressure in the noncompliant left atrium.[22] Thus, despite the clinical utility of color Doppler flow mapping for evaluation of patients with known or suspected valvular regurgitation, this qualitative measure of regurgitant severity is not ideal. Efforts to derive more quantitative and clinically applicable measures of regurgitant severity are ongoing.

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Volumetric Methods Regurgitant fraction can be calculated from the difference between flow rates determined at two separate intracardiac sites using the continuity equation. Total stroke volume is measured as antegrade flow across the regurgitant valve, whereas net forward stroke volume is measured as antegrade flow across a competent valve.[23] The combined use of twodimensional echocardiography with conventional pulsed-wave Doppler and continuous wave Doppler allows the estimate of volumetric flow across any of the cardiac valves using the following equation: SV = CSA × TVI (1) where SV is stroke volume, CSA is cross-sectional area of the annulus, and TVI is time velocity integral measured as the area under the Doppler spectral velocity curve. Volumetric quantification of intracardiac flow using the continuity equation is based on the following assumptions: a constant cross-sectional valve area, a flat velocity profile, and a circular flow area. Although mitral and tricuspid annuli are nearly circular, optimal accuracy requires consideration of their elliptical shape by modifying the equation for stroke volume using an elliptical cross-sectional area: CSA = π(D1 ·D2 )/4 (2) where D1 and D2 are annular diameters measured in two orthogonal views.

When the cross-sectional area is presumed to be circular, for example, in the left ventricular outflow tract, cross-sectional area is calculated as [24]

CSA = πr2 (3)

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To quantitate mitral regurgitant volume (RV), net forward stroke volume (SV) is measured from the aortic annulus and subtracted from the total stroke volume measured at the mitral annulus, as follows: RV = Total SV − Forward SV (4) Total stroke volume can also be obtained by subtracting end-systolic from end-diastolic volume obtained by two-dimensional echocardiography.[25] Regurgitant fraction (RF) is then calculated from the ratio of regurgitant volume to total stroke volume: RF = RV/Total SV (5) Good correlation has been observed between volumetric and angiographic regurgitant fractions for isolated mitral or aortic regurgitation (r = 0.91).[26] Although correlation with angiographic grading is poor, the limitations of using qualitative angiography as a reference standard for assessing the severity of valvular regurgitation have been well documented. [27] The volumetric method is usually applied to left-sided regurgitant lesions, although it is theoretically possible to substitute flow across a competent pulmonary or tricuspid valve for aortic flow in patients with concomitant aortic insufficiency.

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Figure 17-1 Two-dimensional echocardiogram (left) and Doppler spectral velocity envelope (right) demonstrating proper positioning of the Doppler sample volume at the mitral annulus for accurate time-velocity integral measurement to calculate stroke volume. (Courtesy of Brad Roberts, RDCS.)

Although the volumetric method has been validated in a large series of patients with valvular regurgitation, overestimation of mitral regurgitation is a potential limitation of this approach.[28] Improper positioning of the Doppler sample volume may result in overestimation of the mitral timevelocity integral because of the increase in velocity from the annulus to the tip of the leaflets.[29] However, this potential limitation can be avoided by meticulous positioning of the sample volume at the level of the mitral annulus so that diameter and flow velocity are measured at the same anatomic site (Fig. 17-1) . [28] Aortic flow may be underestimated if there is a nonparallel intercept angle between the ultrasound beam and the direction

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of blood flow.[30] Again, this limitation is minimized by careful patient positioning and use of multiple ultrasonographic windows with meticulous adjustment of transducer position to obtain the highest velocity signal. Perhaps the most common source of error in Doppler flow calculations is inaccuracy in the measurement of mitral or aortic annulus cross-sectional area. [31] Because the two-dimensional echocardiographic diameters are squared in order to calculate an elliptical or circular cross-sectional area, small errors in diameter measurement result in large errors in crosssectional area. Moreover, the assumption of a constant maximal flow area using the pulsed Doppler volumetric method does not acknowledge the temporal changes in flow area during the cardiac cycle and contributes to overestimation of regurgitant flow. Errors in diameter measurement can be minimized by using an ultrasonographic window that provides a perpendicular intercept angle between the anatomic structure and the ultrasound beam, by careful attention to gain and other instrument settings, and by averaging several beats. When combined, these potential sources of error may contribute to reported regurgitant fractions up to 20% in normal subjects.[26]

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Indirect Markers of Regurgitation Severity Although indirect markers of regurgitation severity do not provide quantitative estimates of regurgitant volume, they provide valuable information regarding the hemodynamic impact of the regurgitant lesion on atrial pressure and left ventricular end-diastolic pressure.[32] Mitral Regurgitation Pulmonary Venous Patterns

Pulsed Doppler sampling of the pulmonary vein results in a spectral envelope that consists of three distinct waves. A systolic antegrade wave followed by a smaller diastolic antegrade wave represent pulmonary venous inflow during ventricular systole and diastole, respectively. Following the electrocardiographic P wave, there is a small negative wave that represents atrial reversal during atrial contraction. With increasing mitral regurgitation severity, the systolic phase of pulmonary inflow progressively decreases, with eventual reversal of flow in systole when severe mitral regurgitation is present (Fig. 17-2) . [33] Several studies have examined the value of reversal of systolic pulmonary venous flow as a marker of severe mitral regurgitation (Fig. 17-3) .[33] [34] There is an inverse correlation between the ratio of systolic to diastolic pulmonary venous flow velocity time integrals and the mitral regurgitant fraction in patients with normal left ventricular systolic function (ejection fraction > 45%).[35] In patients with left ventricular systolic dysfunction, a normal pulmonary venous systolic flow pattern indicates a small (<0.3 cm2 ) regurgitant orifice area.[34] Conversely, pulmonary vein systolic flow reversal predicts a large (>0.3 cm2 ) regurgitant orifice, consistent with severe regurgitation. However, blunted systolic flow is much less predictive, as it may be associated with a broad spectrum of regurgitant severity, ranging from trivial to severe regurgitation (Fig. 17-4) .

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To optimize the sensitivity of pulmonary venous systolic flow reversal as an indirect marker of mitral regurgitation severity, it is important to sample both right and left pulmonary veins, since jet direction can influence the pulmonary venous flow pattern.[36] Discordant flow patterns have been observed in the right and left pulmonary veins, with systolic flow reversal demonstrated more 370

Figure 17-2 Summary of the relationship between left atrial pressure hemodynamic and pulmonary venous flow Doppler profiles in 2+, 3+, and 4+ mitral regurgitation (MR). As MR increases, the v wave and v-y descent increase, and the a wave and x-y descent decrease, which is coincident with decreased pulmonary venous systolic (S) flow, increased diastolic (D) flow, and reversed systolic flow (RSF) in 4+ MR. AR, atrial reversed flow velocity. (From Klein AL, Stewart WJ, Bartlett J, et al: J Am Coll Cardiol 1992;20:1345–1352. Reprinted with permission from the American College of Cardiology.) Figure 17-3 Reversal of systolic flow by pulsed Doppler sampling of the pulmonary vein during transesophageal echocardiography in a patient with severe mitral regurgitation.

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Figure 17-4 Regurgitant orifice area and regurgitant stroke volume in three different pulmonary venous flow patterns. Open triangles, normal flow; open circles, blunted flow; solid circles, reversed patterns. Dashed lines indicate regurgitant orifice area of 0.3 cm2 . (From Pu M, Griffin BP, Vandervoort PM, et al: J Am Soc Echocardiogr 1999;12:736–743.)

often in the right pulmonary vein.[33] [34] Other limitations of this indirect method include the influence of other factors on pulmonary venous flow pattern, in addition to left ventricular systolic and diastolic function, including atrial fibrillation, mitral stenosis, ventricular loading conditions, left atrial compliance, and left atrial contractile function.[37] [38] In an effort to account for these other factors, it has been proposed that the systolic component of the pulmonary inflow pattern be expressed as a percentage of

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the total (systolic and diastolic) velocity time integral and then corrected for left atrial filling volume measured from single-plane transthoracic echocardiography. This approach correlated well with Doppler-derived regurgitant fraction[39] however, it remains unclear whether this combined method can be used reliably in patients with acute severe mitral regurgitation, patients with eccentric jets, or patients in atrial fibrillation. Peak E Wave Velocity

Early diastolic mitral inflow is represented by the E wave velocity, which is directly related to the pressure gradient between the left atrium and the left ventricle at the time of mitral valve opening. The added regurgitant volume in mitral regurgitation increases the initial atrial-to-ventricular pressure gradient, thus increasing the peak E wave velocity.[40] A recent retrospective study showed a modest positive predictive value (75%) for an E velocity greater than 1.2 m per second for identifying patients with severe chronic mitral regurgitation. This relationship was independent of other variables such as heart rate, age, and restrictive left ventricular diastolic function.[41] However, increased mitral inflow velocity has also been observed in patients with severe aortic regurgitation.[42] Moreover, the predictive value of this marker has not been tested in patients with acute mitral regurgitation. Therefore, although peak E wave velocity may be a simple screening method for hemodynamically significant mitral regurgitation, it should be not used in isolation to judge regurgitant severity. Aortic Regurgitation Pressure Half-Time

The pressure half-time index represents the time for the peak gradient across the aortic valve in diastole to decay to half of its initial value. Doppler velocity and catheterization pressure half-times have been demonstrated to be linearly related (r = 0.91), with Doppler pressure halftime inversely related to the angiographic grade of aortic regurgitation.[43] Patients with severe aortic regurgitation have a shortened pressure half-time because of the rapid rate of decline in aortic diastolic pressure and rise in left ventricular diastolic pressure, resulting in rapid equalization of aortic and left ventricular pressures (Fig. 17-5) . A Doppler pressure half-time of 400 msec separates mild (1+, 2+) from significant (3+, 4+) aortic regurgitation by angiographic grading with a specificity of 92% and positive predictive value of 90%.[43] Aortic regurgitant severity may be overestimated, however, if the left ventricular end-diastolic pressure is

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elevated because of depressed left ventricular systolic function resulting in a significant overlap in pressure half-times between patients with mild, moderate, and severe regurgitation.[43] In addition, other factors such as stroke volume, aortic and left ventricular compliance, and systemic vascular resistance influence the pressure half-time.[44] Pressure half-time is most useful as an additional method to classify and monitor progression of chronic aortic regurgitation when color flow Doppler methods are discrepant. [45] Deceleration Slope

With increased severity of aortic regurgitation, the diastolic aortic pressure falls rapidly while left ventricular filling pressure rises rapidly, resulting in a steeper deceleration slope on a continuous wave Doppler echocardiogram. Although deceleration slope and pressure half-time both are measured from the continuous wave Doppler curve, deceleration slope is not dependent on the initial pressure gradient. Deceleration slope has been reported to be a better index of regurgitant severity than pressure halftime, demonstrating a close correlation with angiographic grade of regurgitation even in patients with associated aortic stenosis, mitral valve disease, or low cardiac output.[46] A deceleration slope greater than 3 m/sec2 suggests severe aortic regurgitation. Unfortunately, a deceleration slope less than 3 m/sec2 can be seen with mild, moderate, or severe regurgitation. [46] [47] Left ventricular compliance influences the reliability of deceleration slope as an index of aortic regurgitant severity, since a steep slope can be observed in a patient with only mild aortic 372

Figure 17-5 (color plate.) Color Doppler image (A) and continuous wave Doppler image (B) demonstrate severe aortic regurgitation with a pressure half-time of 49 msec and deceleration slope of 18 m per second2 resulting from rapid equalization of pressure between the aorta and left ventricle. (Courtesy of Brad Roberts, RDCS.)

regurgitation but a stiff left ventricle. As with pressure half-time, deceleration slope is influenced by systemic vascular resistance.[44] Thus, pressure half-time and deceleration slope are unreliable methods to assess changes in aortic regurgitation severity in response to vasodilators. However, these approaches may be helpful in assessing whether aortic regurgitation is chronic and well-compensated (flat slope), as compared

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with the steep slope in patients with acute, decompensated regurgitation. Diastolic Flow Reversal

Severe aortic regurgitation is associated with diastolic reversal of flow in the aorta (Fig. 17-6) [48] as well as Figure 17-6 Diastolic flow reversal demonstrated by pulsed Doppler interrogation of the descending aorta in the same patient shown in Figure 17-5 with severe aortic regurgitation. (Courtesy of Brad Roberts, RDCS.)

systolic augmentation of flow within the central aorta.[49] Pandiastolic reversal of flow in the superior abdominal aorta using pulsed Doppler echocardiography from a subcostal window is highly specific and sensitive for predicting severe aortic regurgitation.[50] It is possible to calculate aortic regurgitant fraction from the ratio of reversed to forward flow in the aortic arch using M-mode measurements to account for the systolic and diastolic changes in aortic diameter.[49] However, diastolic flow reversal in the aorta is directly related to aortic compliance, as well as to regurgitant volume. Abnormal diastolic flow patterns can be observed in subjects with abnormal compliance in the proximal aorta or in patients with left to right shunt from the aorta 373

(such as a patent ductus arteriosus).[49] Compared with the ascending aorta, pulsed Doppler interrogation of the descending aorta has been reported to more reliably reflect severity of aortic regurgitation, owing, in part, to the more uniform velocity profiles more distally in the aorta.[51] Other Indirect Markers

High left ventricular diastolic pressure associated with severe acute aortic regurgitation results in echocardiographic findings such as premature closure of the mitral valve or diastolic mitral regurgitation.[52] However, these markers of severe aortic regurgitation are poorly sensitive, being present in fewer than half of the patients with this condition.[42] [52] Increased E/A ratio was reported to be more sensitive for severe symptomatic aortic regurgitation, with greater sensitivity than pressure half-time, M-mode, or color flow mapping for predicting regurgitant severity. [42] [52]

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Tricuspid Regurgitation A reliable marker of severe tricuspid regurgitation is systolic reversal of flow in the hepatic veins and venae cavae (Fig. 17-7) .[53] Another index of severe tricuspid regurgitation is an associated annular diameter greater than 34 mm or greater than 21 mm/m.[28] Intracardiac Pressure Gradients Continuous wave Doppler echocardiography can be utilized to measure instantaneous and mean pressure gradients to assess the hemodynamic effects of regurgitant valvular lesions by using the modified Bernoulli equation. Left atrial pressure can be derived from the mitral regurgitant Doppler signal by subtracting the peak gradient from systolic blood pressure.[54] Similarly, left ventricular end-diastolic pressure can be calculated from the diastolic blood pressure and the aortic regurgitant enddiastolic pressure gradient.[47] [55] However, Doppler consistently overestimates left ventricular end-diastolic pressure because of suboptimal angulation of the interrogating ultrasound beam, resulting in underestimation of the peak velocity and gradient. [47] Therefore, the main limitation of this technique is suboptimal angulation and the inability to obtain a complete high-quality Doppler spectral envelope. When there is a rapid rise in left atrial pressure (V wave), the mitral regurgitant jet may appear asymmetric and cut off in late systole (Fig. 17-8) . Although right ventricular systolic pressure can be estimated from continuous wave Doppler interrogation of flow across a regurgitant tricuspid valve, [54] it is of little value in assessing the severity of tricuspid regurgitation, since increased regurgitant severity results in increased right atrial pressure and decreased peak tricuspid velocity and pressure gradient.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Quantitative Analysis of the Proximal Flow Convergence Region Principle of Conservation of Mass Accelerating laminar flow patterns have been observed proximal to stenotic, regurgitant, and shunt orifices by Doppler color flow mapping by transthoracic and transesophageal echocardiography.[56] [57] [58] [59] [60] Regurgitant flow rate can be calculated from these laminar flow patterns based on the conservation of mass, which assumes that fluid converges uniformly and radially toward a restrictive orifice, forming a series of concentric isovelocity layers. These isovelocity surfaces are hemispheric for orifices that are small relative to the region of acceleration.[61] Compared to the turbulent downstream jet, this more predictable pattern of flow in the proximal flow convergence region makes quantitation of regurgitant severity possible. By Doppler color flow mapping, the radius (r) of the isovelocity surface is measured as the distance from the orifice to the point of color aliasing (Fig. 17-9) . Instantaneous flow rate can be calculated as the product of the aliasing velocity VA at any of these hemispheric contours times the surface area (2πr2 ) of that shell: Peak flow rate = VA (2πr2 ) (6) This calculation is based on the conservation of mass, which assumes that the accelerating flow through each isovelocity surface equals flow through the regurgitant orifice, since all flow through the isovelocity surface must pass through the orifice.[57] It is also assumed that the isovelocity hemispheric shells in the proximal flow convergence region demonstrate increasing velocity and decreasing surface area as the regurgitant orifice is approached. Each shell is associated with a particular velocity relative to its surface area. In theory, the proximal isovelocity surface area (PISA) derived from this zone of accelerating laminar flow is less dependent on

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instrument[62] and hemodynamic factors that influence the spatial extent of the regurgitant jet in the receiving chamber. Furthermore, unlike the volumetric method, the PISA method has the practical advantage of being independent of other associated regurgitant lesions. Initial in vitro and animal studies have demonstrated the validity of the hemispheric assumption for proximal isovelocity surfaces of small planar orifices relative to the acceleration zone.[57] [59] [63] There have been several clinical studies in patients with mitral or tricuspid regurgitation validating the PISA method using two-dimensional and quantitative Doppler techniques[64] [65] or color Doppler flow mapping.[66] The cause of mitral regurgitation did not affect the correlation of proximal flow acceleration estimates with angiography and quantitative Doppler calculations.[67] The PISA method was less useful in patients with aortic regurgitation in whom the Doppler beam angle exceeded 30 degrees.[66] By multiplane transesophageal echocardiography, comparison of flow rate calculations from the proximal convergence zone with angiographic grades of mitral regurgitation revealed that the proximal flow convergence method better distinguished severe from mild regurgitation than color Doppler area 374

Figure 17-7 (color plate.) Systolic flow reversal in the hepatic veins demonstrated by M-mode (A) and pulsed Doppler images (B) in a patient with severe tricuspid regurgitation. (Courtesy of Brad Roberts, RDCS.)

375

Figure 17-8 Continuous wave Doppler with V wave cut-off sign in severe mitral regurgitation (A) with simultaneous hemodynamic tracings (B) demonstrating the pressure relationship that causes the alteration in the deceleration slope of the time-velocity signal (arrows). Note the dark signal intensity of the Doppler signal. In the same patient, increased E wave velocity in A is additional evidence for severe mitral regurgitation. (Courtesy of Rick Nishimura, MD.)

and ratio of systolic to diastolic pulmonary venous flow velocities.[68]

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Technical Considerations The accuracy of the proximal flow convergence method is highly dependent on precise measurement of the PISA Figure 17-9 (color plate.) Color Doppler image of a patient with severe tricuspid regurgitation illustrating the proximal flow convergence zone with the hemispheric blue-to-yellow aliasing contour (blue-yellow interface or Nyquist limit) on the ventricular side of the tricuspid leaflets. (Courtesy of Brad Roberts, RDCS.)

radius, which requires high-resolution imaging and zoom magnification.[63] Furthermore, the proximal flow convergence region is not optimally visualized in all patients with regurgitant lesions, particularly in those with mild regurgitation. [66] [67] , [69] [70] Regurgitant Flow Rate and Aliasing Velocity

Adequate visualization of proximal flow acceleration thus depends on the severity of regurgitation and the aliasing velocity. Patients with very mild mitral regurgitation (regurgitant flow rate less than 20 m per second or regurgitant stroke volume less than 4.5 mL) do not have a visible proximal acceleration zone at the typical Nyquist velocity (VN ) of 49 to 58 cm per

second.[67] Because flow rate is underestimated unless the Nyquist velocity is much less than the orifice velocity, the hemispheric assumption for calculating regurgitant flow rate cannot be used with larger Nyquist velocities.[61] In in vitro models, the measured radius is always higher at lower aliasing velocities for a given flow rate (Fig. 17-10) . [69] Thus, the hemispheric model is most accurate with larger volume flow rates or with lower aliasing velocities. To improve accuracy, the aliasing velocity can be optimized to better define the hemispheric contour. [71] [72] Regurgitant flow rate is systematically overestimated furthest from the orifice and underestimated closest to the orifice because of progressive flattening of the flow convergence region (Fig. 17-11) . Therefore, the hemielliptical model may more accurately reflect flow rates closer to the orifice.[69] In the hemielliptical PISA method, radii from the orifice to the aliasing boundary are measured from long-axis (minor) and short-axis (major) views. This method correlates well with actual volume flow rates under

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376

Figure 17-10 (color plate.) In this patient with severe mitral regurgitation, the radius of the proximal flow convergence zone appears larger at a lower aliasing velocity of 22 cm per second (A) compared with an aliasing velocity of 33 cm per second (B). (Courtesy of Brad Roberts, RDCS.)

both constant and pulsatile flow conditions. When a flattened proximal convergence zone exists near the orifice, with a major-to-minor axis ratio greater than 2.0, the hemispheric model underestimates the actual volume flow rate by more than 50%. [69] Based on in vitro models, correction factors have been proposed to adjust for errors in flow rates calculated by the PISA method. [61] Orifice Size and Shape

The initial assumption that fluid converges toward an orifice in concentric hemispheric shells applies to an infinitesimally small orifice but cannot be applied to the finite orifice size of regurgitant orifices. In vitro models have demonstrated that the velocity distribution is independent of orifice size if measured at least two orifice diameters from the orifice, in situations in which the hemispheric assumption is valid.[61] In the clinical setting, a discrete Figure 17-11 Diagram of flow converging toward a finite orifice (bottom) showing the streamlines (dotted lines) and the consecutive isovelocity contours (solid lines), illustrating progressive contour flattening as the orifice is approached. (From Vandervoort PM, Thoreau DH, Rivera JM, et al: J Am Coll Cardiol 1993;22:535–541. Reprinted with permission from the American College of Cardiology.)

circular regurgitant orifice is rarely seen. Moreover, irregular or multiple orifices may make application of the PISA method more difficult. It has been proposed, however, that the PISA method can be consistently applied with irregular or multiple orifices if the measurements are obtained at greater distances (at least two orifice diameters) from the orifice.[59] [63] These studies conclude that measurements obtained far from the regurgitant orifice eliminate the influence of orifice size and shape. Other studies have demonstrated that orifice shape does not influence the accuracy of flow rate calculations if the aliasing velocity is small (<5%) relative to the orifice velocity.[61]

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Surrounding Geometry

In the setting of nonplanar surrounding geometry, the isovelocity shells cannot develop as full hemispheres and are effectively truncated as the orifice is approached.[56] [73] Distortion of the flow field is most pronounced when the constraining wall is positioned close to the regurgitant orifice, resulting in overestimation of the calculated flow rates. This situation can be observed with regurgitation caused by a posterior mitral leaflet flail (Fig. 17-12) . [74] Therefore, in the setting of mitral valve prolapse or flail, the following correction factor adjusts the calculated flow rate for the proximal flow convergence angle (α) (Fig. 17-13) : 2π(α/180) (7) Effective Regurgitant Orifice Area Experimental[75] [76] and clinical studies[77] have indicated that the effective regurgitant orifice area (EROA) provides unique quantitative information about the severity of regurgitation and is less influenced by hemodynamic variables than regurgitant volume and fraction.[75] [78] EROA 377

Figure 17-12 (color plate.) Posterior mitral leaflet flail (left) is demonstrated on transesophageal echocardiography with proximal flow convergence and a severe eccentric jet of regurgitation by color Doppler imaging (right) (see also color plate).

was initially calculated by the PISA method in an in vitro model using the following equation: EROA = (2πr2 VA )/VO = Q/VO (8) where VA is the velocity at a distance r from the orifice and VO is the orifice

velocity obtained by continuous wave Doppler.[79] Thus, in vitro and animal models demonstrated that EROA calculated by the PISA method demonstrated good correlation to actual EROA and to regurgitant stroke volume and fraction (Fig. 17-14) .[79] [80] Alternatively, if mitral regurgitant velocity is assumed to be about 5 m per second and the Nyquist limit is set to 40 cm per second, this equation can be simplified to

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EROA = r2 /2 (9) By comparison to angiographic grades of mitral regurgitation, grade I was associated with an EROA of less Figure 17-13 (color plate.) Flail posterior leaflet by transesophageal echocardiography demonstrating proximal flow convergence with wall constraint because of the proximity of the posterior wall. To adjust for the predictable overestimation caused by this geometric distortion, regurgitant flow rate and orifice area are adjusted by α/180. LA, left atrium; LV, left ventricle. (From Breburda CS, Griffin BP, Pu M, et al: J Am Coll Cardiol 1998;32:432–437. Reprinted with permission from the American College of Cardiology.)

than 10 mm2 and grade III with an EROA of greater than 25 mm2 . [79] In subsequent clinical studies, EROA measured by the PISA method correlated well with EROA measured by quantitative Doppler and twodimensional echocardiographic methods for tricuspid,[81] mitral,[82] and aortic regurgitation.[83] Limitations of EROA calculation by the PISA method include underestimation of aortic EROA in patients with an obtuse (>220-degree) proximal flow convergence angle [83] and overestimation in patients with mitral valve prolapse.[82] Overestimation of EROA in patients with mitral valve prolapse can be explained in part by dynamic changes in the effective orifice area.[84] [85] The PISA method provides instantaneous measurement of regurgitant flow and EROA and thus may not accurately reflect the overall severity of mitral regurgitation over the entire cardiac Figure 17-14 Line plot showing the correlation between effective regurgitant orifice area calculated by the proximal flow convergence method (y-axis) and the Doppler echocardiographic method (x-axis) in the clinical setting of mitral regurgitation. (From Vandervoort PM, Rivera JM, Mele D, et al: Circulation 1993;88:1150–1156.)

378

Figure 17-15 Typical examples of the types of dynamic changes in the

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regurgitant orifice area obtained by the electromagnetically determined flow method (EM). The regurgitant orifice size usually increases to maximal size in early to mid-systole (arrow) and decreases in late systole. (From Shiota T, Jones M, Teien DE, et al: J Am Coll Cardiol 1995;26:528–536. Reprinted with permission from the American College of Cardiology.)

cycle. Furthermore, the dynamic changes in EROA do not necessarily parallel the changes in regurgitant volume.[84] In late systole, despite continued increase in EROA, there is a decrease in the ventriculoatrial gradient and regurgitant velocity.[53] Experimental and clinical data further support the observation that the mitral regurgitant orifice changes dynamically during systole (Fig. 17-15) .[80] [86] Furthermore, the temporal variation in mitral regurgitant orifice area during systole varies according to the underlying cause.[86] Thus the PISA method of calculating EROA has the potential advantage of identifying the dynamic changes in regurgitant orifice area during the cardiac cycle. Changes in EROA are measured sequentially during the cardiac cycle by color M-mode echocardiography from the zenith of the isovelocity hemisphere.[80] [85] [86] The clinical implications of these data are that the EROA is not completely independent of hemodynamic variables and its changes may explain the beneficial effects of vasodilator therapy on functional mitral regurgitation.[77] In contrast, the existence of dynamic changes in aortic regurgitant orifice area is controversial.[87] [88] Dynamic changes have also been observed in the tricuspid regurgitant orifice area using the proximal flow convergence method.[89] Regurgitant Volume Although the calculation of regurgitant flow rate by the PISA method is relatively simple, requiring only the measurement of the isovelocity radius and aliasing velocity in a single view, it estimates peak, but not mean, flow rate. The measurement of regurgitant volume (RV) may be more accurate and clinically useful because the inclusion of the time velocity integral (TVI) by continuous wave Doppler may better reflect regurgitant jet dynamics during the cardiac cycle[64] [90] [91] RV = EROA × TVI (10) When regurgitant volume and flow rate by the PISA method are compared with angiographic grading of mitral regurgitation, PISA-derived regurgitant volume is better than flow rate at distinguishing 4+ mitral regurgitation from the other regurgitant grades.[71]

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In addition to the technical considerations that affect the validity of the hemispheric assumption of the PISA method, there are a number of limitations of this method for estimating regurgitant volume and flow rate. Since the PISA method relies on color Doppler to identify the region of proximal flow convergence, it is limited by technical factors that influence the accuracy of color Doppler flow mapping. Of these factors, the angle between the Doppler beam and direction of blood flow is most critical. The angle of the central PISA radius and the ultrasound beam must approach zero for optimal accuracy.[66] Other technical factors to be optimized include wall filter settings, interrogation depth, pulse-repetition frequency, and spatial beam expansion.[92] Furthermore, translational motion of the valve annulus affects the apparent PISA velocity, with overestimation with movement in the same direction[93] and underestimation with movement away from the PISA velocity shift.[94] Moreover, when the entire flow crossing the aliasing boundary does not pass through the restrictive orifice, as in ventricular septal defects,[93] the conservation of mass principle is not strictly applicable. Although attempts have been made to standardize the PISA method to calculate regurgitant flow, the optimal instrument settings for aliasing velocity and its corresponding radius remain unclear.[72] [91] [95] Furthermore, the accuracy of the PISA method is highly dependent on precise measurement of the radius from the orifice. Theoretically, the higher frequency imaging of transesophageal echocardiography provides improved spatial resolution and lower color aliasing velocity, which should improve the accuracy of the radius measurement.[96] Although attempts have been made to better define the radius by high-resolution imaging with zoom magnification, the exact position of the regurgitant orifice may still remain elusive.[70] [97] Errors in measurement of the PISA radius could result in significant errors in the estimation of volume flow. Vandervoort et al[97] propose an automated algorithm to locate the regurgitant orifice from a computer-simulated flow field, but this approach is not widely available.

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Vena Contracta Width Experimental and Clinical Validation The vena contracta width is defined as the narrowest diameter of regurgitant flow immediately downstream from the flow convergence region (Fig. 17-16) . Although, like proximal jet size, it is relatively unaffected by flow rate and driving pressure,[21] [98] vena contracta width is not identical to proximal jet size, since vena contracta width requires measurement of the diameter at the narrowest portion of regurgitant flow between the flow convergence region and the downstream turbulent jet.[99] Furthermore, the vena contracta width more directly reflects 379

Figure 17-16 (color plate.) Transesophageal imaging in the long-axis view demonstrates the vena contracta width as the narrowest extent of regurgitant flow immediately downstream from the flow convergence region in this patient with severe mitral regurgitation.

changes in the size of the regurgitant orifice.[100] Unlike proximal jet width, vena contracta width remains accurate in the presence of eccentric jets (Fig. 17-17) . [99] [101] [102] [103] [104] [105] The feasibility of measuring the vena contracta is 92% to 97% in patients with mitral regurgitation with minimal inter-observer variability.[100] [104] [106] Multiplane transesophageal echocardiography was shown to be more accurate than single plane imaging.[106] [107] Thus, the vena contracta method has been proposed to be a simple yet accurate method of assessing mitral regurgitant severity intraoperatively.[107] [108] Furthermore, vena contracta width is more predictive of the severity of mitral regurgitation than color Doppler jet area, left atrial size, and pulmonary venous flow.[104] Since mitral regurgitation worsens in the anteroposterior

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Figure 17-17 Linear regression plot showing good correlation between vena contracta width in the parasternal long-axis view and regurgitant volume (left) and regurgitant orifice area (right). Solid circles represent eccentric mitral regurgitation jets; open circles central jets. (From Hall SA, Brickner ME, Willett DL, et al: Circulation 1997;95:636–642.)

direction of the mitral valve orifice, accurate measurement of the vena contracta is obtained from long-axis views by transthoracic and transesophageal echocardiography. [100] [104] , [106] For mitral regurgitation, a vena contracta width of 5 mm or greater identifies severe mitral regurgitation, and a vena contracta width of 3 mm or less identifies mild mitral regurgitation.[104] In clinical and animal studies of aortic regurgitation, the vena contracta width correlates well with quantitative Doppler and electromagnetic flowmeter measurements, [103] [105] so that a vena contracta width of 6 mm or greater predicts severe aortic regurgitation, whereas mild aortic regurgitation is identified by vena contracta width of less than 5 mm.[105] EROA is estimated from the vena contracta width (VCW) by the following equation: EROA = π(VCW/2)2 (11) The estimated EROA and regurgitant volume flow correlated well with reference measurements by electromagnetic flowmeter (Fig. 17-18) .[103] A vena contracta width of 6.5 mm or greater predicts severe tricuspid regurgitation and correlates with EROA significantly better than visual estimates of jet area, which are influenced by right atrial pressure.[99] Clinical Considerations Accurate measurement of the vena contracta width is critically dependent on imaging with optimized axial resolution. Imaging views with poor lateral resolution result in artifactual widening of the flow signal and overestimation of regurgitant lesion severity. Precise imaging of the vena contracta requires smaller sector angles, high frame-rates, high resolution, appropriate color and tissue priority, and zoom mode magnification. However, the vena contracta width may be difficult to measure with poor acoustic windows, orifice movement, or rapid divergence of the jet beyond the orifice. Vena contracta width is not a direct measurement of regurgitant orifice area and is actually smaller than the anatomic orifice by a factor 380

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Figure 17-18 Correlation between peak regurgitant flow rates calculated by color Doppler vena contracta and electromagnetic flow meter methods. (From Ishii M, Jones M, Shiota T, et al: Circulation 1997;96:2009–2015.)

of 0.8 (coefficient of contraction). There is considerable overlap of actual regurgitant orifice areas in the intermediate mitral regurgitant vena contracta width range between 3 and 5 mm.[104] Therefore, regurgitant lesions in the intermediate vena contracta range may require additional methods of quantitation to more fully assess regurgitant severity.[109] In addition, the vena contracta width as a single measurement does not reflect dynamic changes in the regurgitant orifice during the cardiac cycle. In the presence of an irregular regurgitant orifice, multiple vena contracta width measurements in more than one plane may be necessary to improve accuracy.[103] [106] [109] , [110] Three-dimensional imaging of the vena contracta area accurately measures mitral regurgitant orifice by transesophageal echocardiography intraoperatively and may become the approach of choice as three-dimensional methods become clinically feasible.[108] The value of vena contracta width in the presence of multiple or diffuse regurgitant jets or atrial fibrillation is not known.

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Conservation of Momentum Theoretical Background Based on experimental studies of fluid dynamics of turbulent jet flow, the velocity distribution of the jet in the receiving chamber is best characterized by its momentum, which combines several factors such as flow rate, driving pressure, orifice velocity, and orifice area.[111] In the absence of a pressure gradient within the receiving chamber because of an adjacent wall or counterflow from another orifice, momentum should remain constant within the turbulent jet.[112] The principle of momentum conservation states that the momentum measured anywhere in the downstream jet is the same as the momentum of the jet at its orifice: Momentumorifice = Momentumjet (12) At the orifice, momentum is calculated by the product of jet velocity (Vo ) and flow rate (Q):

Momentumorifice = Vo Q (13) Thus, the regurgitant orifice flow rate (Q) can be calculated from jet momentum (M) measured anywhere along the extent of the jet, divided by orifice velocity (Vo ), measured by continuous wave Doppler[113] Q = M/Vo (14) Methods for Quantitation of Momentum In an in vitro model, when jets are formed through 0.005 to 0.5 cm2 orifices at a driving pressure of 1 to 81 mm Hg, the velocity distribution

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downstream conforms to a gaussian (bell-shaped) profile with the centerline velocity decaying inversely with distance from the orifice.[113] Jet momentum (M) flux can be calculated across the transverse plane of the jet by integrating flow velocity (v) across the area (A) of the jet in that plane: M = ∫A v2 dA (15) For an axisymmetric jet (circular cross section), momentum can be calculated from a single velocity profile across the jet: M = 2 π∫0 ∞v2 rdr (16) where r is the radial distance from the jet centerline to a point at which each velocity is measured. Thus, orifice flow rate can be accurately calculated by dividing momentum by the orifice velocity using equation 14. Effective regurgitant orifice areas then can be calculated by dividing momentum by the square of the orifice velocity: EROA = M/Vo 2 (17) An alternative approach, based on data from an in vitro pulsatile model, is to measure only the centerline velocity (Vc ), which is inversely proportional to the distance (x) from the orifice[114]

Vc (x) = 7.8√M/x (18) Then flow rate (Q) can be calculated by recording a single centerline velocity (Vc ) at a distance x from the orifice as well as orifice velocity

(Vo ):

Q = Vc 2 x2 /60.8Vo (19) The flow convergence centerline velocity/distance methods correlated well with reference methods in small

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381

clinical[115] and animal[116] studies that quantitated mitral and aortic regurgitation. The proposed benefit of the centerline velocity method over the PISA method is that the use of several data points instead of a single velocity data point improves accuracy.[116] Clinical Practice In spite of experimental validation and proposed theoretical advantages of using jet momentum or centerline velocity methods to quantitate valvular regurgitation, these methods are rarely used in the clinical setting for several reasons. First, since it has been reported that free jets are observed in only 60% to 70% of patients with mitral regurgitation,[10] the critical assumption of a free axisymmetric jet may not apply to a significant number of patients with eccentric jets in whom momentum is not conserved because of jet impingement on an adjacent wall or interference from pulmonary venous counterflow. It has been demonstrated that eccentrically directed jets are significantly underestimated by the momentum quantification method.[117] Moreover, application of the centerline velocity profile method requires accurate resolution of velocities within the turbulent jet, which is difficult because aliasing due to high velocities is often seen with mitral regurgitation. The considerable variation in the instantaneous velocity and position of the jet axis during the cardiac cycle requires data averaging using the simplified centerline velocity equation. Finally, the applicability of these methods is not known with varying size and compliance of the receiving chamber. Thus, these practical considerations limit the routine use of these momentum-based methods of quantification in the clinical setting.

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Amplitude-Weighted Mean Velocity Amplitude-weighted mean velocity is a nonvolumetric method for calculating the ratio of flow in shunt and regurgitant lesions based on the theory that the amplitude of the recorded Doppler signal is proportional to the number of erythrocytes contributing to the backscattered signal. This approach assumes a hematocrit within the normal range.[118] The amplitudeweighted mean velocity is calculated as the sum of the individual velocities of the erythrocytes within the continuous wave Doppler spectrum multiplied by their respective signal amplitudes.[118] Therefore, the basis of this approach is that each velocity is weighted according to the strength of its signal. Applying this concept over the cardiac cycle, the flow volume during a given time interval is proportional to the time integral of the average weighted mean velocity. Therefore, regurgitant fraction (RF) can be calculated as follows:

where the amplitude-weighted mean flow (AWMF) is measured at the regurgitant valve (regurg. valve) and at a competent reference valve (ref. valve). [119] The advantages of this method are that measurement of valvular surface areas is not necessary and its accuracy is not impaired in the presence of mitral valve prolapse. Regurgitant fraction calculated by the amplitudeweighted mean velocity method has been shown to correlate with ventriculographic[118] [120] and quantitative Doppler and two-dimensional echocardiographic findings.[119] There are technical considerations that limit the amplitude-weighted mean velocity method for calculation of regurgitant severity, however. These include the requirements that the continuous wave Doppler beam be of adequate width to include the entire area of the regurgitant signal (for example, the entire mitral annulus). In addition, the beam must be directed

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properly to avoid inclusion of adjacent flows, and the transducer must be maintained in the same position throughout the recording period to avoid translational motion from one valve to another. Furthermore, determination of the amplitude-weighted mean velocity varies with instrument gain settings and the effect of depth on signal strength. Thus, the ratio of amplitude-weighted mean velocity from the mitral valves to that from the aortic valves may not yield a value of 1.0, even in the absence of valvular regurgitation.[119] In addition to requiring a normal hematocrit, this method is applicable only in the setting of isolated regurgitant lesions, since separation of erythrocytes from blood plasma may falsely elevate the signal amplitude recorded from stenotic lesions.[118] Because the amplitude-weighted mean velocity is dimensionless, its measurement does not represent a physiologic variable and does not allow calculation of regurgitant volume or regurgitant orifice area. Thus, amplitude-weighted mean velocity may best be used as an adjunctive tool to quantitate valvular regurgitation. Finally, the requirement of special software limits the use of this approach in the clinical setting.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Three-Dimensional Echocardiography Three-dimensional echocardiography is an evolving technique that has been applied for the assessment of intracardiac anatomy,[121] [122] for quantification of intracardiac volumes, [123] and to better characterize mitral valve morphology by multiplane transesophageal echocardiography.[124] Initial three-dimensional reconstruction of color Doppler flow mapping for shunts and valvular regurgitant jets could only be visualized in gray scale and did not include quantitative information or comparison with actual flow rates.[125] [126] However, more recent in vitro studies have demonstrated that regurgitant flow may be accurately quantitated by three-dimensional reconstruction for bioprosthetic valves[127] and for varying native valve orifice shapes and jet morphologies.[110] In a preliminary clinical study, three-dimensional reconstruction has also been shown to accurately quantitate mitral regurgitant orifice area compared with the proximal flow convergence method intraoperatively in patients undergoing mitral valve repair.[108] Although early attempts to obtain color-coded images from threedimensional reconstruction required manual digitization of Doppler flow signals,[125] more recent studies 382

have demonstrated three-dimensional reconstruction of Doppler signals in original color coding by using direct digital data, which allows separate visualization of intracardiac flow and cardiac structures.[128] [129] These threedimensional images reveal the complex geometry of eccentric regurgitant jets in patients with mitral valve prolapse and demonstrate how misleading two-dimensional visual assessment or planimetry of regurgitant jets can be ( Fig. 17-19 and Fig. 17-20 ).[128] , [129] Since recent three-dimensional volumes are measured by an automated segmentation and voxel count procedure, they are independent of manual planimetry or subjective

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estimation. The technical and hemodynamic factors that influence color Doppler flow imaging also influence three-dimensional Doppler images.[129] However, the main limitation of three-dimensional echocardiography is the need for stable positioning of the transducer during image acquisition or a method to continuously track transducer position relative to cardiac structures. Another limitation is that three-dimensional reconstruction is time consuming, and the presence of irregular heart rhythms such as atrial fibrillation can significantly prolong the process. Furthermore, the timerelated changes of three-dimensional jet Figure 17-19 (color plate.) A, Transesophageal color Doppler images in a patient with a mitral regurgitant jet recorded at different rotational angles (0 and 90 degrees). B, Three-dimensional reconstruction of the central regurgitant jet in a patient with atrioventricular septal defect. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

areas and volumes have not yet been characterized. Some of these limitations will be overcome in the future with the advent of real-time three-dimensional echocardiography.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Clinical Implications The quantitation of valvular regurgitation is important, not only for the early detection of hemodynamically significant lesions but also for monitoring of therapeutic success. It has been suggested that not all patients respond favorably to vasodilator therapy, and quantitative methods can thus assist in differentiating patients by their response to therapeutic interventions.[130] [131] [132] However, the quantitative assessment of valvular regurgitation is a far more complex issue than the measurement of such variables as regurgitant volume, regurgitant fraction, and regurgitant orifice area. In addition to the anatomy of the regurgitant lesion, its hemodynamic impact should also be taken into account, since symptoms are not necessarily related to regurgitant severity.[32] [133] A semiquantitative index has been proposed that incorporates variables reflecting 383

Figure 17-20 (color plate.) A, Transesophageal color Doppler images show a wall-impinging mitral regurgitant jet at different angles (0 and 90 degrees). None of these conventional views is able to visualize the regurgitant jet entirely. B, Three-dimensional Doppler reconstructions show that the regurgitant jet resembles a spoon. The lower panel shows the convex face of this spoon jet. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.)

384

TABLE 17-1 -- Calculation of the Mitral Regurgitant Index Characteristic Jet penetration

Score Description 0 No jet

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1 2

PISA

CW jet

3 0 1 2 3 0 1 2 3

Pulmonary artery pressure Pulmonary venous flow

0 1 2 3 0

Central jet that does not impinge on lateral wall in any view Eccentric jet that extends to the pulmonary vein Eccentric jet that encircles the atrium No PISA visualized PISA ≤0.5 cm radius PISA 0.5–1.0 cm PISA ≥1.0 cm No jet detected Incomplete jet envelope Complete envelope, jet density 20%–50% of mitral inflow Complete envelope, jet density 50%–70% of mitral inflow <25 mm Hg 25–30 mm Hg 31–45 mm Hg >45 mm Hg Systolic flow exceeds diastolic flow by ≥50%

1 Systolic flow exceeds diastolic flow by <50% 2 Diastolic flow > systolic flow 3 Systolic flow reversal Left atrial 0 None enlargement 1 Mild 2 Moderate 3 Severe The mitral regurgitant index = total score/number of variables CW, continuous wave Doppler ultrasonography; PISA, proximal isovelocity surface area. From Thomas L, Foster E, Hoffman JIE, et al: J Am Coll Cardiol

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1999;33:2016–2022. the hemodynamic impact as well as characteristics of the regurgitant jet (Table 17-1) .[133] The same regurgitant volume may be associated with changing valve structure and varying degrees of chamber dilation and function. Furthermore, echocardiographic signs of severe chronic regurgitation may not be applicable in the acute setting. Although volumetric and proximal isovelocity surface area methods have been validated both clinically and experimentally, these methods are rarely applied in routine clinical practice because they are time consuming and highly dependent on operator experience. Indirect TABLE 17-2 -- Proposed Doppler Criteria for Identifying Severe Valvular Regurgitation by the Transesophageal Approach Mitral Regurgitation Jet area/left atrium area >40% Regurgitant fraction >40% Vena contracta width >5.5 mm Systolic pulmonary vein flow reversal Present Aortic Regurgitation Vena contracta width >12 mm Pressure half-time of regurgitant flow <350 msec End-diastolic flow velocity in the descending aorta >18 cm/sec Modified from Tribouilloy C, Shen WF, Leborgne L, et al: Éur Heart J 1996;17:272–280.

TABLE 17-3 -- Summary of Echocardiographic Methods to Quantify Valvular Regurgitation Method Doppler color flow mapping

Volumetric Doppler

Limitations Jet area represents velocity not volume and is influenced by driving pressure, receiving chamber compliance, regurgitant orifice size, and instrument factors. Underestimation of severity occurs with eccentric jets. Accurate in experienced hands, yet time consuming. Greatest measurement of mitral or

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aortic cross-sectional area. Requires competent valve to measure forward stroke volume. Pulmonary venous In addition to severe MR, systolic-to-diastolic flow pulmonary flow ratio may be influenced by other variables, such as LV function, LA compliance, atrial fibrillation, mitral stenosis, loading conditions, sampling of left vs. right pulmonary vein. AR pressure half-time Both markers are less reliable when systemic and deceleration slope vascular resistance is altered or in the presence of LV dysfunction with significant overlap of values for varying degrees of AR severity. Aortic diastolic flow Related to regurgitant volume and aortic reversal compliance. Proximal flow Relies on hemispheric geometric assumptions. convergence Requires selection of optimal aliasing velocity and identification of the orifice for precise measurement of the radius. Overestimation of flow is observed with eccentric jets. Vena contracta width Simple and accurate but requires optimal axial resolution and imaging plane for clear definition. Limited with rapidly divergent jets and overlap in lesion severity between 3–5 mm. Momentum Measures flow rate and ROA from a single velocity profile across an axisymmetric jet. Validated in vitro but rarely used clinically. Not applicable to eccentric jets. Amplitude-weighted Nonvolumetric method for calculating ratio of flow mean velocity based on the amplitude of the Doppler signal. Requires special software. Three-dimensional Reveals the complex geometry of regurgitant echocardiography lesions. Requires stable positioning of transducer and patient during image acquisition, which may be time consuming. AR, aortic regurgitation; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; ROA, regurgitation orifice area.

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markers are affected by other variables and should not be used in isolation to determine regurgitant severity (Table 17-2) . Although there are many proposed echocardiographic methods to quantify valvular regurgitation (Table 17-3) , the main limitation has been the lack of a true gold standard for comparison.[27] [134] The challenge to future investigations in this area is to develop a better gold standard for quantifying valvular regurgitation by extracting more reproducible yet accurate spatial, temporal, and velocity information from color Doppler imaging.

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389

Chapter 18 - The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation David J. Meier MD Carolyn K. Landolfo MD Mark R. Starling MD

The optimal timing of surgical intervention in patients with chronic mitral and aortic regurgitation remains controversial and challenging. Historically, mitral and aortic regurgitation have been considered hemodynamically equivalent as conditions of left ventricular (LV) volume overload.[1] Although mitral regurgitation is a condition of primary LV volume overload, aortic regurgitation generates both a pressure and a volume overload on the left ventricle. In both conditions, preload is elevated because of excess volume, resulting in the development of eccentric hypertrophy. In aortic regurgitation, however, afterload is also increased secondary to LV pressure overload, resulting in the development of concomitant concentric hypertrophy. These fundamental hemodynamic differences are responsible for the observed differences between mitral and aortic regurgitation in the natural history of the disease processes, mechanisms for LV systolic dysfunction, response to surgery, and the appropriate timing of surgical intervention.

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After a long asymptomatic period, often lasting several years, prolonged mitral or aortic regurgitation inevitably leads to LV pump dysfunction, which is characterized by decreased LV ejection fraction and contractile dysfunction. [2] [3] [4] [5] [6] [7] [8] In assessing LV pump performance in valvular regurgitation, it is important to distinguish between ejection performance and contractile performance of the left ventricle. Left ventricular ejection performance, commonly measured by indices such as ejection fraction and percent fractional shortening, refers to the global pumping capability of the left ventricle. Because LV ejection phase indices are affected by multiple variables, such as contractility, heart rate, preload, and afterload, an abnormal LV ejection fraction does not necessarily imply abnormal contractility. Likewise, LV ejection fraction may be normal, despite significant underlying contractile dysfunction. Left ventricular contractility, on the other hand, refers specifically to the performance of the contractile apparatus of the left ventricle, independent of loading conditions. Although both mitral and aortic regurgitation eventually lead to LV pump dysfunction, the mechanisms underlying decreased LV pump performance differ between the two conditions. Wisenbaugh et al[9] evaluated the hemodynamic characteristics of patients with severe aortic regurgitation (n = 9) and severe mitral regurgitation (n = 8) and compared the findings to those of normal subjects (n = 7) (Fig. 18-1) . Despite a similar volume of regurgitation between the patients with aortic and mitral regurgitation, afterload (end-systolic stress) was found to be significantly increased above control in patients with aortic regurgitation, but not in patients with mitral regurgitation. Conversely, LV contractile dysfunction, measured by the ratio of end-systolic stress to end-systolic volume index, was found to be more depressed in patients with mitral regurgitation than in patients with aortic regurgitation, despite comparable reductions in LV ejection fraction. These data suggest that the mechanism for decreased LV pump performance in aortic regurgitation is afterload excess, in contrast to mitral regurgitation, in which LV contractile dysfunction is the primary mechanism. Because 390

Figure 18-1 The relationship between left ventricular ejection fraction (EF) and end-systolic stress, constructed from the data of Wisenbaugh et al,[9] is illustrated for normal subjects and patients with mitral (MR) or aortic (AR) regurgitation. End-systolic stress or afterload is increased only in the AR group. (From Devlin WH, Starling MR: Cardiol Rev 1994;3:16–28.)

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of the favorable loading conditions in mitral regurgitation, however, ejection phase indices of LV systolic performance often remain normal, thereby masking the severity of LV contractile dysfunction. Although afterload excess is the primary mechanism for LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to decreased LV pump performance, but typically as a late manifestation of severe, prolonged regurgitation.[11] These hemodynamic differences between mitral and aortic regurgitation have very important clinical implications, both in terms of disease progression and in response to corrective surgery. Because afterload excess is responsible for the early decline in LV pump performance in aortic regurgitation, the decrease in afterload that follows aortic valve replacement favors improvement in LV systolic performance, even when preoperative LV ejection phase indices are depressed.[12] [13] [14] [15] [16] [17] Later in the course of the disease, however, significant contractile dysfunction also develops, resulting in progressive and potentially irreversible LV failure. In contrast, contractile dysfunction develops relatively early in the natural history of mitral regurgitation, but it may be masked by the favorable preoperative loading conditions and the compensatory activation of the sympathetic nervous system with resultant beta-adrenergic stimulation.[18] [19] [20] [21] [22] [23] [24] Postoperatively, as loading conditions change with elimination of the regurgitant leak into the low-resistance left atrium, this underlying contractile dysfunction becomes unmasked, resulting in a decreased in LV ejection fraction.[5] [6] [7] [16] [25] [26] [27] [28] [29] Patients with mitral regurgitation who have even a mildly depressed LV ejection fraction preoperatively often have severe contractile dysfunction and are, therefore, at risk for significant LV systolic dysfunction, congestive heart failure, and death in the postoperative period.[4] [5] [6] [7] [8] However, in patients with occult contractile dysfunction marked by a mildly elevated end-systolic dimension in the presence of a normal LV ejection fraction, recovery of contractile function often does occur postoperatively.[30] Thus, these data highlight the clinical imperative in mitral regurgitation to identify early, occult, but potentially reversible contractile dysfunction to optimize the long-term results of mitral valve surgery. This is important because there appear to be two populations of patients: those in whom contractility improves and those in whom contractility does not improve following mitral valve surgery.

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Therefore, because reduced LV ejection fraction reflects more severe contractile dysfunction in mitral compared with aortic regurgitation, a greater degree of preoperative LV pump dysfunction is tolerated without adverse clinical outcome in aortic regurgitation, provided that the duration of LV pump dysfunction is brief. Prolonged LV pump dysfunction reflects severe contractile dysfunction in both mitral and aortic regurgitation and is associated with an adverse postoperative outcome. The ability to identify contractile dysfunction and correct the regurgitant lesion before contractile dysfunction becomes irreversible is critical to the timing of surgical intervention for both regurgitant valve lesions. Although contractile dysfunction is the mechanism for the early decrease in LV ejection fraction in mitral regurgitation, the type of operation performed also significantly affects the degree of postoperative LV pump dysfunction. [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] LV ejection fraction almost always declines after conventional mitral valve replacement with removal of the submitral apparatus, even when preoperative indices of LV pump performance are normal.[31] [32] [33] [36] [37] This decline of LV ejection fraction has been attributed to an alteration in LV geometry resulting from transection of the chordae tendineae and removal of the papillary muscles. Conversely, LV ejection fraction is not decreased to the same extent after mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] , [40] Therefore, because mitral valve reconstruction preserves LV pump performance and can be performed with a low operative morality rate and low risk for thromboembolism and endocarditis, earlier surgical intervention has been advocated in all patients in whom valve repair is feasible, particularly those with reduced LV pump performance. [42] The major challenge in the management of patients with valvular regurgitation is the ability to identify contractile dysfunction and to correct the regurgitant lesion before irreversible contractile dysfunction develops. The purpose of this chapter is to present the echocardiographic parameters that can be used to guide timing of surgical intervention in aortic and mitral regurgitation. Because LV contractility dysfunction is the most important determinant of survival and postoperative outcome in valvular regurgitation, the primary goal guiding the timing of surgical intervention is assumed to be preservation of contractility. Unfortunately, many noninvasive variables currently used to guide surgical intervention identify patients likely to do poorly after surgery, but they do not pinpoint the onset of occult, reversible contractile dysfunction when timely operative

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intervention would be warranted. [11] [18] , [26] [28] The proposed algorithms presented in this chapter for the evaluation of patients with valvular regurgitation incorporate clinical, hemodynamic, and echocardiographic variables into rational guidelines for 391

appropriate timing of surgical intervention directed toward the long-term preservation of contractility.

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Pathophysiologic Mechanisms Although LV volume overload is the primary hemodynamic abnormality in mitral regurgitation, both pressure and volume overload exist in aortic regurgitation. [1] Significant elevations in preload caused by increased regurgitant volume in both mitral and aortic regurgitation lead to the development of eccentric hypertrophy, characterized by LV enlargement and increased myocardial mass.[2] [3] [20] The degree of hypertrophy is commensurate with the degree of LV dilation, maintaining the ratio of LV mass to end-diastolic volume within the normal range. In addition to eccentric hypertrophy, increased systolic wall stress (afterload) in aortic regurgitation also leads to the development of concentric hypertrophy.[1] [9] The differences in the compensatory mechanisms of the left ventricle to pure volume overload in mitral regurgitation and both pressure and volume overload in aortic regurgitation account for the observed difference in disease progression, changes in LV pump performance, and response to operation. Mitral Regurgitation Acute Mitral Regurgitation.

The pathophysiologic mechanisms underlying mitral regurgitation have been well reviewed by Carabello.[43] [44] Left ventricular ejection fraction increases in acute mitral regurgitation as a result of increased preload and decreased afterload. In acute mitral regurgitation, the left ventricle compensates for the sudden increase in volume by increasing sarcomere diastolic length (preload). Left ventricular end-diastolic volume increases, leading to augmentation of LV stroke work by the Frank-Starling mechanism. In addition to increased preload, systolic ejection of blood through the incompetent mitral valve into the low-impedance left atrium lowers systolic wall stress (afterload). Decreased afterload, in turn, augments ventricular emptying, resulting in reduced end-systolic volume,

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increased total stroke volume, and increased ejection fraction. In acute mitral regurgitation, therefore, the left ventricle compensates for the volume overload by emptying more completely. Chronic Compensated Mitral Regurgitation.

The transition from the acute to the chronic state of mitral regurgitation is characterized by LV enlargement and compensatory eccentric hypertrophy, resulting in an increase in LV end-diastolic volume and mass. The increase in LV end-diastolic volume enables augmentation of total stroke volume, helping to return forward stroke volume toward the normal range. With the development of eccentric hypertrophy, the radius of the left ventricle increases without a significant change in wall thickness, increasing wall stress into the normal range, in accordance with the law of Laplace. As wall stress increases into the normal range, LV emptying decreases and endsystolic volume increases. In the compensated phase, therefore, the increase in LV end-diastolic volume produced by increased preload and the increase in end-systolic volume result in an ejection fraction that is within the normal range, but less than that of the acute stage. Chronic Decompensated Mitral Regurgitation.

As a result of these compensatory mechanisms and the stimulation of the sympathetic nervous system, patients with chronic mitral regurgitation may remain asymptomatic for long periods of time and LV ejection phase indices may remain normal, despite underlying contractile dysfunction. Eventually, contractility declines beyond the compensatory capabilities of the left ventricle and the sympathetic nervous system.[24] With LV decompensation, ejection fraction decreases because of an increase in endsystolic volume. Left ventricular end-diastolic pressure increases, resulting in further eccentric hypertrophy and LV dilation. With progressive increases in the radius of the left ventricle, wall stress increases above normal, resulting in a significant increase in end-systolic volume. A vicious cycle thus evolves, leading to a progressive decline in LV pump performance. Response to Operation.

In compensated mitral regurgitation, correction of the regurgitant lesion results in a decrease of LV end-diastolic volume and end-diastolic dimension into the normal range. Although postoperative end-systolic stress remains normal, LV ejection fraction decreases in nearly all patients

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after mitral valve replacement with removal of the submitral apparatus.[45] Left ventricular ejection fraction generally remains unchanged in patients with compensated mitral regurgitation who undergo mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] [34] , [40] In decompensated mitral regurgitation, there is marked preoperative LV enlargement, elevation in end-systolic wall stress, and decreased fiber shortening. [45] Postoperatively, the left ventricle remains persistently dilated, end-systolic wall stress increases, and ejection fraction declines significantly. Interestingly, in children and young adults, the early postoperative course of LV systolic dysfunction is similar to that in adults, but the long-term occurrence of LV systolic dysfunction is significantly different. In a recent study by Krishnan et al,[46] long-term postoperative LV systolic dysfunction was found to be rare, but it occasionally occurred. Better clinical postoperative results were associated with a shorter duration of mitral regurgitation. Aortic Regurgitation Acute Aortic Regurgitation.

In acute aortic regurgitation, because the normal LV chamber cannot acutely adapt to the large regurgitant volume, forward stroke volume is reduced, resulting in significant elevation in LV end-diastolic pressure.[47] Prolonged regurgitation eventually leads to the development of LV dilation and eccentric hypertrophy.[20] Chronic Compensated Aortic Regurgitation.

In the transition from acute to chronic compensated aortic regurgitation, LV dilation and eccentric hypertrophy accommodate a larger end-diastolic volume. [20] [48] The increased LV end-diastolic volume, in turn, allows for 392

increases in both total and forward stroke volume, thereby returning LV filling pressures to normal. These compensatory mechanisms maintain LV ejection fraction and end-systolic volume within the normal range. In addition, vascular adaptation, as measured by total arterial elastance, has been found to occur in response to chronic aortic regurgitation. This LV-

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arterial coupling occurs in a heterogeneous pattern. In some patients it decreases, thereby maximizing LV work and performance, whereas in others it increases, causing "double loading" of the left ventricle and progressive pump dysfunction. [49] Concentric hypertrophy also develops in aortic regurgitation in response to pressure overload.[1] [9] [20] Unlike mitral regurgitation, in which the excess volume is unloaded into the low-impedance left atrium, in aortic regurgitation, the forward and regurgitant volume must be pumped into the higher pressure arterial system, resulting in an increase in end-systolic pressure and wall stress.[50] In accordance with the Laplace relationship, an increased end-systolic wall stress results in concentric hypertrophy, leading to an increase in wall thickness, returning the ratio of cavity radius to wall thickness to within the normal range. Chronic Decompensated Aortic Regurgitation.

The transition to decompensated aortic regurgitation is characterized by progressive LV dilation and deterioration in LV pump performance resulting from intrinsic contractile dysfunction.[2] [51] At this stage, the left ventricle has reached its limit of compensation and can no longer increase wall thickness to compensate for increases in preload. The ratio of cavity dimension to wall thickness increases, resulting in elevated end-systolic wall stress and afterload mismatch. Total and forward stroke volumes decrease and end-systolic volume increases, resulting in a decline in ejection fraction and elevation in left-sided filling pressures. Response to Operation.

In chronic compensated aortic regurgitation, valve replacement results in a reduction in end-diastolic volume and regression of LV hypertrophy. [16] [17] , [52] [53] [54] [55] [56] [57] Afterload also decreases, resulting in improved LV pump performance, even if LV ejection fraction was reduced preoperatively. In chronic decompensated aortic regurgitation, there is marked LV enlargement, significant elevation in end-systolic wall stress, and decreased LV pump performance.[59] [60] Despite successful valve replacement, LV dilation and hypertrophy persist, end-systolic wall stress remains elevated, and systolic performance remains depressed, indicating the development of irreversible contractile dysfunction.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Assessment of Left Ventricular Function in Valvular Regurgitation Although the pathophysiologic mechanisms differ between the two regurgitant valve lesions, LV pump performance is the most important determinant of survival and postoperative outcome in both mitral and aortic regurgitation. As a result, most of the variables used to predict outcome in valvular regurgitation relate to LV ejection phase indices. How, then, is LV systolic performance best evaluated in chronic valvular regurgitation? Ejection Phase Indices. Left ventricular pump performance is often gauged by indices such as ejection fraction and percentage of fractional shortening. These LV ejection phase indices can be altered dramatically, however, by changes in loading conditions, heart rate, and contractility.[18] Alteration in any one of these factors can change LV ejection fraction without necessarily implicating abnormal contractility as the mechanism.[22] Likewise, LV ejection fraction can remain normal, despite markedly impaired contractility. [26] [28] Because mitral and aortic regurgitation are states of altered load, LV ejection phase indices may not accurately assess contractility in these conditions. End-Systolic Indices. To overcome the limitations of LV ejection phase indices in the assessment of contractile state in valvular regurgitation, investigators have alternatively used load-independent variables.[18] [21] [22] [23] [46] Because preload is elevated in valvular regurgitation, preload-independent variables, particularly the end-systolic indices, are commonly employed to assess contractility in mitral and aortic regurgitation.[19] [61] [62] [63] [64] [65] [66] [67] [68] [69] The endsystolic indices have been classified according to those that measure afterload, including end-systolic stress and end-systolic pressure; and those that indicate LV size, including end-systolic volume and end-systolic

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dimension. The ratio of end-systolic stress (or end-systolic pressure) to endsystolic volume (or end-systolic dimension) are preload-independent indices of contractility that also correct for afterload. The basic principle underlying the use of these indices of contractility is that for a given afterload, a ventricle that can shorten to a smaller end-systolic volume has greater contractility than a ventricle with a larger end-systolic volume. End-Diastolic Indices. End-diastolic indices, including end-diastolic dimension and end-diastolic wall stress (the product of end-diastolic pressure and dimension divided by the wall thickness) have also been used to evaluate LV performance in valvular regurgitaton. [59] [66] Left ventricular end-diastolic dimension increases in valvular regurgitation in response to volume overload. In mitral regurgitation, end-diastolic dimension increases without significant changes in wall thickness, whereas in aortic regurgitation both end-diastolic dimension and wall thickness increase. Progressive increases in enddiastolic dimension and end-diastolic wall stress are suggestive of decompensation in both conditions of valvular regurgitation. Pressure-Volume Relationship. The slope of the LV end-systolic pressure-volume relationship has also been used as a load-independent measure of contractility.[11] [20] [21] , [26] [69] [70] [71] Unfortunately, determination of this slope requires measurement of endsystolic volume at different levels of afterload, typically using pharmacologic stress during cardiac catheterization. In most clinical settings, therefore, the pressure-volume relationship cannot be used as a routine tool for serial assessment of contractility in valvular regurgitation. Importantly, however, it can be used to provide insights into the occurrence of contractile dysfunction that can be translated into better use of ejection phase indices to determine the appropriate timing of surgical intervention, particularly in mitral regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Chronic Mitral Regurgitation 393

Traditionally, surgery for chronic mitral regurgitation has been delayed until the onset of symptoms. Unfortunately, by the time symptoms have developed, severe irreversible contractile dysfunction may already be present. Contractile dysfunction typically develops during the asymptomatic period when ejection phase indices of LV pump performance remain within the normal range. Because survival is reduced in patients with mitral regurgitation who have irreversible contractile dysfunction, current management strategies have been directed toward the timing of surgery to prevent progression to irreversible contractile dysfunction. Advances in detection of occult contractile dysfunction, better knowledge of the preoperative predictors of surgical outcome, reduction in mortality for mitral valve replacement using chordal-sparing techniques, and advances in mitral valve repair are leading to earlier surgical intervention in this population of patients. Etiology The mitral valve apparatus consists of the annulus, the anterior and posterior leaflets, the chordae tendineae, and the papillary muscles. Mitral regurgitation develops from alterations in one or more components of the mitral apparatus. [72] Causes of chronic mitral regurgitation are listed in Table 18-1 .[73] The most common causes of pure isolated mitral regurgitation include myxomatous degeneration (62%) (Fig. 18-2) , ischemia-related papillary muscle dysfunction (30%), infectious endocarditis (5%), and rheumatic disease (3%).[72] Changing Etiology of Mitral Regurgitation.

The spectrum of surgical mitral valve disease has changed significantly

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since the 1970s, with a decline in surgical referral for rheumatic valvular disease and an increase for myxomatous degenerative disease.[74] [75] [76] [77] In one review, TABLE 18-1 -- Causes of Chronic Mitral Regurgitation Mechanism Condition Inflammatory Rheumatic heart disease Systemic lupus erythematosus Takayasu's arteritis Scleroderma Degenerative Myxomatous degeneration of mitral valve leatlets Mitral valve annular calcification Marfan's syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Infectious Bacterial endocarditis Structural Ruptured chordae tendineae Rupture or dysfunction of the papillary muscles Dilation of the mitral valve annulus Hypertrophic cardiomyopathy Paravalvular prosthetic leak Congenital Mitral valve clefts or fenestrations Parachute mitral valve abnormality Adapted from Haffajec CI: Chronic mitral regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown. 1987, pp 111–119. Figure 18-2 (color plate.) Transesophageal echocardiogram in the longitudinal plane (two-chamber view) from a patient with myxomatous degenerative mitral valve disease who presented with a 3-month history of dyspnea. Demonstrated is mitral valve prolapse (A) with a flail posterior leaflet secondary to a ruptured chordae tendineae, resulting in severe mitral regurgitation (B).

rheumatic valvulitis accounted for 46% of all surgically treated cases of

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mitral regurgitation from 1970 through 1974, but only 15% from 1985 through 1989. Conversely, myxomatous degenerative disease accounted for only 37% of cases in the earlier years, but it represented 60% of cases in the latter years.[75] Changes in the etiology of mitral regurgitation have been paralleled by changes in surgical therapy for the disease. The number of valves being repaired has steadily increased, particularly in centers experienced in valve reconstruction. At the Cleveland Clinic, 80% of patients referred for correction of mitral regurgitation in 1988 underwent valve repair (see Chapter 19) .[74] Because of the potential for valve repair, the specific anatomic defect responsible for mitral regurgitation, defined by twodimensional and transesophageal echocardiography, has become an integral part of the evaluation of patients with mitral regurgitation. The potential to repair myxomatous degenerative valves has been further stratified according to the specific anatomic defect. Because operative mortality and overall complication rates are lower with mitral valve repair procedures,[72] [77] the ability to repair a valve favors earlier surgical intervention to prevent development of occult contractile dysfunction. Natural History Importance of Left Ventricular Pump Performance.

394

The natural history of mitral regurgitation is variable and depends on multiple factors, including the volume of regurgitation, LV pump performance, contractile state, and the underlying etiology of the disease.[3] [78] [79] The most important determinant of survival, however, is LV contractile state. Chronic mitral regurgitation represents a state of volume overload in which elevated preload and compensatory eccentric hypertrophy maintain overall LV ejection fraction within the normal range for extended periods of time.[43] [44] In addition, recent evidence suggests that LV pump performance in chronic mitral regurgitation is also maintained by activation of the sympathetic nervous system. Nagatsu and colleagues[24] used a canine model to show that indices of LV ejection and contractile performance could be maintained in the normal or near-normal range by beta-adrenergic stimulation in surgically created chronic mitral regurgitation, despite the

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presence of significant underlying contractile dysfunction.[49] This implied that by the time contractile dysfunction is detected in the absence of betaadrenergic blockade, severe contractile dysfunction is already present. In human subjects, Mehta and colleagues[80] [81] found that the sympathetic nervous system was activated in proportion to the increase in LV endsystolic volume and the reduction in ejection fraction, rather than the severity of mitral regurgitation (Fig. 18-3) . Activation of the sympathetic nervous system was found to increase and was clearly evident at echocardiographic LV end-systolic dimensions of 40 mm or more. Despite the initial compensatory function of beta-adrenergic stimulation in mitral regurgitation, chronic stimulation may have adverse effects on LV contractility. Canine models of surgically created mitral regurgitation have shown that sustained beta-adrenergic blockade resulted in Figure 18-3 The relationship between the extravascular norepinephrine release rates (NE2 ) and echocardiographically determined left ventricular end-systolic dimension (ESD) is shown. Note that sympathetic tone is markedly elevated in mitral regurgitation patients with a left ventricular ESD of greater than 40 mm. (From Mehta RH, Supiano MA, Oral H, et al: Am J Cardiol 2000;86:1193–1197.)

improved LV pump performance. This effect was associated with an improvement in cardiocyte contractility secondary to an increased number of contractile elements in isolated cardiocytes.[82] These compensatory mechanisms allow patients to remain asymptomatic for many years. Eventually, a transition phase ensues, during which time insidious contractile dysfunction begins to develop. During this transition phase, however, patients generally remain asymptomatic or are just beginning to develop mild symptoms of fatigue. The development of atrial fibrillation often heralds the onset of this decompensation.[83] [84] By the time patients become overtly symptomatic, with exhaustion, decreased exercise tolerance, and congestive heart failure, severe irreversible contractile dysfunction may have already developed.[3] , [78] It is important to understand that, despite significant and potentially irreversible contractile dysfunction, LV ejection fraction may be reduced to only 40% to 50%. [26] [28] Right heart failure, characterized by congestive hepatomegaly, ascites, and peripheral edema, may develop late in the course of the disease.[77] [85] Medical versus Surgical Therapy.

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Overall survival in chronic mitral regurgitation appears to be improved with surgical therapy in patients with normal or reduced LV pump performance. Because the natural history of severe mitral regurgitation has been significantly altered by surgical advances, only a few studies exist that directly compare medical with surgical therapy[86] [87] [88] [89] (Table 18-2) . Rapaport[86] studied the natural history of 70 patients with mitral regurgitation treated medically over a 5- and 10-year period. The survival rate at 5 and 10 years was reported to be 80% and 60%, respectively, for patients with isolated mitral regurgitation. Hammermeister et al[87] reported much lower 5- and 9- to 10-year survival rates for 36 medically treated patients at 55% and 22%, respectively. Survival was significantly improved in the 61 patients who underwent mitral valve replacement, with 5- and 9to 10-year survival rates of 72% and 63%, respectively. Delahaye et al[89] also reviewed the outcomes of 216 patients with chronic mitral regurgitation. Actuarial survival at 8 years for the surgical group (n = 116) was 74%, compared with 33% for the medical group (n = 54). For mixed mitral regurgitation and stenosis, survival with medical therapy has ranged from 45% to 65% at 5 years and 27% to 32% at 9 to 10 years. Surgery also improves mortality in this subset of patients, with survival rates reported at 61% to 84% at 5 years and 75% at 9 to 10 years. Although survival is reduced in patients with impaired LV pump performance, overall mortality is improved with surgery compared with medical therapy. [87] Therefore, surgery should not be withheld in patients with chronic mitral regurgitation on the basis of reduced LV ejection fraction. Mitral Valve Replacement Importance of Preservation of the Submitral Apparatus.

Left ventricular ejection fraction frequently decreases after surgical correction of chronic mitral regurgitation, 395

TABLE 18-2 -- Survival in Chronic Mitral Regurgitation: Comparison Surgical Therapy Medical Therapy

Sur

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PATIENTS, Study Condition n MR 70 Rapaport[86] MR/MS 102 Hammermeister MR 36 [87] et al MR/MS 22 99 Munoz et al[88] MR/MS Delahaye et al MR 54

9- TO 10YEAR 5-YEAR SURVIVAL, SURVIVAL, PATIENTS, % % n 80 60 65 32 55 22 61 63 45 33

27

45 45 116

[89]

MR, mitral regurgitation; MS, mitral stenosis. even if preoperative indices of LV pump performance are normal.[16] [25] [29] Traditionally, it was believed that afterload (end-systolic wall stress) was decreased in mitral regurgitation by systolic "unloading" into the lowimpedance left atrium. Correction of mitral regurgitation with elimination of the low-resistance leak into the left atrium was thought to acutely increase afterload, resulting in the decrease in LV ejection fraction observed postoperatively.[29] It is now known that for the majority of patients with severe mitral regurgitation, afterload is normal before surgical correction. Furthermore, changes in afterload are not solely responsible for the observed decrease in LV pump performance after surgical correction of mitral regurgitation. Rather, primary contractile dysfunction, resulting from chronic volume overload, and alterations in LV geometry secondary to removal of the submitral apparatus during conventional mitral valve replacement are also responsible for the post-operative decline in LV pump performance. Conventional mitral valve replacement with transection of the chordae tendineae and removal of the subvalvular apparatus almost always results in a postoperative decline Figure 18-4 Preoperative (PRE) and postoperative (POST) left ventricular (LV) ejection fractions depicted for patients undergoing mitral valve replacement with transection (open squares) and preservation (solid circles) of the chordae tendineae. Data for individual

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patients are represented by smaller symbols; mean ± SEM is represented by larger symbols. Mitral valve replacement with transection of the chordae tendineae resulted in a decrease in LV ejection fraction, but mitral valve replacement with chordal preservation did not. (From Rozich JD, Carabello BA, Usher BW, et al: Circulation 1992;86:1718–1726.)

in global and regional LV ejection fraction, even when preoperative indices of LV pump performance are normal.[90] LV ejection fraction decreases immediately after removal of the subvalvular apparatus[34] and persists over the long term after excision.[89] For the majority of patients, however, this decline in LV ejection fraction does not occur with mitral valve reconstruction[34] [91] [92] or mitral valve replacement with preservation of the chordae tendineae and papillary muscles [31] [33] , [40] (Fig. 18-4) . In addition to preservation of LV systolic performance, postoperative survival and exercise capacity have been shown to improve in patients who undergo mitral valve replacement with chordal preservation.[37] The mechanisms for preservation of LV pump performance after mitral valve replacement with chordal preservation have been defined by Rozich et al[40] using two-dimensional echocardiography. Disruption of the functional components of the submitral apparatus during conventional mitral valve replacement disturbs the continuity between the mitral annulus and LV wall through the leaflets, chordae tendineae, and papillary muscles, resulting in significant increases in end-systolic volume and 396

end-systolic stress. In addition, the ratio of the LV major axis to minor axis dimension decreases significantly, suggesting a loss of LV geometry with assumption of a more spherical shape.[33] [40] [45] Mitral valve replacement with chordal preservation maintains LV systolic performance by preserving LV geometry, resulting in a smaller LV cavity and a decrease in endsystolic wall stress.[35] Although the decline in LV pump performance after conventional mitral valve replacement can be attributed, at least in part, to disruption of LV geometry after removal of the submitral apparatus, underlying contractile dysfunction secondary to long-standing volume overload is still the major determinant of postoperative LV pump dysfunction. Left ventricular pump performance declines postoperatively in patients with significant preoperative LV enlargement, despite mitral valve replacement with preservation of the submitral apparatus. Wisenbaugh et al[93] demonstrated

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that patients with an end-systolic diameter of greater than 50 mm had a poor long-term outcome after mitral valve replacement, despite chordal preservation. Similar data have been reported by Enriquez-Sarano et al[5] for patients undergoing mitral valve reconstruction, with a decline in postoperative LV ejection fraction demonstrated for patients with a preoperative LV ejection fraction of less than 60%. These data confirm the fact that occult contractile dysfunction secondary to long-standing volume overload is an important mechanism for the observed postoperative decline in LV ejection fraction after correction of mitral regurgitation. Mitral Valve Reconstruction Left Ventricular Systolic Performance.

The long-term success of mitral valve reconstruction for mitral regurgitation has been reported in numerous series.[37] [77] [79] , [91] , [94] [95] [96] [97] [98] [99] [100] [101] [102] [103] [104] [105] [106] [107] [108] In addition to preservation of LV geometry, mitral valve reconstruction has been shown to confer additional operative and long-term survival advantages over mitral valve replacement for chronic mitral regurgitation. The reduction in LV pump performance that has been observed after conventional mitral valve replacement has not been observed with mitral valve reconstruction, provided that the preoperative contractile state remains intact (Table 18-3) . TABLE 18-3 -- Preoperative and Postoperative Ejection Fraction: A Comparison of Mitral Valve Repair and Mitral Valve Replacement with Chordal Transection and Preservation

Study Duran et al[91] David et al[33] David et al[31] Goldman et al[34] Hennein et al[37] Sakai et al[92]

Repair, % PREOP POSTOP 47 54 63 63 44 65

49 68

Replacement with Chordal Transection, % PREOP POSTOP 54 47 62 51 55 48 64 40 46 31 64 57

Replacement with Chordal Preservation, % PREOP POSTOP 64 53

65 52

50

54

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Rozich et al[40] 60 63 54 69 Enriquez-Sarano et al[5] Preop, preoperative; Postop, postoperative.

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36 49

63

61

Mortality.

Operative mortality and long-term survival rates are also better after mitral valve repair compared with mitral valve replacement (Table 18-4) . Mitral valve reconstruction has been compared to replacement in several studies. The first large retrospective study was reported by Duran et al [91] in 1980 for 562 patients undergoing mitral valve surgery predominantly for rheumatic heart disease. Operative mortality for the 255 patients undergoing mitral valve repair was 1.9% compared with 11.4% for the 307 patients in the replacement group. Survival at 2 years was better for the repair group (98.3%) than for the replacement group (92.9%), largely due to the differences in operative mortality. Only one prospective trial exists comparing mitral valve reconstruction with replacement. Perier[110] studied 400 patients with mitral regurgitation predominantly of rheumatic origin. Patients were divided into four groups of 100 patients each, with one group undergoing mitral valve repair and the remaining three groups treated with valve replacement using different prostheses. The 7-year survival rate was 82% for the repair group versus 56%, 61%, and 60% for the three replacement groups. Yacoub et al[108] reported long-term results for mitral valve reconstruction versus replacement for the "floppy mitral valve syndrome." Survival rates at 5 and 10 years were 91% and 81%, respectively, for the repair group, versus 81% and 39% for the replacement group. In addition to preservation of LV pump performance, therefore, mitral valve reconstruction also confers a survival advantage over mitral valve replacement. Thromboembolism.

In addition to the decreased operative mortality and increased long-term survival associated with mitral valve repair, the thromboembolic and hemorrhagic complications associated with mitral valve reconstruction are also significantly decreased compared with mitral valve replacement. Several studies have reported that approximately 95% of patients are free from thomboembolic complications at 5 to 10 years after surgery.[111] In contrast, 10% to 35% of patients with mechanical prostheses have thromboembolic events within 5 to 10 years of surgery.[112]

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Hemorrhage.

Because only a minority of patients who undergo valve reconstruction are maintained on chronic anticoagulation therapy, the incidence of significant bleeding complications is also extremely small,[101] [111] in contrast 397

TABLE 18-4 -- Operative Mortality and Long-Term Survival: Mitral Valve Repair versus Replacement Operative Mortality

Long-Term Survival YEARS AFTER

REPAIR, REPLACEMENT, REPAIR, REPLACEMENT, n (%) n (%) OPERATION % % Study Duran et 255 1.8 307 11.4 4 96 81 [91] al 86 3.1 46 7.0 5 91 62 Yacoub [108] et al Oliveira 82 4.9 101 5.0 6 88 68 [106] et al Adebo 21 0 44 6.8 5 85 78 and Ross [96]

100 2.0 100(SE)

13

100(BS) 100(BP) 131 6.1 106

12 12 7.5

7

82

5

92

60(BS) 56(BP) 72

222

4.0

5

76

56

Angell et 112 5.4 72 al[95] 75 4.0 63 Cohn et [97] al

18.1

5/10

90/75

55/40

3.0

3

94

85

Perier et al[110]

Orszulak et al[107] Sand et al

48 0

61(SE)

[94]

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Galloway 280 2.0 169(ME) et al[101] 975(BP) Craver et 65 1.5 65 al[99] Kawachi 43 2.3 48 [103] et al Enriquez- 151 1.3 175 * * Sarano et al[7]

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6.6

5

76

72(ME)

8.5 4.6

4

84

69(BP) 82

8.3

5/8

91/91

82/75

5.7

9

79; EF > 60

71; EF > 60

48; EF < 60 68

50; EF < 60

Enriquez- 44 † 6.8 39 † 30.8 10 52 Sarano et al[5] BP, bioprosthesis; BS, Björk-Shiley; EF, ejection fraction; ME, mechanical; SE, Starr-Edwards. *Age ≤ 75 years. †Age > 75 years.

to relatively frequent episodes of bleeding after valve replacement.[112] Endocarditis.

The risk of endocarditis is also decreased after mitral valve repair compared with replacement. In the series of Duran et al,[91] infectious endocarditis occurred at a rate of 0.4% per year after repair and at 2.2% per year after replacement. Late endocarditis after mitral valve reconstruction is negligible, in contrast to the 3% to 6% incidence after mitral valve replacement. [111] Predictors of Postoperative Outcome and Survival As previously stated, patients with mitral chronic regurgitation who have reduced LV pump performance prior to surgery are at risk for a suboptimal postoperative outcome, characterized by persistent LV systolic dysfunction, congestive heart failure, and death. Presumably, operation in such patients

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is being performed late in the hemodynamic course at a time when severe, irreversible contractile dysfunction has already developed. So, should surgery be performed "prophylactically" in all asymptomatic patients to prevent occult contractile dysfunction? The optimal time for surgery is at the onset of LV contractile dysfunction, justifying the surgical risk, but early enough in the course to be reversible. If it were possible to pinpoint this critical moment in the natural history of chronic mitral regurgitation, then it would be simple to plan the timing of surgery in these patients. Unfortunately, no variable that can be routinely measured in the clinical setting is able to define the precise onset of reversible contractile dysfunction in chronic mitral regurgitation. Several markers, however, have been identified that predict a poor outcome after mitral valve surgery. These variables, in conjunction with those that have recently been identified to predict an optimal outcome, can be used to provide a rational framework for the timing of surgery in this valve disease for the purpose of preservation of contractility. Table 18-5 summarizes the preoperative clinical, hemodynamic, angiographic, and echocardiographic parameters that have been used to predict postoperative outcome in patients with mitral regurgitation. Clinical Predictors.

Among 177 surgically treated patients with mitral valve disease, Hammermeister et al[87] found age to be the only independent predictor of survival after mitral valve replacement. Patients older than 61 years had a 5-year survival rate of 40%, compared with 74% in patients 41 to 60 years old and 87% in patients younger than 40 years. In a study by Phillips et al,[8] patient age was also found to predict survival. Patients younger than 60 years at the time of surgery had a 5-year survival rate of 91%, compared with 72% for those 61 years old or older. In several studies by EnriquezSarano and colleagues,[5] [7] age was also found to be an important predictor of operative morality in patients undergoing mitral valve surgery. Operative mortality in elderly patients (older than 75 years) was 30.8% for valve replacement and 6.8% for valve repair versus 5.7% for valve replacement and 1.3% for valve repair in patients younger than 75 years of age. In addition to age, Enriquez-Sarano and colleagues[5] [6] [7] also found the following clinical variables to be predictive of overall survival, operative mortality, and postoperative LV ejection fraction in patients undergoing mitral valve replacement or reconstruction: creatinine (no level specified), New York Heart Association (NYHA) functional class greater than II, atrial

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fibrillation, and concomitant coronary artery disease. Recently, in a study of 576 consecutive postoperative survivors, Dujardin et al[113] found that preoperative LV ejection fraction (<60%) and concomitant 398

TABLE 18-5 -- Surgery for Mitral Valve Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Clinical Age

Value

NYHA functional class Atrial fibrillation Coronary artery disease Hemodynamic Mean pulmonary artery pressure Cardiac index LV end-diastolic pressure Catheterization LV ejection fraction End-systolic volume index

ES stress

> 60 years > 75 years > Class II

8 5 5–7, 114, 116 5–7 5–7

> 20 mm Hg

4

< 2.0 L/m/m2 > 12 mm Hg

116

≥ 30 mL/m2

116 8 19 4

≥ 50 mL/m2

62

≥ 60 mL/m2

64

< 50%

< 2.6 dyne × 103 /cm2

ES volume index Echocardiography LV ejection fraction

References

mL/m2 < 50% < 60% < 63%

6 7 25

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Fractional shortening End-diastolic dimension End-systolic dimension

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< 31% > 70 mm > 50 mm > 45 mm ≥ 40 mm

69 25 25, 93 6, 7 30 69

End-systolic dimension > 2.6 cm/m2 index End-systolic stress index > 195 mm Hg 69 Doppler-derived LV dP/dt < 1343 mm Hg/sec 118 Radionuclide Right ventricular ejection < 30% 119 fraction ES, end systolic; LV, left ventricular; NYHA, New York Heart Association.

coronary artery disease were each positively associated with postoperative mortality and congestive heart failure. Ramanthan et al[114] likewise found NYHA functional class to be an important predictor of survival in medically treated patients with mitral regurgitation followed for a 4-year period, with mortality rates of 53% and 44% for class III and class IV patients, respectively. Similarly, in a recent study of 478 patients with organic mitral regurgitation corrected surgically, Tribouilloy et al[115] found preoperative functional class III/IV symptoms to be independently associated with decreased immediate and long-term postoperative survival. The excess mortality associated with NYHA class III/IV as compared to class I/II was demonstrated regardless of LV ejection fraction (Fig. 18-5) . These researchers concluded that surgical intervention should be considered when no or minimal symptoms are present in low operative risk patients. Salomon et al[116] retrospectively analyzed multiple patient-related risk factors to determine survival after mitral valve replacement in 897 patients, 240 with mitral stenosis, 352 with mitral regurgitation, and 305 with mixed stenosis and regurgitation. In addition to patient age of less than 60 years, preoperative NYHA class of III or lower, cardiac index of 2.0 or greater, and LV end-diastolic pressure of 12 or less were also found to predict improved perioperative as well as long-term survival. Similarly, Crawford et al[4] found that a mean preoperative pulmonary artery pressure of 20 mm Hg or greater predicted a reduced LV ejection fraction after

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mitral valve replacement. Left Ventricular Ejection Fraction.

Although it does not identify asymptomatic patients with early contractile dysfunction, LV ejection fraction has been used extensively to predict outcome after surgery. As mentioned earlier, Dujardin et al[113] found, in a study of 576 consecutive postoperative survivors of mitral valve surgery, that Figure 18-5 Overall survival is compared between patients in New York Heart Association (NYHA) class I/II and those in class III/IV who had a preoperative left ventricular ejection fraction (EF) of 60% or greater (A) or less than 60% (B). (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1995;91:1022–1028.)

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Figure 18-6 Postoperative survival following mitral valve surgery on organic mitral regurgitation based on patients' preoperative left ventricular ejection fraction is shown. (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1994;90:830–837.)

LV ejection fraction of 60% or greater was associated with improved survival (adjusted risk ratio 0.49) and reduced incidence of congestive heart failure (adjusted risk ratio 0.30). In a study by Enriquez-Sarano et al[7] of 409 patients with isolated mitral regurgitation undergoing mitral valve surgery, preoperative LV ejection fraction was found to be the most important predictor of long-term survival. Survival at 10 years was 72% for patients with a mean preoperative LV ejection fraction of 60% or greater, 53% for patients with an ejection fraction in the range of 50% to 60%, but only 32% percent for those with an ejection fraction of less than 50% (Fig. 18-6) . Enriquez-Sarano et al[6] also reviewed the echocardiographic predictors of postoperative LV pump performance in 266 patients undergoing mitral valve replacement for mitral regurgitation. Independent predictors of postoperative LV pump dysfunction (defined as an ejection fraction of less than 50%) included a preoperative LV ejection fraction of less than 50% or an end-systolic dimension of greater than 45 mm. Postoperative LV pump

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dysfunction (ejection fraction of less than 50%) was associated with an increased mortality rate evidenced by an 8-year survival rate of 38% in patients with decreased postoperative LV ejection fraction, compared with 69% for patients with a postoperative LV ejection fraction of greater than 50%. In a study of 150 patients undergoing mitral valve replacement for isolated mitral regurgitation, Phillips et al[8] also demonstrated the value of preoperative LV ejection fraction in predicting long-term survival. Fiveyear survival rates for patients with a preoperative LV ejection fraction of 50% or greater, 40% to 49%, and less than 40% were 89%, 71%, and 38%, respectively. These data suggest that by the time LV ejection fraction had decreased to below the lower limits of normal, severe contractile dysfunction had already developed, and recovery was unlikely after surgery. Reduced LV ejection fraction, therefore, identifies patients who are likely to do poorly after surgery, but a normal LV ejection fraction does not distinguish between patients with normal contractility and those with occult early contractile dysfunction, who might benefit from prompt surgical intervention. Crawford et al[4] studied 48 patients with mitral regurgitation and 23 patients with mixed mitral stenosis and regurgitation to determine the role of LV size, pump performance, and clinical status in predicting survival and LV pump performance after mitral valve replacement. Mortality and increased NYHA functional class due to congestive heart failure were significantly higher in patients with mitral regurgitation and a postoperative LV ejection fraction of less than 50% and in patients with mixed stenosis and regurgitation and postoperative LV enlargement, defined by an enddiastolic volume index of greater than 101 mL/m2 . The strongest predictor of postoperative LV ejection fraction was the preoperative ejection fraction. Preoperative predictors of postoperative LV enlargement included an endsystolic volume index of greater than 50 mL/m2 and a mean pulmonary artery pressure of greater than 20 mm Hg. Similarly, Starling[30] studied 15 patients with chronic mitral regurgitation with micromanometer LV pressures and radionuclide angiograms for LV volumes over a range of loading conditions before and 1 year after successful mitral valve surgery. This study demonstrated that LV contractile impairment is reversible in many patients with chronic mitral regurgitation and that the best predictors of this reversibility include a normal preoperative LV ejection fraction and less LV dilation as manifest

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by end-systolic volume (Fig. 18-7) . Thus, following mitral valve surgery for chronic mitral regurgitation, LV contractility improved in those patients with an average preoperative LV ejection fraction of 0.63 ± 0.09 and an end-systolic volume index of 44 ± 12 mL/m2 , whereas it remained abnormal in those patients with an LV ejection fraction of 0.49 ± 0.12 and an end-systolic volume index of 89 ± 28 mL/m2 . This implies that early surgical intervention can preserve LV contractility and portend an excellent long-term outcome in some patients with mitral regurgitation.

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Figure 18-7 The left ventricular (LV) end-systolic pressure-volume relationship (Ees ) both before and after successful mitral valve surgery uncorrected (A) and corrected (B) for LV size is shown. A substantial increase in contractility occurs on the postoperative study compared with the preoperative study in the majority of patients, although a small group of patients shows either a decline or no change in this contractile index. *P < .05. (From Starling MR: Circulation 1995;92:811–818.)

The percentage of fractional shortening has also been used to assess LV pump performance in mitral regurgitation. Zile et al[69] found that a preoperative fractional shortening of less than 31% predicted postoperative congestive heart failure and death after mitral valve replacement in patients with mitral regurgitation. Despite the fact that survival is decreased in patients with reduced LV pump performance, patients with a decreased LV ejection fraction have improved survival with surgery over medical therapy.[87] The 5-year survival rate in patients with a reduced LV ejection fraction (31% to 50%) was 82% with valve repair or replacement, compared with 45% for the medically treated group. The 10-year survival rate was 82% for the repair group, 74% for the replacement group, and less than 20% for medically treated patients. Therefore, despite reduced overall survival in patients with mitral regurgitation and impaired LV pump performance, mitral valve surgery, particularly valve repair, should not be withheld in this subset of patients, as survival is significantly worse with medical therapy alone. End-Systolic Dimension.

Using two-dimensional echocardiography, Schuler et al[25] demonstrated the

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importance of the preoperative LV end-systolic dimension as a predictor of postoperative LV pump dysfunction in 16 patients with mitral regurgitation who underwent conventional mitral valve replacement. Group I consisted of those patients with a normal preoperative LV ejection fraction and mild LV enlargement; group II included those patients with a low normal LV ejection fraction and moderate LV enlargement. Postoperatively, at a mean follow-up of 15 months, group I patients demonstrated a significant decrease in mean echocardiographic LV end-diastolic and end-systolic dimension, a slight decline in LV ejection fraction, and regression of LV hypertrophy. In contrast, group II patients had no significant decrease in LV end-diastolic dimension, an increase in end-systolic dimension, and a marked reduction in LV ejection fraction. A preoperative LV end-diastolic dimension of greater than 70 mm, end-systolic dimension of greater than 50 mm, and LV ejection fraction of less than 55% identified the majority of patients with postoperative LV pump dysfunction and lack of regression of LV hypertrophy. Wisenbaugh et al[93] evaluated the outcome of 66 patients after mitral valve replacement with preservation of the submitral apparatus. At a mean follow-up period of 24 months, postoperative death or severe heart failure were predicted by a preoperative echocardiographic end-systolic dimension of 50 mm or greater. A preoperative LV end-systolic dimension of less than 40 mm identified all patients with an excellent postoperative outcome. The importance of echocardiographic end-systolic dimension in predicting adverse postoperative outcome has also been reported by Enriquez-Sarano and associates[6] [7] for an end-systolic dimension of greater than 45 mm and by Zile et al[69] for an end-systolic dimension index of greater than 26 mm/m2 . Similarly, in a recent study by Flemming et al,[117] 27 patients were evaluated with micromanometer LV pressures, radionuclide angiography, and echocardiographic parameters prior to and at 3 and 12 months after mitral valve surgery. They found that the most predictive echocardiographic indicator of early occult LV contractile dysfunction was an end-systolic dimension of 40 mm or more (Fig. 18-8) . This index was also able to predict a unique response to mitral valve surgery that was characterized by a short-term fall in LV pump performance, but a long-term recovery to normal LV pump performance, possibly because of a recovery of LV contractile function. They concluded that this measure may be useful to separate those with and without early occult LV contractile dysfunction and normal LV pump performance and to identify those patients who may

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benefit from early mitral valve surgery with or without mild symptoms to preserve LV systolic performance. End-Systolic Volume.

Borow et al[19] have evaluated the 401

Figure 18-8 Receiver operator characteristic curves were generated using sensitivity and 100-minus specificity for echocardiographic left ventricular (LV) end-systolic dimension (ESD), fractional shortening (FS), and end-diastolic dimension (EDD) to identify contractile dysfunction in mitral regurgitation (MR) patients with a normal LV ejection fraction. An LV ESD of 40 mm or greater was optimal for identifying patients with MR and a normal LV ejection fraction and early occult contractile dysfunction. (From Flemming MA, Oral H, Rothman ED, et al: Am Heart J 2000;140:476–482.)

role of the preoperative end-systolic volume index as a predictor of postoperative LV pump performance and survival in chronic mitral regurgitation. Abnormal postoperative LV pump performance was predicted by a preoperative end-systolic volume index of greater than 60 mL/m2 . Furthermore, a preoperative end-systolic volume index of greater than 90 mL/m2 predicted increased postoperative mortality. Specifically, four of five patients with an end-systolic volume index of greater than 60 mL/m2 died in the perioperative period, whereas no patients with an endsystolic volume index of less than 60 mL/m2 died of cardiac failure. All patients with an end-systolic volume index of less than 60 mL/m2 achieved NYHA class I or II postoperatively. In the study by Crawford et al,[4] an end-systolic volume index of 50 mL/m2 or greater was similarly found to predict postoperative LV pump dysfunction. End-Systolic Wall Stress.

In addition to an echocardiographic LV end-systolic dimension index of greater than 26 mm/m2 and percentage fractional shortening of less than 31%, Zile et al[57] have also demonstrated that an echocardiographic LV end-systolic wall stress index of greater than 195 mm Hg can be used to predict postoperative congestive heart failure and death after mitral valve replacement for chronic mitral regurgitation.

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End-Systolic Wall Stress/End-Systolic Volume Index.

Variables predictive of reversible LV contractile dysfunction have been identified in mitral regurgitation, but such measurements have required complex invasive hemodynamic protocols. In a study of 21 patients with mitral regurgitation, Carabello et al[64] found that the ratio of end-systolic wall stress to end-systolic volume, a preload-independent index of contractility, was the best predictor of outcome after mitral valve replacement for mitral regurgitation. The end-systolic wall stress to endsystolic volume index was 5.6 in normal subjects, 3.3 in patients with a favorable postoperative outcome (NYHA class II or lower), and 2.2 in patients with an unfavorable postoperative outcome, including NYHA class III or IV symptoms or death. The fact that the absolute value of the ratio of LV end-systolic wall stress to end-systolic volume index was lower in patients with a favorable postoperative outcome than in normal subjects suggests that preoperative contractility was abnormal in this subset of patients with mitral regurgitation, but to an extent that did not adversely affect postoperative outcome. A significant decrease in the LV end-systolic wall stress to end-systolic volume index, on the other hand, appeared to identify a patient group with severe, irreversible contractile dysfunction. The LV end-systolic wall stress to end-systolic volume index may, therefore, be useful in identifying patients with early contractile dysfunction in whom timely operative intervention would be warranted. In a subsequent study, Carabello et al [62] further demonstrated that an endsystolic wall stress to end-systolic volume index ratio of 2.6 or less predicted poor surgical outcome, defined as postoperative death or NYHA class III or IV symptoms. Pressure-Volume Relationship.

Starling et al[26] have demonstrated that the slope of the end-systolic pressure-volume relationship (chamber elastance), a load-independent measure of contractility, can be used to identify occult reversible contractile dysfunction in patients with mitral regurgitation who have a normal LV ejection fraction. Patients with a normal preoperative LV ejection fraction but impaired contractility (reduced elastance) had an initial decline in ejection fraction in the immediate postoperative period, but it improved within 1 year of surgery. In contrast, patients who had both impaired contractility and a reduced ejection fraction preoperatively had persistent postoperative LV pump dysfunction. These data suggested that the combination of abnormal elastance and normal ejection fraction can identify a patient group in whom contractile dysfunction is present but still

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reversible. In this particular group of patients, prompt surgical intervention is indicated to avoid progression to irreversible dysfunction. Unfortunately, because measurements of elastance require complex hemodynamic protocols, elastance cannot be used as a routine tool for serial assessment of patients with mitral regurgitation. However, the information gained using elastance has helped to interpret the clinical data used to determine the appropriate timing for surgical intervention in patients with mitral regurgitation. In a preliminary analysis of patients with mitral regurgitation and normal LV ejection fraction, patients with impaired contractility could be separated from those with normal contractility on the basis of echocardiographic indices of LV size and performance.[117] An LV end-systolic dimension of greater than 40 mm approximated a reasonable separation of these patients and may, therefore, represent a reasonable surrogate for the elastance concept in patients with mitral regurgitation. Doppler-Derived dP/dt.

The spectral velocity pattern of mitral regurgitation obtained by continuous wave Doppler echocardiography can also be used to assess LV systolic performance in mitral regurgitation. The spectral velocity curve represents the instantaneous pressure difference between the left ventricle and the left atrium. When systolic performance is reduced, the rate of rise of LV 402

Figure 18-9 Spectral Doppler signal of mitral regurgitation from a patient with depressed left ventricular function, demonstrating a slow rate of acceleration to peak regurgitant velocity, reflecting a low dP/dt. The dP/dt is estimated from the time interval (dt) required for the mitral regurgitant velocity to rise from 1 to 3 m per second. In this case, the dP/dt measured 800 mm Hg per second.

pressure is decreased, resulting in a concomitant decrease in the rate of increase in the velocity of mitral regurgitation. The slope of the mitral regurgitant velocity curve, designated as dP/dt, is decreased when LV systolic performance is decreased (Fig. 18-9) . Pai et al [118] studied the Doppler-derived index of the rate of LV pressure rise (dP/dt) in 25 patients with mitral regurgitation before and 6.5 weeks after mitral valve surgery. The LV dP/dt was found to be the best independent predictor of postoperative LV ejection fraction. A preoperative dP/dt of 1343 mm Hg

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per second or less predicted a postoperative ejection fraction of 50% or less. Right Ventricular Ejection Fraction.

Hochreiter et al[119] assessed the prognostic importance of right ventricular ejection fraction in 35 medically treated and 21 surgically treated patients with chronic mitral regurgitation. Patients with a right ventricular ejection fraction of 30% or less had a markedly reduced 4-year survival rate (18%) when treated medically compared with those treated surgically (84%). Left Atrial Size.

Reed et al[120] studied the role of left atrial size in predicting postoperative outcome in 176 symptomatic patients who underwent mitral valve replacement with a mean follow-up of 3.8 years. An abnormal left atrial size index (defined as the product of the major and minor atrial dimensions measured in the apical four-chamber view) was found to predict postoperative death. The left atrial size index, however, predicted mortality independent of LV systolic performance only in patients with a supernormal LV ejection fraction (>75%). Since patients with an LV ejection fraction in this range have an excellent prognosis, regardless of the left atrial size, this index appears to offer no additional prognostic information to LV systolic performance. Timing of Surgery Before discussing a rational approach to the proper timing of surgical intervention for chronic mitral regurgitation, the following key points should be emphasized: 1. Chronic severe mitral regurgitation leads to a progressive decline in LV pump performance. 2. Patients may remain asymptomatic with a normal LV ejection fraction for extended periods of time. 3. Occult contractile dysfunction generally develops at a time when patients remain asymptomatic and LV ejection fraction remains normal, and it may be reversible after surgical intervention. 4. Patients with normal LV ejection fraction and occult reversible contractile dysfunction who undergo mitral valve replacement or reconstruction have a favorable long-term prognosis. 5. Patients with LV pump dysfunction and irreversible contractile dysfunction are at risk for postoperative LV systolic dysfunction,

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6.

7. 8. 9.

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death, and congestive heart failure. Although reduced LV pump performance is associated with an overall decrease in long-term survival for patients with mitral regurgitation, survival is improved with surgical therapy compared with medical therapy. Compared with conventional mitral valve replacement, mitral valve reconstruction preserves LV pump performance and reduces mortality and comorbid complications. If feasible, mitral valve reconstruction should be the procedure of choice in patients with reduced preoperative LV pump performance. Long-term postoperative LV pump dysfunction due to mitral regurgitation in children and young adults is rare, but it does occur. However, a shorter duration is associated with improved postoperative results.

Since long-term survival in chronic mitral regurgitation is dependent on the contractile state of the left ventricle, the primary goal of surgical intervention should conceptually be to preserve contractility. All symptomatic patients with mitral regurgitation should be referred promptly for valve repair or replacement. It is often difficult for clinicians to justify referral of asymptomatic patients for surgical procedures that have a finite risk for death, even when the risk is small. The immediate operative and postoperative risks, on the one hand, must be balanced by the risk for progression to severe, irreversible contractile dysfunction and, thus, reduced long-term survival. Table 18-6 presents a proposed algorithm for the timing of surgery in patients with chronic mitral regurgitation, based on a system in which points are assigned to the different clinical variables that normally play a role in the decision-making process. The major components of the decision analysis, depicted in part A of the algorithm, include clinical and hemodynamic parameters, LV size and pump performance, and the feasibility of valve repair. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were selected on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. The ability to repair a valve should be determined based on the anatomic and pathologic defects of the valve as defined by transesophageal echocardiography. The feasibility of valve repair, based on the echocardiographic findings, should then be determined in consultation with a surgeon experienced in valve reconstruction. In general, symptomatic patients with congestive heart

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TABLE 18-6 -- Proposed Algorithm for Timing of Surgery in Patients with Mitral Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size EJECTION * FRACTION, END-SYSTOLIC Feasibility of Valve Clinical DIMENSION, mm Repair Points Symptoms % 0 None > 60 < 40 None 1 I/II 50–60 40–45 Possible 2 III/IV < 50 > 45 Definite Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; recommend clinical and echocardiographic followup at 12 months 2 Borderline; recommend clinical and echocardiographic follow-up at 6 months ≥ 3 Proceed with surgery Part C: Although not essential for decision analysis, additional predictors of adverse outcome, all of which can be measured by twodimensional echocardiography, can also be used to support decisions. Additional Predictors of Adverse Outcome in Aortic Regurgitation † Value Fractional shortening < 31% End-systolic volume index > 30 mL/m2 End-systolic stress index End-diastolic dimension Doppler dP/dt of mitral regurgitant jet Right ventricular ejection fraction

> 195 mm Hg > 70 mm < 1343 mm Hg/sec < 30%

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*Add one point for age > 60 and coronary artery disease; add three points for history of atrial arrhythmias. †Add two points for each predictor present.

failure, decreased exercise tolerance, or atrial arrhythmias should be referred for surgery, regardless of the status of the left ventricle, particularly when mitral valve reconstruction can be performed. Asymptomatic patients with an LV ejection fraction in the low-normal range (<55%) or LV dilation with an end-systolic dimension of greater than 40 mm are likely to have contractile dysfunction and should, therefore, be referred for surgery. Asymptomatic patients with a high-normal LV ejection fraction (>60%) and small (<40 mm) end-systolic dimension can be followed clinically with serial echocardiography every 6 to 12 months for evidence of reduced exercise tolerance, declining LV ejection fraction, or increased end-systolic dimension. Any change from baseline may indicate the onset of contractile dysfunction, and patients should be referred for prompt surgical intervention. Parenthetically, symptoms in patients with chronic mitral regurgitation are sometimes subtle and difficult to elicit. They are normally fatigue, not dyspnea. Based on the outcome data, patients with early symptoms should also undergo surgery even if they do not meet these LV size and performance criteria. Recently, the natural history of chronic mitral regurgitation and its surgical correction were evaluated in children and young adults.[121] Although the early postoperative course of LV pump dysfunction in children parallels the course in adults, children usually demonstrate a late improvement in LV systolic performance. Thus, early surgical intervention in children without symptoms or LV pump dysfunction is not necessary for most children. However, the duration of mitral regurgitation is correlated with outcome; and for those children who will inevitably require mitral valve repair, operative intervention should be entertained prior to the onset of heart failure. Included in the algorithm in Table 18-6 are additional parameters that identify patients at high risk for contractile dysfunction and, therefore, can be used to strengthen decisions for surgical intervention. Although some of these predictors were validated using nonechocardiographic techniques, all parameters included in this part of the algorithm can be measured using two-dimensional echocardiography. Because more detailed measurements

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and computations are required, most are not included as part of a routine echocardiographic report. These variables are not requisite components of the algorithm and should be considered adjunctive to decision making. Two case studies illustrate how this algorithm can be applied in the clinical setting. The first patient was a 32-year-old aerobics instructor referred for an evaluation of an asymptomatic murmur. Transesophageal echocardiography revealed mitral valve prolapse with a flail posterior leaflet and severe mitral regurgitation. The LV ejection fraction measured 65%, and the end-systolic dimension measured 38 mm. Using step A of the algorithm, this patient would be given a total of 2 points, based on the high feasibility of mitral valve repair. Given the normal LV end-systolic dimension and the high-normal ejection fraction, the possibility of occult contractile dysfunction in this patient was thought to be very small; therefore, surgery was deferred in this patient with follow-up performed 404

every 6 months. At 1-year follow-up, although the patient remained asymptomatic, the LV ejection fraction had decreased to 60% and the endsystolic dimension had increased to 42 mm, suggesting the onset of early contractile dysfunction. This patient was then referred for successful mitral valve reconstruction. The second patient was a 50-year-old woman with a history of rheumatic heart disease who presented with atrial fibrillation. Echocardiography revealed an LV ejection fraction of 55%, mild mitral stenosis with mild leaflet thickening, and severe mitral regurgitation. According to the proposed algorithm, the development of atrial fibrillation and the LV ejection fraction of 55% resulted in a total of 3 points, justifying operative intervention. Mitral valve repair in this particular case of rheumatic mitral regurgitation was considered possible but not definite; hence, this patient was referred for possible valve repair to be followed by valve replacement if reconstruction was unsuccessful.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Chronic Aortic Regurgitation Despite significant volume and pressure overload on the left ventricle, patients with aortic regurgitation typically remain asymptomatic for extended periods of time.[122] Symptoms of dyspnea, orthopnea, nocturnal angina, and syncope develop relatively late in the course of the disease. Aortic valve replacement has clearly been shown to prolong survival and improve functional class in patients with severe symptoms.[12] [123] [124] The optimal timing for valve replacement in asymptomatic or minimally symptomatic patients, however, is less concrete. Progression to contractile dysfunction may precede symptom onset; therefore, if symptom onset is used as the sole guide for surgical intervention, a small subset of patients will be at risk for LV dilation and pump dysfunction and, thus, congestive heart failure and death in the postoperative Figure 18-10 The relationship between left ventricular (LV) ejection fraction and total vascular load is shown in aortic regurgitation (AR) patients with normal LV contractility (solid circles) and depressed contractility (open circles). There was a significant difference between the slopes of these two relationships, indicating that in patients with AR and contractile dysfunction, the sensitivity of LV ejection fraction to total vascular load was greater than in patients with preserved contractility. (From Devlin WH, Petrusha J, Briesmiester K, et al: Circulation 1999;99:1027–1033.)

period.[14] Fortunately, in contrast to mitral regurgitation, LV pump performance often improves postoperatively in patients with aortic regurgitation, even if depressed preoperatively.[1] [17] [125] , [126] Because afterload excess is primarily responsible for the initial decline in LV pump performance in aortic regurgitation, the decrease in afterload after aortic valve replacement favors postoperative improvements in LV systolic performance in the majority of patients. Although developing relatively late in the natural history of the disease, contractile dysfunction also contributes to LV pump dysfunction in aortic regurgitation and is associated with an

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increased risk for postoperative morbidity and mortality. It is also apparent from one recent study[49] that LV loading conditions have a greater effect on LV pump performance in patients with contractile dysfunction compared with those with preserved LV contractility (Fig. 18-10) . So, should prophylactic aortic valve replacement be performed to preserve LV contractility? The benefits of preserving contractility, on the one hand, must be weighed against the immediate operative risks and the potential for bleeding, thromboembolism, and endocarditis associated with prosthetic valves.[127] [128] Ideally, to justify the surgical risk, the appropriate timing of surgery in patients with aortic regurgitation is at the onset of LV pump dysfunction, yet early enough to avoid the development of irreversible contractile dysfunction. Etiology Aortic regurgitation results from primary pathologic abnormality of the aortic valve leaflets (Fig. 18-11) or of the wall of the aortic root, or a combination of both abnormalities. [129] [130] Aortic root disease accounts for approximately one third of all patients with isolated aortic regurgitation, who ultimately undergo valve replacement. The 405

Figure 18-11 (color plate.) Transesophageal echocardiogram in the longitudinal plane (long-axis view) from a patient who presented with dyspnea on exertion several years after having been treated for aortic valve endocarditis. Demonstrated are focally thickened aortic valve leaflets with prolapse of the leaflets into the left ventricular outflow tract (A), resulting in severe aortic regurgitation (B).

etiology of aortic regurgitation, grouped by the mechanism of regurgitation, is given in Table 18-7 . Natural History of Medically Treated Patients The clinical history of patients with chronic aortic regurgitation is characterized by a long asymptomatic phase, often lasting several decades, followed by a symptomatic phase with a relatively rapid progressive deterioration in clinical status.[86] [131] [132] [133] All patients with aortic regurgitation have reduced survival with medical therapy, with approximately 75% of patients alive at 5 years and 50% alive at 10 years after the initial diagnosis has been made.[79]

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Asymptomatic Patients.

Asymptomatic patients with normal LV pump performance have an excellent long-term prognosis.[61] In a study of 77 asymptomatic patients with a normal LV ejection fraction, 90% of patients remained asymptomatic at 3 years; 81% at 5 years; and 75% at 7 years (Fig. 18-12) . The percentage of patients requiring aortic valve replacement was less than 4% per year. Data suggest that vasodilator therapy with nifedipine reduces LV dilation and hypertrophy in asymptomatic patients with aortic regurgitation who have normal LV TABLE 18-7 -- Mechanisms and Etiology of Aortic Regurgitation Mechanism Inflammatory

Structural

Destructive

Congenital

Condition Rheumatic fever Syphilis Systemic lupus erythematosus Ankylosing spondylitis Reiter's syndrome Behçet's syndrome Takayasu's arteritis Methysergide therapy Unicuspid, bicuspid, quadricuspid valves Annular dilation from aortic aneurysm Sinus of Valsalva aneurysm Fenestrated valve Infectious endocarditis Trauma Aortic dissection Marfan's syndrome Ventricular septal defect Pseudoxanthoma elasticum Osteogenesis imperfecta Mucopolysaccharidoses Ehlers-Danlos syndrome

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Abnormal loading conditions

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Hypertension

Renal failure Adapted from Alpert JS: Chronic aortic regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown, 1987, pp 283–318. systolic performance.[133] [134] [135] [136] [137] [138] [139] [140] Furthermore, these beneficial hemodynamic effects have significantly delayed the need for aortic valve replacement in this subset of patients. Because afterload excess is the primary hemodynamic abnormality leading to LV pump dysfunction in chronic aortic regurgitation, the beneficial unloading effects of nifedipine can be anticipated in this setting. Figure 18-12 The clinical course of 77 asymptomatic patients with chronic aortic regurgitation and normal left ventricular (LV) function is presented from the time of initial diagnosis. Clinical end points include onset of symptoms or development of LV pump dysfunction. (From Bonow RO, Rosing DR, McIntosh CL, et al: Circulation 1981;68:509–517.)

406

In contrast to the excellent long-term prognosis of asymptomatic patients with normal LV pump performance, approximately 66% of asymptomatic patients with impaired LV function are likely to require surgery within 2 to 3 years.[13] [129] [130] Symptomatic Patients.

Severely symptomatic patients with aortic regurgitation have a poor prognosis with medical therapy.[141] [142] [143] Only 4% of patients with NYHA class III or IV symptoms of congestive heart failure are alive at 10 years. Similarly, patients with both symptomatic congestive heart failure and LV pump dysfunction generally die within 2 years without surgical intervention. Patients with right-sided congestive heart failure have a particularly poor prognosis, with less than 10% of patients alive at 4 years. [144]

Natural History of Surgically Treated Patients

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Survival.

Although there have been no randomized trials directly comparing medical therapy with surgery, surgical intervention appears to improve survival and functional class in patients with symptomatic aortic regurgitation. Rapaport [86] reported 5- and 10-year survival rates of 75% and 50%, respectively, for medically treated patients with aortic regurgitation. Operative and inhospital mortality rates for symptomatic patients with chronic aortic regurgitation have ranged from 4% to 10%.[12] [124] [144] [145] Increased operative mortality after aortic valve replacement for aortic regurgitation is associated with advanced functional class (class III or higher), creatinine level greater than 3.0 mg/dL, and atrial fibrillation.[146] [147] Long-term survival after aortic valve replacement for aortic regurgitation is displayed in Table 18-8 . The observed variability in survival with surgery predominantly reflects the year of surgery, improvements in surgical technique in the later years, especially with regard to myocardial preservation using cardioplegic arrest, differences in patient populations, and the presence of concomitant coronary artery disease. Five-year survival rates after aortic valve replacement from studies published in the mid1980s have ranged from 82% to 83%.[12] [68] [148] The 10-year survival rate reported in only one of these studies was 65%.[148] Clinical Improvement.

Aortic valve replacement results in significant relief of symptoms in the majority of TABLE 18-8 -- Survival After Aortic Valve Replacement for Aortic Regurgitation Study Hirshfeld et al[147] Roberts et al[154] Forman et al[123] Clark et al[150] Greves et al[124] Acar et al[144] Louagie et al[148] Bonow et al[12]

Patients, n 3-YEAR 88 55 26 76 90 79 17 61 36 85 126 85 114 90 80 90

Survival Rate, % 5-YEAR 8- TO 10-YEAR. 48 48 65 58 — — — — 85 — 70 49 82 65 83 —

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62

88

83

—

patients.[12] [143] Whereas 70% to 80% of patients will have improvement in functional class, approximately 40% of patients will become completely asymptomatic. In contrast to the situation for chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation demonstrate clinical improvement, despite NYHA class III or IV symptoms of congestive heart failure and a decreased LV ejection fraction.[149] Left Ventricular Pump Performance.

Left ventricular pump performance typically improves after aortic valve replacement with correction of the volume and pressure overload.[14] [58] [150] , [151] Patients with normal preoperative LV ejection fraction generally have normal postoperative LV pump performance and an excellent long-term prognosis.[12] [14] [151] Unlike patients with chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation who have a decreased preoperative LV ejection fraction often demonstrate significant improvements in LV pump performance after correction of the volume and pressure overload.[12] [15] [17] [58] , [63] [151] There is, however, a smaller subset of patients who have persistent LV systolic dysfunction postoperatively, suggesting the presence of irreversible contractile dysfunction.[12] [14] [15] [60] This group of patients has an extremely poor prognosis, with death often occurring from progressive congestive heart failure. Predictors of Outcome and Survival Clinical Predictors.

Several clinical factors, the majority of which indirectly reflect longstanding volume and pressure overload on the left ventricle, have prognostic significance in chronic aortic regurgitation (Table 18-9) . Heart volume, indicated by the cardiothoracic ratio on the chest radiograph, has been shown to predict long-term survival.[126] [144] [152] In one study, patients with a cardiothoracic ratio of 0.58 or greater had a 5-year survival rate of only 48%, compared with 90% for patients with a ratio of less than 0.58. Earlier studies from the 1970s suggested that an age older than 65 years,[144] [153] electrocardiographic evidence of marked LV hypertrophy,[154] [155] NYHA class III or IV,[126] [154] and elevated systolic blood pressure (>140 mm Hg) or decreased diastolic pressure (<40 mm Hg)[156] identified patients at increased risk for postoperative death. In a recent study by Klodas et al [157] comparing postoperative survival in functional class I or II patients with

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functional class III or IV patients, preoperative 407

TABLE 18-9 -- Surgery for Aortic Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Clinical Age Cardiothoracic ratio NYHA functional class Poor exercise tolerance Prolonged LV dysfunction Electrocardiographic evidence of LV hypertrophy Hemodynamic LV end-diastolic pressure Cardiac index Catheterization LV ejection fraction End-systolic volume index Peak systolic pressure/End-systolic volume index Echocardiography Percentage fractional shortening

End-systolic dimension

Value > 65 years ≥ 0.58 ≥ Class III < 8 METs > 18 mo > 18 mo

> 20 mm Hg < 2.5 L/m/m2 < 50% ≤ 45% ≥ 60 mL/m2 ≤110 mL/m2 ≥ 1.72 mm Hg/mL/m2 < 25% < 28% < 29% > 50 mm

References 144, 153 126, 144, 152 126, 153 14, 158 15 147, 156

144 123, 124 123 124 19 62, 168 169

60 66 155 66

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> 55 mm > 60 mm End-systolic dimension index

> 2.6 cm/m2 End-systolic wall stress > 235 mm Hg End-systolic dimension > 80 mm > 72 mm End-diastolic dimension (R) ≥ 3.2 End-diastolic wall thickness (th) ≥ 4.0 LV, left ventricular; NYHA, New York Heart Association.

60 63 59 66 59, 60 66 66 59

functional class III or IV symptoms were found to be independent risk factors for increased early and long-term postoperative mortality, suggesting that the onset of symptoms should warrant a rapid consideration of surgery. This is particularly true for women. Hemodynamic Predictors.

Hemodynamic predictors of adverse postoperative outcome have also been used to stratify patients prior to aortic valve replacement. The 2-year survival rate in patients with a reduced cardiac index ( 2.5 L/m/m2 ) has been reported to be 72%, compared with 94% for those with a normal index.[144] In two other studies,[123] [124] survival rates at 3 and 5 years in patients with a cardiac index of 2.5 L/m/m2 or less were reported to be 63% and 66%, respectively. Elevated LV end-diastolic pressure of 20 mm Hg or greater has also been associated with increased mortality after aortic valve replacement.[144] Indices of Left Ventricular Systolic Performance in Symptomatic Patients Ejection Phase Indices!

Left ventricular pump performance has been shown to be the most important determinant of survival in symptomatic patients with aortic regurgitation. [123] [124] , [153] Forman et al[123] found preoperative LV ejection fraction to be the most important determinant of survival in 90 patients with chronic aortic regurgitation who underwent valve replacement. Patients with an ejection fraction of less than 50% had a poor 3-year survival rate (64%) when compared with those with an LV ejection fraction of 50% or greater (91%). Greves et al[124] similarly demonstrated an adverse outcome

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in patients with a reduced LV ejection fraction secondary to aortic regurgitation, reporting a 5-year survival rate of 54% in patients with an ejection fraction of 45% or less, compared with 87% for those with an ejection fraction of greater than 45%. Duration of Left Ventricular Systolic Dysfunction.

In addition to decreased LV pump performance as an important predictor of adverse outcome in chronic aortic regurgitation, Bonow et al[15] have also demonstrated the impact of the duration of preoperative LV pump dysfunction in determining survival (Fig. 18-13) . Despite comparable reductions in LV fractional shortening and similar exercise tolerance, patients with prolonged LV systolic dysfunction (≥18 months) had a survival rate of only 45%, compared with 100% for patients with a more brief (<14 months) duration of LV pump dysfunction. Percentage of Fractional Shortening.

Percentage of fractional shortening, an ejection phase index of LV systolic performance derived using two-dimensional or M-mode echocardiography, has also been used to predict postoperative death and LV systolic dysfunction in symptomatic patients with aortic regurgitation. Cunha et al [155] found that the postoperative 5-year survival rate was 100% in patients with a fractional shortening of greater than 35 percent, compared with a rate of 91% for a fractional shortening in the range of 31% to 35%, and a rate of 78% for a fractional shortening of 30% or less. In a study conducted by the National Institutes of Health,[14] a fractional shortening of less than 29% was associated with a 3-year survival rate of 62%, compared with 91% for a fractional shortening of 29% or greater. Similar data have been reported for a fractional shortening of less than 25%[60] and of 28% or less. [66]

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Figure 18-13 Survival in aortic regurgitation after aortic valve replacement as a function of the duration of left ventricular (LV) dysfunction, demonstrating significantly reduced survival in patients with prolonged (>18 months) LV pump dysfunction. (From Bonow RO, Picone Al, McIntosh CL, et al: Circulation 1985;72:1244–1256.) Exercise Capacity.

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Preoperative exercise capacity has been shown to provide additional prognostic information to LV pump performance in aortic regurgitaton.[14] [158] Poor exercise tolerance (defined by the National Institutes of Health protocol, equivalent to approximately 8 metabolic equivalents [METs]) also predicts survival in symptomatic patients with aortic regurgitation. The 3year survival rate in patients with preserved exercise capacity was 100%, compared with 52% for patients with reduced exercise tolerance. Exercise capacity further stratifies patients with concomitant LV pump dysfunction into low- and high-risk groups. Decreased exercise tolerance in patients with a decreased fractional shortening (<29%) identified a patient subgroup at significantly higher risk for postoperative LV pump dysfunction and death secondary to congestive heart failure (Fig. 18-14) . Survival at 3.5 years was 32% in this particular subgroup of patients. In addition to exercise capacity, the LV ejection fraction response to exercise has been used to evaluate functional reserve in symptomatic patients with aortic regurgitation.[47] [159] [160] [161] [162] [163] [164] [165] [166] [167] The majority of symptomatic patients with aortic regurgitation have an abnormal LV ejection fraction response to exercise; however, no specific level of reduced exercise performance has clearly been shown to predict survival or LV pump dysfunction in this patient population. Hence, the LV ejection fraction response to exercise in symptomatic patients provides no prognostic information in addition to resting LV ejection fraction and exercise capacity in determining outcome in chronic aortic regurgitation. The difficulty in assigning a specific cut-off level for exercise performance in aortic regurgitation relates to the fact that ejection phase indices of LV systolic performance are highly dependent on heart rate, preload, afterload, and contractility, all of which are altered during exercise.[18] End-Systolic Dimension.

Henry et al[58] prospectively studied 50 patients with symptomatic aortic regurgitation prior to aortic valve replacement to define echocardiographic predictors of adverse postoperative outcome. Left ventricular end-systolic dimension of greater than 55 mm predicted postoperative congestive heart failure and death after aortic valve replacement. The survival rate at 3.5 years was 83% for patients with an end-systolic dimension of less than 55 mm, but only 42% for an end-systolic dimension of greater than 55 mm. Left ventricular end-systolic dimension of greater than 55 mm and a percentage fractional shortening of less than 25% identified a patient group at high risk for adverse outcome, with death occurring in 9 of 13 patients (69%) (Fig. 18-15) . More recently, Carabello et al[63] showed that

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symptomatic patients with impaired LV pump performance and an endsystolic dimension of less than 60 mm have an excellent long-term survival and experience improvement in LV ejection fraction after aortic valve replacement. In patients 409

Figure 18-14 Survival in symptomatic patients with aortic regurgitation and reduced preoperative echocardiographic left ventricular (LV) fractional shortening (<29%) presented as a function of the preoperative exercise capacity. Patients able to complete 22.5 minutes of the National Institutes of Health protocol had significantly improved survival compared with patients with impaired exercise capacity, despite similar reductions in LV function. (From Bonow RO, Rosing DR, Kent KM, et al: Am J Cardiol 1982;50:325– 336.)

with a reduced LV ejection fraction preoperatively, an end-systolic dimension of less than 60 mm correlated with a postoperative ejection fraction of 55%. End-Systolic Volume Index.

Borow et al[19] studied 41 symptomatic patients with mitral or aortic regurgitation and found that a normal preoperative LV end-systolic volume index predicted normal postoperative LV pump performance and improvement in symptoms to NYHA functional class I or II. For the subset of patients with chronic aortic regurgitation, an end-systolic volume index of 90 mL/m2 or greater identified patients at higher risk for postoperative death and persistent LV pump dysfunction. Similar findings were reported by Carabello et al[62] Figure 18-15 The relationship between preoperative echocardiographic left ventricular (LV) fractional shortening and end-systolic dimension in determining prognosis in symptomatic patients after aortic valve replacement for chronic aortic regurgitation is illustrated. The 97% confidence intervals for normal subjects are indicated by the elliptical area. The highrisk area defined by an LV end-systolic dimension of greater than 55 mm and fractional shortening of less than 25% identifies patients at risk for postoperative death. (From Henry WL, Bonow RO, Borer JS, et al: Circulation 1980;61:471–483.)

for an end-systolic volume index of greater than 110 mL/m2 and by Taniguchi et al[168] for an end-systolic volume index of greater than 200

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mL/m2 . In these two studies, the greater degree of preoperative LV pump dysfunction tolerated without adversely affecting outcome has been attributed to improved surgical techniques in more recent years, particularly with regard to myocardial preservation during cardiopulmonary bypass. End-Diastolic Dimension.

Echocardiographic LV end-diastolic dimension has also been used to determine prognosis in aortic regurgitation, but it is less sensitive than endsystolic dimension in predicting postoperative outcome. A preoperative end-diastolic dimension of greater than 80 mm has been shown to identify a subset of patients with severe preoperative LV enlargement at risk for persistent postoperative LV dilation and congestive heart failure.[59] [60] Although it is less useful as a preoperative predictor, a postoperative enddiastolic dimension of greater than 70 mm identified patients at significant risk for postoperative death from congestive heart failure.[60] End-Diastolic Radius–to–Wall Thickness Ratio.

The end-diastolic radius–to–wall thickness ratio, measured by twodimensional echocardiography, has also been used to predict outcome in aortic regurgitation. The ratio of LV dimension reflected in radius (r) to wall thickness (th) at end-diastole is linearly related to the ratio of LV volume to mass and has been used to determine the degree to which mass is appropriate for a given volume. In patients with chronic aortic regurgitation, the degree of LV dilation may exceed the limit of compensatory LV hypertrophy, resulting in significant LV dilation and pump dysfunction and an increase in the r/th ratio. Gaasch et al,[59] in 12 patients with chronic aortic regurgitation who underwent aortic valve replacement, found that a r/th ratio of 4.0 or greater identified all four patients who showed no reduction in LV dimension or mass postoperatively. Similarly, Kumpuris et al [66] demonstrated that a r/th ratio of 3.2 or greater predicted persistent postoperative LV dilation. Pressure-Volume Relationship.

410

The slope of the LV end-systolic pressure-volume relationship is a loadindependent measurement of contractility that is commonly employed to assess contractile state in valvular regurgitation. Starling et al[11] have used the slope of the pressure-volume relationship and the circumferential stress-

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shortening relationship (the ratio of end-systolic stress to ejection fraction) in patients with aortic regurgitation to differentiate reversible from irreversible LV pump dysfunction. As noted previously, although afterload excess is responsible for the early decline in LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to pump failure, but late in the course of the disease. Starling et al[11] demonstrated that the severity of preoperative contractile dysfunction determined recovery of LV ejection fraction. LV pump performance recovered postoperatively in the group of patients with less severe contractile dysfunction, in whom afterload excess predominated, but failed to recover in patients with more severe contractile dysfunction. Unfortunately, measurements of the slope of the end-systolic pressure-volume relationship and circumferential stressshortening relationship require complex, invasive, hemodynamic protocols; therefore, these indices cannot be routinely applied in most clinical settings. However, assessment of contractility using these techniques is important in that it provides the framework for timing of surgery using noninvasive modalities. To simplify the measurement of the end-systolic pressure-volume relationship, the ratio of the peak systolic pressure to end-systolic volume generated from a single point at rest has also been used to demonstrate abnormal contractility in patients with aortic regurgitation.[70] [169] Pirwitz et al[169] found the ratio of peak systolic pressure to end-systolic volume to be the strongest predictor of postoperative outcome in 27 patients with aortic regurgitation and LV dilation with an end-diastolic volume of greater than 60 mL/m2 . A ratio of 1.72 mm Hg/mL/m2 or greater identified all patients with postoperative functional class I or II, whereas a ratio of less than 1.72 identified 31% of patients in class III and 8% (n = 1) of patients who died. Indices of Systolic Left Ventricular Performance in Asymptomatic Patients Ejection Phase Indices.

As previously noted, asymptomatic patients with normal LV pump performance have an excellent long-term survival rate, and less than 4% of patients per year require aortic valve replacement.[61] Asymptomatic patients with impaired LV ejection fractions, on the other hand, have a considerably more aggressive clinical course and should be referred for elective aortic valve replacement to avoid progression to irreversible contractile dysfunction. Several investigators have evaluated the LV ejection fraction response

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during exercise as a way of predicting the onset of resting LV pump dysfunction in asymptomatic patients with aortic regurgitation.[160] [166] [170] Using radionuclide angiographic techniques, Borer et al[160] evaluated 22 asymptomatic patients with aortic regurgitation to assess LV ejection fraction reserve during exercise. Of the 21 patients (95%) with a normal resting LV ejection fraction, 9 patients (43%) had an abnormal LV ejection fraction response to exercise. The authors concluded that exercise-induced LV systolic dysfunction may precede the development of symptoms and abnormal resting LV pump performance and, therefore, may be used to follow patients for clinical deterioration. Although a decrease in LV ejection fraction with exercise may precede the onset of resting LV pump dysfunction in patients with aortic regurgitation, an abnormal exercise response does not necessarily portend a poor surgical or adverse postoperative outcome. End-Systolic Dimension.

To predict the subset of asymptomatic patients with aortic regurgitation likely to develop symptoms or require aortic valve replacement, Henry et al [142] studied 37 asymptomatic patients with serial echocardiograms for a mean of 34 months. The need for subsequent operative intervention was best predicted by the preoperative LV end-systolic dimension.[59] Eighty percent of patients with an end-systolic dimension of greater than 55 mm required surgery within the follow-up period, compared with 20% of patients with an end-systolic dimension of less than 55 mm. Left ventricular end-systolic dimension has also been used to predict asymptomatic patients likely to require aortic valve replacement. No patient with an LV end-systolic dimension of 40 mm or less required aortic valve replacement at 4 years, whereas 65% of patients with an end-systolic dimension of greater than 50 mm required surgery within the follow-up period. Pressure-Volume Relationship.

The slope of the LV end-systolic pressure-volume relationship has also been used to demonstrate abnormal contractility in asymptomatic patients with aortic regurgitation.[70] [71] [167] [171] Schuler et al[71] studied 14 asymptomatic patients with chronic aortic regurgitation and found that the slope of the end-systolic pressure-volume relationship could be used to identify contractile dysfunction in patients with preserved exercise tolerance and a normal LV ejection fraction.

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Timing of Surgery in Chronic Aortic Regurgitation In considering the timing for surgical intervention in these patients, several facts should be re-emphasized: 1. Chronic aortic regurgitation leads to a progressive decline in LV pump performance secondary to afterload excess. 2. Subclinical LV contractile dysfunction may develop when the LV ejection fraction remains normal, although unlike in patients with mitral regurgitation, LV ejection fraction in aortic regurgitation generally improves after valve replacement. 3. Asymptomatic patients with a normal LV ejection fraction have an excellent long-term prognosis with medical therapy. 4. Asymptomatic patients with normal LV pump performance should be treated with afterload reduction to delay the progression of LV dilation and the need for aortic valve replacement. 5. Valve replacement in symptomatic or asymptomatic patients with mild or moderately depressed LV pump 411

performance improves survival over medically treated patients with aortic regurgitation. 6. Severe preoperative contractile dysfunction is associated with persistent LV dilation and pump dysfunction, often resulting in postoperative congestive heart failure and death. 7. NYHA functional class III and IV symptoms are independently associated with increased early and long-term postoperative death. TABLE 18-10 -- Proposed Algorithm for Timing of Surgery in Patients with Aortic Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size Clinical END-SYSTOLIC Exercise EJECTION * Points Symptoms FRACTION, % DIMENSION, mm Capacity † 0 None > 60 < 45 Preserved 1 I/II 50–60 45–55 2 III/IV < 50 > 55 Decreased

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Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; clinical and echocardiographic follow-up at 12 mo 2 Borderline; recommend clinical and echocardiographic follow-up at 6 mo ≥ 3 Proceed with surgery Part C: Although not a requisite part of the algorithm, these additional predictors of adverse outcome can also be used in decision analysis. These variables marked with a double-dagger (‡) can be measured by two-dimensional echocardiography. Additional Predictors of Adverse Outcome in Aortic Regurgitation ‡ Value Percentage fractional shortening < 29% End-systolic volume index > 60 mL/m2 End-systolic wall stress End-diastolic dimension End-diastolic dimension (radius) (R)/End-diastolic wall thickness (th)

> 235 mm Hg > 80 mm ≥ 3.2

*Add one point for age > 65; cardiothoracic ratio 0.58; LV hypertrophy on electrocardiogram. †Preserved = ability to complete at least 8 METs on graded exercise treadmill testing or stable exercise performance; Decreased = inability to complete 8 METs on graded exercise treadmill testing or a decline in exercise performance from an established baseline. ‡Add two points for each additional predictor present.

In aortic regurgitation, the timing of surgery in both asymptomatic and symptomatic patients is relatively straightforward. In general, the majority of symptomatic patients have improved survival, functional class, and LV pump performance with aortic valve replacement; therefore, they should be referred promptly for aortic valve replacement, regardless of the status of LV ejection fraction. Asymptomatic patients with impaired LV pump

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performance have a rapidly progressive course and are likely to develop symptoms and require aortic valve replacement within 2 to 3 years. These patients should be referred for elective aortic valve replacement. Asymptomatic patients who have normal exercise tolerance and preserved LV pump performance can be treated medically and followed closely with serial noninvasive assessments of LV ejection fraction. Left ventricular end-systolic dimension and exercise capacity are parameters that can be used to serially assess asymptomatic patients with aortic regurgitation for the development of LV pump dysfunction. A poor or decreasing exercise tolerance, defined as the inability to complete approximately 8 METs on a graded exercise treadmill test or any decline in LV pump performance from a previously established baseline, may signal the onset of LV decompensation. Similarly, patients who develop a progressive increase in end-systolic dimension likely have contractile dysfunction and, therefore, should be referred for surgery. Given that functional class III and IV symptoms are independent predictors of early and long-term postoperative mortality, patients with class II symptoms should be referred for surgical correction before class III or IV symptoms develop. Table 18-10 presents guidelines in the form of an algorithm for timing of surgery in patients with chronic aortic regurgitation based on a system in which points are assigned to different clinical variables. The major components (part A) of this algorithm include hemodynamic variables, including LV ejection fraction, LV size, and exercise capacity. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were chosen on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. Included in this algorithm (part B) are additional parameters, all of which can be measured using two-dimensional echocardiography, that identify patients at high risk for contractile dysfunction. These parameters may, therefore, be used to confirm a decision to proceed with surgery, but they are not considered requisite components of the algorithm. These variables should be considered only supplemental to the decision-making process. The use of this algorithm to gauge the appropriate 412

timing of surgical intervention in aortic regurgitation is illustrated in the following case study. The patient was a 45-year-old construction worker

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with severe aortic regurgitation secondary to a bicuspid aortic valve. At the time of initial evaluation, the patient was able to complete stage III of a Bruce protocol without symptoms. Echocardiographic LV end-systolic dimension measured 45 mm, and the LV ejection fraction measured 55%. According to the algorithm, the patient would be assigned two points, justifying medical therapy with serial clinical and echocardiographic follow-up. The patient was treated with a vasodilator and followed every 6 months for 1 year, and then yearly thereafter. At 5 years after the initial diagnosis, although the patient remained asymptomatic, echocardiography revealed an increase in the LV end-systolic dimension to 55 mm and a decrease in the LV ejection fraction to 48%, resulting in a total of 3 points. The patient was then referred for successful aortic valve replacement.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Summary After a long asymptomatic period, often lasting several years, severe, chronic mitral and aortic regurgitation eventually lead to reduced LV pump performance. In aortic regurgitation, decreased LV ejection performance is predominantly caused by afterload excess until late in the course of the disease, when contractile dysfunction supervenes. In contrast, contractile dysfunction occurs early in the course of mitral regurgitation, but it is masked by the favorable preoperative loading conditions. For both conditions, the development of irreversible contractile dysfunction is associated with increased risk for postoperative LV pump dysfunction and death from congestive heart failure. To justify the risk of surgery, the ideal timing for surgical intervention in patients with valvular regurgitation is, therefore, at the onset of contractile dysfunction, yet early enough to prevent the development of irreversible contractile dysfunction. Two-dimensional echocardiography, in conjunction with a thorough history and physical examination, provides an accurate, reproducible, and costeffective methodology for the serial screening for the development of contractile dysfunction in patients with valvular regurgitation. In this chapter, all of the major predictors of clinical outcome in valvular regurgitation, including those validated from nonechocardiographic methodologies, have been integrated to create the pathophysiologic framework necessary to develop algorithms for timing of surgical intervention using echocardiographic tools. The proposed algorithms for timing of surgery in patients with chronic mitral and aortic regurgitation guide operative intervention to preserve contractility and thereby improve long-term postoperative outcome and minimize unnecessary risk.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

417

Chapter 19 - Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Brian P. Griffin MD William J. Stewart MD

The advent of transesophageal echocardiography (TEE) and innovations in ultrasound technology have led to progressive improvement in the outcomes of valve surgery, especially mitral valve repair. Echocardiography has been used extensively in the operating room since the early 1980s. It is an essential element of every valve reconstruction operation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Indications for Intraoperative Echocardiography Intraoperative echocardiography has both diagnostic and monitoring functions that are useful in mitral valve repair and other valve-sparing operations. The diagnostic functions are used before cardiopulmonary bypass (prepump) to determine the mechanism and severity of the mitral valvular dysfunction, identify lesions of other valves, and refine the surgical mission. The diagnostic functions are used after cardiopulmonary bypass (postpump) to determine the success of the surgical mission. Intraoperative echocardiography is essential in performing valve repair, aortic homograft, and pulmonary autograft implantation.[1] In addition to its use in valve surgery, the diagnostic function of intraoperative echocardiography also is used in the surgical management of congenital heart disease, [2] [3] hypertrophic cardiomyopathy,[4] [5] reconstruction of the ascending aorta,[6] [7] and many other surgeries (Table 19-1) . [8] The monitoring function of intraoperative echocardiography is used to determine the hemodynamic status of the patient before and after surgery, for assessing intravascular volume, and ventricular contractility. Perioperative monitoring of left ventricular function is important in patients with impaired contractility who are undergoing any kind of cardiac surgery, including myocardial revascularization, [9] [10] and in those with significant cardiac disease undergoing high-risk noncardiac surgery such as reconstructive surgery of the descending thoracic and abdominal aorta[11] [12] [13] (see Chapter 3) . Intraoperative echocardiography also is used to help position intravascular and intracardiac catheters,[14] , [15] including those used for retrograde cardioplegia via the coronary sinus. When postpump echocardiography detects intracardiac air, [16] [17] this can be cleared by further venting of the cardiac chambers to prevent embolization to the coronary blood vessels[18] 418

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TABLE 19-1 -- Indications for Intraoperative Echocardiography Mitral Disease Assess feasibility and success of mitral repair for mitral regurgitation. Assess feasibility and success of commissurotomy for mitral stenosis. Determine need for mitral surgery in patients undergoing revascularization or aortic surgery. Assess presence of disease of other valves or other cardiac structures. Aortic Disease Assess feasibility and success of aortic valve repair. Assess size of prosthesis. Assess feasibility and success of homograft implantation or Ross procedure. Tricuspid Disease Assess need for and feasibility and success of tricuspid repair. Prosthetic Function Determine presence and site of paravalvular leak. Assess perivalvular tissue for abscesses or infection. Assess site and presence of pannus or thrombus. Revascularization Assess regional wall motion and global left ventricular function before and after revascularization. Determine sequence of graft placement. Detect and assess complications of infarction (ventricular septal defect, mitral regurgitation). Surgery on Aorta Assess size and extent of aneurysm. Determine the mechanism and severity of associated aortic regurgitation. Determine presence and complications of aortic dissection. Determine presence and extent of aortic atheroma. Transplantation/Devices

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Assess left ventricular function and suture lines postoperatively. Assess appropriate sizing, function, and hemodynamic changes with ventricular assist devices. Congenital Heart Surgery Determine connections (ventriculoarterial, atrioventricular). Assess systemic and nonsystemic ventricular size and function. Assess anatomy of shunts and valvular anatomy. Monitoring Assess ventricular volume and function. Monitor drug effects on ventricular function. Diagnose presence and location of ischemia. or the brain.[19] In patients who are difficult to wean off cardiopulmonary bypass or who remain hypotensive in the early postoperative period, echocardiography is a useful diagnostic and monitoring tool.[20] [21] More recent indications for intraoperative echocardiography include use in patient selection and monitoring for alternative surgical approaches such as the use of smaller incisions, port access techniques for cannulation, and offpump coronary artery grafting without cardiopulmonary bypass. [22] [23] The most frequent indication for intraoperative echocardiography is the postpump assessment of valve reconstruction surgery to determine whether the desired surgical result has been obtained. The availability of online feedback concerning the adequacy of the surgical result has allowed surgeons to become more innovative in repair techniques. Immediately after valve repair and before the chest is closed, the echocardiographer can determine whether the repair is adequate or if there is residual regurgitation or other complications present, requiring further repair or prosthetic implantation. Making this determination before the chest is closed allows the surgeon to perform further surgical procedures during a second run of cardiopulmonary bypass (a "second pump run") to optimize the surgical outcome. This second pump run eliminates the need for another surgical procedure at a later time, which would require another thoracotomy and create an increased mortality risk for the patient. In one study, 11% of patients undergoing valve surgery had inadequate results based on postpump echocardiographic imaging and required further surgery.[24] In our experience, intraoperative echocardiographic findings require a second pump run in 6% of cases.[1]

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It is axiomatic that all elective patients undergoing cardiac surgery have a full diagnostic work-up and a definite surgical plan before arriving in the operating room. Despite this, there are findings on the prepump echocardiogram that alter management by refining the preoperative diagnosis and the surgical mission. In our unpublished series of 436 consecutive prepump echocardiograms in patients with various valve problems, the surgical procedure was changed in 40 cases (9.2%). In a series of 154 consecutive patients undergoing valvular surgery, 29 patients (19%) had significant new findings by prepump intraoperative echocardiography. These findings changed the operative plan in 14 patients (9%). The changes were more common in mitral than aortic operations. The most frequent additional finding in this study was an increase in the severity of the valvular regurgitation compared with preoperative studies.[24] Even in patients in whom no major change in plan occurred, the prepump echocardiogram provided an updated understanding of the specific valvular anatomy and the mechanism of dysfunction, which helped to refine the surgical technique. These changes result from the improvement in resolution of TEE over preoperative transthoracic echocardiography (TTE) or cardiac catheterization and from changes in hemodynamic conditions or ischemia between the time of preoperative testing and the time of surgery. A 1999 study of 1918 consecutive cases in which intraoperative echocardiography was used showed a very low prevalence (2.5%) of discordant findings by echocardiography compared with operative findings. In only 0.3% of patients were the discrepancies sufficiently severe to warrant a change in the operative procedure. [25]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technique of Intraoperative Echocardiography Intraoperative echocardiography may be performed from either the transesophageal or epicardial imaging windows (Table 19-2) . Transesophageal Echocardiography TEE is the most widely used technique for intraoperative echocardiography. Figure 19-1 illustrates the experience with intraoperative echocardiography at the Cleveland Clinic Foundation from 1984 through 1999. TEE became available in 1987 and progressively supplanted the epicardial route for most studies. Compared with epicardial echocardiography, TEE has the advantage of allowing image acquisition without interfering with the surgical field or procedure. Immediately after induction 419

TABLE 19-2 -- Relative Advantages of Epicardial and Transesophageal Approaches to Intraoperative Echocardiography INDICATIONS

TRANSDUCER ADVANTAGES

Epicardial LVOT gradients; HOCM; congenital, aortic atheroma; TEE impossible or nondiagnostic 3.5–7.5 MHz transthoracic (standard TTE) sector scan Excellent images, especially of LVOT and septum; rapid imaging in emergency

Transesophageal All others

3.5–7.5 MHz transesophageal Does not interfere with sterile field; continuous imaging possible

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DISADVANTAGES Requires plastic covers for May be difficult to sterile preparation of probe; intubate esophagus once patient is draped; interferes with operative field and procedure; imaging occasionally impossible to obtain images (e.g., due to of posterior structures hiatal hernia, air), imaging difficult with prosthetic of anterior structures shadowing; may interfere difficult with hemodynamics; requires >1 person HOCM, hypertrophic obstructive cardiomyopathy; LVOT, left ventricular outflow tract; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. of anesthesia and endotracheal intubation, the TEE probe is inserted and left in place throughout the operation. Although the technique of intraoperative TEE is similar to its use in the echocardiography laboratory, there are additional potential pitfalls. First, it is occasionally difficult to pass the probe, particularly if the patient has been draped and the ether screen has been positioned. Usually, Figure 19-1 Cleveland Clinic Foundation experience with intraoperative echocardiography from 1984 to 1999. The total number of intraoperative echocardiograms per year is shown (bars).

this problem can be overcome using a laryngoscope and direct vision. Inadequate imaging occurs with the transesophageal approach for a number of reasons. Anatomic causes include a hiatal hernia or the presence of an echodense structure such as a mechanical valve prosthesis can cause shadowing of other cardiac structures. With all TEE studies, there is a "blind spot" approximately 2 to 4 cm in size in the middle portion of the ascending aorta caused by interposition of the trachea between the esophagus and the ascending aorta. Interference from electrical apparatus such as electrocautery leads to distortion of two-dimensional imaging and renders spectral and color Doppler signals impossible to interpret. Fortunately, imaging may be resumed once the electrocautery is discontinued. Another potential cause of ultrasonic probe dysfunction in the operating room is the thermistor in the transesophageal probe, which can sense an elevated esophageal temperature and cause the probe to stop

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functioning. This safety feature, designed to minimize the risk of esophageal damage from excess heat buildup in a malfunctioning probe, may deactivate the TEE transducer while the heart is being rewarmed after surgery. Newer probes have a mechanism whereby the probe temperature can be reset to take into account the patient's temperature. Finally, while the heart is on cardiopulmonary bypass, the absence of cardiac motion causes suboptimal images until the heart is filled with blood again and starts to eject during rewarming. Epicardial Echocardiography In epicardial imaging, images of the heart are acquired by placing a standard transthoracic transducer directly on the epicardium. Sterility is maintained using a double plastic sleeve. Intervening air is eliminated by using sterile acoustic gel inside the layers of plastic and by moistening the epicardial surface. An acoustic standoff such as a sterile bag or glove filled with saline is sometimes used if the structures of interest are superficial, in the first centimeter of depth below the probe. Epicardial echocardiography often provides better image quality than TEE of structures such as the ascending aorta, aortic arch, and left ventricular outflow tract, and it is especially accurate in measuring the outflow tract velocities. We use an epicardial approach when images obtained by TEE are inadequate during an open-chest procedure. Similarly, TTE can be used when needed during closed-chest procedures, including most types of noncardiac surgery. In addition, epicardial imaging is needed in infants who are too small for the available TEE probes. In the experience at the Cleveland Clinic Foundation, progressively fewer procedures are performed using an epicardial imaging window. The major current indication for an epicardial approach is in the evaluation of the ascending aorta of patients with suspected ascending atheroma, on the basis of clinical suspicion, calcification on chest x-ray study, or palpation by the surgeon. Identification of the severity and location of atheroma helps the surgical team optimize the location and methods of cannulation, 420

including the use of an alternative cannulation site such as the subclavian artery. In 1987 we described the following four standard imaging windows (Fig. 19-2) to be useful for epicardial imaging:[26]

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1. Parasternal equivalent. The transducer is placed on the most anterior portion of the heart, the right ventricular outflow tract. Image planes are similar to those for transthoracic imaging from the left parasternal imaging window. Both long-axis and short-axis views are obtained. The heart is scanned in the short axis from base to apex. By imaging more medially, the tricuspid valve and right ventricle also may be imaged. 2. Aorta-pulmonary sulcus. The transducer is placed in the sulcus between the pulmonary artery and ascending aorta, with the long side of the transducer against the left side of the ascending aorta. This view provides excellent images of the left ventricular outflow tract, aorta, aortic valve, mitral valve, and left atrium. 3. Subcostal equivalent. The transducer is at the most inferior portion of the thoracotomy incision against the most inferior portion of the right ventricular free wall. The four-chamber view is used to evaluate all four chambers, mitral and tricuspid valves, pulmonary artery, and the systemic veins. Angling medially allows imaging of the venae cavae, atria, and atrial septum. Angling superiorly visualizes the right ventricular outflow tract. Angling laterally brings in the left ventricular apex. 4. Aorta-superior vena cava position. The long side of the transducer is placed against the right side of the ascending aorta, pointing inferiorly and to the left, to image the left ventricular outflow tract and the aortic and mitral valves. This view is the best way to determine left ventricular outflow gradients with the continuous wave Doppler beam parallel to flow. The left atrium is also well seen from this view. Figure 19-2 The four standard positions for epicardial transducer placement. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

The epicardial window allows excellent imaging of intracardiac structures such as the cardiac valves and myocardium. High-velocity jets may be measured by continuous wave Doppler either with an imaging transducer or a stand-alone, nonimaging transducer. The epicardial window also has some disadvantages: 1. It enters the operative field and interrupts the operation itself. For this

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reason, a more limited time is available for imaging. 2. Imaging of structures in the near field may be difficult unless a good acoustic standoff is achieved. 3. Most surgeons and individuals that are accustomed to scrubbing for surgery are not adept at image acquisition with a hand-held transducer or echocardiographic anatomy, which requires a substantial learning curve. 4. If the probe is applied too heavily against the heart, it may cause arrhythmias or transiently interfere with cardiac filling. Equipment Ideally, an ultrasound machine devoted solely to intraoperative echocardiography should be available. In addition to interfacing with transesophageal and transthoracic transducers, the machine should be capable of recording M-mode and two-dimensional imaging and all Doppler modalities. A facility should be available near the operating room for cleaning and disinfecting the probes. Transthoracic probes from 3.0 to 7.5 MHz may be useful for different purposes, depending on the objectives of the study, using the lower frequency for general cardiac imaging and the higher frequency for infant congenital cases and aortic atheroma investigation. A stand-alone continuous wave Doppler probe should also be available. Sterile sleeves and acoustic gel should be available for epicardial imaging. The ultrasonic machine should have a capability for cineloop display and retrieval to compare prepump with postpump images. Videotapes or digital storage media should be available for archival of each study, an important consideration for medical-legal purposes. Cables should be available to input the electrocardiographic signal from the operating room monitoring system into the ultrasound machine. Many institutions have the capability of transmitting images from the operating room to a remote site such as the echocardiography laboratory in order to allow oversight or second opinions to be obtained in selected cases. Increasingly, digital storage of images is possible, which allows rapid retrieval to demonstrate findings to the surgical personnel and facilitates comparison of the preoperative and postoperative images.[27] Personnel Intraoperative echocardiography is a highly demanding technical field requiring specialized personnel skilled in transesophageal and epicardial imaging. This field requires

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421

familiarity with the phases of cardiac surgery and their effects on hemodynamics as manifested by echo and Doppler studies. The American Society of Echocardiography suggests that those learning TEE be in the phase of developing level 3 experience, which is equivalent to experience in performing at least 300 echocardiographic studies. In busy operating rooms in which a large volume of intraoperative studies are being undertaken, an echo technologist or other ancillary support person, working under the aegis of the echocardiographer, can facilitate and improve the efficiency of acquiring multiple studies, some of which may be needed simultaneously. Intraoperative Echocardiography Examination Intraoperative echocardiography should be performed in a standard comprehensive manner so that the acquisition of critical information is not omitted. It is important to do a complete TEE study, using imaging planes that allow good views of each intracardiac valve and chamber as well as the great vessels.[28] The entire prepump examination should be recorded on videotape or digitally to provide a durable record of the examination, especially as a reference for postpump studies and for medical-legal purposes. In cases in which comparison with postpump findings is likely, storing key images in a cineloop facilitates rapid comparison at the end of the operation. In diagnostic (as opposed to monitoring) studies, the structure of interest to the primary surgical mission should first be examined thoroughly in multiple planes, using imaging and Doppler modalities. If the echo study must thereafter be abbreviated because of pressing demands of the surgical agenda or the need to limit anesthetic and cross-clamp time, the primary concern, the raison d'être of the echo study, has at least been addressed. Other structures of interest should then be examined, including long- and short-axis views of all four chambers, all four valves, and the great vessels. The entire aorta should be examined in all cases. We also advocate a routine intravenous contrast injection to look for intracardiac shunting. The number of times the probe is passed through the gastroesophageal junction should be minimized, as should all unnecessary manipulation of the probe, to reduce the risk of mucosal trauma, esophageal tears, and pharyngeal trauma that are reported in a very small percentage of cases.[29] Once the prepump study is completed, a written report of the examination detailing significant findings should be made. Although ultrasound has not

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been demonstrated to cause any significant damage to cardiac structures during prolonged examinations,[29] it is advisable to put the machine on freeze so that no ultrasound energy is transmitted when imaging is not required. After cessation of cardiopulmonary bypass, a second comprehensive examination should be carried out and a second or updated report generated. The intraoperative examination has several aspects that are different from a TEE or TTE study in the outpatient echocardiography laboratory: 1. The echocardiogram is performed simultaneously with the operation; therefore, the room conditions, including the lighting and the space for the machine, may be suboptimal. For example, radiofrequency interference from other machines may mar the quality of images for long periods. 2. The hemodynamic milieu may change quickly, and the echocardiographic appearance may differ from images acquired outside the operating room. Changes in hemodynamics, such as intravascular volume, preload, and afterload, substantially affect the severity of valvular lesions. If necessary, the hemodynamic situation may be manipulated to match "street conditions" in order to determine the true or potential severity of a valvular lesion. 3. The surgeon who requests the intraoperative study may request online interpretation. Care must be maintained to make only diagnoses and conclusions that have been verified by examination from multiple imaging planes under appropriate imaging and hemodynamic conditions.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prepump Intraoperative Echocardiography in Patients Undergoing Valve Repair for Mitral Regurgitation The prepump echocardiogram assessment of mitral regurgitation (Table 193) usually merely confirms findings made previously by preoperative echocardiography or cardiac catheterization. TEE, however, often can improve on the accuracy and resolution of preoperative TTE because of improved resolution of the component structures, the mitral valve and the regurgitant jet. There are four main goals of intraoperative echocardiography in mitral valve disease: 1. To assess the severity of mitral regurgitation and determine the need for mitral valve surgery. 2. To assess the mechanism of mitral regurgitation and determine if a repair rather than prosthetic replacement is feasible and to determine the technique of repair. 3. To determine the presence of other significant valvular 422

disease that may require surgical attention, such as tricuspid regurgitation or aortic valve disease. 4. To assess left and right ventricular function in order to be able to compare with the postpump study. TABLE 19-3 -- Intraoperative Assessment of Repair and Reconstructive Valve Operations Prepump Assess severity of stenosis/regurgitation. Assess mechanism of regurgitation and potential reparability of valve.

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Measure dimensions of annulus, chambers, valves. Assess whether lesions other than the primary lesion require surgery. Determine biventricular function. Postpump Assess severity and mechanism of residual regurgitation/stenosis. Detect systolic anterior motion of the mitral valve and left ventricular outflow obstruction. Determine change in severity of other valve lesions. Assess biventricular function. Detect iatrogenic complications. Severity of Mitral Regurgitation The severity of mitral regurgitation is assessed by intraoperative echocardiography in the same manner as the use of echocardiography for other applications in other parts of the hospital (see Chapter 1) .[30] [31] [32] [33] [34] Several have indicated that the intraoperative assessment of mitral regurgitation agrees with the preoperative assessment by contrast ventriculography or TTE.[35] [36] In patients with ischemic mitral regurgitation, agreement between preoperative studies and the intraoperative assessment is less, possibly because of changes in hemodynamics or the degree of ischemia. One study of patients with ischemic mitral regurgitation showed that in 11% of patients the preoperative and intraoperative assessments of mitral regurgitation severity differed by more than one grade, with discordance occurring in both directions.[37] Discordance was more common in patients with clinical instability or those who received thrombolysis. It is important to remember that mitral regurgitation is dynamic and is affected by loading conditions. Reduction of afterload or intravascular volume at the time of the operation may reduce the true severity of the regurgitation. When less mitral regurgitation is found than expected, the intravascular blood volume should be expanded and systemic vascular resistance increased transiently using repeated boluses of IV phenylephrine. The velocity of mitral regurgitation, and therefore display of its jet by color Doppler, depends on the pressure difference between the left atrium and left ventricle, which is higher with hypertension. The size of the jet in the left atrium is also very sensitive to changes in color gain (directly proportional) and pulse repetition frequency (inversely proportional) (see Chapter 17) .

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The transesophageal imaging window has advantages over epicardial imaging in the assessment of mitral regurgitation. A mitral prosthesis or severe mitral calcification causes acoustic shadowing of the regurgitant jet when the transducer is placed anteriorly, such as in epicardial imaging or TTE. Excellent agreement, however, has been reported between the epicardial and transesophageal approaches in assessing mitral regurgitation. [38]

Semiquantitation of mitral regurgitation on a scale from 0 to 4+[30] [31] is determined based on a weighted average of several criteria: 1. The size of the left atrial flow disturbance, based on the depth of penetration and area of the regurgitant jet in the left atrial cavity assessed in multiple imaging planes; a multiplane probe facilitates this process, especially in eccentric jets. 2. The geometry of the jet; eccentric jets tends to have a higher regurgitant volume than free jets of the same area.[32] 3. The size of the proximal convergence zone, also called the proximal isovelocity surface area (PISA) technique. More severe regurgitation is associated with a larger radius of the proximal flow convergence.[33] Flow convergence can be used to calculate regurgitant flow, orifice area, and volume (see later). 4. The width of the proximal portion of the regurgitant jet on the left atrial side of the orifice is also useful and may be less load sensitive than mapping of the regurgitant jet in the atrium.[39] 5. The pulmonary venous pulsed Doppler tracing. Severe mitral regurgitation often leads to systolic reversal of flow in the pulmonary veins,[34] which is 69% sensitive and 98% specific in predicting a regurgitant orifice area of greater than 0.3 cm2 .[40] Blunting of pulmonary vein flow is somewhat reliable in predicting severe mitral regurgitation for patients in normal rhythm with normal left ventricular function but is unreliable in patients with severe left ventricular dysfunction or atrial fibrillation. A normal pulmonary vein flow pattern is useful in excluding severe mitral regurgitation and predicting a regurgitant orifice area of less than 0.3 cm2 . Importantly, in patients in which the right and left pulmonary vein flow pattern is discordant (23% of patients), the more abnormal pattern is most predictive of mitral regurgitation severity. 6. Quantification of mitral regurgitant volume (RV) from the difference between Doppler echocardiography measurements of antegrade flow through the mitral and the aortic valves. Regurgitant fraction (RF) is

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the proportion of total mitral flow (MF) that is regurgitant: RF (%) = RV/MF Mitral and aortic valve flow can be assessed by the product of annular cross-sectional area derived from echo and velocity derived from pulsed Doppler measurements at the same site. Mitral cross-sectional area is derived from two orthogonal diameters of the annulus, which is elliptic in shape.[41] This method has not been used routinely because of the timeconsuming nature of the measurements required and the ease and general reliability of semiquantitative techniques (see Chapter 17) . Other methods of assessing the severity of mitral regurgitation in the operating room include surgical palpation of the left atrium for the thrill of a mitral regurgitant jet, evaluation of the size of v waves on the left atrial pressure tracing, fluid filling of the arrested left ventricle, and contrast echocardiography. These methods lack sensitivity and are not as reliable or as convenient as color flow Doppler techniques.[36] [42] [43] The size of the regurgitant orifice area can be derived from Doppler echocardiography techniques in the operating room,[44] using either the antegrade flow difference method or the flow convergence method. The maximum regurgitant orifice area is calculated by dividing regurgitant flow rate by the maximum mitral regurgitant flow velocity (Vmax ) obtained from continuous wave Doppler. The regurgitant orifice area is greater than 0.4 cm2 in severe mitral regurgitation and greater than 0.25 cm2 in moderately severe mitral regurgitation. The flow convergence, or PISA, technique analyzes flow proximal (on the left ventricular side) to the regurgitant orifice, assuming a hemispheric shape.[44] [45] In this area, blood accelerates predictably as it moves toward the 423

regurgitant orifice and forms a series of concentric shells of decreasing area and increasing velocity that are depicted clearly as easily measured hemispheres on the color image because of the color aliasing of the accelerating flow. Because the surface area of a hemiellipse can be calculated from 2πr2 for blood flow moving at velocity v and at a radius r from the regurgitant orifice (Fig. 19-3) , flow rate Q can be calculated as

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follows: Q = 2πr2 v The PISA method provides excellent estimation of regurgitant flow when the flow convergence is centrally located, well away from the walls; however, this method overestimates regurgitant flow when the proximal flow is constrained by the left ventricular wall. Use of appropriate correction factors can compensate for this problem.[46] Automated analysis of digital velocity maps in the echocardiographic machine is feasible and has the potential to further simplify this technique.[47] The PISA method of determining the regurgitant orifice area (ROA) may be simplified without significant loss of accuracy. If the aliasing velocity of the color Doppler is set to approximately 40 cm per second and the mitral regurgitation by continuous wave Doppler (Vmax ) is assumed to be 5 m per second (500 cm per second), then the formula becomes

ROA = (2πr2 v)/Vmax ROA

[2(3.14)(r2 )(40 cm/s)]/(500 cm/s)

ROA

250 r2 /500

ROA

r2 /2

This method has particular merit in the operating room where rapid quantification is often helpful. Mechanism of Mitral Regurgitation Assessment of the cause (Fig. 19-4) and mechanism (Fig. 19-5) of mitral regurgitation is of great importance Figure 19-3 (color plate.) Proximal convergence zone of a patient with severe mitral regurgitation. The hemisphere produced by flow at an aliasing velocity of 51 cm per second is shown (arrow). The radius of the hemisphere is 1 cm.

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Figure 19-4 Feasibility of mitral repair by etiology of valve disease at the Cleveland Clinic Foundation. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

in determining the suitability of the mitral valve for repair. Mitral valve repair is most likely in patients with mitral regurgitation due to myxomatous degeneration and is least likely in patients with regurgitation due to endocarditis. Repair is now successful in greater than 90% of all patients with myxomatous disease. The probability of repair, however, is affected by the mechanism of regurgitation, especially whether the posterior leaflet, the anterior leaflet, or both leaflets are involved. Repair is most likely with posterior prolapse or flail, whereas bileaflet involvement and isolated anterior leaflet prolapse reduce the likelihood of successful repair substantially.[48] An Organized Approach to Imaging the Mitral Valve

To adequately assess the pathophysiologic mechanism responsible for mitral regurgitation, it is essential to perform Figure 19-5 Feasibility of mitral valve repair by mechanism of regurgitation in myxomatous mitral valve disease. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.)

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a thorough examination of the mitral valve and mitral apparatus and to determine the origin and geometry of the regurgitant jet. The long-axis imaging planes are best for determining which mitral leaflet is involved. Long-axis views of the mitral valve are obtained by imaging from midesophageal TEE planes. Figure 19-6 shows the "multiplane protractor" with all of the multiplane angles superimposed on the mitral valve. Most basilar long-axis views around the entire multiplane sweep allow portions of both leaflets to be examined individually. At approximately 50 to 60 degrees in most patients, the imaging plane parallel to a line between the commissures, is very useful for determining which portion of the anterior or posterior leaflet is involved. Imaging at a multiplane angle of about 135 degrees cuts perpendicular to this intercommissural line.

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The short-axis views also are useful for determining which portion of the anterior or posterior leaflet is involved. These views may be obtained from either the transgastric short-axis view or the epicardial parasternal shortaxis equivalent view.[49] The posterior leaflet has three divisions or scallops: the medial, middle, and lateral. The anterior leaflet is not segmented but has a central portion known as the bare area between the insertions of the chordae from the anterolateral and posteromedial papillary muscles. In a similar way the posterior leaflet is also supported, about half each by chordae from the anterolateral and posteromedial papillary muscles. The papillary muscles lie below each mitral commissure. The papillary muscles and chordae usually are well visualized from the transgastric long-axis views of the left ventricle using biplane or multiplane probes.[50] In assessing the mitral valve and in providing the results to the surgeon, giving an accurate localization of the abnormality is important. A prospective study of 50 patients used a segmental approach to the mitral valve, breaking each leaflet into three segments, and found that TEE was 96% accurate for localization compared with surgical findings.[51] Other Figure 19-6 The short-axis view of the mitral valve in systole from a transverse transgastric view. The medial and lateral commissures (COMM) and the positions of the medial (MED), middle (MID), and lateral (LAT) scallops of the posterior leaflet are shown. ANT, anterior. (From Stewart WJ; Griffin B, Thomas JD: Am J Cardiol Imaging 1995;9:121–128.) Figure 19-7 Transgastric short-axis view of the mitral valve in a patient with severe prolapse of the middle scallop of the posterior leaflet (arrow). ANT, anterior leaflet.

researchers have shown that localization of the defect to the posterior leaflet by TEE is 78% sensitive and 92% specific in myxomatous disease, with accuracy being least when the medial rather than the lateral or middle scallop is involved.[52] Assessment of the mechanism of mitral regurgitation is performed by analyzing the motion of the valve leaflets with twodimensional echocardiography (Fig. 19-7) and the direction of the regurgitant jet with color flow imaging [53] (Table 19-4) . Three types of leaflet motion (Fig. 19-8) may be associated with mitral regurgitation: (1) excessive motion, as seen with prolapse or flail valve caused by chordal rupture or elongation, (2) restricted motion, as seen in rheumatic disease and papillary muscle infarction, and (3) normal motion, as seen with leaflet perforation and ventricular-annular dilation.

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Intraoperative echocardiography has been shown to be highly sensitive and specific in determining the mechanism of mitral regurgitation in patients undergoing mitral TABLE 19-4 -- Determination of the Mechanism of Mitral Regurgitation from Analysis of Jet Direction and Leaflet Mobility Jet Direction Anterior Posterior

Leaflet Motion RESTRICTIVE NORMAL

EXCESSIVE Prolapse/flail of posterior leaflet Prolapse/flail of anterior leaflet

Restriction of posterior > anterior leaflet Equal restriction of both leaflets

Central

Prolapse/flail of both leaflets

Commissural

Rupture of commissural chordae or papillary muscle

Eccentric origin

Apical tethering from LV dilation Apical tethering from LV dilation, annular dilation

Leaflet perforation or cleft

LV, left ventricular.

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Figure 19-8 Morphology and echocardiographic appearance of normal, excessive, and restricted motion of the mitral valve, each of which can cause mitral regurgitation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

valve surgery. In a study of 286 patients undergoing mitral valve surgery in whom the echocardiography mechanism was correlated with the surgical findings, echocardiography was highly accurate (86%) in determining the mechanism of mitral regurgitation.[53] Echocardiography was least accurate in ascertaining the mechanism of mitral regurgitation in patients with

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leaflet perforation, bileaflet prolapse, or ventricular-annular dilation. Excessive Leaflet Motion.

Excessive leaflet motion occurs with elongation or disruption of any portion of the mitral valve or of the mitral apparatus, including the papillary muscles and chordae. Myxomatous disease, endocarditis, and papillary muscle infarction all can lead to this abnormality. With excessive leaflet motion, the regurgitant jet is directed away from the affected leaflet. Thus, prolapse or flail of the posterior leaflet leads to an anteriorly directed jet (Fig. 19-9) . In bileaflet prolapse, the excessive motion is often asymmetric, and the jet direction is away from the more severely affected leaflet. When the amount of prolapse or flail is completely balanced between both leaflets, a central jet direction occurs. If the chordae to the commissures are ruptured, then a jet originating at the commissures is seen in the transgastric short-axis view. Jets originating at the commissure also are seen in infarction of a papillary muscle, most commonly the posteromedial one.[54] Excess motion with overwhelming mitral regurgitation results when the head of a papillary muscle ruptures in an acute myocardial infarct. This type of rupture may be differentiated from acute chordal rupture by detecting a mass attached to the flail leaflet that is a portion of the muscle and by the appropriate clinical setting (Fig. 19-10) . Precise delineation of which portion of the valve has excess motion is important in planning the surgical repair. Rupture of the posterior chordae is the most common abnormality and is repaired by quadrilateral resection of the posterior leaflet (Fig. 19-11) . Elongation of the chordae is repaired by chordal transfer or by implantation of artificial chordae. Papillary muscle elongation or disruption may be repaired by reimplantation, supporting, or shortening the affected muscle.[48] Postoperative prognosis is best in those with excessive leaflet motion. Restricted Leaflet Motion.

This pattern is seen most commonly in rheumatic disease, but it also can occur in regurgitation from ischemic heart disease, the chronic phase of lupus, or acquired valvular disease caused by certain drugs such as ergot derivatives and anorexigenic drugs such as the fen-phen combination (fenfluramine and phentermine). In rheumatic, lupus, and drug-induced diseases, the leaflets are thickened. If both leaflets are equally affected by the pathologic process, the jet direction is central. More commonly in rheumatic disease, the posterior leaflet is more severely affected than the

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anterior leaflet, and the relatively normal anterior leaflet "over-rides" the restricted posterior leaflet. The direction of the regurgitant jet in this situation is posterior, toward the affected leaflet. The surgical approach to this condition includes débridement of the valve tissue and chordae, commissurotomy, and annuloplasty. This type of repair is more technically demanding and is less often successful. In ischemic heart disease, the posterior leaflet is typically restricted in motion owing to apical displacement of the posteromedial papillary muscle. The displacement results from ischemia or infarction of this papillary muscle or the muscle to which it is attached and which is usually in the perfusion territory of the right or circumflex coronary artery. The leaflets themselves are normal and are not thickened but fail to coapt adequately (Fig. 19-12) . In extreme cases the leaflets may not touch at all. The surgical approach to this problem usually involves placement of an annuloplasty ring to reduce the size of the mitral annulus and coronary revascularization. Use of a figureof-eight or Alfieri stitch either alone or in combination with annuloplasty ring also has been used. The Alfieri 426

Figure 19-9 (color plate.) Posterior leaflet prolapse (A) with severe mitral regurgitation (B) before mitral valve repair and no mitral regurgitation after successful mitral valve repair (C).

stitch effectively converts the mitral valve into a doubleorifice valve by attaching the leaflets at their midpoint. Surgical treatment of ischemic regurgitation with restricted leaflet motion is less successful in that residual regurgitation is often more significant than after myxomatous valve repair. Figure 19-10 Papillary muscle rupture with resulting severe mitral regurgitation. The rupture portion of muscle is seen prolapsing into the left atrium (arrow). Normal Leaflet Motion.

Perforation of the valve leaflet causing mitral regurgitation occurs most commonly because of endocarditis or because of a congenital cleft in the valve. Occasionally it is iatrogenic, after attempted repair. The jet origin is eccentric, arising from the midportion of the leaflets rather than from the coaptation line. The

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Figure 19-11 Quadrilateral resection of the posterior leaflet of the mitral valve with annular ring implantation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.)

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Figure 19-12 Ischemic mitral regurgitation with restricted posterior leaflet motion and posteriorly directed jet of mitral regurgitation.

prejet flow acceleration also may be seen away from the coaptation line, along the affected leaflet. Leaflet perforation may be repaired in some instances by suture closure or with pericardial patch.[55] Normal leaflet motion is commonly seen in patients with mitral regurgitation secondary to left ventricular dilation of any cause, such as disease of other valves, dilated cardiomyopathy, or severe ischemic cardiomyopathy. We have previously termed this category ventricularannular dilation. Ventricular enlargement causes displacement of the mitral coaptation point toward the apex with resultant impaired coaptation. Annular dilation is seen in these patients, but it occurs in proportion to left ventricular dilation, in contrast to myxomatous or rheumatic mitral regurgitation patients whose annulus size is often abnormally large. Annuloplasty with ring insertion is commonly used in the surgical management of these patients. An Alfieri stitch to support the valve also has been used instead of or in addition to the annuloplasty. There has been an upsurge in interest in the surgical management of severe mitral regurgitation in patients with dilated cardiomyopathy. Excellent functional improvement with a relatively low operative mortality has been reported even in selected patients with severe mitral regurgitation and severe left ventricular dysfunction. One study of 248 patients undergoing mitral valve surgery showed that TEE was greater than 90% accurate for definition of the mechanism of regurgitation, localizing the origin of regurgitation, and in detecting a flail segment. TEE was 88% accurate in detecting ruptured chordae. The TEE findings of valve function were highly predictive not only of valve reparability but also of long-term survival, which were independent of age,

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gender, ejection fraction, and coronary artery disease. [56] Other Valve Disease and Biventricular Function During Mitral Repair The severity of aortic and tricuspid valvular disease is assessed by intraoperative TEE using color flow mapping to determine the severity of the dysfunction and the necessity of valve surgery. These decisions should be made preoperatively, but diagnostic information should be refined intraoperatively, as mentioned earlier. Intraoperative diagnosis is particularly important in patients with active endocarditis. Significant tricuspid or aortic regurgitation usually requires operative intervention; however, intraoperative echocardiography tends to underestimate the degree of tricuspid regurgitation because of optimization of the hemodynamics that usually results in a reduction of right-sided pressures and volume. Because the preoperative echocardiogram is generally performed under ambulatory conditions, it is a better guide to decision making with regard to tricuspid valve repair, as opposed to the intraoperative findings alone. Regional and global left ventricular function is best assessed using TEE from long- and short-axis transgastric views and various midesophageal long-axis views. The long- and short-axis views from any epicardial imaging window also show the left and right ventricle well. Right ventricular function is assessed by TEE in the midesophageal 45-degree view at the level of the short axis of the aortic valve, from the midesophageal transverse four-chamber view, or from a longitudinal transgastric view rotated clockwise to obtain a long-axis image of the right ventricle.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Determining the Need for Mitral Valve Surgery in Patients Undergoing Cardiac Surgery for Other Reasons Intraoperative echocardiography increasingly is used to determine the need for a mitral valve operation in patients undergoing aortic valve surgery or revascularization procedures; this is especially true in the assessment of patients in whom the severity of the mitral regurgitation preoperatively is significantly different by cardiac catheterization and echocardiography, when the severity of mitral regurgitation over time is variable (such as in ischemic heart disease), and when the mitral regurgitation is of moderate severity. The following questions must be considered when determining the need for mitral valve surgery in addition to the primary surgery: 1. How severe is the mitral regurgitation? 2. Is there a primary abnormality of the mitral valve (such as a torn chord or prolapse)? 3. Will the mitral regurgitation change as a consequence of the primary operation? 4. Is the valve repairable or is prosthetic replacement necessary? 5. What is the additional risk imposed by the additional mitral valve procedure? The final decision on surgery is made by the surgeon; however, when the surgical objectives are changed in the operating room, telephone consultation with the referring cardiologist is advisable. In many patients, especially those in whom the regurgitation is secondary to ischemia or left ventricular dilation, 428

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the severity of the regurgitation may be variable. Sometimes, the severity of regurgitation detected at the time of operation is different from that recorded preoperatively. Frequently the difference in severity is due to a true physiologic change. Compared with ambulatory conditions, the loading conditions during surgery often entail a lower intravascular volume and less peripheral vasoconstriction, both of which may reduce the severity of valvular regurgitation and reduce stenotic valve gradients. On other occasions this discrepancy reflects the superior ability of esophageal and epicardial echocardiography to visualize mitral regurgitation. When approaching patients whose regurgitation is 2+ or less, we often purposely increase the afterload with multiple boluses of 100 µg of phenylephrine to determine the severity of regurgitation at a mean arterial pressure that is transiently as high as 120 mm Hg. Patients with 3+ or more mitral regurgitation at rest, or during this afterload stress test, are generally considered candidates for a mitral valve operation. The threshold for surgery on the mitral valve also is affected by other factors, including whether there is a primary structural abnormality of the valve. If the valve appears to be repairable, the threshold for surgery is lower, given the relatively low morbidity and mortality associated with repair as compared with valve replacement, whereas the threshold for surgery is higher in patients with valves that are not reparable. In patients undergoing surgery for aortic stenosis, improvement in the severity of the mitral regurgitation can be expected postoperatively. Therefore, the threshold for concomitant mitral surgery is higher.[57] [58] A postpump assessment of the mitral regurgitation is made regardless of whether a surgical intervention on the mitral valve has been performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Postpump Intraoperative Echocardiography in Mitral Repair The most significant indication for intraoperative echocardiography in mitral valve repair (see Table 19-3) is to determine the competency of the repair immediately after cardiopulmonary bypass. If the repair is inadequate, further repair or replacement can be performed immediately during the same thoracotomy. Timing Return of the patient to normal loading conditions is necessary to make valid assessments of valvular performance. It is also best to make valvular assessments after ventricular function has reached its postoperative plateau. The most appropriate time to image after repair is when the patient is off cardiopulmonary bypass, the intravascular volume is replete, and the loading conditions are similar to those in the ambulatory state. Imaging can be initiated after the aortic cross clamp is off and when the left ventricle is at least partially filled, but abnormal findings at this time may result from abnormal left ventricle geometry. The surgeon should not act on these findings unless they are subsequently confirmed by further imaging after the cessation of cardiopulmonary bypass. Intraoperative Findings In most cases, with an experienced surgeon, mitral valve repair leads to a competent mitral valve with mild or no residual mitral regurgitation; however, there are potential complications of mitral valve repair that are readily recognized by postpump intraoperative echocardiography. Many of these complications may not be apparent clinically or may take longer to accurately diagnose without echocardiography. If left untreated, these complications may interfere with the long-term success of the procedure and require early reoperation. Complications seen after mitral valve repair by intraoperative echocardiography are shown in Table 19-5 .

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Incomplete Mitral Repair Significant residual mitral regurgitation is the most common postpump problem detected by intraoperative echocardiography. The incidence of this complication varies with the cause of the valvular regurgitation, the complexity of the repair, the experience of the surgeon, and the threshold of the operative team to accept a suboptimal result. Frequently, if the echocardiographer can define the mechanism of the residual regurgitation, further repair of the valve leads to an improved result with reduction or elimination of mitral regurgitation. In some patients, TABLE 19-5 -- Management of Abnormal Findings on Doppler Echocardiography after Mitral Valve Repair Complication Residual mitral regurgitation

Management Define mechanism. If ≤1 +, accept. If 2 +, give phenylephrine to recheck MR with increased afterload; if >2 +, further surgery is required. Systolic anterior motion with Assess LVOT gradient and MR. LVOT obstruction Increase ventricular volume, stop positive inotropes, and increase afterload. If these measures are not successful, further surgery is needed to revise repair. Dehisced ring or leaflet perforation Another pump run is needed to fix annuloplasty. Residual mitral stenosis Quantify severity. If mean gradient >5 mm Hg or area < 1.5 cm2 , consider further surgery. Significant tricuspid regurgitation If 3 + or more, consider further repair. Regional left ventricular Assess intracardiac air; if not resolved dysfunction after further time on pump, consider coronary bypass. Global (right or left) ventricular Assess volume status, afterload, and dysfunction response to medications. LVOT, left ventricular outflow tract; MR, mitral regurgitation.

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429

further repair is impossible or fails, and the patient requires another pump run to implant a prosthesis. Moderate (2+) or more mitral regurgitation, either at rest or following afterload challenge with phenylephrine as previously described, is generally considered excessive after mitral repair and is an indication for a further surgical procedure. If the regurgitation is mild (1+) or less, then the result is usually accepted, though individual surgeons vary in their willingness to accept even mild grades of regurgitation. The severity of mitral regurgitation detected by immediate postpump intraoperative echocardiography correlates well with angiographic or TTE and TEE estimates of severity obtained later.[59] [60] Rarely, changes in the early postoperative period such as chordal rupture, suture dehiscence, or early postoperative endocarditis may cause acute worsening of the mitral regurgitation. Thus, intraoperative echocardiography is a reliable measure of the severity of mitral regurgitation and the need for further intervention. Other considerations in deciding whether residual mitral regurgitation should be accepted or subjected to another surgical procedure include the mechanism of the mitral regurgitation, the overall condition of the patient, and left ventricular function. Postpump determination of the mechanism of the residual mitral regurgitation helps the surgeon to determine whether a further reparative procedure could lessen the regurgitation and yet conserve the valve. More mitral regurgitation than is usually desirable might be accepted when other surgical procedures such as aortic valve replacement or coronary artery bypass grafting also have been accomplished, particularly in elderly patients or those with significant left ventricular dysfunction. For example, in patients with extensive mitral annular calcification, mitral prosthetic insertion may be technically more difficult and more hazardous for the patient than accepting a 2+ or even 3+ mitral regurgitation.[61] In one study of 100 patients undergoing mitral valve repair, 8% needed a second pump run, and 3% had persistent mitral regurgitation that was greater than 2+. Further repair in all three patients led to an improvement in regurgitation. [35] In another study of 309 patients undergoing mitral valve repair, 26 (8%) had immediate failure and required further cardiopulmonary bypass. Ten of those patients (3.2%) had excessive residual regurgitation. Two of the 10 patients subsequently had mitral prosthetic implantation, and eight had further repair. The further repair

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included chordal shortening in three patients, annuloplasty in four patients, and both procedures in one patient. Residual mitral regurgitation after the second repair was mild or absent in all patients. In this study, inadequate repair was associated with a degenerative cause of the mitral regurgitation and with the absence of an annuloplasty ring implantation at the time of initial repair.[62] In another study, residual mitral regurgitation caused by inadequate repair was seen in 4% of patients immediately postpump. In this study, need for reoperation because of inadequate repair or systolic anterior motion of the mitral valve was more common in patients with anterior mitral leaflet or bileaflet prolapse, as opposed to those with posterior prolapse.[63] Impact on Clinical Outcome The severity of residual mitral regurgitation after mitral valve repair is important for prognosis, as shown by several studies. In one of these studies, moderate or greater mitral regurgitation was associated with a higher incidence of congestive heart failure, repeat valve surgery, or postoperative death.[37] In a study of ischemic mitral regurgitation, residual regurgitation by postpump intraoperative echocardiography was a strong predictor of survival after mitral valve repair.[24] Residual mitral regurgitation in ischemic heart disease, however, correlates more with the degree of permanent contractile impairment rather than the technical success of the repair procedure. In another study, two patients with 3+ mitral regurgitation as determined by postpump intraoperative echocardiography who did not undergo a further pump run at the time of initial surgery required reoperation within 5 days because of hemodynamic instability and the inability to wean off mechanical ventilation.[35] Patients who undergo a second pump run for an initially inadequate repair have an in-hospital complication rate that is similar to that of patients who require a single pump run.[64] In one study, residual mitral regurgitation of 1+ or 2+ did not increase hospital complications when compared with trivial or no regurgitation postoperatively. There was a trend for patients with 1+ or 2+ mitral regurgitation, however, to need more reoperations in late follow-up than those with trivial or no mitral regurgitation.[65]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Other Complications of Mitral Valve Repair Systolic Anterior Motion of the Mitral Valve Significant left ventricular outflow obstruction caused by systolic anterior movement of the mitral valve (SAM) has long been recognized as a complication of mitral valve repair.[66] [67] This abnormality simulates that seen in hypertrophic cardiomyopathy, even though septal hypertrophy is absent. Similar to outflow obstruction in hypertrophic cardiomyopathy, SAM after mitral repair is dynamic and exacerbated by reducing the size of the ventricular chamber or augmenting the contractile state. SAM may cause pressure gradients of 100 mm Hg or more, severe hypotension, severe mitral regurgitation, and inability to wean the patient from cardiopulmonary bypass. Fortunately, this series of complications is readily recognized and quantified by an experienced echocardiographer on the postpump echocardiogram study (Fig. 19-13) . SAM has been reported in 2% to 9% of patients undergoing mitral valve repair.[35] [63] [68] Several mechanisms have been proposed to explain SAM following mitral valve repair. These mechanisms include anterior displacement of the posterior ventricular wall, anterior displacement of the posterior mitral leaflet, and narrowing of the angle between the mitral and aortic valves.[69] It is clear that SAM occurs primarily in patients 430

Figure 19-13 (color plate.) Series of images indicating the presence of systolic anterior motion at the end of the first pump run (A, arrow) leading to severe mitral regurgitation (B) and outflow obstruction (C). The maximal velocity measured in the outflow tract was 4.6 m per second, giving a pressure gradient of 85 mm Hg.

with degenerative mitral valve disease, those with large mitral leaflets, and

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in the presence of a hyperdynamic small ventricle.[63] SAM is usually seen only after annuloplasty ring insertion, but it has been reported after a suture annuloplasty.[63] It is seen more commonly with stiff than flexible annuloplasty rings.[63] [68] One quantitative study has shown that SAM is associated with anterior displacement of the mitral coaptation line. The anterior displacement is reduced or disappears after successful revision of the repair and elimination of SAM.[69] More recently, the ratio of the length of the anterior and posterior leaflet in the coapted state and the distance from the coaptation point to the septum were shown to be predictors of systolic anterior motion on preoperative TEE. The smaller the ratio between anterior and posterior leaflet and the narrower the distance between the coaptation point and the septum, the greater the likelihood of SAM.[70] When severe, SAM is easily recognized and may involve both leaflets. The left ventricular outflow gradient and the severity of mitral regurgitation are important indicators of the hemodynamic severity. The deep transgastric imaging window with the heart in an orientation similar to a transthoracic apical five-chamber image provides the best transesophageal window for assessing the left ventricular outflow tract gradient with continuous wave Doppler. When this examination cannot be reliably performed with the transesophageal approach, an epicardial study may be needed. The initial management of this condition should be to increase intracardiac volume by fluid repletion and to stop any positive inotropic agents that are being administered.[63] Systemic afterload can be supported by a pure alpha agonist (phenylephrine), avoiding any beta agonists. If these measures are inadequate to reduce the severity of SAM, another pump run to improve the SAM is indicated. Further procedures to improve SAM include (1) a sliding posterior leaflet advancement (sliding plasty), which reduces the anteriorposterior height of the posterior leaflet; (2) insertion of an annuloplasty of larger size; and (3) removal of the annuloplasty ring. Sliding annuloplasty is currently used as a component of the primary operative procedure on patients who are considered at risk for developing SAM and has significantly reduced the incidence of this complication in those patients in whom it has been used.[71] [72] If SAM persist despite these maneuvers, the final recourse is mitral prosthetic implantation. Patients in whom SAM is discovered by TTE days or longer after mitral valve repair, obviously a subset selected to have milder obstruction by successful weaning from bypass and extubation, may be treated medically with

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negative inotropic agents. Some patients show a late reduction in the left ventricular outflow gradient, but this may remain inducible by amyl nitrite. [73]

Suture Dehiscence

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Occasionally, suture dehiscence leads to significant mitral regurgitation immediately after mitral valve repair. This complication occurred in 2% of operations in one series.[62] Dehiscence of a suture at the site of the leaflet resection in the posterior leaflet simulates a posterior leaflet perforation and is easily repaired on a second pump run. Another rare complication of mitral valve repair that can be detected by intraoperative echocardiography is partial dehiscence of the annuloplasty ring. The annuloplasty ring shows increased mobility and regurgitation originates outside the ring (Fig. 1914) . Left Ventricular Systolic Dysfunction Some reduction in left ventricular function often is detected after mitral valve repair.[74] [75] When dysfunction occurs, it is most often global and may reflect the unmasking of left ventricular dysfunction present preoperatively that had been concealed by the effects of increased ventricular preload and decreased afterload. In a minority of instances, a regional wall motion abnormality is detected, despite normal coronary vasculature preoperatively. This abnormality is usually caused by passage of air into a coronary vessel, and it can cause transient wall motion abnormalities and occasionally permanent infarction.[18] Because of its anterior position, air is more likely to travel to the right coronary artery in a supine patient, causing inferior wall motion abnormalities. Air within the left ventricular cavity is readily detected by echocardiography because it is echodense. The presence of large amounts of air on echocardiography is an indication for increased surgical venting of the left ventricle to prevent coronary embolization. In minimally invasive operations in which small hemisternotomy incisions are used, surgical venting may be difficult or impossible. In this situation, resumption of cardiopulmonary bypass may be necessary for a period of time in order to allow slow resolution of the air. Fortunately, most instances of air embolization of the coronary vessels resolve without significant long-term

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ventricular dysfunction. A rare complication of mitral valve repair or of any mitral operation is the inadvertent entrapment of the circumflex artery in the annulus sutures, which causes a wall motion abnormality in the Figure 19-14 (color plate.) Ring dehiscence leading to severe mitral regurgitation. The dehisced portion of the ring is shown (arrow).

basilar posterolateral wall that may also be detected echocardiographically. Tricuspid Regurgitation Generally, tricuspid regurgitation that is treated with a ring annuloplasty at the time of mitral surgery should be rechecked on the postpump intraoperative echocardiogram.[76] The success of the tricuspid surgery should be checked only after the intravascular volume status has been normalized. [77] Occasionally, tricuspid regurgitation that did not appear to be significant preoperatively may appear to be more severe on the postpump study and require a further pump run for tricuspid repair. Mitral Stenosis In performing a mitral valve repair in a nonrheumatic valve, the surgeon may remove a significant portion of the leaflet or perform an annuloplasty that reduces the size of the mitral annular orifice. Despite these anatomic derangements, it is unusual to have any significant stenosis in degenerative or ischemic mitral valve repair. The annulus area is 5 to 10 cm2 , varying with the size of the annuloplasty ring inserted. In contrast, residual stenosis of mild degree is common after rheumatic mitral valve repair because of the thickened leaflets and fusion of subvalvular chordae and commissures. The mitral valve gradient should be measured using continuous wave Doppler after every mitral valve repair. A mean gradient in excess of 5 mm Hg should arouse suspicion of some degree of stenosis of the valve.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Mitral Valve Repair Involving Commissurotomy Although balloon valvuloplasty is a common method of treating selected patients with mitral stenosis, mitral repair with open commissurotomy still has a place, especially in patients with moderate amounts of valve calcification or thickening, those with multivalvular disease, or those with combined stenosis and significant regurgitation. Before surgery, intraoperative echocardiography is used to determine the severity of stenosis as a reference to assess the success of surgery. The severity of mitral stenosis is determined by measuring the transmitral pressure gradient and the pressure half-time with continuous wave Doppler.[78] [79] An epicardial approach using a para-sternal short-axis equivalent view may be used to obtain views suitable for planimetry of the mitral orifice if needed, but most TEE short-axis views of the mitral valve from the transgastric short-axis view are not of sufficient quality. The mechanism of the stenosis, whether valvular or subvalvular, should also be determined. A splitability score generated in a manner similar to the transthoracic method used for percutaneous mitral valvuloplasty may help to determine the degree of valvular fibrosis and calcification and whether a valve-sparing procedure is feasible.[80] Because 432

the surgeon can débride the valve under direct vision, open commissurotomy is sometimes possible even with a moderately high splitability score of 9 to 11, when a balloon valvuloplasty is not as likely to be effective or durable (see Chapter 20) . The presence of mitral regurgitation is also determined, and its mechanism, usually restricted leaflet motion, is determined. It is important also to detect left atrial and appendage thrombus preoperatively so that the surgeon can remove it. Postpump mitral valve gradient and area and mitral regurgitation are assessed. The presence of residual mitral regurgitation of 2+ or greater, or a

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mitral valve area of less than 1.5 cm2 is an indication for a further pump run, either to improve the repair or to implant a prosthesis. Frequently, when the patient has a large atrium or atrial fibrillation, the surgeon attempts to ligate the left atrial appendage in an effort to reduce the embolic risk. One study with TEE Doppler has demonstrated that these ligation attempts may be incomplete in up to one third of patients and in these instances blood still may enter and leave the appendage.[81] Patients with incomplete ligation remain susceptible to left atrial appendage thrombus formation and even thromboembolism. It has not been demonstrated that TEE evaluation of the competency of the ligation at the time of surgery improves the outcome.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions The acquisition and storage of digital images is available on many of the current echocardiographic machines and opens up new vistas for intraoperative echocardiography. This storage method preserves image quality better than does videotape. Retrieval of digital images also is more facile, but it depends on how and where the data is stored. Comparing previously performed studies directly with the current study provides a more reliable detection of change. Digital storage and retrieval of previously performed studies may reduce the need for prepump intraoperative studies, or at least shorten their duration. Appropriate training of additional personnel is changing intraoperative echocardiography for the better. Cardiac anesthesiologists are quickly learning the requisite skills, which could reduce the need for dedicated cardiology support to the cardiac operating rooms except to consult when specific problems arise. Online consultation is increasingly feasible with the availability of digital archival and retrieval of images on a common server. Additionally, training of cardiac surgeons in epivascular imaging of the aorta has the potential to reduce the involvement of other echocardiographers directly in image acquisition. New technology is constantly becoming available both in terms of the echocardiographic machines themselves and in terms of the available transducers. Image quality has improved remarkably, from faster computers and parallel processing circuitry. New technology including Doppler myocardial imaging, harmonic imaging, and contrast analysis software provides improved physiologic analysis. On the other end of the spectrum, smaller hand-held machines having many of the capabilities of bigger machines will soon become available in cardiac operating rooms, although they likely will need to be supplemented by more sophisticated technology for cases with significant diagnostic needs. As yet, these smaller machines have not had transesophageal capability, nor has their use in the operating

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room been reported. Newer transducers that are currently being evaluated include transnasal probes.[82] These smaller transducers, inserted through the nasopharynx, lessen the risk to teeth and the interference with the endotracheal tube. Currently, these probes are not available with multiplane capabilities. They are therefore at a disadvantage compared with standard multiplane TEE probes. Three-dimensional echocardiography has tremendous potential in any analysis of complex cardiac morphology, including the assessment of lesions in which repair or reconstruction is being considered[83] (see Chapter 10) . The complex three-dimensional geometry of some valvular and congenital lesions is easier to display and understand using three-dimensional echocardiography.[84] , [85] Threedimensional reconstruction may allow more appropriate selection of patients, help determine the most appropriate surgical procedure, and potentially allow the surgeon to map out the reconstruction ahead of time in three-dimensional computer space. Recently, the feasibility of intraoperative three-dimensional TEE has been shown, with acquisition time less than 3 minutes and reconstruction possible in greater than 90% of patients. Three-dimensional data yielded incremental information to TEE in up to 25% of patients but only led to a change in the operative plan in one of 60 patients studied.[86] Three-dimensional imaging for reconstruction of some structures has already been accomplished, including the regurgitant orifice area in patients with severe mitral valve prolapse.[87] Although realtime three-dimensional echocardiographic acquisition hardware is now a reality, transesophageal applications are not currently available and the exigencies imposed by the data acquisition render the image quality inferior to current two-dimensional echocardiographic images. Real-time acquisition of three-dimensional data has the potential to further expand echocardiographic abilities intraoperatively by allowing rapid changes in volume and structure to be quantified online and in allowing multiple slices of structure to be generated at a later time from one stored data set.

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Chapter 20 - Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Cheryl L. Reid MD

Historical Background and Technique of Mitral Balloon Commissurotomy Mitral stenosis in the adult occurs most commonly as the late result of rheumatic fever. Rarely, mitral stenosis may be caused by congenital or mitral annular calcification, particularly in the elderly patient. The natural history of rheumatic mitral stenosis is progressive symptomatic deterioration owing to reduction in the mitral valve orifice area. In the 10 to 20 years following an initial bout of rheumatic fever, the effective mitral valve area decreases because of fusion of the commissures, thickening and calcification of the mitral leaflets, and fibrosis and retraction of the chordae tendineae. The normal mitral valve area of 4.0 to 5.0 cm2 gradually decreases to 2.0 cm2 or less, at which time symptoms begin to develop usually with moderate to severe exercise. When the mitral valve area is reduced to 1.5 cm2 or less, symptoms may become severe and complications may develop.

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Mechanical intervention for the treatment of mitral stenosis, either open or closed mitral commissurotomy, has evolved in the past 40 years. Surgery, which has been shown to be highly effective, is usually performed for the relief of symptoms. Surgical replacement of the mitral valve may be necessary in patients with rigid, calcified mitral valves or severe mitral regurgitation in whom results with commissurotomy are suboptimal. Early experience with surgical commissurotomy showed that M-mode echocardiography could be helpful in selecting patients who would have a successful surgical mitral commissurotomy. It is important to identify patients who will have a successful commissurotomy because of the wellrecognized complications of valve prostheses, including thromboembolism, endocarditis, and higher operative mortality. The percutaneous approach to dilate a stenotic mitral valve was first reported by Inoue et al[1] in 1984, with subsequent evolution of catheter design and technique since the initial description. Simply stated, the technique consists of the percutaneous insertion of a dilating balloon into the right atrium. Using a trans-septal approach, the balloon catheters are then positioned across the stenotic mitral orifice and inflated at high pressures (1 to 2 atm). The desired result from inflation of the balloons is splitting 436

Figure 20-1 Technique of double-balloon valvuloplasty of the mitral valve. Top left, Two trans-septal sheaths from the right femoral vein are advanced to the left atrium (LA). Top center, Two end-hole balloon wedge catheters are positioned in the apex of the left ventricle (LV). Top right, Two curved exchange guidewires are inserted through the balloon catheters, which are then withdrawn. Bottom left, Two dilation balloon catheters are placed across the mitral valve orifice and into the LV apex. Bottom center, Two dilating balloon catheters are then fully inflated. Bottom right, Valve dilation balloons are removed. AO, aorta; IVC, inferior vena cava; RA, right atrium. (From McKay CR, Kawanishi DT, Rahimtoola SH: JAMA 1987;257:1753–1761, with permission. Copyright © 1987 American Medical Association.)

of the fused mitral commissures with resultant increases in the mitral valve orifice area. The procedure can be performed using either the doubleballoon or Inoue technique (Fig. 20-1) . In the double-balloon technique, two balloons are positioned side by side across the mitral valve orifice and then simultaneously inflated to achieve the desired result. The Inoue technique uses a unique self-seating single balloon that sequentially inflates

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from the distal to proximal end of the balloon. In recent years, the technical complexity and potential for serious complications (specifically, cardiac rupture inherent with the double-balloon technique) have largely lead to the abandonment of the double-balloon technique in favor of the Inoue technique. Early results of the procedure showed that the increase in mitral valve area is comparable to that obtained with surgical mitral commissurotomy.[2] [3] [4] Mitral balloon commissurotomy is now considered the procedure of choice for the treatment of symptomatic mitral stenosis in selected patients. Twodimensional Doppler echocardiography has played a major role in the evolution of mitral balloon commissurotomy, guiding our understanding of the mechanism by which the mitral valve area is increased. It is essential for the evaluation and selection of patients before the procedure and for the assessment of complications following the procedure. Hemodynamic measurement of the severity of the mitral stenosis and associated valve disease before the procedure, immediate hemodynamic changes during the procedure, and long-term follow-up can be reliably estimated with Doppler echocardiography (Table 20-1) .

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Evaluation of the Patient Before Mitral Balloon Commissurotomy Mechanisms of Increase in Mitral Valve Area Studies performed by two-dimensional echocardiography have shown that the primary mechanism for the increase in mitral valve area following mitral balloon commissurotomy is splitting of the fused commissures (Fig. 20-2) .[5] Tears of either the anterior or posterior mitral valve leaflet rarely occur and usually result in moderate to severe mitral regurgitation. In contrast to open, surgical commissurotomy in which the fused and retracted chordae can be manually separated, it is unclear that mitral balloon commissurotomy has a significant effect in dilating the subvalvular apparatus. Fortunately, the subvalvular region is rarely the primary orifice in patients with mitral stenosis.

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TABLE 20-1 -- Role of Two-Dimensional Doppler Echocardiography in the Evaluation of Patients Undergoing Mitral Balloon Commissurotomy Initial studies Severity of valve disease Mitral valve gradient Mitral valve area Mitral regurgitation Initial valve morphology Left atrial thrombus During mitral balloon commissurotomy

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Balloon position or trans-septal catheterization Changes in valve area or gradient Changes in mitral regurgitation Complications (rupture, atrial septal defect, etc.) Immediate results Changes in valve function Complications Long-term results Restenosis Mitral regurgitation Atrial septal defects Pulmonary artery pressure Ventricular size and function Other valve disease Mitral Valve Morphology The pathologic processes of rheumatic heart disease include (1) fusion of the commissures, (2) thickening and calcification of the valve leaflets, and (3) fusion and shortening of the chordae tendineae. These processes result in varying degrees of involvement of the mitral apparatus. Given that the mechanism of the increase in mitral valve area by surgical or percutaneous techniques is splitting of the commissures, it is expected that the morphology of the mitral valve apparatus will influence the results of the procedure. Experience with both surgical mitral commissurotomy and mitral balloon commissurotomy has confirmed this expectation. The characteristic feature of rheumatic mitral stenosis on two-dimensional echocardiography is doming of the body of the mitral valve leaflets during diastole caused by the fused commissures. As blood flows from the left Figure 20-2 Two-dimensional echocardiogram in the parasternal shortaxis view at the level of the mitral valve during early diastole. A, Before double-balloon catheter balloon valvuloplasty the transverse diameter was 20 mm. Calcification of the posterior commissure was present. B, After catheter balloon valvuloplasty the transverse diameter increased to 27 mm. The increase in

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transverse diameter suggests that the split occurred at the commissures. Figure 20-3 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis. The mitral valve is mobile with doming of the anterior leaflet. Minimal valve thickening and no subvalvular disease is noted. Right, Transesophageal echocardiogram in the midesophagus fourchamber transverse view from the same patient. The mitral valve morphology in this patient is ideal for mitral balloon commissurotomy and excellent results would be expected. LA, left atrium.

atrium to the left ventricle through the narrowed mitral orifice, the body of the leaflets balloon apically. The mobility of the leaflets (amplitude of doming) reflects the degree of calcification of the leaflets and commissural fusion. Both qualitative and semiquantitative criteria have been proposed for evaluation of leaflet morphology. [6] [7] In patients in whom the transthoracic echocardiogram is inadequate, transesophageal echocardiography can provide a similar analysis of the mitral valve morphology, although nonstandard image planes may complicate interpretation ( Fig. 20-3 and Fig. 20-4 ). [8] [9] In addition, subvalvular thickening and calcification may be underestimated on transesophageal imaging because of masking of the subvalvular region from thickening and calcification in the mitral valve leaflets. To some extent, these limitations can be avoided by use of biplane or multiplane transesophageal echocardiography with imaging of the subvalvular region in the transgastric longitudinal imaging plane. Total echocardiographic scoring systems based on leaflet morphology have been proposed as a guide to the selection of patients for mitral balloon commissurotomy. Although studies using these methods have been shown Figure 20-4 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis undergoing evaluation for mitral balloon commissurotomy. The mitral valve is heavily calcified with decreased excursion of the mitral leaflets during diastole. Right, Transesophageal echocardiogram in the midesophagus transverse view, which again shows a heavily calcified immobile mitral valve. The assessment of the morphologic features of the mitral valve are similar between the transthoracic and transesophageal echocardiographic examinations. The increase in mitral valve area from mitral balloon commissurotomy in this patient would be expected to be minimal. LA, left atrium.

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Figure 20-5 The anatomic features of the mitral valve in relationship to the resultant mean mitral valve area immediately after catheter balloon valvuloplasty are shown for the presence or absence of calcification, subvalvular disease, and pliable or rigid mitral valves. The mean mitral valve area was greater in the groups with pliable mitral valves without calcification or subvalvular disease.

to correlate with the immediate results, the wide scatter of the data makes their value questionable in an individual patient for predicting the hemodynamic results of the procedure ( Fig. 20-5 and Fig. 20-6 ). These criteria should be used, therefore, only as a guide to the severity of the individual morphologic variables of the mitral valve. Table 20-2 is a summary from the literature of the morphologic features of the mitral valve and the criteria used in assessment before mitral balloon commissurotomy. The single best echocardiographic morphologic variable that predicts the results of mitral balloon commissurotomy is leaflet mobility, which reflects the extent of commissural fusion and calcification of the mitral leaflets.[10] In the studies of the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry and Reid et al,[6] [10] leaflet mobility was the only independent echocardiographic variable to predict the results of mitral balloon commissurotomy (Table 20-3) . The presence of calcification and the involvement of one or both commissures assessed in the twodimensional echocardiography parasternal short-axis view may also be helpful in predicting the success of commissural Figure 20-6 Total morphology score by echocardiography versus mitral valve area (MVA) measured by cardiac catheterization after mitral balloon commissurotomy (MBC). There is significant (P < .001) but weak negative correlation (r = -0.24).

splitting by the balloon dilation (see Fig. 20-2) .[11] In asymmetric involvement of the commissures, in which one commissure is heavily fibrosed or calcified, splitting occurs in the opposite commissure. If both commissures are equally fused without marked calcification, both commissures are expected to split. In one study, if at least one commissure split, 89% of patients had a good hemodynamic result.[11] The presence of severe subvalvular fibrosis and calcification may also result in suboptimal results from mitral balloon commissurotomy because it is unclear that balloon dilation is able to split chordal fusion. Isolated subvalvular disease,

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however, rarely occurs and is usually associated with extensive fibrosis and calcification of the commissures and valve leaflets. The best hemodynamic result based on echocardiographic evaluation is expected in a patient with a highly mobile mitral valve without evidence of calcification or severe subvalvular disease (see Fig. 20-3) . In this group of patients, a mean resultant mitral valve area greater than 2.0 cm2 is predicted.[6] Mitral valve morphology, however, should not be used alone in the selection of patients to undergo mitral balloon commissurotomy. In occasional patients, satisfactory hemodynamic and clinical improvement can occur with more severe mitral valve disease. Other variables that have been shown to influence the results of the procedure and should be considered in the selection of patients include evidence of long-standing disease such as a low cardiac output, baseline mitral valve area, and left atrial size and technical factors such as the balloon diameter used in the dilation. Assessment of Left Atrial Size and Left Atrial Thrombi As a result of chronic pressure overload, the response of the left atrium is progressive enlargement. With long-standing mitral stenosis, an extremely large or "giant" left atrium (>6.5 cm anteroposterior diameter) may result. The 439

TABLE 20-2 -- Two-Dimensional Echocardiographic Assessment of Mitral Valve Morphology Predicted Results SUBOPTIMAL Variable OPTIMAL Leaflet Highly mobile with restriction Minimal forward motion of motion of only leaflet tips and H/L leaflets in diastole or H/L ratio ≥ 0.45 ratio ≤ 0.25 Leaflet Leaflets < 4–5 mm or Leaflets > 8.0 mm thick or a thickening MV/PWAo ratio of 1.5–2.0 MV/PWAo ratio ≥ 5.0 Subvalvular Thin, faintly visible chordae Thickening and shortening disease tendineae with only minimal of chordae to papillary thickening below valve muscle; areas with echo

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density greater than endocardium Commissural Homogeneous density of both Both commissures heavily calcium commissures calcified H, height of doming of mitral valve; L, length of dome of mitral valve; MV, mitral valve; PWAo, posterior wall of aorta. Data from Reid CL, Chandraratna PAN, Kawanishi DT, et al: Circulation 1989;80:515–524; and Abascal VM, Wilkins GT, Choong CY, et al: J Am Coll Cardiol 1988;2:257–263. enlarged left atrium can compress the inferior vena cava, resulting in increased Doppler flow velocities and an increased incidence of hepatomegaly.[12] Other well-recognized complications associated with an enlarged left atrium include the development of atrial fibrillation and blood stasis within the enlarged left atrium with thrombus formation. Left atrial thrombi occur in approximately 25% of patients with mitral stenosis and are seen even in patients in normal sinus rhythm. [13] In the majority of cases, the thrombi are confined to the body of the left atrial appendage, but they may also protrude into the body of the left atrium or attach to the left atrial wall or interatrial septum (Fig. 20-7) . In patients undergoing mitral balloon commissurotomy, the size of the left atrium has been noted to have a significant influence on outcome.[14] In patients with large left atria (>6 cm), technical difficulties may be encountered in performing the trans-septal puncture and crossing the mitral valve orifice. Enlarged left atria also are more frequently associated with a suboptimal increase in the resultant mitral valve area, perhaps because of technical difficulties or as an index of more severe and chronic disease. Conversely, smaller left atria are more frequently associated with the development of an atrial septal defect after mitral balloon commissurotomy. In such patients, shorter balloon sizes should be used or care taken during the procedure to prevent slippage of the balloon catheter against the interatrial septum. Systemic embolization has been reported in 0 to 4% TABLE 20-3 -- Predictors of Mitral Valve Area Variable NHLBI-BVR[10]

R2 0.31

P value <.001

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Pre-MBC MVA <.001 Cardiac output .004 Leaflet mobility .01 Left atrial size .01 Balloon diameter .02 0.65 .0001 REID et al[6] Leaflet motion .0001 EBDA .03 Cardiac output .002 EBDA, effective balloon dilating area; MBC, mitral balloon commissurotomy; MVA, mitral valve area; NHLBI-BVR, National Heart Lung, and Blood Institute Balloon Valvuloplasty Registry. of patients undergoing mitral balloon commissurotomy.[15] Because the dilating balloon catheters must traverse the left atrium to be positioned across the stenotic mitral orifice, the risk of embolization is increased if a left atrial thrombus is present. Transesophageal echocardiography has been shown to be more sensitive than transthoracic echocardiography in the identification of left atrial thrombi, especially for imaging of the left atrial appendage where most thrombi occur. Furthermore, by transthoracic echocardiography the left atrium lies in the far field of the ultrasound beam, thus the image quality is suboptimal. In contrast, the left atrium is the structure closest to the ultrasound beam by transesophageal echocardiography and thrombi therefore can be accurately located and characterized by size and shape. Identification of left atrial thrombi is especially important in patients who are undergoing mitral balloon commissurotomy because of the risk of systemic embolization.[16] Although some of these episodes are undoubtedly from left atrial thrombi, other sources also must be considered, such as atherosclerotic debris and catheter thrombi.[17] The role of transesophageal echocardiography in patients before mitral balloon commissurotomy is controversial. Although mitral valve morphology and hemodynamic Figure 20-7 Transesophageal echocardiograms from two patients undergoing evaluation for thrombi before mitral balloon

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commissurotomy. Recordings were made at the midesophagus in a four-chamber view. Left, The interatrial septum through which the dilating balloon catheter is inserted is thin and without evidence of clot. Right, The interatrial septum is markedly thickened with evidence of a layer clot along the left atrial side of the septum (arrows). LA, left atrium; RA, right atrium.

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assessment of the severity of the mitral valve disease can be reliably predicted in most patients by transthoracic echocardiography, only transesophageal echocardiography can accurately exclude the presence of a left atrial thrombus. Obviously, if a left atrial thrombus is detected by transthoracic echocardiography, then a transesophageal echocardiogram is not usually necessary. Although the presence of a left atrial thrombus is not an absolute contraindication for mitral balloon commissurotomy, it should only be considered in patients that are at high risk for surgical commissurotomy. In such patients, monitoring by transesophageal echocardiography during the mitral balloon commissurotomy can be used to help guide the placement of the balloon catheters to avoid the thrombus. [18] A layered thrombus along the interatrial septum is a particularly high risk because of the trans-septal puncture. If no contraindication to anticoagulant therapy is present, it is prudent to treat the patient with anticoagulants for 1 to 3 months before the mitral balloon commissurotomy because some thrombi may resolve with anticoagulant therapy. Transesophageal echocardiography should then be performed in close temporal relationship to the mitral balloon commissurotomy. If a left atrial thrombus is present, anticoagulant therapy may be continued if the patient is clinically stable to attempt to resolve the thrombus or the patient should be referred for surgical mitral commissurotomy. Although anecdotal cases of patients having successful mitral balloon commissurotomy with thrombi confined to the atrial appendage have been noted, the procedure should be considered in patients only after thorough consideration of the risks and potential benefits.

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Hemodynamic Assessment of the Patient Undergoing Mitral Balloon Commissurotomy Hemodynamic assessment of the severity of mitral valve disease in the patient undergoing mitral balloon commissurotomy can be measured reliably by Doppler and two-dimensional echocardiography. The severity of the stenosis can be quantitated by measurement of the mitral valve area and gradient and the presence, and the severity of mitral regurgitation can be assessed by two-dimensional echocardiography in combination with spectral and color Doppler data. TABLE 20-4 -- Comparison of Mitral Valve Areas by Doppler Echocardiography with Gorlin-Formula Mitral Valve Areas Before and After Mitral Balloon Commissurotomy

Author Reid et al[6]

Method T½ 2D echo Abascal et al T½

MVA, Mean ± SD (cm2 ) r Value AFTER BEFORE AFTER BEFORE 1.0 ± 0.2 1.9 ± 0.4 0.73 0.42 1.0 ± 0.2 2.2 ± 0.4 0.71 0.34 0.9 ± 0.2 1.5 ± 0.4 0.75 0.46

[7]

2D echo 0.9 ± 0.3 1.8 ± 0.4 0.81 0.75 Nakatani et al Continuity 0.9 ± 0.3 1.6 ± 0.4 0.77 0.86 [27] equation 0.8 ± 0.2 2.4 ± 0.6 0.81 0.84 Chen et al[30] T½ MVA, mitral valve area; SD, standard deviation; T½, pressure half-time; 2D echo, two-dimensional echocardiography.

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Mitral Stenosis Severity Pressure Gradients

The mean diastolic mitral valve gradient is measured from Doppler flow velocity tracings based on the modified Bernoulli equation. In patients undergoing mitral balloon commissurotomy, Doppler gradients are accurate as shown by simultaneous measurement of mitral valve gradient before and after mitral balloon commissurotomy in comparison to cardiac catheterderived gradients (r = 0.70 and 0.89, respectively). [19] Pressure gradients across stenotic valves depend on the volume flow rate and orifice size. Thus, the pressure gradient varies depending on the hemodynamic state of the patient. If the volume flow rate increases, such as with exercise, the gradient increases. Conversely, if the patient is dehydrated, the gradient may be low. Because of this flow rate dependency, calculation of mitral valve area is essential. Mitral Valve Area Two-Dimensional Echocardiographic Planimetry of Mitral Valve Orifice.

Two-dimensional echocardiography or Doppler echocardiography is used for determination of the mitral valve area in patients with mitral stenosis. By two-dimensional echocardiography, the mitral valve orifice can be directly planimetered when visualized in the parasternal short-axis view. * Careful scanning by two-dimensional echocardiography of the mitral valve apparatus must be performed to identify the smallest or most restrictive orifice. The gain settings of the machine must be adjusted to prevent "blooming" because of the presence of calcification. The accuracy of this method in patients before mitral balloon commissurotomy has been confirmed in several studies with r values of two-dimensional echocardiography compared to cardiac catheterization ranging from 0.71 to 0.81 (Table 20-4) . The mitral valve area estimated by two-dimensional echocardiographic planimetry of the mitral valve orifice before mitral balloon commissurotomy, in reported series, ranges from 0.9 to 1.0 cm2 , with a resultant increase immediately following the procedure to 1.8 to 2.2 cm2 .[6] [7] After mitral *See Otto CM (ed): Textbook of Clinical Echocardiography, 2nd ed. Philadelphia, WB Saunders, 2000, pp 229–264. 441

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balloon commissurotomy, the correlation ranges from an r value of 0.51 to 0.75.[19] [20] [21] [22] Similar to patients after surgical commissurotomy, in patients following mitral balloon commissurotomy the orifice becomes more irregular and technically difficult to planimeter, especially if calcium is present. Because of the accuracy of this technique, two-dimensional echocardiography measurement of the mitral valve area should be performed in all patients undergoing mitral balloon commissurotomy in whom it is technically feasible. Doppler Pressure Half-Time Mitral Valve Area.

Doppler spectral tracings are used to estimate mitral valve area based on the pressure half-time method described by Hatle et al.[23] The pressure halftime (T1/2 ) is defined as the rate at which the initial mitral valve gradient declines to one half of the initial value, with mitral valve area (MVA) calculated as: MVA = 220/T1/2 (Fig. 20-8) . Although several clinical studies have validated the accuracy of this method, there are limitations to the technique, some of which are unique to patients undergoing mitral commissurotomy. Factors that influence the accuracy of the Doppler pressure half-time method are both technical and hemodynamic. The accuracy of Doppler flow velocity tracings for hemodynamic measurements depends on the Doppler beam being parallel to the direction of blood flow. In patients with mitral stenosis, Doppler flow velocity recordings typically are made in the apical four-chamber view with the Doppler beam directed through the center of the mitral stenotic jet. Adequate tracings can be recorded in most patients with the aid of Doppler color flow to identify the stenotic jet even in patients for whom two-dimensional echocardiography is inadequate. In the rare patient in whom transthoracic flow velocity tracings cannot be obtained, transesophageal echocardiography can be performed to obtain the flow velocity tracings from a high esophageal position in a four-chamber view. Another technical limitation to the Doppler pressure half-time method is difficulty in identifying the diastolic deceleration slope. In some patients, the diastolic flow is Figure 20-8 Doppler transmitral flow velocity from a patient with mitral stenosis. The pressure half-time (T1/2 ) is the time required for the

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initial gradient to decrease to one half. This point is identified on the diastolic slope of the transmitral flow tracing. Figure 20-9 Transmitral Doppler flow velocity tracing from a patient with nonlinear flow (arrow). In this circumstance the mid-diastolic flow, which is more linear, should be extrapolated back to obtain the maximal initial velocity (dashed line).

nonlinear (Fig. 20-9) . If linear flow cannot be obtained by careful angulation and placement of the Doppler beam, the mid-diastolic flow, which is more linear, should be used and the slope extrapolated back to obtain the initial maximum velocity.[24] In patients with rapid heart rates who are in sinus rhythm the A wave may be superimposed on the diastolic slope, making identification impossible. Similarly, rapid atrial fibrillation and atrial flutter may preclude identification of the early diastolic slope. Hemodynamic considerations in the application of the Doppler pressure half-time method include the effects of coexisting valve disease. When aortic regurgitation is present, the increased diastolic filling may result in a more rapid rise of the left ventricular end-diastolic pressure. As a result, the pressure half-time may be shorter than expected for the valve area; therefore, the severity of the mitral stenosis may be underestimated.[25] The severity of the aortic regurgitation can be assessed by color Doppler flow and, if mild or moderate, the pressure half-time method may be applied. If the aortic regurgitation is severe or acute (which is unusual in mitral stenosis patients), the limitation of the pressure half-time method should be recognized and an alternative method applied for estimation of the mitral valve area. One of the major limitations of the Doppler pressure half-time method is calculation of the mitral valve area when hemodynamics are changing rapidly. With the advent of mitral balloon commissurotomy, it was recognized early that calculation of the mitral valve area immediately following mitral balloon commissurotomy might be inaccurate.[5] The Doppler pressure half-time method assumes that the left atrial and left ventricular compliances are stable (Fig. 20-10) .[26] This assumption is not valid following relief of the mitral stenosis by balloon dilation because there are rapid changes in the left atrial pressure and left ventricular filling with consequent changing compliances of both the left atrium and left ventricle. The mitral valve

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Figure 20-10 Left atrial (LA) and left ventricular (LV) compliance curves showing the relative changes in LV and LA pressures and volumes before and after percutaneous mitral valvuloplasty (PMV). The LA pressurevolume relationship (top) shifts to the left after PMV because of reduced LA size and pressure, whereas the LV pressure-volume relationship (bottom) shifts to the right because of increased diastolic ventricular filling. Despite these significant shifts in individual chamber compliance, the net compliance remains almost constant before and after valvuloplasty. (From Thomas JD, Wilkins GT, Choong CY, et al: Circulation 1988;78:980–993.)

area by the pressure half-time method also varies directly with the square root of the initial pressure gradient across the mitral valve, further complicating post-mitral balloon commissurotomy data as pressures rapidly fall. It should be noted, however, that the widely accepted catheter-derived mitral valve area based on the Gorlin formula also may be inaccurate following mitral balloon commissurotomy because of significant mitral regurgitation and the presence of an atrial septal defect leading to inaccurate measurement of transmitral volume flow.[27] In patients before mitral balloon commissurotomy, the noninvasive estimation of mitral valve area correlates well with invasive estimates (see Table 20-4) , with a standard error of the estimate ranging from 0.15 to 0.11 cm2 (r = 0.71-0.81) for Doppler pressure half-time method, 0.22 cm2 (r = 0.77) for the continuity equation method, and 0.17 cm2 (r = 0.71-0.81) for the twodimensional echocardiographic planimetry method.[19] [20] [21] [22] [23] [27] Immediately following mitral balloon commissurotomy, however, the Doppler pressure half-time method correlates less well with invasive data or with two-dimensional echocardiographic planimetry of valve area (see Table 20-4) . This inaccuracy is multifactorial and includes the rapid hemodynamic changes and the development of an atrial septal defect in many patients post mitral balloon commissurotomy.[28] In this setting, the pressure half-time method may overestimate the mitral valve area and depends on the magnitude of the shunt. In one study, occlusion of the atrial septal defect in patients after mitral balloon commissurotomy decreased the difference in the mitral valve area calculated by hemodynamic measurements and by the Doppler pressure half-time method.[29] This difference was due largely to a decrease in the mitral valve area calculated by the Gorlin formula when the atrial septal defect was occluded.

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The accuracy of the Doppler pressure half-time method has been shown to improve with time from the procedure. At 24 to 48 hours, hemodynamic equilibrium may be reached and the Doppler pressure half-time accuracy improves.[27] Furthermore, the mitral valve area calculated by the continuity equation decreases slightly at 24 hours probably because of a loss of "stretch" of the mitral valve. Because of these many considerations, caution should be taken in estimating the noninvasive mitral valve area immediately following mitral balloon commissurotomy. Doppler Continuity Equation Mitral Valve Area.

The calculation of mitral valve area by the continuity equation is based on the law of conservation of mass. The mitral valve area is calculated as MVA = (AVA [or PVA] × TVIa [or TVIp ])/TVIm where MVA is mitral valve area, AVA (PVA) is aortic (pulmonary) valve area measured from two-dimensional echocardiography, TVIa (TVIp ) is time velocity integral of the aortic (pulmonary) flow, and TVIm is time velocity integral of transmitral flow. One advantage of the continuity equation is that it is theoretically independent of transvalvular gradient and compliance. The continuity equation method, however, is much more difficult to perform. In addition, application of the continuity equation requires that the flow across the stenotic valve and another valve must be equal, based on the conservation of mass. In patients with associated mitral regurgitation, particularly if greater than mild, the stroke volume across the valves is different. Similarly, if greater than mild aortic regurgitation is present, pulmonary flow should be used. If the continuity equation is used to calculate the mitral valve area in the presence of mitral stenosis and an atrial septal defect, the transaortic Doppler flow should be used to avoid the effect of shunt flow volume. Other limitations of the technique include difficulty in measuring accurate pulmonary and aortic diameters. Regardless of the technical difficulty, studies have shown the method to be accurate in the calculation of mitral valve area with a correlation of r = 0.81 before mitral balloon commissurotomy and r = 0.84 after mitral balloon commissurotomy.[30] Stress Doppler Echocardiography

The clinical decision on interventional therapy for the relief of mitral stenosis must take into consideration the patient's symptoms in addition to the severity of the stenosis based on area and gradient. In some patients, symptoms of mitral stenosis caused by the elevated left atrial pressure and

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pulmonary congestion may be present 443

only during exercise. The transmitral gradient is dependent on flow volume and, thus, the severity of the mitral stenosis is underestimated in patients with low cardiac output at rest. Exercise hemodynamics have been used in patients with mitral stenosis to determine whether the mitral stenosis limits the transmitral flow and contributes to the patient's symptoms.[31] [32] Stress testing in patients with mitral stenosis is performed during supine bicycle or pharmacologic stress, which allows recording of the Doppler flow velocity. The calculation of mitral valve area by Doppler methods is controversial and the reliability of the pressure half-time in this setting is questionable.[32] [33] Calculation of the mitral valve area by the continuity equation in this setting is technically difficult. The severity of the mitral stenosis still can be reliably assessed by measurement of the transmitral gradient and pulmonary artery systolic pressure and assessment of the patient's symptoms. Studies have shown that mitral flow dynamics are improved in patients who have undergone mitral balloon commissurotomy with a decrease in the transmitral gradient and heart rate at maximal stress. [34] [35]

Associated Lesions Mitral Regurgitation

Mitral regurgitation, in varying degrees of severity, is commonly associated with mitral stenosis. The severity of associated mitral regurgitation can be assessed using standard Doppler echocardiography techniques (see Chapter 17) . Because most patients undergoing mitral balloon commissurotomy have transesophageal echocardiography, the variability in assessing the severity of mitral regurgitation by transesophageal and transthoracic echocardiography should be recognized. Because of the closer proximity of the transesophageal probe to the flow, shallower depth setting, decreased attenuation of the Doppler signals, and higher transducer frequency, the flow disturbance by the mitral regurgitation appears larger by transesophageal echocardiography.[36] [37] [38] Thus, there is a tendency to overestimate the severity of the mitral regurgitation when assessed by transesophageal echocardiography. Caution must be taken in estimating the severity of the mitral regurgitation in association with mitral stenosis.

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Patients with severe mitral regurgitation associated with mitral stenosis are not considered candidates for either balloon or surgical commissurotomy. In patients with moderate mitral regurgitation (grade 2+), commissurotomy should only be undertaken based on the patient's symptoms and the degree of mitral stenosis. Mild mitral regurgitation is not considered a contraindication to mitral balloon commissurotomy. In patients with associated mild or moderate mitral regurgitation, however, left atrial size is greater, which may cause more technical difficulties during the procedure. Pulmonary Hypertension

In patients with severe, long-standing mitral stenosis, the elevated left atrial pressure results in pulmonary hypertension and elevated pulmonary vascular resistance. Initially, the increase in pulmonary artery pressure is "passive" because of the increased resistance to the pulmonary venous drainage within the left atrium. With chronic elevation of the left atrial pressure, the pulmonary hypertension becomes "reactive" with an increase in the pulmonary vascular resistance.[39] Secondary effects of pulmonary hypertension include the development of right ventricular hypertrophy, right ventricular enlargement and dysfunction, and tricuspid regurgitation because of annular dilation. Estimation of the degree of pulmonary hypertension can be made based on the velocity of the tricuspid regurgitant jet.[40] The simplified Bernoulli equation applied to the peak tricuspid regurgitant jet velocity can be used to calculate the right ventricular peak systolic pressure when added to the estimate of right atrial pressure. In patients without right ventricular outflow tract obstruction, the right ventricular systolic pressure reflects pulmonary artery systolic pressure. Pulmonary vascular resistance, however, cannot be determined directly with Doppler echocardiography techniques. The severity of the pulmonary hypertension and pulmonary vascular resistance shows a significant relationship to the mitral valve area (Fig. 20-11) . Because of the wide variation in pulmonary pressures observed with a any given degree of mitral obstruction, however, specific predictors of pulmonary hypertension cannot be identified based solely on the severity of the mitral stenosis.[39] In patients in whom the pulmonary hypertension is out of proportion to the severity of the mitral stenosis, other possibilities, such as coexisting pulmonary disease, should be considered. In patients undergoing mitral balloon commissurotomy, there is a significant decrease in the pulmonary artery pressure as estimated by Doppler echocardiography immediately following mitral balloon

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commissurotomy despite the presence of severe pre-existing pulmonary hypertension.[40] Following mitral balloon commissurotomy, there is an immediate decrease of approximately 10 mm Hg in pulmonary artery pressure. The decrease in pulmonary hypertension following mitral balloon commissurotomy, however, cannot be predicted based on baseline characteristics. [39] Despite the initial improvement in pulmonary artery pressures, Doppler estimate of right-sided pressures should be followed closely for evidence of persistently elevated or increasing pressures.[41] Associated Other Valve Disease

Rheumatic heart disease affects not only the mitral valve but also the aortic valve and to a lesser incidence the tricuspid valve. The severity of these lesions can be assessed using standard Doppler echocardiography techniques. Patients that have significant stenosis of the aortic or tricuspid valve can be considered for concurrent dilation with the mitral valve. The symptomatic improvement in patients with aortic stenosis, however, may be limited because of the less than favorable results with balloon aortic valvuloplasty. Associated aortic regurgitation of mild or moderate severity does not significantly affect the hemodynamic and 444

Figure 20-11 Mitral valve area at catheterization on x-axis versus pulmonary vascular resistance on y-axis with inverse curve fit. (From Otto CM, Davis KB, Reid CL, et al: Am J Cardiol 1993;71:876. Reprinted with permission from Excerpta Medica Inc.)

symptomatic improvement obtained with mitral balloon commissurotomy. [42] The severity of the tricuspid regurgitation can be semiquantitated, similar to mitral regurgitation, based on the size of the regurgitant jet. Increasing severity of tricuspid regurgitation is directly related to the severity of the mitral stenosis. Patients with severe tricuspid regurgitation have a less favorable long-term result from mitral balloon commissurotomy than patients with mild or moderate regurgitation. [43] Ventricular Function The presence of mitral stenosis results in a chronic restriction in left ventricular diastolic filling. Left ventricular volumes are reduced in patients

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with isolated mitral stenosis compared with normal patients.[44] Left ventricular systolic function is normal. Increased left ventricular diastolic volumes suggests the presence of concomitant mitral or aortic regurgitation. Following successful mitral balloon commissurotomy, left ventricular end-diastolic volume and mass increase without significant change in end-systolic volume or ejection fraction. [45] Right ventricular end-diastolic volumes are increased in patients with severe mitral stenosis. Right ventricular volumes and function in patients with mitral stenosis are affected by the increased afterload because of pulmonary hypertension and the presence and severity of associated tricuspid regurgitation. Successful mitral balloon commissurotomy significantly improves but does not normalize right ventricular function.[46]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Role of Doppler Echocardiography in Predicting Results and Complications of Mitral Balloon Commissurotomy Patient Selection Doppler echocardiography plays a major role in the selection and evaluation of patients to undergo mitral balloon commissurotomy (see Table 20-1) . In patients with symptomatic mitral stenosis (mitral valve area < 1.5 cm2 ), the ideal candidate for mitral balloon commissurotomy based on the Doppler echocardiographic examination is one in whom the mitral valve is highly mobile without significant calcification of the leaflets or subvalvular apparatus. The presence of mitral regurgitation of greater than 2+ severity and a large left atrial thrombus within the left atrium or attached to the interatrial septum is considered a contraindication to mitral balloon commissurotomy. Immediate and long-term results are less successful in patients with evidence of long-standing disease such as large left atrium (>6 cm) or low cardiac output, although results vary in individual patients. The presence of significant other valvular disease such as critical aortic stenosis or severe aortic or tricuspid regurgitation and coronary artery disease may warrant consideration for surgical referral. The decision to perform mitral balloon commissurotomy in patients considered to be high risk for surgery because of other medical diseases, suboptimal mitral valve morphology, or a left atrial thrombus must be based on consideration of the risk-to-benefit ratio and the patient's desire. During Mitral Balloon Commissurotomy Doppler echocardiography plays a major role not only in the selection and evaluation of patients before mitral balloon commissurotomy but also is a useful adjunct during the procedure (see Table 20-1) . Doppler echocardiography equipment should therefore be available during the procedure to assess the immediate results and potential complications.

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Imaging by two-dimensional echocardiography of the interatrial septum can be performed to confirm and aid in the proper location of the transseptal catheter in difficult circumstances. Variability in the location of the interatrial septum may occur because of aortic root dilation, right atrial dilation, or cardiac deformity owing to scoliosis, 445

and in these settings, fluoroscopy may be misleading. Echocardiography can be useful in this setting by visualization of the interatrial septum and confirming by contrast saline injection the location of the needle within the left atrium once the trans-septal puncture is performed.[15] The identification of the needle tip may be difficult if it is out of the imaging plane, but it can be assessed indirectly by the "tenting" of the interatrial septum. Following the trans-septal puncture, two-dimensional echocardiography can aid in positioning the catheters across the stenotic mitral orifice. This positioning is important if the double-balloon technique is used. The Inoue balloon technique involves a unique self-seating design, which makes positioning of the balloon catheter easier. Echocardiography is helpful to prevent inadvertent inflation within the left atrium, which may result in an atrial septal defect if it butts against the interatrial septum. In patients with left atrial thrombi considered high risk for surgical commissurotomy, transesophageal echocardiography may be beneficial in preventing inadvertent migration of the catheter into the left atrial appendage. Two-dimensional echocardiography can also be used during the procedure to assess the affects of sequential balloon dilation. The transmitral gradient and changes in mitral regurgitation can be rapidly assessed to determine the need for further inflations. If the mitral regurgitation increases by one or more grades the procedure should be terminated. The success of mitral balloon commissurotomy has been shown to be related to the mitral anulus–to–balloon diameter ratio.[47] The mitral anulus by two-dimensional echocardiography can be measured to aid in selecting the appropriate balloon sizes. The increase in mitral valve is directly related to the mitral anulus–to–balloon diameter ratio. If the balloon diameter is too large, however, excessive tearing of the commissures or mitral leaflets may occur resulting in significant mitral regurgitation. In patients undergoing doubleballoon dilation, a ratio of the sum of diameters of the two dilating balloons to mitral anulus of ≥1.1 is associated with a significant increase in mitral regurgitation without further increase in mitral valve area.

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Complications of Mitral Balloon Commissurotomy Complications that may occur with mitral balloon commissurotomy are those known to be associated with invasive procedures, including death, myocardial infarction, stroke, bleeding, and heart failure. In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry, the incidence of serious complications was 12% and inhospital deaths 1%.[48] The reported complications of mitral balloon commissurotomy that can be detected by Doppler echocardiography are shown in Table 20-5 . Doppler echocardiography provides a rapid method for the early detection of complications and a noninvasive technique for serial evaluation. Atrial Septal Defects

The creation of an atrial septal defect in patients undergoing mitral balloon commissurotomy results from the TABLE 20-5 -- Complications of Mitral Balloon Commissurotomy Detected by 2D Doppler Echocardiography Event Thrombus (systemic embolization) Cardiac perforation (tamponade) Left-to-right shunt (atrial level) Valve related Acute mitral regurgitation (requiring early surgery) Increase in MR

Incidence (%) 2 4 10 3 12 36

Inadequate result (MVA < 1.5 cm2 ; ≥ 2 + increase MR) Restenosis ? MR, mitral regurgitation; MVA, mitral valve area. Data from National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry Participants: Circulation 1992;85:448–461, 2014– 2024. trans-septal approach. The reported incidence of atrial septal defects depends on the method of detection. By oximetry immediately following mitral balloon commissurotomy, the reported incidence ranges from 7% to 33% depending on the type of balloons used and diagnostic criteria.[3] [49] [50]

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Transesophageal echocardiography is the most sensitive method for detection of left-to-right shunting after mitral balloon commissurotomy and defects have been reported in 87% of patients examined within 24 hours of the procedure.[52] Transthoracic echocardiography detects left-to-right shunting in about half of the patients immediately following mitral balloon commissurotomy.[53] [51]

The detection of left-to-right shunting after mitral balloon commissurotomy requires a thorough evaluation of the interatrial septum in any patient who has undergone mitral balloon commissurotomy. The optimal view of detecting defects of the interatrial septum is obtained from the subcostal approach (Fig. 20-12) . In this position, the cardiac flow is parallel to the ultrasound beam, which is optimal for detection by color Doppler. The characteristic Doppler flow pattern is a continuous or late systolicholodiastolic left-to-right flow caused by the high pressure gradient between the right and left atrium in patients with mitral stenosis. The size of the defects range from 0.3 to 1.5 cm in diameter. By color Doppler, a jet width less than 0.5 cm is not likely to be detected by oximetry. Atrial septal defects greater than 1.0 cm are associated with significant right heart oxygen stop-ups. Shunt flow volumes calculated by Doppler echocardiographic methods range from 0.08 to 4.87 L per minute. The highest incidence of atrial septal defects is reported immediately after mitral balloon commissurotomy. Defects that are less than 0.7 cm in diameter usually close within 6 months.[54] Factors that have been associated with the development of atrial septal defects after mitral balloon commissurotomy include smaller increases in mitral valve area, the presence of mitral valve calcification, and smaller left atria. Atrial septal defects have also been reported to be initially detected during follow-up. Persistence of an atrial septal defect during follow-up is associated with larger sizes, a decrease in mitral valve area, and an increase in the mitral valve gradient. Clinically, significant problems are not associated with small atrial 446

Figure 20-12 (color plate.) Two-dimensional echocardiogram in the subcostal view from a patient after mitral balloon commissurotomy. Color Doppler flow mapping shows flow from the left to right atrium through a large atrial septal defect. The defect created by the dilating balloons measured 0.9 cm in diameter. RA, right atrium; LA, left atrium.

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septal defects. The effect on the right heart hemodynamics of large atrial septal defects with or without restenosis of the mitral valve remains to be determined. Mitral Regurgitation

Mitral regurgitation is a frequent complication of mitral balloon commissurotomy (Fig. 20-13) . The presence and severity of the mitral regurgitation should be carefully Figure 20-13 (color plate.) Transthoracic and transesophageal echocardiograms from a patient who had undergone mitral balloon commissurotomy (MBC). A, Transthoracic apical four-chamber view before MBC, which by color Doppler flow mapping shows a small blue jet in the left atrium during systole (arrow) consistent with mild mitral regurgitation. B, Same echocardiographic view obtained during the procedure following the first balloon inflation. The Doppler flow mapping shows turbulent flow into the left atrium. The mitral regurgitant jet is directed along the lateral wall and wraps around, almost completely filling the left atrium. C, Transesophageal echocardiogram from the midesophagus longitudinal view, which shows both the anterior and posterior leaflets of the mitral valve are flail with ruptured chordal attachments. LA, left atrium; LV, left ventricle.

evaluated by Doppler echocardiography using standard techniques before mitral balloon commissurotomy so that any change in severity can be recognized and evaluated immediately. Creation of new or an increase in pre-existing mitral regurgitation has been reported in 19% to 85% of patients undergoing mitral balloon commissurotomy.[5] [55] [56] [57] [58] [59] In most patients, however, the increase in mitral regurgitation is mild. An increase of greater than 2 grades in mitral regurgitation occurs in only 3% to 10% of patients. [48] [55] [56] [57] [58] [59] In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry early surgery for mitral valve replacement owing to severe mitral regurgitation occurred in 2% of patients.[55] This rate is comparable to results of surgical mitral commissurotomy. Although some patients who develop severe mitral regurgitation require urgent surgery for mitral valve replacement, others may tolerate the mitral regurgitation acutely. The mechanisms in the development of mild increases in mitral regurgitation differs significantly compared with the mechanisms of severe mitral regurgitation.[58] [59] [60] [61] [62] Echocardiographic studies of patients who develop mild increases in mitral regurgitation have shown that the

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regurgitant jet originates from the split commissures. Severe mitral regurgitation following mitral balloon commissurotomy, however, results from tearing of the valve leaflets or rupture of the chordal attachments. In one study of patients having balloon commissurotomy with the Inoue technique, the incidence of severe mitral regurgitation was 7.5%.[59] The most common cause was rupture of the chordae tendinae to the anterior or posterior leaflet in 43% of cases. A heavily calcified posterior leaflet resulted in tearing of the leaflet in 30%. Other variables that have been associated with the development of severe mitral regurgitation include severe calcification of both commissures and extensive subvalvular disease. [60] Splitting of the commissures, which most commonly is associated with mild increases in mitral regurgitation, can, if "excessive," result in severe regurgitation owing to incomplete coaptation of the valve leaflets during systole.

447

Unfortunately, the development of severe mitral regurgitation in patients undergoing mitral balloon commissurotomy cannot be reliably predicted from baseline characteristics, valve morphology, or technical factors during the mitral balloon commissurotomy procedure. The incidence of severe mitral regurgitation is not significantly different between patients undergoing double-balloon or Inoue techniques.[48] [56] [57] [58] [59] [60] [61] [62] [63] Similarly, stepwise inflation with the Inoue balloon technique has not reduced the frequency of severe mitral regurgitation. Indeed, inadvertent inflation of the Inoue balloon within the subvalvular apparatus, which may occur because of the unique design of the balloon catheter, can result in rupture of the chordal attachments or tear of the leaflets. Care must be taken in the positioning of the catheter before inflation. In one study, calcification of the posterior leaflet of the mitral valve resulted in a tear of the leaflet in the region of the calcification.[62] After each sequential balloon inflation, Doppler echocardiography should be performed to evaluate changes in mitral regurgitation. Two-dimensional echocardiography in the parasternal short-axis view permits evaluation of commissural splitting to assess the need for subsequent balloon inflations. Cardiac Perforation

Perforation of a cardiac chamber can occur during mitral balloon commissurotomy and is a major cause of death in these patients (see Table 20-5) . Atrial perforation can occur during the trans-septal catheterization

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and left ventricular perforation during the balloon inflations. The incidence of cardiac perforation is directly related, in part, to the dilation technique. In the Balloon Valvuloplasty Registry of patients undergoing mitral balloon commissurotomy with either a single- or double-balloon technique, the incidence of perforation was 4%. Perforation was the most common cause of death during the procedure, usually left ventricular perforation, and the most frequent indication for emergency cardiac surgery.[48] Cardiac perforation with the Inoue technique is much less common (<2%).[56] [61] [62] Left ventricular perforation occurs in the relatively thin apex owing to the positioning of the catheters and guidewires used in the technique. Manipulation of the catheters can then result in puncture of the apex. Perforation of the left ventricle usually results TABLE 20-6 -- Follow-up by Doppler Echocardiography of Patients Undergoing Mitral Balloon Commissurotomy Mean F/U No. of Author Method Patients 2D 235 Vahanian et al[63] Desideri et al[65] T½ 57 T½ 33 Georgeson et al

MVA (cm2 )

Mo RANGE BEFORE AFTER 18 1–48 1.1 2.0 19 9–33 1.0 2.2 17 1–38 1.1 2.0

F/U 1.9 1.9 1.7

[41]

Park et al[67] Hernandez et al

2D T½ 2D T½

59(I) * 13 61(D) † 561 39

— —

1.1 0.9 0.9 1.0

1.9 1.8 1.9 1.8

1.7 1.6 1.7 1.7

[70]

F/U, follow-up; MVA, mitral valve area; T½, pressure half-time; 2D, two-dimensional valve area. *Inoue balloon technique. †Double-balloon technique.

in abrupt hemodynamic collapse. Prompt recognition of this complication is essential. The role of echocardiography in the early diagnosis of this devastating complication is the most commanding reason for availability of echocardiographic equipment during the procedure. Echocardiography can

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identify the presence of cardiac tamponade caused by the perforation and guide the pericardiocentesis required to stabilize the patient. Although the incidence of left ventricular perforation has been reduced with the Inoue technique, the risk of perforation of the atria is common to both procedures. This risk is due to the need for trans-septal catheterization to position the balloons across the mitral orifice. Perforation of the atria, however, usually has less devastating consequences and can frequently be treated with pericardiocentesis or careful observation.

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Long-term Outcome The reported follow-up of patients who have undergone mitral balloon commissurotomy for mitral stenosis have ranged from 6 to 69 months.[40] [41] [57] [64] [65] [66] [67] [68] [69] [70] [71] , Early improvement in functional status occurs in approximately 90% of patients with the majority being in New York Heart Association functional class I or II. Sustained clinical improvement in functional status has been shown to be predicted by baseline characteristics.[64] [65] [67] [68] [69] [70] [71] [72] Patients with noncalcified valves by echocardiography and an excellent result from the mitral balloon commissurotomy (mitral valve area > 2.0 cm2 , < 2 + mitral regurgitation) have an event-free survival rate of 79% at 5 years.[67] Noninvasive testing with Doppler echocardiography eliminates the need for repeat cardiac catheterization in the hemodynamic evaluation of these patients during long-term follow-up. In the limited reported studies, the mitral valve area by Doppler echocardiography has shown a small decrease in valve area but remains significantly greater than that measured before the procedure (Table 20-6) . Restenosis (loss of 50% of the initial increase and a valve area of < 1.5 cm2 ) occurs in 6% to 21% at a mean follow-up of 19 to 22 months depending on the type of valve anatomy.[64] [66] Clinical and echocardiographic variables that have been shown to predict a poor long-term result are shown in Table 20-7 . The strongest predictor of the long-term 448

TABLE 20-7 -- Baseline Variables Associated with Poor Long-term Results Following Mitral Balloon Commissurotomy Clinical

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Advanced Age Higher NYHA Previous commissurotomy Hemodynamics Lower initial valve area Presence of MR Poor valve morphology or calcification Severe tricuspid regurgitation Higher pulmonary artery pressure Immediate Hemodynamic Results

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64, 67, 69 43, 67, 69 43, 63 63 43, 64, 68 43, 64, 65, 66, 67, 69, 70, 71 43 67 67, 69

Poor initial result (MVA ≤ 1.5 cm2 ) 43, 63, 65, 67, 70 Severe MR (> 2T) 63, 70, 71 Procedural EBDA 67, 68 EBDA, effective balloon dilating area; MR, mitral regurgitation; NYHA, New York Heart Association functional class. results, as with the immediate results of mitral balloon commissurotomy, is the degree of valve deformity. Patients with severe calcification of the mitral valve have both a poorer immediate result and long-term outcome than patients with more favorable valve anatomy. Other predictors of an adverse outcome include a lower initial valve area, the presence of mitral regurgitation or severe tricuspid regurgitation, and a higher pulmonary artery pressure. Increases in mitral regurgitation, which are common following mitral balloon commissurotomy, are generally well tolerated during follow-up. Although patients who develop severe mitral regurgitation usually require valve replacement during short-term follow-up, the changes in the mild to moderate mitral regurgitation are variable. The degree of mitral regurgitation by color Doppler echocardiography in reported series remains unchanged in 46% to 60%, decreases in 30%, and increases in 20% to 10% of patients.[64] [66] Multivariate analyses, however, have shown that the

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presence of mitral regurgitation both before and after mitral balloon commissurotomy is associated with a lower event-free survival.[65] [68] Thus, patients with either pre-existing or new mitral regurgitation should be followed closely after mitral balloon commissurotomy with clinical and echocardiographic evaluation for the development of symptoms or changes in valve function. The long-term effects of atrial septal defects is yet undetermined. Small defects close in about two thirds of patients during follow-up, and small defects that persist are generally well tolerated. Factors that are associated with the persistence of an atrial septal defect are a pulmonary-to-systemic shunt ratio of greater than 1.5, elevated right and left atrial pressures, smaller mitral valve area following mitral balloon commissurotomy, and evidence of restenosis.[66] These findings are not unexpected because elevation of left atrial pressures either caused by a poor initial result or restenosis would favor shunting through the atrial septal defect and perhaps prevent healing of the atrial septum. The long-term effects of the right ventricular volume overload is unknown. If the patient requires mitral valve surgery during follow-up, the atrial septum should be carefully examined and any defect surgically closed. Difficult management problems, however, occur in patients who have a successful mitral valve dilation but in whom a significant atrial septal defect results. Unfortunately, the hemodynamic burden of mitral stenosis in these patients is exchanged for an iatrogenic Lutembacher's syndrome. Importantly, these patients should be closely evaluated by Doppler echocardiography during follow-up to evaluate the atrial septal defect and evidence of developing right ventricular volume overload or restenosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Technical Limitations and Alternate Approaches The technique of mitral balloon commissurotomy has proved that sustained clinical and hemodynamic improvement occurs in most patients treated for symptomatic mitral stenosis. The immediate results are equal to those obtained with surgical commissurotomy. The technique is not, however, without its limitations. Suboptimal results and complications occur in a number of patients regardless of whether the double-balloon or Inoue technique is used. Doppler echocardiography has been invaluable in the evaluation of patients and the technique as mitral balloon commissurotomy has evolved. Patients with mitral stenosis who require intervention can be identified and the results predicted by careful Doppler echocardiographic evaluation. Before intervention, patients with mitral stenosis can be evaluated reliably by the pressure gradient, valve area, severity of valvular regurgitation, and indirect evidence such as chamber size and intracardiac pressures. Thus, the majority of patients with isolated mitral stenosis do not require more invasive testing with cardiac catheterization. In older patients, in whom the presence of coronary artery disease is a consideration, coronary angiography should be performed. Furthermore, cardiac catheterization, either as the initial evaluation or in patients in whom restenosis is suspected, should be reserved for those patients in whom there is a discrepancy between the physical or clinical signs and the Doppler echocardiographic examination. The choice of mitral balloon commissurotomy or surgical commissurotomy in patients identified who require intervention depends on a number of factors. Presently, mitral balloon commissurotomy should be considered the procedure of choice in patients with isolated mitral stenosis with favorable mitral valve anatomy because it is cost-effective and safe. In other patients, mitral balloon commissurotomy may be required if the patient refuses surgery or the medical condition makes surgery high risk. In

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patients with less favorable valve anatomy, the decision for mitral balloon commissurotomy or surgical commissurotomy must be made based on the consideration of risks and benefit of each procedure. Mitral balloon commissurotomy, however, should only be considered a palliative procedure, which may delay the time in which surgical 449

intervention may be required for mitral valve replacement.

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Future Directions Although the immediate and current follow-up of patients undergoing mitral balloon commissurotomy is favorable and comparable to surgical commissurotomy, several issues remain. Potential long-term questions remain unresolved. For example, does the presence of persistent small atrial defects significantly alter the clinical course of patients? In order to answer this question and others, continued follow-up of patients who have undergone mitral balloon commissurotomy is required. Further refinements in the technique and in the development of balloon catheters also may be expected; however, whether these changes will result in significant improvement in the expected outcome depends on careful patient selection. The development of intracardiac echocardiography also may be of benefit in the guidance of the procedure.[73] Regardless of these considerations, mitral balloon commissurotomy has become a proven technique and will continue to play a major role in the treatment of patients with symptomatic mitral stenosis.

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451

Chapter 21 - Clinical Decision Making in Endocarditis Nelson B. Schiller MD

Infection of the endocardium walls or lining layer of the heart—whether on valve leaflets or chordae, congenital defects, chamber walls, paraprosthetic tissue, or the attachment of implanted shunts or conduits—is known as infective endocarditis. The major milestones in our understanding of infective endocarditis include availability of diagnostic blood culture techniques in the first decades of the 20th century; reversal of its invariably fatal course with antibiotics; palliation of potentially fatal valvular complications with surgery; and, most recently, immediate and accurate diagnosis of its anatomic and hemodynamic manifestations with echocardiography. Although no technique in isolation can always establish this diagnosis, echocardiography has a very high sensitivity for detection of valvular vegetations and complications of infective endocarditis. Thus, echocardiography is the only imaging modality that has a significant role in the clinical diagnosis and treatment of infective endocarditis. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the clinical application of echocardiography (Table 21-1) indicate that echocardiography is an essential technique in the diagnosis and treatment of endocarditis and is mandatory in nearly all patients with this disease. [1] This chapter discusses the use of echocardiography in infective endocarditis

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with emphasis on both clinical applications and utility in research studies. The weaknesses and pitfalls of the technique are discussed, particularly how these factors might cause the performance of echocardiography in practice to fall short of published data.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Basic Principles Underlying a discussion of the use of echocardiography in patients with suspected infective endocarditis must be an attempt to come to terms with a clinical definition of the diagnostic criteria of the syndrome. First, should the diagnostic criteria include echocardiography? The studies that initially evaluated the role of echocardiography in the diagnosis of infective endocarditis could not, of course, use an echocardiographic definition of this disease. Instead, TABLE 21-1 -- ACC/AHA Guidelines for Use of Echocardiography in Patients with Infective Endocarditis CLASS I (Evidence or general agreement that echocardiography is definitely indicated) Detection and characterization of valvular lesions, their hemodynamic severity, and/or ventricular compensation * Detection of vegetations and characterizations of lesions in patients with congenital heart disease suspected of having infective endocarditis Detection of associated abnormalities (e.g., abscesses, shunts) * Re-evaluation studies in complex endocarditis (e.g., virulent organism, severe hemodynamic lesion, aortic valve involvement, persistent fever or bacteremia, clinical change, or symptomatic deterioration) Evaluation of patients with high clinical suspicion of culture-negative endocarditis * CLASS IIA (Conflicting data, but the weight of evidence/opinion is in favor of the usefulness of echocardiography) Evaluation of bacteremia without a known source * Risk stratification in established endocarditis * CLASS IIB (Conflicting data, but efficacy is less well established) Routine re-evaluation in uncomplicated endocarditis during antibiotic

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therapy CLASS III (Not indicated) Evaluation of fever and nonpathologic murmur without evidence of bacteremia Modified from Cheitlin MD, Alpert JS, Armstrong WF, et al: J Am Coll Cardiol 1997;29:862–879. *Transesophageal echocardiography (TEE) may provide incremental value in addition to information obtained by transthoracic echocardiography. The role of TEE in firstline examination awaits further study.

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TABLE 21-2 -- Clinical Definition of Infective Endocarditis Definite Direct evidence based on histology from surgery or autopsy or bacteriology by Gram stain or culture of valvular vegetation or arterial embolus Probable A. Persistently positive blood cultures plus one of the following: 1. New regurgitant murmur or 2. Predisposing heart disease and vascular/immunologic phenomena (e.g., splinter hemorrhages, Osler's nodes, glomerulonephritis) B. Negative or intermittently positive blood cultures (<2 of 2 or 3 of 3 or 70% positive if more than four obtained) plus all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena Possible A. Persistently positive blood cultures plus one of the following: 1. Predisposing heart disease or

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2. Vascular phenomena B. Negative or intermittently positive blood cultures with all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena C. For Streptococcus viridans cases only: At least two positive cultures without an extracardiac source and fever Rejected A. Infective endocarditis unlikely and alternative diagnosis apparent B. Infective endocarditis possibility warrants antibiotic therapy C. Culture-negative infective endocarditis diagnosed but excluded by autopsy Modified from Von Reyn CF, Levy BS, Arbeit RD, et al: Ann Intern Med 1981;94(part 1):505–518. most studies adopted or modified the criteria of Von Reyn et al[2] (Table 212) . These somewhat complex criteria have been useful in developing the literature that has established echocardiography as a required part of the clinical work-up, but they now have been replaced by criteria incorporating echocardiographic findings. New criteria ( Table 21-3 and Table 21-4 ) that incorporate echocardiographic findings in the diagnostic criteria for endocarditis have been developed by the Duke Endocarditis Service and have been prospectively tested at several centers.[3] [4] [5] [6] [7] [8] [9] [10] [11] In the initial Duke study, each of 405 retrospectively reviewed suspected cases was classified as definite/probable, possible, or rejected using both the old (nonechocardiographic) and new (echocardiographic) criteria. Only 51% of the pathologically definite cases were detected using the older Von Reyn criteria compared with 80% using the newer Duke criteria. Confirming these findings, in a small prospective study of 63 patients admitted to a nonreferral hospital with a diagnosis of suspected endocarditis,[4] [5] the detection rate for pathologically confirmed cases increased from 50% to 100% when echocardiographic data were used for diagnosis. In this study, all patients had both transthoracic

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echocardiography (TTE) and transesophageal echocardiography (TEE). In the 17 cases with echocardiographic evidence of a vegetation, TABLE 21-3 -- Definitions of Terminology in Duke Criteria for Endocarditis Major Criteria I. Positive blood culture for infective endocarditis Typical microorganism for infective endocarditis from two separate blood cultures (Streptococcus viridans, Streptococcus bovis, HACEK group, community-acquired Staphylococcus aureus or enterococci) in the absence of a primary focus or Persistently positive blood cultures of an infective endocarditis consistent organism recovered from a. Cultures drawn at least 12 hours apart or b. The majority of four cultures spanning more than an hour II. Evidence of endocardial involvement Echocardiogram positive for infective endocarditis by 1. Oscillating mass on valve or apparatus or in jet pathway or on implanted material in absence of alternative explanation or 2. Abscess or 3. New prosthetic dehiscence or III. New valve regurgitation (increase or change in pre-existing murmur not sufficient) Minor Criteria I. Predisposition: predisposing heart condition or intravenous drug history II. Fever ≥ 38°C III. Vascular phenomena: major arterial emboli, septic pulmonary embolism/infarction, mycotic aneurysm (with and without hemorrhage), conjunctival hemorrhage, and Janeway lesions IV. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor V. Microbiologic evidence: positive blood culture but not meeting major criteria (excludes coagulase-negative staphylococci and organisms not causing infective endocarditis) or serologic evidence of infective

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endocarditis organism VI. Echocardiogram consistent with but not meeting major criteria for endocarditis Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. the process was detected only by TEE in 7 cases (41%) (Table 21-5) . In the past 5 years, the Duke criteria have received extensive confirmation. [6] [7] [8] [9] [10] [11] Some studies have suggested ways of improving the criteria while confirming that they TABLE 21-4 -- Duke Criteria for Endocarditis Using Definitions in Table 21-3 I. Definite infective endocarditis Pathologic criteria Microorganisms: demonstrated by culture or histology in a vegetation (in situ or embolized) or in an intracardiac abscess Pathologic lesions: vegetation or intracardiac abscess confirmed active by histology Clinical criteria using definitions in Table 21-3 2 major criteria or 1 major and three minor or 5 minor II. Possible infective endocarditis Findings consistent with but falling short of I Definite but not III Rejected III. Rejected Firm alternative diagnosis for manifestations Resolution of manifestations with 4 days or less of antibiotics No surgical or pathologic evidence with 4 days or less of antibiotics Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209.

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TABLE 21-5 -- Clinical versus Echocardiographic-Based Criteria: Results of Two Trials Retrospective Duke Trial * Clinical criteria identified 51% of pathologically definite infective endocarditis Echocardiographic/clinical criteria identified 80% Prospective Harbor/UCLA Trial † Clinical criteria identified 50% Echocardiographic/clinical criteria identified 100% (41% by TEE only) *Data from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. †Data from Bayer AS, Ward JI, Gintzon LE, Shapiro SM: Am J Med 1994;96:211– 219; Bayer AS: Clin Infect Dis 1996;23:303–304.

are the preferred systematic diagnostic approach. One suggestion is to eliminate minor criterion status for a nondiagnostic echocardiogram[12] based on the widespread use of TEE. Another suggestion is to consider a positive Staphylococcus aureus blood culture or Q fever seropositivity as major criteria. However, regardless of possible modifications of the Duke criteria, these studies provide compelling evidence for the inclusion of echocardiography as an integral element in the diagnosis of infective endocarditis. The remainder of this chapter concentrates on the details of the echocardiographic approach to the patient with infective endocarditis by discussing the strengths and weaknesses of each component of the echocardiographic examination as it relates to the detection and analysis of vegetations and complications and the estimation of prognosis.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Vegetations The first goal of the echocardiographic examination is identification, characterization, and localization of valvular vegetations. For many reasons, the process is one of integrating circumstantial findings and epiphenomena, and, through indirect (albeit compelling) evidence, reaching a reasonable conclusion that a given echocardiographic set of observations has identified the pathologic hallmark of endocarditis, the vegetation. Once a vegetation has been identified, criteria can be applied to judge clinical prognosis. This diagnostic process first depends on a solid knowledge of the normal appearance of cardiac structures seen in a variety of technically mediated circumstances. These circumstances include the choice of transducer frequency, variations among commercial ultrasound instruments, the unique technical characteristics of each patient, the settings of the instrument, variations in technique among technicians, and the duration and intensity of the examination as influenced by the level of pretest and intratest index of suspicion regarding the likelihood of disease (Table 21-6) . Qualitative and Technical Factors Transducer Frequency

Lower frequency transducers (i.e., nominal center line frequency of approximately 2.5 MHz) are the type most commonly employed in adult patients because they combine superior penetration with optimal color flow and spectral Doppler sensitivity. Although the images obtained at lower frequencies are easier to acquire, they are lower in resolution than those obtained at higher frequencies, particularly in the middle and far fields of the image where beam spread causes image degradation. From the precordial window, the mitral valve lies in the middle field, and from the apical window, it lies in the far field. At these distances, a normal valve examined with low frequency insonation tends to take on an irregular or

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lumpy appearance. If present, small vegetations tend to be obscured and normal irregularities magnified. For these reasons, sequential use of both a lower frequency and higher frequency transducer is recommended for routine examinations in order to develop familiarity with the normal appearance of cardiac structures generated under both circumstances and to promote recognition of genuine pathologic changes. Harmonic imaging has become widely available and will soon become the standard modality for most examinations. In this technique, insonation is accomplished by transmission at a standard frequency, but with detection of the reflected signal at its harmonic frequency (one-half the transmitted value). For example, if 3.5 MHz is used for transmission, the received signal is analyzed at 1.75 MHz. The technique provides greater sensitivity for the low-level signals arising from the endocardium, allowing better evaluation of regional ventricular wall motion. Tradeoffs for this beneficial increase in contrast resolution include accentuation of normal leaflet irregularities and homogenation of valve texture; both tend to reduce specificity for identifying a mass as vegetation. The chordal attachment points are particularly likely to take the appearance of small lumps. At the time of this writing, the technique is not available with TEE because it has not been possible to adapt it to the higher frequencies at which TEE examinations are conducted. It is, therefore, not uncommon to perform a TEE examination at 7 MHz in a patient with a "lumpy" mitral valve on transthoracic harmonic imaging but find that the valve is absolutely normal in appearance on TEE. Commercial Instruments and Instrument Setting Variation

Dynamic range options, pre- and postprocessing algorithms among instruments, and changes in these settings within instruments alter the appearance of valves. Depth settings, probe frequency, deployment of electronic focusing, and sector width have differing influences on the frame rate at which the image is displayed. At greater TABLE 21-6 -- Technical Factors Affecting Detection of Valvular Vegetations Transducer frequency (particularly low-frequency imaging) Instrument characteristics and settings (especially harmonic imaging) Patient characteristics Pretest expectations and probability

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depth settings (e.g., 20 cm), slower frame rates, especially in the far field, may obscure the characteristic rapid vibrations of many vegetations. Some devices offer "B color" tagging of tissue images. This method expands the dynamic range of the display and may influence the appearance of valve pathology. The highly reflective nature of calcific degeneration may be easier to differentiate from the tissue or thrombus-like appearance of vegetations when using this type of image postprocessing. Patient Physical Characteristics

Obesity, hyperinflated lungs, narrow interspaces, valvular and annular calcification, and valve prostheses impede the transmission of ultrasound between the transducer and the heart. A tall patient may have greater distance from the apical impulse location to the mitral valve. All of these factors can obscure a vegetation that might have been seen under other circumstances. TEE is less sensitive to these constraints and nearly always provides an excellent examination. The difference between TTE and TEE must be considered when analyzing the endocarditis literature or when choosing the ideal imaging modality for a given patient. Pretest Expectations

The physician or sonographer begins each examination with some notion about what is being sought in each patient. If there is strong suspicion of endocarditis, it is only natural to scrutinize the valves with augmented intensity using a complete array of probes and processing algorithms. Under such circumstances, maximal "performance" of the technique may be approached. However, as sensitivity rises, specificity must fall pari passu. Under the magnification of increased surveillance, small, normally unseen irregularities, anatomic variants, and artifacts may be mistaken for vegetations. When only transthoracic imaging was available, considerable time and care was taken to visualize the valve structures in patients with suspected endocarditis with reported sensitivities for detection of valvular vegetations much higher than in subsequent studies comparing TEE with TTE. The lower sensitivities in these studies may possibly be due to a shifting of attention to the TEE arm of the study. Nonetheless, these lower sensitivities are probably more representative of what may be expected in daily clinical practice.

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M-mode Echocardiography M-mode echocardiography was the first ultrasound imaging modality widely applied in endocarditis. With M-mode imaging, the smallest size of vegetation that can be detected is estimated to be about 5 mm.[13] Although the role of M-mode imaging is less important when two-dimensional imaging is used, the M-mode approach remains useful in specific situations. M-mode echocardiography offers high sampling rates and fine resolution when compared with two-dimensional imaging (>1000 Hz vs. two-dimensional echocardiography at 30 to 60 Hz). M-mode imaging not only allows recognition of vegetations that prolapse (by location) but also can detect their characteristic tissue level images and typical vibrations. These vibrations occur as the prolapsing mass, composed of platelets, thrombus, bacteria, inflammatory cells, and disrupted valve tissue, is caught in the regurgitant jet. Although it is normal for the aortic valve to vibrate slightly during systole, diastolic vibrations almost certainly indicate that the mass is a vegetation, a torn leaflet, or both (Fig. 21-1A) (Figure Not Available) . Similarly, systolic vibrations of the mitral leaflet are highly suggestive of a vegetation, ruptured valve, or both (see Fig. 21-1B) (Figure Not Available) . In seeking to confirm a mass as a vegetation, it is useful to employ these specific but insensitive signs,[14] but when doing so, to remember that in modern ultrasound equipment their sensitivity has been diluted by lowered resolution and the limited frame rate of the video display in comparison with a single crystal probe combined with a strip chart recorder. Two-Dimensional Echocardiographic Imaging of Vegetations In a meta-analysis of 16 early studies (641 patients) O'Brien and Geiser[15] reported a mean sensitivity of 79% for two-dimensional echocardiography in the detection of vegetations in infective endocarditis. M-mode imaging sensitivity from the same series was only 52%. In one of the first reports of two-dimensional echocardiography in definite (autopsy/surgery) cases of infective endocarditis, Gilbert et al[14] noted good agreement between the location and identity of large vegetations and pathologic findings but encountered difficulties when comparing exact ultrasound measurements to pathologic reality. More importantly, this study found that "several" small vegetations of less than 3 mm in maximum dimension were undetectable by two-dimensional echocardiography. This lower size limit on vegetation detection continues to be a current problem in the use of TTE. In the decade since the Gilbert et al study, the sensitivity

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of TTE has dropped despite major improvements in ultrasound equipment (Table 21-7) . For example, on review of 7 studies performed between 1989 and 1994[16] [17] [18] [19] [20] [21] [22] [31] the mean sensitivity for TTE was 62%, whereas for TEE it was 92%. As stated, the reason for the decrease in TTE sensitivity is probably a combination of more rigorous and less biased case selection in the contemporary studies and less intense scrutiny of the patient with TTE than with TEE. TABLE 21-7 -- Two-Dimensional Echocardiography versus M-mode Echocardiography versus TEE: Sensitivity for Detecting Vegetations Meta-Analysis of 16 Early Studies M-mode, 52% Two-dimensional echocardiography, 79% Meta-Analysis of 7 More Recent Studies Two-dimensional echocardiography, 62% Transesophageal echocardiography, 92%

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Figure 21-1 (Figure Not Available) A, M-mode image of a disrupted aortic valve showing coarse systolic vibrations (arrowheads) specific for vegetation, disruption, or both. Very fine systolic vibrations are normally seen and can be barely discerned. B, M-mode image of an infected mitral valve showing increased thickness and systolic vibrations specific for vegetation, disruption, or both.

The accuracy of the measurement of structures in echocardiographic images is limited by resolution. Because TTE underestimates the size and complexity of large vegetations and fails altogether to detect small vegetations (<3 mm in diameter), it is reasonable to conclude that if knowledge of the size and behavior of vegetations is predictive of prognosis and useful in guiding therapy, TTE underachieves as a prognostic and therapeutic guide. Furthermore, in a review of the literature of infective endocarditis, none of the studies stated the carrier frequency of the transthoracic transducer. From this omission, it may be inferred that there is considerable variation in performance of TTE within and among studies, weakening the use of size criteria in clinical practice. In a comprehensive published study of the prognostic value of the

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morphologic details of TTE images of vegetations, Sanfilippo et al[23] retrospectively studied 204 patients who met clinical criteria of infective endocarditis. Documented clinical events were correlated with echocardiographic vegetation characteristics. The events or complications were as follows: 1. Failure of febrile illness to respond to an appropriate course of antibiotics so that a change in treatment was required 2. Congestive heart failure on or after admission 3. Pulmonary, systemic, or peripheral embolization 4. Surgery 5. Death Valvular vegetations were defined as "a discrete mass of echogenic material adherent at some point to a leaflet surface and distinct in character from the remainder of the leaflet." Separate classifications were made for nonspecific thickening ("diffuse irregularities"), aortic valve disease, mitral valve disease, mitral prolapse, prosthetic valve, and no evidence of vegetations. If a mass was identified as a vegetation (Table 21-8) , it was analyzed according to four properties: Size: Two largest orthogonal diameters perpendicular and orthogonal to the leaflet (Fig. 21-2) (Figure Not Available) Mobility: Grade 1, fixed; grade 2, fixed base, free edge; grade 3, pedunculation; grade 4, prolapsing (Fig. 21-3) (Figure Not Available) Density: Grade 1, calcified; grade 2, partially calcified; grade 3, more dense than myocardium but not calcified; grade 4, equivalent to myocardium Extent: Grade 1, single; grade 2, multiple on a single leaflet; grade 3, multiple leaflets; grade 4, extending to extra valvular structures The overall incidence of complications was 55%, with equivalent rates for native and prosthetic valves and for clinical endocarditis in nonspecifically thickened valves. Unexpectedly TABLE 21-8 -- Five Characteristics Allowing a Valve Mass to Be Designated a Vegetation Texture

Gray scale and reflectance of myocardium

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Location Characteristic motion Shape Accompanying abnormalities

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Upstream side of valve in path of jet Chaotic and orbiting Lobulated and amorphous Abscess and pseudoaneurysm Fistulas Prosthetic dehiscence Paravalvular leak: significant pre-existing or new regurgitation

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Figure 21-2 (Figure Not Available) Vegetation size is measured in two axes or diameters. D1 is the maximum size of the vegetation perpendicular to the leaflet; D2 is the maximum extent of the vegetation parallel to the leaflet surface. The larger of the two dimensions was used for analysis. Ao, aorta; LA, left atrium; LV, left ventricle. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191– 1199. Reprinted with permission from the American College of Cardiology.)

high rates of complications were found for tricuspid endocarditis (77%) and studies with no abnormality (27%). There tended to be more complications with higher grades of mobility and lesion extent. Vegetation consistency did not predict complications except that those with calcified vegetations had no clinical complications (Fig. 21-4) (Figure Not Available) . Size was perhaps the most powerful predictor of complications. The probability of sustaining a complication was 10% in 6-mm vegetations, 50% in 11-mm vegetations, and almost 100% at 16-mm vegetations in maximum dimension (Fig. 21-5) (Figure Not Available) . Sanfilippo et al also proposed a "score" for risk, calculated as the sum of the scores for size, mobility, and extent (each grades 1 to 4). The highest possible score Figure 21-3 (Figure Not Available) A vegetation mobility grading scheme is illustrated (see text). (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) Figure 21-4 (Figure Not Available) Complication rates by the extent of a graded vegetation abnormality: mobility, extent, and consistency. The numerator above each

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subgroup refers to the number of patients with a given complication, and the denominator refers to the total number in that subgroup. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

for any valve is 12. As Figure 21-6 (Figure Not Available) (mitral) and Figure 21-7 (Figure Not Available) (aortic) show, a high score is always present in patients with complications (i.e., high sensitivity), but only half or less of those with high scores actually develop complications (i.e., low specificity). There is a trend for aortic valve endocarditis to have a higher complication rate, but the statistical significance is not clear from this study. These figures are reproduced here because they may prove useful in clinical decision making; however, their "exportability" to TEE findings is uncertain. Because a given vegetation on TEE is likely to appear larger, a higher score may be required for a given level of risk when using the newer modality. Seeking to improve on this study, De Castro et al[24] examined 57 patients with large (>10 mm) vegetations and no previous embolic events at the time of the study using both TTE and multiplane TEE. In the course of the Figure 21-5 (Figure Not Available) Complications relative to vegetation size. Note that this graph is not limited to any one complication such as peripheral embolization but plots all complications relative to size. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

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Figure 21-6 (Figure Not Available) Mitral valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

study, 44% sustained clinically apparent embolic events. Although this study confirmed that large vegetations define a high-risk population, within this group, no single characteristic of vegetation location, mobility, or appearance predicted embolization. Millaire et al[25] used advanced imaging techniques (e.g., magnetic resonance imaging, computed tomography, and other modalities) in 102 patients meeting the Duke criteria for infective endocarditis. Combining the

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results of imaging with a 21-month follow-up, the investigators found that 51% had imaging evidence of embolization and that many were clinically inapparent. There was a trend toward higher mortality in those with emboli (20% versus 12%), but the trend did not reach statistical significance. From these data it was concluded that demonstrable embolization is far more common than previously thought; therefore, a study seeking to predict events by vegetation characteristics needs to use advanced imaging as a reference standard. There is no evidence that such a study has been performed, and the question of the capability of echocardiography to predict outcome remains unsettled. Transesophageal Echocardiography When two-dimensional imaging supplanted M-mode echocardiography as the imaging mode of choice, some published cases still suggested suboptimal sensitivity even with two-dimensional echocardiography.[26] These suspicions were shown to be well founded when TEE was applied to the study of patients with suspected endocarditis.[27] It was not until almost a decade later, however, when a number of studies addressed the marked differences in sensitivity between TTE and TEE[19] ( Fig. 21-8 , Fig. 21-9 , Fig. 21-10 ). The role of TEE in endocarditis is a direct result of its high sensitivity in detecting the defining manifestation of Figure 21-7 (Figure Not Available) Aortic valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.)

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Figure 21-8 Discrepancy between TTE and TEE. Left, Apical fourchamber view showing only subtle changes in the posterior leaflet of the mitral valve (arrow). Right, TEE shows a flail, thickened valve with evidence of a vegetation at the tip of the posterior leaflet (pML). The anterior leaflet (aML) has normal thickness and is normally positioned. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Figure 21-9 Four small vegetations (small arrows) arrayed along the

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anterior mitral leaflet. By transthoracic echocardiography, only one of these (large arrow) was suspected.

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Figure 21-10 A, Four-chamber TEE view taken in the transverse plane. Small solitary vegetation (Veg, arrow) is seen at the coaptation of the anterior and posterior mitral leaflets (aML, pML) but was not apparent on transthoracic echocardiography. Note the gray texture of the mass, which closely resembles myocardium. This appearance is typical of a vegetation. Ao, aorta. B, Larger vegetation detected by TTE but found to be 3 mm larger by TEE. C, Transverse plane view of the base of the heart from TEE. The left atrial (la) appendage (laa) is occupied by an irregular mass whose shape, location, and motion are typical of thrombus (thr). Note that the gray texture of the mass is indistinguishable from that of vegetation. Thus, vegetations and thrombi are identified by circumstantial rather than direct evidence.

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TABLE 21-9 -- Reported Sensitivity and Specificity of TEE for Native Valve Endocarditis TTE (%)

TEE (%)

Sample Size (n) SENSITIVITY/SPECIFICITY SENSITIVITY/SPECIFICITY Shively et al 66 44/98 94/100 [19] (1991) Pedersen et 24 50/— 100/— [31] al (1991) 61 Birmingham et al (1992) [28]

Aortic Mitral Sochowski and Chan

25/— 50/— 105 —/—

88/— 100/— 91/—

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(1993)[21] 64 60/91 87/91 Shapiro et al [30] (1994) TOTAL 256 46/95 93/96 TTE, transthoracic echocardiography; TEE, transesophageal echocardiography. the disease, valve vegetations. The comparison of the sensitivity of TTE to that of TEE is an important issue because if the two methods are similar in this regard, the less invasive and less expensive modality will be used. Five studies that address the differences in sensitivity between TTE and TEE in detecting vegetations[19] [28] [29] [30] are presented in Table 21-9 . Generally, patients reported in these studies are considered to have vegetations when a valve abnormality (mass) has the characteristics that allow it to be identified as a vegetation with a "high degree of certainty."[23] These characteristics include the texture of the mass, its location, characteristic motion, shape, and accompanying abnormalities. In general, experienced readers recognize a vegetation as having a gray scale and a low level of reflectance similar to myocardium (Fig. 21-11) . Vegetations are usually positioned on the upstream side of the valve (e.g., on the atrial side of the mitral valve and on the ventricular side of the aortic valve) and concentrated at the point where a regurgitant or stenotic jet impinges on the valve or wall. The mass is usually lobulated, amorphous, and mobile. The mobility Figure 21-11 TEE image of a bulky vegetation involving the atrial surface of the mitral valve and the annulus. Note the amorphous shape and gray texture, which resembles myocardium. This patient also had moderate to severe mitral regurgitation. LA, left atrium.

may be chaotic, appear to orbit around the valve, or have fine vibrations imparted by the jet of abnormal flow. Abnormalities that accompany vegetations include periannular abscesses (solid or cystic), fistula formation, and severe regurgitation (Fig. 21-12) . In prosthetic endocarditis, paravalvular leaks, valve dehiscence, and occasional obstruction are seen (Fig. 21-13) . Vegetations also characteristically prolapse into the upstream chamber: mitral vegetations into the atrium in systole, aortic vegetations into the left ventricular outflow

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tract during diastole. As stated, they tend to flank the regurgitant jet or form on a jet target. Characteristics that identify an abnormal mass as being unlikely to be a vegetation include high reflectivity, bistable appearance (white not gray), fibrillar appearance with narrow base of attachment (Fig. 21-14) , and lack of associated regurgitation (Table 21-10) . These characteristics are used by experienced readers regardless of whether a transthoracic or transesophageal window is used. Their appearance on TEE, however, is considerably more vivid, and the resolution for very small vegetations is higher. The superior sensitivity of TEE is clearly and consistently documented by the studies listed in Table 21-9 , in which the differences between modalities were strongly significant statistically. From these findings and from the study of Lowry et al[32] it can be concluded that a transesophageal echocardiogram with a negative result makes the probability of endocarditis very low; it does not, however, eliminate the possibility, and the physician must always temper interpretations with clinical judgment. For example, it may be appropriate to repeat an initial TEE examination with a negative result after 1 to 2 weeks if the clinical suspicion and disease course continue to suggest endocarditis. As the sensitivity of a test increases, specificity is likely to decrease. Falsepositive findings in TEE arise because small, previously invisible irregularities and degenerative processes are clearly seen in magnified format. A two-center study, in which this researcher participated as an "expert" blinded reader, compared TTE with TEE in infective endocarditis. Although no false positives occurred, some minor irregularities were encountered.[19] For example, tiny mobile strands on either valve are frequently encountered. These strands probably represent a normal degenerative process and are known as Lambl's excrescences. Strands, possibly from the same source, can arise on the sewing ring of prosthetic valves. Occasionally, a suture end can be visualized and might be mistaken for a pathologic finding. Redundant chordae or false tendons in the left ventricle as well as Chiari's remnant on the TABLE 21-10 -- Characteristics of a Mass Not Likely to Be a Vegetation Texture Location Shape

Reflectance of calcium/pericardium (appears white) Outflow tract attachment, downstream surface of valve Stringy or hairlike strands with narrow

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attachment Lack of accompanying No regurgitation abnormalities

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Figure 21-12 Endocarditis of the mitral and aortic valves leading to abscess (Ab)/pseudoaneurysm, aortic and mitral vegetations (veg), severe aortic insufficiency (AI), and fistula formation (not shown) between the aorta (Ao) and left atrium (LA). A, Contiguous vegetations on both aortic and mitral leaflets. B, Thick-walled, expansile abscess of the aortic root. C (color plate.), Broad jet of aortic insufficiency filling the outflow tract. D (see color plate), Width and timing of jet seen in C documented by color M-mode echocardiography. Wide jets that occupy more than 65% of the left ventricular outflow tract are indicative of severe regurgitation. LVOT, left ventricular outflow tract; RA, right atrium.

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Figure 21-13 (color plate.) Prosthetic dehiscence due to endocarditis. Note that the ring of this mechanical prosthesis is displaced from its expected plane and separated from the posterior aortic (Ao) root (top). Bottom, Color flow documents that the site of aortic insufficiency (AI) is paraprosthetic.

right side may pose as vegetative masses. All of the masses mentioned in this paragraph have a tendency to be highly reflective in appearance with the approximate echodensity of pericardium or aortic root.

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Prosthetic Valve Endocarditis Prosthetic valve endocarditis is a special case (Table 21-11) . The materials used to construct these devices usually do not allow passage of ultrasound and, as a result, these valves shadow or obscure structures lying between the valve and the transducer. For example, it is usually impossible to image the atrial side of the mitral prosthesis or the arterial side of the aortic prosthesis from an apical TABLE 21-11 -- Prosthetic Valve Endocarditis: A Special Case Both transesophageal echocardiography and transthoracic echocardiography must be used to circumvent shadowing— Ventricular side of mitral valve: Transthoracic echocardiography Atrial side of mitral valve: Transesophageal echocardiography Two or three prostheses: Shadow one another

TABLE 21-12 -- Prosthetic Valve Endocarditis: Comparison of TEE to TTE Sensitivity

Daniel et al (1993)[33] Zabalgoitia et al (1993)[35] Bioprostheses Abscess

TEE TTE Sample Size Sensitivity Sensitivity (n) (%) (%) 33 82 36 44 4

86 100

44 25

TTE approach. TEE solves this problem in mitral prostheses and improves it in aortic prostheses. When both mitral and aortic devices are present, however, shadowing from the mitral device tends to obscure the region of

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the aortic prosthesis. Multiplanar TEE probes allow improved imaging in this situation, but some areas may remain obscured; therefore, a combination of TTE and TEE imaging may be needed for complete visualization of the valvular structures. Tricuspid and pulmonic devices pose similar problems, but they are effectively evaluated by TEE. Daniel et al[33] reported on 33 cases of prosthetic endocarditis studied with both TEE and TTE and found sensitivities of 82% and 36%, respectively. Alton et al[34] reported similar findings but with smaller numbers. In a study of TEE in 44 patients with bioprosthetic valves who were going to surgery, Zabalgoitia et al[35] found that TTE had a sensitivity of 44%, whereas TEE had a sensitivity of 86% (Table 21-12) . In abscess identification, TEE was 100% sensitive, whereas TTE was only 25% sensitive (Fig. 21-15) . Figure 21-14 Ruptured chordae tendineae (rct) of the posterior mitral leaflet. This prolapsing mass is thin and brighter in appearance than a vegetation (similar to the aortic root and anterior leaflet). Although this condition was associated with severe mitral regurgitation, there were no other clinical features of endocarditis.

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Figure 21-15 Large posterior abscess in a bioprosthesis. A, TEE image of a thick-walled abscess with an abscess cavity or pseudoaneurysm posterior to the aortic root and protruding into the left atrium. The arrow points to the collapsed cavity during diastole. Note that the cavity is contiguous with the posterior stent of the aortic prosthesis. B, Systolic expansion of the cavity (arrow). Note the anterior shadowing of structures that lie beyond the prosthesis. C, Transthoracic echocardiography in the same patient showing little more than the sewing ring (sr) of the prosthesis and a vague outline of the aortic ring (short arrow). The large gulf in resolution between these two modalities is illustrated here. a, anterior; p, posterior.

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Prediction of Clinical Outcome Once a native valve vegetation is identified, the attending physician is obligated to estimate the risk that the process poses to the patient's recovery or survival and to decide on an appropriate therapeutic plan. Unexpectedly, the bacteriology of the responsible organism was not found to be of prognostic importance in the Sanfilippo et al[23] or Mugge et al[16] studies. Prognostic estimations and decisions, however, can be made by a careful analysis of the clinical and TEE presentation. There are interesting and provocative studies that the clinician can use in making these decisions.[16] [36] [37] [38]

Using TTE to predict embolic events, researchers at Duke[38] looked at the site, size, mobility, shape, and attachment of vegetations. They found high interobserver agreement on the presence and location of vegetations but less agreement on the size, mobility, and shape. A vegetation size of greater than 10 mm was associated with an embolic rate of greater than 50%, whereas a vegetation size of less than 10 mm was associated with an embolic rate of 42%. In contrast to the study by Sanfilippo et al,[23] these researchers found that characteristics of vegetations from TTE were not helpful in predicting complications. In applying TEE to the same question, Mugge et al[16] concurred with the lack of correlation between site, mobility, shape, and attachment of the vegetation and prediction of embolic events. Mugge et al, however, probably owing to the increased sensitivity of TEE imaging, found a stronger association between vegetation size and embolic events than did researchers of the Duke study, particularly if the vegetation was present on the mitral valve. A vegetation size of greater than 10 mm was associated with an embolic rate of 46%, whereas vegetation size less than 10 mm was associated with only a 20% risk (P < .001). These observations are not comparable to the TTE study of Sanfilippo et al,[23] in which all complications were related to vegetation characteristics: the use of

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vegetation characteristics to predict specific complications such as systemic embolism was not examined. Also, if all studies had employed TEE and surveillance imaging for subclinical embolic events, perhaps a better correlation between size and outcome would have been demonstrated. In one of the most interesting and useful studies, Rohmann et al[36] performed serial TEE in 83 patients and found that if a vegetation size increased or remained static during 4 to 8 weeks of therapy, prognosis was much worse than if vegetation size decreased with therapy. These differences were striking and included incidence of valve replacement (45% versus 2%), embolic events (45% versus 17%), abscess formation (13% versus 2%), and mortality (10% versus 0%) (all P < .05). These data suggest that it may be logical to temporize by performing serial studies in patients who have not experienced complications and who present with large vegetations that tempt early surgical intervention. They also dispel somewhat the concern that a shrinking vegetation is tantamount to embolization of a fragmenting mass. When indicated, it is appropriate to repeat the TEE after 7 days of antibiotic therapy and compare the size of the vegetations. Although this time scale is considerably shorter than the 4 464

TABLE 21-13 -- TEE Vegetations and Outcome Size Mugge et al (1989) >10 mm: 46% emboli [16]

Heinle et al (1994) [38]

>10 mm: >50% emboli

Temporal Behavior Rohmann et al (1991)[36] Serial TEE at 4–8 wk: Static or enlarged vegetation Valve replacement 45% Embolic events 45% Abscess formation 13%

<10 mm: 20% <10 mm: 40%

(P < .001) (P = ns)

Smaller vegetation 2% 17% 2%

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Death

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10%

0%

(P < .05 for all)

to 6 weeks in the Rohmann et al study, dramatic decreases in vegetation size may be seen after only 1 week of treatment. A prospective study is needed to determine the shortest time interval required between the first observation at the beginning of treatment and the second observation to reliably establish a patient as a responder or nonresponder to antibiotic therapy (Table 21-13) . It is also important to consider the implications of a TEE examination that fails to show vegetations in a patient with suspected infective endocarditis (Table 21-14) ; Shively et al[19] found a negative predictive value of 98% for a TEE study with a negative result in patients with suspected endocarditis. Sochowski and Chan,[21] however, using monoplane TEE, found 65 of 105 patients with suspected infective endocarditis with a negative finding on initial examination. Of these, 56 patients never developed definite endocarditis, but in five patients, infective endocarditis was eventually documented. In three of these five, repeat TEE demonstrated new vegetations. The most common type of patient with infective endocarditis in whom initial TEE fails to detect a vegetation is one with an aortic prosthesis. Although a false-negative TEE examination occurs in only 5% or less of patients with infective endocarditis, all negative studies impose an obligation on the physician to follow patients until a sustained afebrile status is confirmed. Under some circumstances it may be permissible to withhold antibiotics while monitoring for signs of infective endocarditis.

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Intracardiac Complications of Endocarditis In the process of bacterial infiltration and proliferation in valve tissue, the integrity of the leaflet may be destroyed. This TABLE 21-14 -- Implications of an Initial TEE with a Negative Result Shively et al (1991)[19] 98% negative predictive value Sochowski and Chan 65 of 105 suspected cases had a negative result on initial examination (1993)[21] 56 never developed infective endocarditis 5 eventually developed disease (3 showed vegetations on repeat examination) Aortic prosthetic endocarditis was most likely to be negative destruction leads to regurgitation of varying severity. Etiology makes little difference in the echocardiographic features of severe mitral regurgitation. There is a distinct feature of valves in infective endocarditis, however, that merits consideration; that is, it is very difficult to differentiate a disrupted, prolapsing, and flail segment of leaflet from a mobile prolapsing vegetation. Both have the same motion during the cardiac cycle and the same visual tissue characteristics, and both may be simultaneously present in the same location. Measuring a flail leaflet that has been mistaken for a vegetation may lead to miscalculation of risk level, or worse, an incorrect diagnosis of endocarditis. TEE substantially improves the likelihood of distinguishing leaflet from vegetation; this ability probably contributes to its advantages as a prognostic and diagnostic tool. Beyond this feature, the principles that govern the Doppler and two-dimensional evaluation of the severity of valvular regurgitation remain the same and are discussed thoroughly elsewhere in this book. When the endocardial infectious process spreads beyond the valve leaflets

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or endocardium it invades the continuous basal myocardium and tissue of the fibrous cardiac skeleton. Early in this process, the contagion produces cellulitis. If tissue necrosis and white cell activity continue, the central portion of this process undergoes pyogenesis and forms an abscess cavity ( Table 21-15 ; see also Fig. 21-12 , Fig. 21-15 , and Fig. 21-16 ). Because the abscess wall is under considerable pressure, the weakened necrotic tissue may disrupt, resulting in communication with a ventricle, atrium, or great vessel (Fig. 21-16) . In the setting of this fistulous communication the abscess cavity can also be viewed as a pseudoaneurysm,[39] particularly if it involves the aortic wall directly. Examples of fistulous communications include aorta to left atrium (associated with a new continuous murmur) and left ventricle to right atrium. If the abscess extends into the septum, the conduction system may be interrupted or slowed and a right bundle branch block with first-degree A-V block may ensue. [40] In a landmark study of the effectiveness of TEE in detecting abscesses in endocarditis, Daniel et al[20] studied 118 cases and found evidence of abscess formation in 37%. The mortality rate among those with abscess was 23% versus 14% for those without. The sensitivity and specificity of TTE imaging was 28% and 99%, respectively, whereas TEE imaging had a sensitivity and specificity of 87% and 95%, respectively, for detection of paravalvular 465

TABLE 21-15 -- TEE Myocardial Abscess Leung et al (1994) [20]

Sample Size Abscess Formation Detection by TTE Sensitivity Specificity Detection by TEE Sensitivity Specificity

Daniel et al (1991) n = 118 44 (37%)

[41]

n = 34 (all aortic) 11 (32%)

28% 99%

36% 100%

87% 95%

100% 100%

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Mortality With abscess Without abscess Staphylococcus aureus With abscess Without abscess Site of Infection Native aortic root Para-aortic prosthesis

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23% * 14% * p = NS

5/11 (45%)

52% † 16% † p <.001 14/44 (32%) 12/44 (27%)

*P = ns. †P < .001.

abscess. Karalis et al[40] found a similar disparity in sensitivity between TTE and TEE. From these data it is also evident that abscess-related lesions are relatively common in endocarditis (especially when the infecting organism is S. aureus) and patients with a demonstrable abscess on echocardiography represent a subgroup that is at high risk for death. In one study the mortality rate was as high as 45% when an abscess was detected.[41] Because of proximity to the transducer, TTE is most effective in detecting an anterior abscess at the aortic septal junction and least effective in detecting those that lie more posteriorly. Its overall adequacy is insufficient for detection of abscesses because its Figure 21-16 (color plate.) Aortic root abscess in communication with the aortic root. In this case of aortic endocarditis, there is a large vegetation on a partly destroyed aortic valve (AV) and a root abscess (Ab). Note that color flow imaging demonstrates both severe aortic regurgitation (right, large arrow) and flow into the abscess cavity (arrowheads). LA, left atrium; RVOT, right ventricular outflow tract; SVC, superior vena cava.

sensitivity is far too low and the extent of the lesion is unlikely to be fully

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Right-Sided Infective Endocarditis Vegetations of the tricuspid valve are commonly encountered in populations of intravenous drug users. Most reported series use TTE to study this group of patients. Hecht and Berger[42] collected 132 instances of right-sided infective endocarditis in 121 intravenous drug users. S. aureus was the organism in 82% (108 of 132). The tricuspid valve was the site in 127 patients, the pulmonic valve in 4 patients, and both valves in 1 patient. In 80% the vegetation was 1 cm or greater in diameter. There was a strongly significant association between vegetation size greater than 2 cm and mortality rate (33% in those with a vegetation > 2 cm vs. 1.3% in those with a vegetation < 2 cm; P > .001). San Roman et al[43] studied 48 intravenous drug users suspected of having infective endocarditis with both TEE and TTE. Both techniques were equally sensitive and specific, each identifying the same 22 vegetations. In no instance did TEE find a vegetation that was overlooked by TTE. In 63%, however, the vegetation was better characterized by TEE. From this study San Roman concluded that TEE did not confer sufficient advantage to justify its routine use in intravenous drug users with suspected right-sided endocarditis. This study met with criticism because it was mostly conducted with monoplane equipment. In my own experience, the use of multiplane TEE in these cases has increased the yield of pulmonic vegetations[44] ( Fig. 21-17 and Fig. 2118 ). Another concern is the possibility of left-sided involvement in patients with right-sided vegetations. If the duration of medical therapy would be affected by the presence of left-sided vegetations, TEE may be needed. It remains to be seen whether further experience will justify an expanded role for TEE in right-sided endocarditis. For the moment, the issue remains unsettled.

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Figure 21-17 (color plate.) Four-chamber view from TEE in a patient with a tricuspid valve vegetation. The color flow image of tricuspid regurgitation (arrow) obscures the vegetation. Note that the interatrial septum is bulging abnormally from right to left, confirming the severity of the regurgitant lesion. Figure 21-18 Transverse (left) and longitudinal (right) plane images of a pulmonic valve vegetation (Veg). The use of multiplane TEE was probably responsible for the identification of this vegetation, because it was very difficult to appreciate in the transverse plane. LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract.

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TABLE 21-16 -- Key Points in Echocardiographic Evaluations of Patients with Endocarditis 1. Echocardiography has a central role in diagnosis and management of infective endocarditis 2. All patients with infective endocarditis should undergo serial TTE 3. Most if not all patients with infective endocarditis should undergo TEE at least once 4. Technical factors are paramount 5. Experienced operators and readers are essential 6. High-frequency probes and biplanar/multiplane TEE are required

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Summary In summary (Table 21-16) , echocardiography has an unassailable place in the diagnostic evaluation and management of infective endocarditis. TTE and TEE are complementary from the point of view of comprehensively evaluating hemodynamics and anatomy. TEE is superior to surface imaging by dint of its greater sensitivity in detecting native valve vegetations, prosthetic valve vegetations, paravalvular abscesses, and other pyogenic complications. A negative finding on a TEE study makes endocarditis unlikely, and a large vegetation that fails to shrink during therapy connotes a poor prognosis. Based on these considerations and clinical experience, it is an established medical fact that all patients with infective endocarditis should undergo TTE, and it is the firm opinion of most experts that these patients should also have at least one TEE examination.

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469

Chapter 22 - Aortic Stenosis Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making David M. Shavelle MD Catherine M. Otto MD

Evaluation of Stenosis Severity The echocardiographic evaluation of the patient with valvular aortic stenosis focuses on quantitation of stenosis severity and assessment of the left ventricular response to chronic pressure overload. However, complete evaluation also includes quantitation of coexisting aortic and mitral regurgitation, estimation of pulmonary artery pressures, assessment of left ventricular diastolic function, measurement of the degree and extent of aortic root dilation, and evaluation of any other coexisting cardiac abnormalities. Evaluation for concurrent coronary artery disease may require additional diagnostic procedures. The basic clinical echocardiogram includes measurement of maximum aortic jet velocity and calculation of continuity equation aortic valve area, as detailed in the Textbook of Clinical Echocardiography. [1] Although echocardiographic measures of stenosis severity have been well validated, it still is the responsibility of each echocardiographer to be aware of the

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theoretical basis of these techniques and potential pitfalls in their clinical application. In some clinical situations, other measures of stenosis severity may be helpful in patient management. In addition, a more detailed assessment of stenosis severity may be important for understanding the natural history of this disease and for assessment of interventions to slow or reverse disease progression. Pressure Gradient versus Jet Velocity The velocity of blood flow through the narrowed aortic orifice is related to the pressure difference across the valve as described by the Bernoulli equation. For valvular aortic stenosis, the simplified Bernoulli equation, ∆P = 4v2 , which ignores the effects of acceleration and viscous losses, has proven to be remarkably accurate as compared with simultaneous invasive pressure gradient measurements. The relationship between Doppler velocity and manometric pressure measurements has been evaluated in in vitro models of a stenotic valve, in animal models of valvular and nonvalvular stenosis, and in patients with clinical disease.[2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] In these studies, simultaneous measurements show a close correlation between Doppler and 470

invasive maximum instantaneous and mean pressure gradients over a wide range of stenosis severity. In addition, the Doppler technique accurately measures changes in pressure gradient with changes in flow rate.[11] [13] [15] Of course, nonsimultaneous recordings of Doppler and manometric data correlate less well, since interval physiologic changes in transaortic volume flow rate and heart rate may result in interval changes in the transaortic gradient. Some clinicians may be confused by the use of Doppler velocity and maximum gradient measurements if the differences between maximum instantaneous, peak-to-peak, and mean systolic gradients are not appreciated. The Doppler maximum velocity corresponds to the maximum instantaneous pressure gradient across the valve (Fig. 22-1) . The "peak-topeak" gradient measured manometrically—the difference between peak left ventricular and peak aortic pressures—does not correspond to a specific Doppler measurement, since these two pressure peaks are not simultaneous and thus this "pressure difference" does not actually occur at any time point in the cardiac cycle. In a physiologic sense, the "peak-to-peak" gradient does not truly exist. Clarity in the echocardiographic report prevents any

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potential confusion on the part of the referring physician in regard to differentiating between the maximum Doppler gradient and the "peak-topeak" catheter gradient. Measurement of Doppler mean gradients is more comparable to the mean gradient measured in the catheterization laboratory because both represent the average pressure difference across the valve during the systolic ejection period. Of note, maximum and mean transaortic pressure gradients (∆P) are linearly related when measured either by Doppler or manometric techniques. The regression Figure 22-1 Relationship of pressures to Doppler velocities in normal and aortic stenosis. Note that the maximum pressure gradient (doubleheaded arrow) corresponds to the maximum Doppler velocity in both situations, but the timing of the left ventricular (LV) to aortic (Ao) pressure gradient is quite different when valve obstruction is present.

equations described for this relationship[16] [17] [18] include the following: Mean ∆P = (max ∆P/1.45) − 2.2 mm Hg and Mean ∆P = 2.4(Vmax )2 where Vmax is maximum aortic jet velocity. These two equations, derived

from separate patient populations, give similar results. It is important to recognize that these equations apply only to native aortic valve stenosis because the close correlation between maximum and mean gradient is dependent on a similar shape of the velocity curve (or pressure difference) with respect to time among the patient population. Given this linear relationship between maximum and mean pressure gradients, it becomes clear that there is little additional information content provided by gradient calculations versus simply reporting the Doppler aortic jet velocity alone. Since maximum and mean gradients are linearly related, and since maximum gradient is related to maximum velocity as stated in the simplified Bernoulli relationship, a given maximum velocity consistently corresponds to a given maximum and mean gradient. For example, a maximum jet velocity of 4 m per second corresponds to a

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maximum gradient of 64 mm Hg and a mean gradient of 38 mm Hg. Similarly, a maximum jet velocity of 5 m per second corresponds to a maximum gradient of 100 mm Hg and a mean gradient of 60 mm Hg. These close relationships between maximum jet velocity, maximum gradient, and mean gradient explain why maximum jet velocity data alone are so useful in clinical decision making in adults with valvular aortic stenosis. The technical aspects of recording aortic jet velocities in patients with valvular aortic stenosis cannot be overemphasized (Fig. 22-2) . The utility of Doppler data in patient management clearly is dependent on accurate data recording. Since the direction of the aortic jet is unpredictable and often eccentric, careful examination from multiple acoustic windows is needed for detection of the highest velocity signal. Use of a small, dedicated continuous wave Doppler transducer, careful patient positioning with an apical "cut-out" in the examination bed, and operator experience all are critical factors in obtaining accurate data. ( See Chapter 9 of the Textbook of Clinical Echocardiography for further details on data acquisition.) Even with an experienced operator and attention to technical details, there is some degree of measurement variability, as for any clinical measurement. In the absence of interval physiologic changes, the coefficient of variability for recording and measuring aortic jet velocity is 3%,[19] so that a change in jet velocity greater than 0.2 m per second and a change in mean gradient greater than 4 mm Hg are outside the range of measurement variability. Another physiologic issue that needs to be considered in the Doppler assessment of pressure gradients in patients with aortic stenosis is the phenomenon of distal pressure recovery.[20] [21] [22] [23] [24] [25] The fluid dynamics of valvular aortic stenosis [26] are characterized by a laminar highvelocity jet in the 471

Figure 22-2 One of the technical pitfalls in recording aortic jet velocities is correct recognition of the velocity signal. In this patient, three high-velocity systolic signals were obtained from an apical transducer position. The aortic stenosis jet (A) is distinguished by a shorter ejection time than either mitral (B) or tricuspid (C) regurgitation. Other factors helpful in identifying the signal include

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the accompanying diastolic flow signal and the shape of the velocity curve. When identification is problematic, use of two-dimensional and color-flow guided continuous wave Doppler echocardiography may be helpful.

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narrowed orifice with the narrowest segment of the flow stream (the vena contracta) occurring downstream from the anatomic valve orifice. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure ("pressure recovery") such that when aortic pressure in measured in the distal ascending aorta, the left ventricular to aortic pressure difference is less than if aortic pressure is measured in the vena contracta. No doubt pressure recovery accounts for some of the discrepancies between Doppler and invasive data reported in the literature. Clinically, however, the observed magnitude of pressure recovery is only 5 to 10 mm Hg, an effect that is unlikely to affect clinical decision making. The magnitude of pressure recovery is greater with a larger valve area and with a smaller aortic root. Thus, patients with severe aortic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and a small or normal aortic root dimension. In any case, the phenomenon of pressure recovery supports the use of Doppler data in evaluation of aortic stenosis patients. Since the maximum aortic jet velocity reflects the pressure difference between the left ventricle and the vena contracta, pressure recovery is a "problem" only in comparing the Doppler data with manometric data measured downstream from the vena contracta. In effect, the Doppler velocity measures the physiologic variable of most importance; it is the manometric data that must be interpreted with caution. The major potential limitation of Doppler velocity data in evaluation of patients with valvular aortic stenosis is that velocities (and pressure gradients) are volume flow rate dependent. When coexisting aortic regurgitation results in a high transaortic volume flow rate, aortic jet velocity may be high even if the degree of valve narrowing is only moderate. Conversely, when transaortic volume flow rate is reduced because of left ventricular systolic dysfunction or coexisting mitral regurgitation, jet velocity may be only moderately elevated despite severe valve narrowing. In an individual patient with aortic stenosis, aortic jet velocity varies with volume flow rate. For example, jet velocity increases with exercise as transaortic volume flow rate increases. Thus, comparisons of stenosis severity at different time points in an individual patient may be

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confounded by interval changes in transaortic volume flow rate. In each of these clinical situations, calculation of valve area, which takes the transaortic volume flow rate into account, is needed. Continuity versus Gorlin Formula Valve Areas: Assumptions and Accuracy Aortic valve areas have traditionally been calculated from invasive hemodynamic data using the formula of Gorlin and Gorlin.[27] Gorlin valve area calculations have provided accurate and important data for clinical decision making since the initial publication of the formula in 1951. More recently, however, Doppler echocardiography has allowed noninvasive calculation of valve area using the continuity equation.[19] [28] [29] [30] [31] [32] Since Gorlin valve areas have been used as the standard of reference for validation of continuity equation valve areas, it is important to review the derivation of these equations to understand the differences between these two approaches (Fig. 22-3) . Aortic valve area (AVA) is calculated using the formula of Gorlin and Gorlin as AVA = (cardiac output) / (C × SEP × ∆Pmean ) where mean ∆P is measured manometrically, SEP is systolic ejection period, and C is a constant. As for any clinical measurement, careful data acquisition is important. Accurate pressure gradient measurements depend on careful attention to frequency response, damping, and catheter positioning. The use of a double-lumen catheter or, alternatively, two separate catheters (with measurements obtained in the left ventricle and in the aorta), as opposed to measurement of the femoral artery pressure as a surrogate of the aortic pressure, provides more accurate results. Cardiac output should reflect transaortic volume flow rate. Although a Fick or thermodilution output can be used for isolated aortic stenosis, when aortic regurgitation is present, an angiographic cardiac output measurement is more appropriate. When both mitral and aortic regurgitation are present, accurate invasive determination of the transaortic volume flow rate in the clinical setting is not possible. The constant in the Gorlin formula, which has been empirically derived, attempts to account for several factors. The Gorlin constant incorporates (1) the coefficient of contraction, which reflects the difference between the

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anatomic valve area and the area of the vena contracta, (2) the coefficient of velocity, which relates to the conversion of potential to kinetic energy, (3) measurement of pressure in mm Hg, and (4) an empirical "correction" factor. Both in vitro and in vivo studies suggest that the Gorlin constant may vary with changes in volume flow rate, orifice shape, and stenosis severity.[33] [34] [35] [36] [37] Despite potential limitations of Gorlin valve areas, alternative reference standards for quantitation of aortic stenosis severity remain problematic. Unlike rheumatic mitral stenosis, in which commissural fusion results in a fixed anatomic orifice that can be measured directly at surgery, calcific aortic valve stenosis is characterized by stiff leaflets that open to a variable degree depending on the force applied by the surgeon's finger. This limits attempts at direct measurement of aortic valve area. Doppler continuity equation valve area calculations provide the advantages of noninvasive data collection and absence of an empirical constant.[3] [13] [28] [29] [31] [38] [39] , , Continuity equation aortic valve area (AVA) can be calculated using either velocity time integrals or maximum velocities (V) as follows: AVA = (VLVOT × CSALVOT ) / VAS-JET where left ventricular

outflow tract (LVOT) diameter is measured from a two-dimensional parasternal long-axis view, parallel and adjacent to the aortic valve plane, for calculation of a circular cross-sectional area (CSA); LVOT flow velocity is measured from an apical approach using pulsed Doppler ultrasonography; and the aortic stenosis jet (AS-JET) velocity is measured with continuous wave 473

Figure 22-3 Comparison of valve areas by the continuity equation (A) and the Gorlin formula (B).

Doppler echocardiography from the echocardiographic window that yields the highest velocity signal (Fig. 22-4) . Continuity equation valve area calculations assume accurate recording of the maximum aortic jet velocity, as discussed earlier for pressure gradients. However, the largest source of variability in continuity equation valve area calculations is in the measurement of the outflow tract diameter. The mean coefficient of interobserver and intraobserver measurement variability is 5% to 8%,

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resulting in a measurement variability for valve area of 0.15 cm2 for a valve area of 1.0 cm2 . In an individual patient, outflow tract diameter remains relatively constant over time, such that a change in valve area greater than 0.1 cm2 most likely represents an actual interval change. Continuity equation valve area calculations depend on accurate measurement of transaortic volume flow rate. In theory, volume flow rate could be measured at any one of several intracardiac sites (pulmonary artery, mitral annulus, left ventricular outflow tract). However, when there is coexisting aortic regurgitation (which is present to some degree in more than 80% of adults with valvular aortic stenosis), volume flow measured across other valves does not equal the volume flow rate across the aortic valve.[19] From a technical standpoint, flow measurements just proximal to the stenotic aortic valve are feasible in nearly all adult patients, whereas volume flow rate calculations at other intracardiac sites often are limited by image quality. Thus, in practice, the left ventricular outflow tract is used for measurement of transaortic volume flow rate in nearly all cases. Volume flow measurement proximal to the stenotic aortic valve assumes that (1) the cross-sectional area of flow is circular in systole and flow fills the anatomic cross-sectional area, (2) the pattern of blood flow is laminar with uniform parallel stream lines of flow, (3) cross-sectional area and flow velocity are measured at the same site, and (4) the spatial flow velocity profile is relatively "flat" during ventricular ejection; that is, flow velocities are the same in the center and at the edges of the flow stream. The assumptions of a circular cross-sectional area with flow filling the anatomic area have been corroborated by careful short-axis two-dimensional and color flow imaging in animal models and in patients with valvular obstruction.[5] Laminar flow is confirmed by recording a narrow band of velocities throughout ejection on the pulsed Doppler spectral tracing. The circular cross-sectional area of the outflow tract is calculated from a two-dimensional parasternal long-axis measurement of mid-systolic diameter, immediately adjacent and parallel to the aortic valve plane. Since the outflow tract is perpendicular to the ultrasound beam from this view, axial resolution provides a more accurate diameter measurement than the use of apical views. Flow velocity is measured from an apical approach, because Doppler measurements are most accurate when the ultrasound beam is parallel to the direction of blood flow. To ensure that the diameter and flow measurements are recorded from the same anatomic site, it is important that both measurements be made as close to the aortic valve as

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possible. On the two-dimensional image, the valve leaflet insertions provide an accurate and reproducible landmark, and on the Doppler recordings, the aortic valve closing click ensures that the sample volume is adjacent to the aortic valve. Although a region of flow acceleration occurs on the left ventricular side of the stenotic aortic valve, this area is spatially small and is easily avoided by recognition of spectral broadening on the Doppler velocity recording. In theory, the spatial flow profile in the outflow tract should be relatively flat because of the tapering of the 474

Figure 22-4 Continuity equation valve area is calculated based on a parasternal left ventricular outflow tract diameter (2.6 cm) for calculation of a circular cross-sectional area (A), placement of a sample volume immediately proximal to the aortic valve in an anteriorly angulated apical four-chamber view (B) with pulsed Doppler recording of laminar flow proximal to the aortic valve with a maximum velocity of 0.9 m per second (C). The highest velocity aortic signal (4.9 m per second) was obtained from an apical approach using continuous wave Doppler (D) in this patient. In this example, the continuity equation valve area is 1.0 cm2 . Ao, aorta; LA, left atrium; LV, left ventricle; SV, sample volume.

outflow tract and acceleration of blood during systole, both of which result in blunt flow profiles at the entrance to large vessels (Fig. 22-5) . Direct examination of the spatial flow profile in the left ventricular outflow tract proximal to the stenotic aortic valve initially was performed with conventional pulsed Doppler by carefully recording flow at sequential sites across the two-dimensional image in both apical long-axis and anteriorly angulated four-chamber views of the outflow tract.[19] [40] A more recent study, using color flow imaging to map the spatial flow profile, showed variable skewing in the spatial flow profile, most often with highest velocities along the septum, in 10 patients with aortic stenosis both before and after aortic valve replacement[41] (Fig. 22-6) . In another study, patients with predominant aortic stenosis were found to have relatively flat flow profiles, whereas normal subjects and patients with aortic regurgitation had skewed velocity profiles, with the highest velocities occurring anteroseptally[42] (Fig. 22-7) . In practical terms, even when the flow profile is somewhat skewed, if the recorded flow velocity is a reasonable approximation of the spatial and temporal flow velocity in the outflow

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tract, then a reasonably accurate volume flow rate will be calculated. It is likely that in most patients, when the Doppler sample volume is positioned near the center of the outflow tract in two orthogonal views, the recorded flow velocity approximates the spatial mean velocity across the outflow tract. Rather than examining the assumptions underlying the Doppler approach to volume flow rate calculations, a more pragmatic approach to validation of the accuracy of transaortic volume flow measurements is to compare 475

Figure 22-5 (color plate.) An apical long-axis view (in the same patient as shown in Fig. 22-4) shows relatively laminar flow in the left ventricular (LV) outflow tract proximal to the stenotic valve (arrow) with a flow disturbance in the ascending aorta (Ao) corresponding to the high-velocity jet and post-jet flow disturbance.

Doppler data with an established standard of reference. This has been difficult in clinical studies because most patients with aortic stenosis have coexisting aortic and mitral regurgitation. Although the degree of regurgitation may not be hemodynamically "significant," when regurgitation is present, neither the forward (Fick or thermodilution) nor the total (angiographic) cardiac output will accurately represent the volume flow rate across the aortic valve. In the research setting, transaortic volume flow rate can be measured directly, with an electromagnetic or transit time flow meter (Fig. 22-8 (Figure Not Available) and Fig. 22-9 (Figure Not Available) ). In both acute and chronic models of valvular aortic stenosis, Doppler transaortic volume flow rates have been shown to be accurate (Table 22-15, 15 ) with a standard error of TABLE 22-1 -- In Vivo Studies of Simultaneous Invasive and Doppler Vo Measurements from Left Ventricular Outflow Tract at Aortic Annulus in Su Aortic Stenosis and Subjects Without Aortic Stenosis Patients, Standard of Study Model N Reference Burwash Chronic 75 Transit time[15] et al valvular flow AS

Cardiac Output Strok RANGE SEE, RA r L/MIN L/MIN r m 0.86 0.9– 0.50 0.86 9 6.2

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(closedand openchest dogs) altered volume flow rate Otto et al Acute 52 Electromagnetic 0.90 0.9– 0.25 0.88 5 [38] valvular flow 3.2 AS (openchest dogs) altered volume flow rate Stewart Normal 33 Roller pump 0.98 0.5– 0.30 NA N ‡ et al (open5.0 chest dogs) altered volume flow rate Lewis et Patients 35 Thermodilution 0.91 2.1– 0.63 0.95 24 † al (no AS) 9.5 Labowitz Patients 31 Thermodilution 0.90 1.6– 0.95 NA N * et al (no AS) 8.4 AS, aortic stenosis; NA, not available; SEE, standard error of the estimate. ‡Stewart et al: J Am Coll Cardiol 1985;6:653. †Lewis et al: Circulation 1984;70:425. *Labowitz et al: Am Heart J 1985;109:327.

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Figure 22-6 Three-dimensional plot of velocity distribution in left ventricular outflow tract close to the level of aortic annulus. Velocity is plotted against position in the left ventricular outflow tract diameter and against time. There are 20msec intervals along the time axis and approximately 2 mm between each observation along the diameter axis. (From Wiseth R, Samseth S, Rossvoll O, et al: J Am Soc Echocardiogr 1993;6:279–285.)

the estimate of 2 to 4 mL for stroke volume and 0.25 to 0.5 L per minute for cardiac output over a wide range of flow rates (Fig. 22-9 (Figure Not Available) and Fig. 22-10 ). In comparing Gorlin and continuity equation valve areas, it is important to bear in mind that although they both describe stenosis severity, they measure different parameters. The Gorlin formula examines the hydraulic load and calculates an anatomic orifice area, whereas the continuity equation describes the physiologic flow area of the vena contracta.[43] [44] Thus, it is neither expected nor essential that these two measurements be identical to each other. In terms of clinical decision making, the precision, reproducibility, and ability to predict patient outcome of these measures are more important than agreement or disagreement between the two approaches. As Gorlin and Gorlin note, "We need not be frustrated when valve areas derived by two different methods are not the same. Rather, we should, like the princes of Serendip, seize upon the difference for what it reveals about the anatomy of the valve orifice as opposed to the physiology of the total obstructing valve tract under active pressure and flow conditions."[45]

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Figure 22-7 (color plate.) The two photos show the color Doppler registrations from a patient with aortic regurgitation: A, three-chamber view; B, five-chamber view. In the left ventricular outflow tract, a line, drawn along the transverse axis from the posterior to the anterior wall in the threechamber view and from the septal to the lateral wall in the five-chamber view, shows the location (x) from where velocity information (v) is obtained. The lower panels show, from top to bottom, the uncorrected and the angle-corrected velocity profile along the two transverse axes as they appear on the computer screen. Below them, the time- (and angle-) corrected spatial velocity profiles from the beginning of the color Doppler sweep are shown. A, anterior wall; AO, aorta; L, lateral wall; LA, left atrium; LV, left ventricle; P, posterior wall; RA, right atrium; RV, right ventricle; S, septal wall. (From Sjöberg BJ, Ask P, Loyd D, Wranne B, et al: J Am Soc Echocardiogr

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1994;7:276–285.)

Other Measures of Stenosis Severity Continuity equation valve areas provide an accurate, reproducible, and useful measure of stenosis severity in patients with valvular aortic stenosis when data are recorded carefully with attention to technical details of data acquisition. However, other measures of stenosis severity may be needed in individual patients if the results of clinical and diagnostic evaluation are discrepant. In these situations, it may be helpful to utilize Gorlin formula valve areas derived from invasive data, other noninvasive measures of stenosis severity, or continuity equation valve areas calculated under conditions of altered transaortic volume flow rate. Even within the physiologic range, the degree of aortic valve opening appears to depend on the interaction between the force applied to the valve leaflets (as reflected in the transaortic volume flow rate) and the stiffness and rigidity of the valve leaflets. Changes in valve area of 20% to 30% can be observed for a 50% change in volume flow rate.[46] [47] [48] [49] [50] [51] [52] This potential flow dependence is of most concern in patients with coexisting left ventricular systolic dysfunction in whom separating the effect of reduced left ventricular force from the effect of leaflet stiffness on the degree of valve opening remains difficult. This clinical dilemma has led to a search for a flow-independent measure of stenosis severity. Several alternative measures of stenosis severity have been proposed, including two-dimensional valve area on transesophageal imaging,[52] [53] left ventricular stroke work loss,[48] [54] valve resistance,[50] [55] [56] [57] changes in aortic valve area during the cardiac cycle,[58] three-dimensional valve area, [59] and scoring of valve calcium.[60] [61] On transthoracic imaging, planimetry of the aortic orifice is limited by image quality. In addition, the anatomy of the stellate stenotic orifice is complex in three dimensions (Fig. 22-11) , so that it is not always possible to obtain a planar image of the valve orifice. Similar considerations apply to the higher quality images obtained on 477

Figure 22-8 (Figure Not Available) Simultaneous volume flow and pressure data in a canine model of aortic stenosis. The electrocardiographic (ECG) recording is displayed on top, instantaneous volume flow rate in the middle, and left ventricular (LV) and aortic (Ao) pressures at the bottom. The recordings on the left demonstrate

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the hemodynamics at one flow rate. The recordings on the right display the hemodynamics at a larger volume flow rate during dobutamine infusion. Pmax , maximum instantaneous pressure gradient; Pmean , mean pressure gradient; SV, stroke volume. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.) Figure 22-9 (Figure Not Available) Typical Doppler echocardiographic recordings made in one subject at two different volume flow rates. The left ventricular outflow tract (LVOT) velocity profile and velocity time integrals (VTI) (A) and aortic stenosis (AS JET) velocity (Vmax ) and velocity time integral (VTI) (C) are displayed at one flow rate. Increases in LVOT velocity (B) and AS JET velocities (D) were observed in the same subject with a dobutamine-induced increase in volume flow rate. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.)

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Figure 22-10 Correlation of simultaneous Doppler echocardiography and ascending aortic transit time-stroke volume (SV) and cardiac output (CO) during 75 separate interventions. (From Burwash IG, Forbes AD, Sadahiro M, et al: Am J Physiol 1993;265:H1734–1743.)

transesophageal imaging. In addition, significant calcification of the valve can limit accurate delineation of the aortic valve orifice.[62] Some investigators have reported favorable correlations between planimetered stenotic orifice areas obtained on multiplane transesophageal echocardiography and continuity equation valve areas and/or Gorlin valve areas, but this approach is likely to be needed Figure 22-11 Anatomic specimen showing calcific aortic stenosis with nodular deposits of calcium within the aortic cusps and no commissural fusion.

in only a small subset of patients.[52] [53] [63] [64] Other investigators have found planimetry of the aortic orifice to be difficult and less accurate than continuity equation valve areas obtained from transthoracic imaging. [65] Multiplane transesophageal echocardiography does appear to provide more accurate determination of aortic valve morphology (bicuspid versus tricuspid valve) than biplane imaging.[66] More recently, Doppler transesophageal echocardiography has been applied using both biplane and

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multiplane imaging from the transgastric view.[67] [68] Aortic valve area as derived from Doppler transesophageal echocardiography was similar to that measured by planimetry but could not be obtained in approximately 70% of patients because of failure to align the Doppler beam adequately.[67] The amount of work expended by the left ventricle in keeping the aortic valve open in systole compared with the amount of work resulting in effective forward blood flow has appeal as a potential measure of stenosis severity. This measure may reflect the intrinsic stiffness of the valve leaflets, and thus be less dependent on volume flow rate.[48] [54] [69] With a normal aortic valve, work calculated from left ventricular or aortic pressure tracings will be nearly identical. However, when aortic stenosis is present, the difference between work calculated from left ventricular pressures versus aortic pressures should be related to the amount of work "lost" in opening the stiff leaflets. To calculate work, a power curve is generated by multiplying instantaneous flow times pressure, with total potential stroke work calculated by integrating power over the systolic ejection period[69] using either left ventricular (for total work) or aortic (for effective work) pressures. The steady component of work is defined as mean systolic pressure times stroke volume; pulsatile work is defined as total minus steady work. Stroke work loss then represents the difference between left ventricular and effective work and can be calculated for total, steady, and pulsatile components[48] as follows:

LV stroke work loss = LV work − effective work Since potential work obviously will increase with increases in flow rate, the potential work loss across the stenotic valve is indexed for volume flow rate and expressed as the percentage of left ventricular stroke work loss: Given that stroke work is calculated as the instantaneous product of pressure and flow, and stroke work loss is simply the ratio of left ventricular to aortic work, this proposed index of stenosis severity also is likely to vary with volume flow rate if the actual degree of valve opening varies. Note that when the ratio of left ventricular to aortic work is calculated, the terms for transaortic volume flow rate cancel each other, so that stroke work loss can be determined from Doppler pressure calculations alone.

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A new index of energy loss that takes body surface area into account and can be calculated from Doppler-derived data was recently evaluated in an experimental model.[70] The model used fixed stenoses and bioprosthetic valves 479

of two sizes that were evaluated at different flow rates. With use of this model, the effective orifice area was compared to the energy loss index. In a retrospective analysis of 138 patients with moderate or severe aortic stenosis, the index and valve area were compared in predicting clinical outcome, defined as death or need for valve replacement. This energy loss index was the better predictor of clinical outcome, with a positive predictive value of 67%. Valve resistance is calculated from invasive or Doppler data as follows[56] [57]

Resistance = (∆Pmean \ Qmean ) × 1333 where ∆Pmean is mean transaortic pressure gradient in mm Hg, Qmean is

mean volume flow rate in milliliters per second, 1333 is a conversion factor, and resistance is in units of dynes per second per cm-5 . Several investigators have observed a curvilinear relationship between valve resistance and valve area (with both invasive and Doppler data[56] [57] ) (Fig. 22-12) . This observation is not surprising given the mathematical derivation of the valve area and resistance concepts. In fact, the concepts of valve area and valve resistance are to some extent mutually exclusive. Valve area calculations with the Gorlin formula assume a quadratic relationship between pressure gradient and flow rate. Conversely, the valve resistance concept assumes a linear relationship between these two variables. Most clinical and experimental data support the concept of a quadratic, rather than linear, relationship between pressure gradient and flow rate across a stenotic valve[71] (Fig. 22-13) (Figure Not Available) . More complete modeling of the interaction between the left ventricle, valve, and peripheral vasculature may enhance our understanding of the hemodynamics of valvular aortic stenosis.[72] Aortic valve resistance has largely been used as a research tool and has not gained widespread acceptance into clinical practice. The reasons for

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Figure 22-12 Relationship between aortic valve resistance and aortic valve area for patients with severe aortic stenosis confirmed at surgery (group I; circles) and the 95% confidence limits of this relation (dashed curves). Values for patients with milder, noncritical stenosis (group II triangles) were plotted against this relation; in seven of eight group II patients, values were outside the confidence limits. (From Cannon JDJ, Zile MR, Crawford FAJ, Carabello BA: J Am Coll Cardiol 1992; 20:1517–1523.) Figure 22-13 (Figure Not Available) Plot of square-law dependence of pressure gradient on flow demonstrated for circular stenoses with orifices from 0.5 to 2.0 cm2 . (From Voelker W, Reul H, Heinhaus G, et al: Circulation 1995;91:1196–1204.)

this are multifactorial and include familiarity of most cardiologists with gradients and valve areas and a lack of consensus among studies in terms of the added information valve resistance provides above more traditional measures of stenosis severity.[56] [73] [74] Aortic valve area changes during the cardiac cycle, and the valve has been shown to open and close more slowly in patients with aortic stenosis than in those with normal valves.[75] The rate of change in the aortic valve area during the cardiac cycle has therefore been proposed as an additional measure of aortic stenosis severity and in predicting disease progression. [58] When the rate of change in the aortic valve area throughout the ejection phase of the cardiac cycle was expressed as a ratio (AVA ratio), patients with a large AVA ratio were found have more rapid disease progression than those with a lower AVA ratio. This new measure may prove useful in patients with valve areas of borderline significance (i.e., 1.0 cm2 ) by identifying patients with a higher probability for rapid disease progression (Fig. 22-14) (Figure Not Available) . Three-dimensional echocardiography has largely been used as a research tool to evaluate left and right ventricular chamber size and structural dimensions of the mitral valve. However, this imaging modality was used to planimeter the inner surface of the aortic valve leaflets in 23 patients undergoing aortic valve replacement.[76] Measurements were feasible in all but one patient, and valve area was comparable to that derived by the Gorlin formula. Progressive calcification of the aortic valve occurs with all causes of aortic stenosis and eventually leads to impaired leaflet mobility and valve obstruction. The degree of aortic valve calcification can be evaluated on the short-axis view with transthoracic echocardiographic imaging. In a recent

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study of 126 asymptomatic patients with severe aortic stenosis (aortic jet velocity of at least 4 m per second), the extent of aortic valve calcification was the only independent predictor of clinical outcome, defined as death or need for valve replacement (Fig. 22-15) .[61] In addition, the combination of severe valve calcification and a rapid increase in aortic jet velocity (at least 0.3 m per second per year) predicted an extremely poor prognosis with 79% of patients undergoing surgery or dying within 2 years. In this study, calcification was graded on a scale of 1 (no calcification) to 4 (extensive thickening and 480

Figure 22-14 (Figure Not Available) Relationship of the change in valve area during the systolic ejection to the rate of progression of aortic stenosis. The aortic valve area ratio (AVA ratio) was calculated as the aortic valve area during the midpoint of deceleration divided by the valve area during the mid-point of acceleration. A larger AVA ratio indicates stiffer aortic valve leaflets. Rapid progression was defined as a decrease in valve area of 0.20 cm2 per year or more. In patients with a baseline AVA of 1.2 cm2 or greater, the number of rapid and slow progressors for a ratio less than 1.25 and 1.25 or greater is shown (A). In patients with a baseline AVA of 1.2 cm2 or greater, the receiver operating curve for AVA ratio (B) indicates the sensitivity and specificity of various AVA ratios for predicting rapid progression of disease. AUC, area under the curve. (From Lester SJ, McElhinney DB, Miller JP, et al: Circulation 2000;101:1947–1952.)

calcification of all cusps). Other studies have also found aortic valve calcification to predict more rapid disease progression.[60]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Physiologic Variability in Measures of Stenosis Severity Exercise Hemodynamics in Valvular Aortic Stenosis Although exercise testing should be performed with caution, if at all, in symptomatic patients with valvular aortic stenosis because of the high risk of complications,[55] studies in asymptomatic patients have provided insight into the relationship between hemodynamic severity and clinical symptoms (Table 22-2) . [46] [47] [48] [49] [51] , [77] [78] [79] [80] In patients with asymptomatic aortic stenosis, exercise is associated with an appropriate rise in heart rate and cardiac output. The increase in cardiac output with upright exercise is mediated almost entirely by heart rate, with little change in stroke volume. However, even though stroke volume does not change, mean and maximum transaortic volume flow rates are increased because of concurrent shortening of the systolic ejection period. Thus, exercise results in an increase in maximum aortic jet velocity, with a corresponding increase in the mean transaortic gradient as predicted by the Bernoulli equation. The continuity equation predicts a linear relationship between maximum volume flow rate (Qmax ) and maximum jet velocity (Vmax ) for any given valve area.[78] This linear relationship has been verified using both invasive and noninvasive data in an animal model of valvular aortic 481

Figure 22-15 Kaplan-Meier analysis of event-free survival among 25 patients with no or mild aortic valve calcification, as compared with 101 patients with moderate or severe calcification. The vertical bars indicate standard errors. All the subjects in this study had an initial aortic jet velocity of at least 4.0 m per second (mean 5.0 ± 0.6 m per second). (From Rosenhek R, Binder T, Porenta G, et al: N Engl J Med, 2000;343:611–617.)

stenosis.[81] In clinical studies, only two data points typically can be

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acquired, but the slope of the change in Vmax relative to Qmax in patients with no change in valve area with exercise parallels the slope predicted by this relationship. In patients with an increase in valve area with exercise, the observed slope is greater than predicted for a fixed valve area. Changes in Aortic Valve Area with Changes in Volume Flow Rate The effect of changes in volume flow rate on Gorlin and continuity equation valve areas also has been examined in in vitro models, in animal models, [82] and in patients with valvular aortic stenosis (Fig. 22-16) . These studies consistently show an increase in valve area with an increase in transaortic volume flow rate for most stenotic aortic valves.[46] [47] [48] [49] [50] [51] [83] [84] [85] Although these apparent increases, to some extent, could be due to errors in the valve area formulas, both in vitro pulsatile flow model data [71] and video imaging of flow-dependent changes in valve opening support the concept that valve area itself, both anatomic and physiologic, varies with transaortic volume flow rate.[86] This conclusion is not all that surprising given the well-known observation that even normal aortic valve leaflets open less when volume flow rate is decreased, for example, in patients with a dilated cardiomyopathy. Change in Other Measures of Stenosis Severity with Change in Volume Flow Rate Although some investigators have suggested that valve resistance is independent of flow rate,[50] [87] other investigators have shown changes in valve resistance with changes in volume flow rate in in vitro models,[71] in animal models, and in patients with asymptomatic aortic stenosis.[15] [83] In part, the relative stability of valve resistance with changes in flow rate observed in some studies[56] [57] may relate to the range of stenosis severity evaluated (see Fig. 22-12) . Because of the curvilinear relationship between resistance and valve area, with "larger" valve areas (right side of 482

TABLE 22-2 -- Physiologic Changes with Exercise in Adults with Valvular Aortic Stenosis Bache et al[47]

Ettinger et al[79]

Otto et al[78]

Martin Burwash et al[49] et al[51]

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Patients, N Measurements

20 10 Invasive Invasive

Type of Exercise

Supine bicycle

Heart Rate, bpm Rest Exercise Systolic Blood Pressure, mm Hg Rest Exercise Stroke Volume, mL Rest Exercise Qmean , mL/sec Rest Exercise

Supine bicycle

28 85 110 Doppler Invasive Doppler echo echo Treadmill Supine Treadmill bicycle

79 ± 3 87 ± 5 112 ± 5 109 ± 5

71 ± 17 71 ± 2 147 ± 28 98 ± 2

63 ± 14 104 ± 23

120 ± 3 118 ± 8 136 ± 3 133 ± 8

139 ± 15 — 155 ± 24 —

143 ± 22 163 ± 29

— —

— —

98 ± 29 89 ± 32

245 ± 14 318 ± 21

— —

300 ± 85 275 ± 8 319 ± 80 366 ± 325 ± 10 400 ± 140 159

Cardiac Output, L/min Rest Exercise

5.4 ± 0.3 8.6 ± 1.1 8.5 ± 0.6 9.2 ± 0.9

Mean Pressure Gradient, mm Hg Rest Exercise

59 ± 4 74 ± 5

37 ± 9 38 ± 11

— —

103 ± 30 96 ± 30

6.5 ± 1.7 6.0 ± 0.2 6.3 ± 1.7 10.7 ± 9.3 ± 0.2 9.9 ± 3.8 4.4

39 ± 20 52 ± 26

37 ± 2 41 ± 2

30 ± 14 41 ± 18

Vmax (m/sec) Rest Exercise

— —

— —

4.0 ± 0.9 4.6 ± 1.1

—

3.6 ± 0.8

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— Aortic Valve Area, cm2 Rest 0.8 ± 0.1 1.8 ± 0.3 Exercise 0.9 ± 0.1 1.9 ± 0.3 Valve Resistance, dyne/sec/cm-5 Rest — — Exercise — — Stroke Work Loss, % Rest — — Exercise — — Left Ventricular EndDiastolic Pressure; mm Hg Rest 12 ± 6 15 ± 3 Exercise 20 ± 2 15 ± 4 Vmax , maximum aortic jet velocity.

4.3 ± 0.8

1.2 ± 0.5 1.1 ± 0.1 1.4 ± 0.5 1.3 ± 0.7 1.3 ± 0.1 1.6 ± 0.7

— —

191 ± 12 137 ± 81 182 ± 12 155 ± 97

— —

26 ± 1 25 ± 1

17 ± 7 20 ± 9

— —

— —

— —

curve) resistance changes very little even with substantial changes in valve area, whereas with smaller valve areas (left side of curve), large changes in resistance are expected with only small changes in valve area. Similarly, left ventricular stroke work loss has been found to vary with changes in volume flow rate.[51] [71] [88] Overall, both total and steady left ventricular stroke work losses correlate inversely with valve area. However, for a specific valve anatomy, work loss increases with an increase in stroke volume despite a concurrent increase in valve area. This suggests that for a given degree of leaflet stiffness, greater opening of the valve is achieved at the expense of greater work loss. Alternatively, since work includes both potential and kinetic energy, a decrease in the percentage of potential work converted to kinetic work would lead to this observation. In studies to date, only potential work has been measured because of the conceptual and technical difficulties in measurement of kinetic work. Changes in the effective frictional loss component with changes in volume flow rate also

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may affect calculated measures of stenosis severity. Which Measure of Stenosis Severity Is Best? The anatomy of degenerative valvular aortic stenosis is characterized by thickened and stiff leaflets without commissural fusion (see Fig. 22-11) . Given this anatomic substrate, it is not surprising that the degree of valve opening varies with the amount of "force" applied to the valve, whether this force is represented by the surgeon's finger, a balloon valvuloplasty catheter, or the rate and volume of blood ejected by the left ventricle. Most investigators to date have found that each proposed measure of stenosis severity, when examined in detail, varies with changes in volume flow rate. These measures include peak left ventricular to aortic pressure gradient, mean transaortic pressure gradient, maximum Doppler aortic jet velocity, Gorlin valve area, continuity equation valve area, left ventricular stroke work loss, and valve resistance. Of note, despite this potential limitation, most clinical decisions can be made with a high degree of reliability using these, albeit imperfect, indices of disease severity. To 483

Figure 22-16 Relationship of rest and continuity equation aortic valve area (A), aortic valve resistance (B), and percentage of left ventricular stroke work loss (C) in 110 exercise studies. The slopes of the regression lines (solid line) are greater than the line of identity (dashed line), demonstrating an increase in all three indexes with exercise. AVA, aortic valve area; LVSW, left ventricular stroke work. (From Burwash IG, Pearlman AS, Kraft CD, et al: J Am Coll Cardiol 1994;24:1342–1350.)

define the "best" measure of stenosis severity, the specific goals in quantitating the degree of stenosis must be clarified. These goals fall into two distinct categories: clinical patient management and research applications. In terms of clinical decision making, the ideal measure of stenosis severity should reflect disease severity and should have an acceptable intraobserver and interobserver reproducibility. In addition, it should be easily applicable, noninvasive, and inexpensive. Most importantly, it should be predictive of clinical outcome. Clearly, Doppler echocardiographic measures of jet velocity and valve area meet these criteria, as discussed subsequently. In the clinical setting, the impetus to derive a flow-independent measure of stenosis severity arises from the relatively unusual clinical situation in

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which there is coexisting left ventricular systolic dysfunction and an anatomically abnormal aortic valve. Potential approaches to this clinical dilemma are discussed in the following sections. For specific research applications, the "best" measure of stenosis severity must possess additional characteristics. One research goal is to explain the paradox of the marked overlap in hemodynamic severity between symptomatic and asymptomatic patients with aortic stenosis. Some patients with hemodynamically severe disease remain asymptomatic, whereas other patients with only moderate valve obstruction develop definite symptoms. [89] [90] [91] Whether these apparent discrepancies between hemodynamic severity and clinical manifestations of disease are related to other factors (such as ventricular diastolic function[92] ) or whether they reflect the inadequacy of available measures of stenosis severity remains unclear. A second and more important research goal is to follow disease severity over time to define the natural history of this disease and to identify factors that predict progression in individual patients. This goal requires measures of stenosis severity that have a high degree of reproducibility over time and among institutions. This application will allow use of Doppler echocardiographic measures of aortic stenosis severity as end points in intervention trials to prevent or slow disease progression.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Left Ventricular Response to Valvular Aortic Stenosis Diastolic Function The initial physiologic response to chronic pressure overload of the left ventricle is impaired early diastolic relaxation as manifested by a prolonged time constant of relaxation (tau), a lengthened isovolumic relaxation time (IVRT), and a reduced early diastolic filling velocity, similar to the changes seen in patients with systemic hypertension ( see Chapter 6 and Chapter 32 ). [93] [94] [95] [96] [97] Changes in diastolic function typically precede evidence of systolic dysfunction and thus may be present early in the disease course. Although some investigators suggest that Doppler measures of early and late diastolic filling velocities (or rates) may not be sensitive for detection of early diastolic dysfunction,[94] others propose that diastolic parameters can distinguish symptomatic from asymptomatic patients.[92] Later in the disease course, decreased diastolic compliance plus a rightward shift on the passive diastolic pressure-volume relationship may result in a filling pattern characterized by a shortened IVRT, increased early diastolic filling velocity, rapid early deceleration slope, and reduced atrial contribution to diastolic filling, a pattern often referred to as pseudonormalization. [96] Wall Stress and Concentric Hypertrophy

484

As the severity of stenosis increases, concentric left ventricular hypertrophy develops in response to the chronic elevation in left ventricular systolic pressure. This increase in myocardial wall thickness allows maintenance of normal wall stress given that wall stress is directly related to chamber pressure and dimension, but inversely related to wall thickness. Left ventricular hypertrophy is assessed most reliably by calculation of left

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ventricular mass from two-dimensional images, although simple chamber dimensions and diastolic wall thickness may be adequate for clinical evaluation in many patients. Meridional and circumferential wall stress can be calculated from two-dimensional echocardiographic data in conjunction with Doppler evaluation of the aortic valve gradient and a cuff blood pressure measurement, as described in Chapter 4 . In general, the time course for development of left ventricular hypertrophy parallels the course of stenosis severity in most patients. In some individuals, the degree of hypertrophy appears out of proportion to the severity of aortic stenosis. In these cases, other causes for hypertrophy, such as hypertension, coexisting hypertrophic cardiomyopathy, or an infiltrative myocardial process should be considered. It is particularly important to evaluate these possibilities carefully on two-dimensional imaging because the clinical presentation of hypertrophic cardiomyopathy may be similar to that of valvular aortic stenosis. Genetic factors also play a role in the degree of left ventricular hypertrophy. For example, a recent study found that certain polymorphisms of the angiotensin-converting enzyme gene were associated with increased left ventricular hypertrophy.[98] Gender Differences in the Left Ventricular Response to Aortic Stenosis Several investigators have found significant gender differences in the left ventricular response to the chronic pressure overload of aortic stenosis. [99] In symptomatic patients referred for aortic valvuloplasty, although women and men had similar valve areas, women had higher transaortic gradients, higher relative wall thicknesses, and a higher prevalence of left ventricular hypertrophy using gender-specific hypertrophy criteria. In addition, women had a lower functional status score for the same degree of aortic valve obstruction.[100] Another study observed higher peak left ventricular pressures, higher ejection fractions, smaller left ventricular end-diastolic dimensions, and a higher relative wall thickness in women, as compared with men, with aortic stenosis.[101] Although left ventricular mass did not differ in women versus men, left ventricular geometry differed as reflected in a lower circumferential wall stress for a given degree of hypertrophy. Similar findings were observed in a consecutive series of asymptomatic aortic stenosis patients.[102] Even though there were no gender differences in aortic stenosis severity, women reported more functional limitation and had smaller left ventricular end-diastolic and end-systolic volumes and mass index, but had a higher relative wall thickness and fractional shortening as compared with men. In addition, women had a shorter treadmill exercise

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duration and a smaller increase in cardiac output with exercise, even though heart rate and blood pressure responses were similar in men and women.[102] The importance of gender differences in the left ventricular response to chronic pressure overload are illustrated by the observation that after aortic valve replacement in patients with depressed left ventricular systolic function (ejection fraction < 45%), women had a greater improvement in ejection fraction at a mean of 1.4 years after valve replacement, although survival was similar between men and women. The ejection fraction increased from 33% ± 8% to 48% ± 15% in women, compared with an increase from 32% ± 9% to 42% ± 15% in men (P < .02).[103] In summary, the degree of increase in left ventricular mass is variable, in both men and women. However, women tend to have small ventricles with thick walls, low wall stress, and normal or hyperdynamic systolic function (Fig. 22-17) . In contrast, men tend to have left ventricular dilation with normal wall thickness, increased wall stress, and depressed systolic function. Systolic Dysfunction Left ventricular systolic dysfunction due to valvular aortic stenosis usually occurs late in the disease course. Given the high ventricular afterload caused by the stenotic valve, left ventricular contractility typically remains normal, despite a low ejection fraction. Relief of the high afterload with valve replacement often leads to rapid normalization of systolic function. In adult patients, however, left ventricular systolic dysfunction may be due to causes other than aortic stenosis, such as coronary artery or myocardial disease. Patients with these conditions often fail to improve with valve replacement. In the patient with a moderate aortic valve gradient, distinguishing poor left ventricular systolic function caused by severe aortic stenosis from that caused by concurrent ischemic or myocardial disease with only moderate aortic valve disease remains a difficult dilemma. One approach to this problem is to use a flow-independent measure of stenosis severity or to look at the change in stenosis severity with a change in volume flow rate; an alternate approach is to utilize a load-independent measure of left ventricular contractility to evaluate myocardial function. Unfortunately, a load-independent measure of contractility has proven as elusive as a flow-independent measure of stenosis severity.[94] [101]

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Evaluation of Coexisting Coronary Artery Disease In the patient undergoing valve replacement for symptomatic aortic stenosis, most cardiac surgeons recommend concurrent coronary artery bypass grafting if significant coronary artery disease is present. Although the need for coronary bypass grafting in the aortic stenosis patient remains somewhat controversial, reported operative mortality 485

Figure 22-17 In this elderly woman with calcific aortic stenosis and mitral annular calcification, severe concentric hypertrophy is present as shown in an end-diastolic image in an apical four-chamber view (A). Aortic jet velocity is 5.1 m per second corresponding to a maximum gradient of 104 and a mean gradient of 62 mm Hg (B). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

in patients with both aortic stenosis and coronary artery disease is only 1.1% to 4.8% when valve replacement plus coronary bypass grafting is performed, versus 4.0% to 13.2% when valve replacement alone is performed.[104] [105] In aortic stenosis patients with angina, the prevalence of significant coronary artery disease ranges from 40% to 80%, so that coronary angiography is needed for planning the operative procedure. Aortic stenosis patients without symptoms of angina also have a prevalence of significant coronary artery disease between 0% and 54% (average 16%). The appropriate diagnostic approach to these patients is less clear. Exercise treadmill testing in aortic stenosis patients is often nondiagnostic for the presence of coronary artery disease because most of these patients (even when asymptomatic) have significant ST segment depression with exercise, possibly related to left ventricular hypertrophy. [78] [106] In addition, it is important to recognize the potential risk of exercise testing in symptomatic aortic stenosis patients.

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The utility of echocardiographic stress imaging for the diagnosis of coronary artery disease in aortic stenosis patients has not been extensively evaluated. Studies on the exercise physiology of aortic stenosis or on the response to inotropic stimulation with dobutamine have focused on Doppler evaluation of aortic stenosis severity and cardiac output rather than on segmental wall motion abnormalities of the left ventricle.[87] A recent study of 50 patients with severe aortic stenosis evaluated the use of adenosine stress echocardiography for the detection of coronary artery disease.[107] The sensitivity and specificity of stress echocardiography were 85% and 97%, respectively. In addition, no major complications occurred during the procedure. Clearly, these observations need confirmation in other studies. In our experience, definite exercise-induced reversible segmental wall motion abnormalities have been seen in a few patients with aortic stenosis in whom subsequent coronary angiography confirmed significant coronary artery disease. More often, however, no definite wall motion abnormalities are seen, even though subsequent catheterization does show greater than 50% narrowing in the coronary arteries. Whether this lack of sensitivity relates to exercise limitation by aortic stenosis itself (the ischemic threshold is not reached), to diffuse subendothelial ischemia obscuring segmental abnormalities, or whether the degree of stenosis being treated with bypass grafting is insufficient to cause ischemia remains unclear. Further studies of stress echocardiography in aortic stenosis patients may clarify this issue. Exercise tomographic thallium imaging in aortic stenosis patients has a sensitivity of 90% and a specificity of 70% for the presence of significant (greater than 50% luminal diameter narrowing) coronary artery disease.[108] Similarly, adenosine thallium stress testing in aortic stenosis patients has a sensitivity of 92% and a specificity of only 71%.[109] When combined with a pretest likelihood of disease (based on gender, age, and cardiac risk factors), the post-test likelihood of coronary artery disease can be helpful in deciding whether coronary angiography is necessary and may result in a reduction in overall costs of patient evaluation.[110] However, many clinicians choose to perform coronary angiography because of the low risk associated with this procedure and the potential impact of the diagnosis on the operative procedure and survival in a specific individual.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Disease Progression Natural History of Aortic Valve Stenosis The natural history of valvular aortic stenosis is characterized by a long time period during which the patient is asymptomatic but there is gradually increasing obstruction 486

to left ventricular outflow (Table 22-3) .[111] [112] The duration of this asymptomatic period is variable. With a congenital unicuspid valve, symptoms typically are recognized in childhood or adolescence. Occasionally, however, young adults may present with symptomatic congenital aortic stenosis, either due to restenosis after a surgical valvotomy as a child or in the absence of previous surgical procedures. In patients with a congenital bicuspid aortic valve, the onset of symptoms typically is at 50 to 60 years of age.[113] [114] In the elderly patient with degenerative valve disease, symptom onset typically is at 70 to 80 years of age, but the interval between observing aortic valve "sclerosis" by echocardiography and clinical evidence of severe stenosis may be only 5 to 10 years. Rheumatic valvular aortic stenosis has a variable course with significant aortic valve obstruction (in conjunction with mitral valve involvement) occurring over a wide age range. Because disease progression results in reduced leaflet opening, the antegrade velocity across the valve increases in direct relation to the degree of valve obstruction. Transaortic pressure gradients increase as predicted by the Bernoulli equation; although it is noteworthy that little increase in the pressure gradient is seen until the valve area is reduced to one half the normal area, whereas an increase in velocity will be noted with only minimal TABLE 22-3 -- Natural History of Valvular Aortic Stenosis

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Study Frank et al[111]

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Entry Criteria ∆Ppeak ≥ 50 mm Hg or AVI < 0.7 cm2 /m2

Chizner et Cardiac cath, al[133] no AVR

O'Keefe et al[134]

Symptom Status 80% symptomatic

Patients, Age, N yrs 15 32– 59

Aortic Mea Stenosis Follo up Severity AVI 0.4 > 2 y ± 0.1 cm2 /m2

76% symptomatic

42 22– AVA 0.7 5.4 y 77 ± 0.3 (0.2–1.1) cm2

Severe aortic Symptomatic stenosis, no AVR, age ≥ 60

50 77 Vmax 4.5 1.7 y

Turina et Cardiac cath, al[91] no AVR

Symptomatic

Asymptomatic

m/sec, AVA 0.6 (0.3–8) cm2

(60– 89) 125 43 Mean ∆P 6.6 y 69 mm Hg AVA 0.56 cm2 (16– 73) 65 Mean ∆P 57 mm Hg AVA 0.76 cm2

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Horstkotte Catheterization Asymptomatic et al[89] for other reasons Catheterization Asymptomatic for other reasons

Refused surgery

Kelly et al Vmax ≥ 3.6 [131]

Symptomatic

Asymptomatic

m/sec

Symptomatic Pellikka et al[132]

Doppler Vmax Asymptomatic ≥ 4 m/sec

142

Mild AS (AVA > 1.5 cm2 ) 236 Moderate AS (AVA 0.8–1.5 cm2 ) 35 Severe AS (AVA < 0.8 cm2 ) 51 63 ± ∆P 68 ± 15 ± 19 19 mos 39 72 ± ∆P 68 ± 11 19 143 72 Vmax 4.4 20 m (4–6.4) m/sec

(40– 94)

18% Kennedy Moderate [135] aortic stenosis asymptomatic et al at cath, no AVR Otto et al Abnormal Asymptomatic [128] valve with Vmax > 2.6

66 67 ± AVA 35 m 10 0.92 ± 0.13 (0.7–1.2) 2.5 y 123 63 ± Vmax < 16 3.0 m/sec

m/sec

Vmax 3–4

m/sec Vmax >

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Rosenhek Abnormal et al[61] valve with Vmax > 4.0

Asymptomatic

4.0 m/sec 128 60 ± Vmax 5.0 27 ± mos 18 ± 0.6 m/sec

m/sec

AS, aortic stenosis; AVA, aortic valve area; AVI, aortic valve index, AVR valve replacement; cath, catheterization; ∆P, pressure gradient; Vmax , maxim jet velocity.

* Event-free survival.

obstruction. Continuity equation valve areas will reflect accurately the degree of impairment of valve opening. In the past, "severe" or "critical" aortic stenosis has been defined in terms of a specific valve area or valve area index. More recent studies[89] [91] [115] have shown marked overlap in hemodynamic severity between symptomatic and asymptomatic patients, indicating that the "critical" degree of valve narrowing varies from patient to patient (Fig. 22-18) . This observation has been confirmed in prospective studies showing that symptom onset occurs with a jet velocity as low as 3.0 m per second or may be delayed until the jet velocity is over 5.0 m second. Similarly, some patients remain asymptomatic with a valve area less than 0.7 cm2 , whereas others have definite symptoms with a valve area greater than 1.0 cm2 . Hemodynamic Progression Until recently, data on the hemodynamic progression of valvular aortic stenosis was limited to studies of patients in whom two cardiac catheterizations had been performed (Table 22-4) . [116] [117] [118] [119] [120] [121] The impact of selection bias on these data is difficult to assess, since only patients who did not die or undergo valve replacement after the first catheterization,

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487

Figure 22-18 Hemodynamically severe aortic stenosis: mean aortic pressure gradient, valve orifice area, cardiac index, and left ventricular end-diastolic pressure in severely symptomatic (open circles) and asymptomatic or mildly symptomatic (closed circles) patients. Mean value (horizontal line) and statistical difference between both groups are indicated. NS, not significant. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–473.)

yet required a second catheterization for clinical indications, are included in these series. In general, these studies showed an average rate of increase in mean pressure gradient between 0 and 12 mm Hg per year and a decrease in valve area between 0.02 and 0.3 cm2 per year. Marked individual variability in the rate of progression was noted, however, and no clear factors were identified that predicted the rate of progression. The availability of an accurate, noninvasive method to evaluate hemodynamic severity has allowed larger and more detailed studies on the rate of hemodynamic progression.[58] [60] , [61] [90] , [115] [122] [123] [124] [125] [126] [127] In these studies, the average rate of increase in aortic jet maximum velocity ranges from 0.2 to 0.4 m per second per year, with an increase in mean gradient of 6 to 7 mm Hg per year and a decrease in valve area of 0 to 0.3 cm2 per year. Again, marked individual variability in the rate of hemodynamic progression Figure 22-19 Change in maximal aortic jet velocity (Vmax ) and pressure gradient during follow-up in 45 patients. (From Faggiano P, Ghizzoni G, Sorgato A, et al: Am J Cardiol 1992;70:229–233.)

was observed ( Fig. 22-19 and Fig. 22-20 ). Although Dopplerechocardiographic studies have the advantage of larger patient numbers and potentially less selection bias (a repeat echocardiographic study is likely to be requested more often than a repeat cardiac catheterization), many of these studies are retrospective, with the data extracted from ongoing clinical databases. Thus, patients with rapid progression, those developing symptoms, or those requiring surgical intervention may be overrepresented. Conversely, repeat studies may not have been performed in clinically stable patients. The results of more recent prospective studies may avoid some of these biases.[61] [128]

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It is important to remember that as the disease progresses, increasing obstruction to left ventricular outflow most often is reflected by both a decrease in valve area and an increase in jet velocity and pressure gradient. However, if there is a concurrent decrease in transaortic 488

TABLE 22-4 -- Hemodynamic Progression of Valvular A

Study Bogart et al[116]

Clinical Status at Entry 2 cardiac caths

Cheitlin et al[117] Wagner and Selzer

2 cardiac caths 2 cardiac caths

Mean Follow up Type of Measurement Patients, Interva Study Method N yr Retrospective Invasive 11 4.9

Retrospective Invasive

29 4

Retrospective Invasive

50 3.5

Retrospective Invasive

26 9

[120]

Jonasson et al[118] Nestico et al[119] Davies et al[121] Otto et al

Calcific AS

2 cardiac Retrospective Invasive caths 2 cardiac Retrospective Invasive caths Asymptomatic Prospective Doppler

29 5.9 47 42 1.7

[90]

Roger et al AS on echo

Retro cohort Doppler

112 2.1

Retrospective Doppler

25 4.8

[123]

Thoreau et AS on echo al[122]

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AS on echo

Peter et al AS on echo

Prospective

Doppler

45 1.5

Retrospective Doppler

49 2.7

Retrospective Doppler

394 6.3

[126]

Brener et al[125] Otto et al

AS on echo

Asymptomatic Prospective

Doppler

123 2.5

Retrospective Doppler

91 1.8

Retrospective Doppler

170 1.9

Prospective

128 1.8

[128]

Bahler et AS on echo al[60] Palta et al AS on echo [127]

Roshenhek AS on echo et al[61] with Vmax

Doppler

>4.0 m/sec

AS, aortic stenosis; AVA, aortic valve area; ∆P, pressure gradient; Vmax , volume flow rate, a decrease in valve area alone may be seen with no change in jet velocity or transaortic gradient. A decrease in transaortic volume flow rate may occur secondary to comorbid disease, such as increasing mitral regurgitation or myocardial infarction, but also may occur late in the disease course of isolated aortic stenosis as left ventricular stoke volume decreases because of the onset of subtle systolic dysfunction (Fig. 22-21) . Conversely, some patients may have an interval increase in jet velocity and pressure gradient with no change in valve area if transaortic stroke volume is increased because of systemic factors (e.g., anemia, fever, pregnancy) or increasing aortic regurgitation. At this point, it is not clear whether the rate of hemodynamic progression in an individual patient is either predictable or "steady." In fact, it is most likely that the rate of progression is nonlinear; that is, a fairly slow rate of Figure 22-20 Maximal aortic jet velocity (Vmax ) is plotted for the initial

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and final Doppler echocardiographic studies in 42 asymptomatic patients. Group means are indicated by the symbol . (From Otto CM, Pearlman AS, Gardner CL: J Am Coll Cardiol 1989; 13:545–550.)

progression may change to a rapid increase in severity when the opposing forces of left ventricular ejection and leaflet stiffness can no longer be balanced. Predictors of Hemodynamic Progression Factors that predict the rate of hemodynamic progression in an individual patient have not been well defined. Clearly, valve anatomy is an important factor in disease progressive, since most patients with a bicuspid stenotic valve require surgical intervention at a younger age than patients with degenerative aortic stenosis.[114] Gender also is important, since the ratio of men to women with aortic stenosis is approximately 2:1. Other factors associated with the rate of disease progression are the severity of aortic stenosis when initially seen (more severe disease 489

Figure 22-21 A 32-year-old man had asymptomatic valvular aortic stenosis with a jet velocity of 5.0 m per second and a continuity equation valve area of 1.2 cm2 (A and B). Over the next year, he developed the onset of exercise intolerance and early symptoms of aortic stenosis. Repeat examination showed a decrease in aortic jet velocity to 4.5 m per second (C) in association with a decreased transaortic volume flow rate (D). Aortic valve area had decreased to 1.0 cm2 . Two-dimensional echocardiography showed normal left ventricular systolic function, but ejection fraction had decreased from 72% to 60%.

leads to symptoms more rapidly than milder disease) and age (older patients have more rapid disease progression than younger patients). Clinical factors such as elevated serum lipid levels, hypertension, smoking, and diabetes have been found to be associated with aortic stenosis.[129] In addition, a recent study found that smoking, hypercholesterolemia, and elevated creatinine and calcium levels were associated with more rapid disease progression.[127] However, further studies are needed to confirm these results. Two recent studies suggested that the amount of aortic valve calcium is an important determinant of disease progression.[60] [61] Despite using different grading scales to evaluate valve calcium, both of these studies found that the rate of disease progression was more rapid when

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more valve calcium was present. These studies also confirmed previous observations that the rate of disease progression is highly variable for individual patients. Given the continued uncertainty regarding which factors predict progression in an individual patient, it is prudent to follow patients with aortic valve thickening closely, monitoring for early symptoms of valve obstruction. Periodic echocardiographic examinations also are warranted, particularly for any change in symptoms or functional status. Uncertainty as to the rate of hemodynamic progression in an individual patient complicates the decision as to whether concurrent aortic valve replacement should be performed in patients with only moderate aortic stenosis who are undergoing coronary artery bypass surgery. Some surgeons recommend "prophylactic" valve replacement, since otherwise reoperation may be needed in less than 5 years.[130] Symptomatic versus Asymptomatic Aortic Stenosis The clinical course of the patient with aortic stenosis changes dramatically once symptoms supervene. The 490

Figure 22-22 (Figure Not Available) A, Event-free survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circle) in severely symptomatic (solid lines and solid symbols) and asymptomatic or mildly symptomatic (dashed lines and open symbols) patients. B, Effective survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circles) in severely symptomatic (solid lines) and asymptomatic or mildly symptomatic (dashed line) patients. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–483.)

asymptomatic patient (regardless of hemodynamic severity) has a low risk of sudden death with an actuarial survival rate no different from that of agematched normal subjects[89] [91] [131] [132] (Fig. 22-22 (Figure Not Available) and Fig. 22-23 ). In contrast, the symptomatic patient has a grim prognosis, with a 5-year actuarial survival rate of only 12% to 50% without surgical intervention. These data were derived from studies of patients who refused surgical intervention.[89] [91] , [111] , [131] [133] [134] [135] In patients with severe, symptomatic aortic stenosis, predictors of survival include the transaortic gradient or velocity, left ventricular systolic function as assessed qualitatively on echocardiography, age, and gender.[136] Of note, patients with a higher transaortic gradient have a better prognosis, most likely

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because when severe stenosis is present, a low gradient indicates a low transaortic stoke volume. In any case, valve surgery for relief of stenosis remains the appropriate treatment for symptomatic patients, even the elderly.[137] [138] Only rarely does severe comorbid disease result in an unacceptably high operative morbidity and mortality.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Role of Echocardiography in Clinical Decision Making Timing of Intervention in the Symptomatic Patient Calcific aortic valve disease is prevalent in the elderly.[139] [140] Most of these patients have a systolic murmur on auscultation, but not all are symptomatic. The first step in the clinical decision making process for the timing of intervention in a patient with valvular aortic stenosis is a careful history as to whether symptoms (angina, exertional dizziness, exercise intolerance, or heart failure) are present or absent ( Table 22-5 ; ; Fig. 2224 ). Most clinicians defer intervention until definite symptoms are present, since the risk of sudden death is very low in the asymptomatic patient.[89] [91] [131] [132] , The presence of moderate or severe valve calcification in combination with a rapid increase in jet velocity over time (i.e., rapid progressors) identifies a subgroup of asymptomatic patients with a very poor short-term prognosis who are likely to develop symptoms soon.[61] If the patient has symptoms that may be due to aortic stenosis, the next step is to confirm the anatomic diagnosis and quantitate the degree of valve obstruction by Doppler echocardiography. The most appropriate standard of reference for the diagnostic utility of echocardiography in the management of symptomatic aortic stenosis patients is survival and functional status (not catheterization results), as our goal is to predict clinical outcome correctly.[16] Based on this reference standard, aortic jet velocity alone is a simple and useful initial diagnostic test. When jet velocity is very high (>4.0 or 4.5 m per second), severe stenosis is confirmed.[140] [141] [142] Some patients with mixed moderate aortic stenosis and aortic regurgitation will have a jet velocity over 4 or 4.5 m per second even though valve area is in the range of 1.0 to 1.5 cm2 . Comparing Doppler data with subsequent clinical outcome suggests that these patients benefit from valve replacement if symptoms of valve disease are present.[40] Decision making in patients with mixed aortic stenosis and aortic regurgitation is confounded by the need to take the degree of left

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ventricular dilation and systolic dysfunction into account as well as the severity of valve obstruction (see Chapter 4) . When jet velocity is very low (<3.0 m per second), severe stenosis is unlikely and valve replacement is not needed.[140] [142] Of course, exceptions do occur in clinical practice and an occasional patient may be seen with a jet velocity less than 3.0 m per second and a valve area less than 1.0 cm2 in association with severely reduced left ventricular systolic function. Similarly, this numerical approach applies only to the symptomatic patient in whom valve replacement is being considered. A high jet velocity in an asymptomatic patient certainly does not mandate surgical intervention. The use of two break points (upper and lower) allows both severity and specificity to be maximized but leaves an intermediate group in whom further evaluation is needed. When the jet velocity is 3 to 4 m per second, calculation of valve area and assessment of the degree of coexisting aortic regurgitation are helpful in clinical decision making. If the valve area is 1.0 cm2 or less and the patient has symptoms of aortic stenosis, valve replacement is indicated. If the valve area is greater than 1.5 cm2 , valve 491

Figure 22-23 Cumulative life table incidence of death in aortic stenosis patients. Asymptomatic persons (closed circles) had a significantly better survival with respect to all-cause mortality, cardiac death, and sudden death than symptomatic patients (open circles). (From Kelly TA, Rothbart RM, Cooper CM, et al: Am J Cardiol 1988;61:123–130.)

TABLE 22-5 -- Clinical Decision Making in Adults with Symptomatic Ao Stenosis Lower V max

Patients, Study N Method Otto 104 Split sample 1988 [40]

Upper V max

Break Break Diag End Point, Point, Accu Point % m/sec Midrange m/sec 9 Surgical <3.0 AVA, AR >4.0 findings plus 1 yr

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mortality Oh 100 Comparison Aortic Single AVA >4.5 1988 with cath data stenosis value [141] severity at cath Galan 510 Observational, Actual <3.0 AVA >4.5 1991 retrospective outcome [3] (AVR) Shah 93 Blinded Actual <3.0 AVA >4.0 1991 decision re: outcome [142] AVR (AVR) AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; Vmax , maximum aortic jet velocity.

6

9

9

replacement is unlikely to be helpful. When the valve area is between 1.0 and 1.5 cm2 , valve replacement may be indicated if there is at least moderate coexisting aortic regurgitation. Again, clinical decision making is problematic in this patient group. One prudent approach in the mildly symptomatic patient is to repeat the Doppler echocardiographic study after a reasonably short time interval (3–12 months). Evidence of disease progression will tip the balance toward intervention, whereas a stable examination and the absence of worsening symptoms argues for further waiting with close clinical follow-up. In clinical practice, the basic echocardiographic examination of a patient with valvular aortic stenosis includes measurement of maximum aortic jet velocity (with optional gradient calculations); continuity equation valve area; assessment of the degree of coexisting aortic regurgitation; evaluation of left ventricular size, hypertrophy, and systolic function; evaluation of the degree of mitral regurgitation; and estimation of pulmonary artery pressures. All of these parameters are included in the clinical decisionmaking process, along with any other specific measurements needed in an individual patient. Aortic Stenosis with Decreased Left Ventricular Function In some patients it is unclear whether valve opening is restricted due to excessive leaflet stiffness or whether there is only mild leaflet sclerosis with limited motion due to low transaortic stroke volume (Fig. 22-25) .

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There have been two basic research approaches to resolving the problem of distinguishing severe aortic stenosis with consequent depressed left ventricular systolic function from only mild to moderate stenosis with reduced leaflet motion due to intrinsic left ventricular dysfunction: (1) a flow-independent measure of stenosis severity or (2) a load-independent measure of left ventricular systolic function. Although significant progress has been made with both of these approaches, as discussed earlier, neither approach has provided a clear answer. A pragmatic clinical approach to this patient group is to (1) look at the valve, (2) look at the patient, (3) look at the options, and (4) consider further diagnostic evaluation (Table 22-6) . Direct assessment of the degree of leaflet thickening and calcification by fluoroscopy, transthoracic or transesophageal echocardiography, or, if 492

Figure 22-24 Flow chart for clinical decision making in aortic stenosis. AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; F/U, follow-up; Vmax , maximum velocity of aortic jet.

Figure 22-25 A 61-year-old man presented with heart failure symptoms. Echocardiographic examination showed a moderately calcified valve with reduced leaflet opening (A) and reduced systolic function (ejection fraction, 20%) in association with marked left ventricular dilation as seen in the apical four-chamber view (B). Transaortic stroke volume was reduced as shown by pulsed Doppler echocardiographic examination of left ventricular outflow velocity in an anteriorly angulated four-chamber view (C). The aortic jet velocity (D) was 3.0 m per second corresponding to a maximum gradient of 36 mm Hg and a mean of gradient of 22 mm Hg. Continuity equation valve area was 0.9 cm2 . After multiple readmissions for heart failure on medical therapy, the patient underwent aortic valve replacement. Postoperatively, there has been no change in left ventricular function and persistent symptoms of heart failure are present. Ao, aorta; AS-jet, aortic stenosis jet; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium; RV, right ventricle.

493

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TABLE 22-6 -- Clinical Decision Making: Aortic Stenosis with Decreased Left Ventricular Function 1. Look at the valve Severely calcified versus Flexible leaflets 2. Look at the patient LV dysfunction due to end-stage ischemic disease or cardiomyopathy versus LV dysfunction due to aortic stenosis 3. Look at the options Risk of surgery Comorbid disease Outcome without surgery 4. Evaluate stenosis severity at two different flow rates (dobutamine or exercise): Increased transaortic flow rate Increased AVA suggests flexible valve leaflets No change in AVA suggests stiff, rigid valve leaflets No change in transaortic volume flow rate Severe AS versus unresponsive myocardium? AS, aortic stenosis; AVA, aortic valve area; LV, left ventricular. necessary, direct inspection at the time of surgery often is very helpful. A heavily calcified valve suggests that valve replacement will be beneficial, whereas thin, flexible leaflets argue against valve surgery. Additional clinical information about the patient may clarify the problem. If left ventricular systolic dysfunction is due to aortic stenosis, improvement is expected after valve replacement. However, if left ventricular dysfunction is due to end-stage ischemic disease or a primary cardiomyopathy, little improvement is expected after aortic valve surgery. Next, the therapeutic options and expected outcomes can be estimated for the individual patient. If the risk of surgery is acceptable or if the patient is having surgery for coexisting coronary artery disease, the threshold for valve replacement is reasonably low. If the risk of valve replacement is excessively high because of comorbid disease, medical therapy may be

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appropriate. If the patient has failed aggressive medical therapy, surgical intervention may be indicated, even if the risk is high. If the clinical decision still remains unclear, evaluation of stenosis severity at two different flow rates may be helpful. With mild to moderate aortic stenosis, augmentation of transaortic volume flow rate with exercise or a positive inotropic agent (e.g., dobutamine) will result in a significant increase (>0.2 cm2 ) in valve area as the flexible leaflets open to a greater extent. Conversely, with critical aortic stenosis, valve area will change little despite increased transaortic volume flow due to stiff, rigid valve leaflets. However, an increase in aortic valve area can be seen in some patients with surgically confirmed severe aortic stenosis, which therefore does not exclude fixed valve disease.[143] If the ventricle fails to respond to inotropic stimulation (i.e., no increase in cardiac output), interpretation is more difficult.[50] [144] [145] The failure of volume flow rate to increase may be due to limitation of flow by a severely stenotic valve or may be due to an unresponsive myocardium. In some patients, it may be preferable to evaluate stenosis severity at baseline and after several weeks of therapy to optimize preload and afterload, rather than using maneuvers to acutely increase volume flow rate. Instead of assessing changes in valve area, another approach is to calculate the end-systolic wall stress to fractional shortening relationship and compare the patient's data with those of published series[101] to assess whether improvement after valve replacement is likely. Unfortunately, despite meticulous diagnostic evaluation, outcome is likely to be poor in patients with aortic stenosis and low output, regardless of the therapy chosen.[146] [147] [148] [149] [150] Patients with reduced systolic function and a history of a prior myocardial infarction experience a particularly poor outcome following valve replacement.[151] A recent study that included patients with a low transvalvular gradient in addition to impaired systolic function found that the ejection fraction improved in the majority of patients following surgery, but that the 30-day mortality rate was 21%.[152] Evaluation of the Asymptomatic Patient Undergoing Noncardiac Surgery In the asymptomatic patient with valvular aortic stenosis undergoing noncardiac surgery, echocardiography allows (1) assessment of disease severity, (2) monitoring of left ventricular function before, during, and after the procedure, and (3) alerting the clinician to the need for invasive

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hemodynamic monitoring. Many of these patients, even with severe obstruction, can be managed without valve replacement if loading conditions are optimized preoperatively and careful invasive monitoring is continued in the postoperative period.[153] [154] Common postoperative complications include pulmonary edema or congestive heart failure associated with tachycardia that usually resolves quickly with rate control and diuresis. Similar considerations apply to the management of the pregnant patient with aortic valve disease (see Chapter 31) . Optimizing the Surgical Approach Once the decision has been made to proceed with relief of stenosis, the echocardiographic examination plays a key role in choosing the optimal surgical approach. Valve replacement remains the standard therapy for relief of valvular aortic stenosis. The optimal valve size and type typically are selected in the operating room based on direct measurement of the annulus by the surgeon. Echocardiographic prediction of prosthetic valve size has been only fair because of the limited number of valve sizes and the goal of implanting a larger valve when possible to improve hemodynamics. [155] For homograft valve replacements, an estimate of the optimal size is more important than for mechanical valves, so that the correct size will be available at the time of surgery.[156] For homograft aortic valves, diastolic left ventricular outflow tract diameter correlates best with implanted valve size. Note that the diastolic outflow tract diameter measurement averages 2 mm smaller than the systolic measurement (which is used in valve area calculations). A dilated aortic root commonly is seen as a result of poststenotic dilation and, in some cases, may be large enough to merit root replacement. In patients with a 494

small aortic annulus, an enlarging procedure may be considered or a specific valve chosen to avoid suboptimal hemodynamics postoperatively. Recognition of a subvalvular membrane, which can be mistaken for valvular stenosis on echocardiography, will alter the surgical approach and may allow resection of the membrane without valve replacement. Coexisting hypertrophic cardiomyopathy, although rare, is important to recognize to avoid postoperative dynamic subaortic obstruction.

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Echocardiographic Evaluation after Valve Replacement for Aortic Stenosis Evaluation of the Valve Replacement Surgical procedures that preserve the native aortic valve have not yet been successful for treatment of valvular aortic stenosis,[157] nor has percutaneous balloon valvuloplasty shown long-term benefit in adult patients. [136] A mechanical or stented tissue prosthetic valve is most often implanted after removal of the stenotic valve leaflets. The fluid dynamics of prosthetic valves, evaluation of valve function, and other postoperative complications are discussed at length in Chapter 23 , Chapter 24 , and Chapter 25 . Newer surgical approaches to treatment of valvular aortic stenosis include the development of stentless tissue valves[158] [159] [160] [161] [162] [163] and the use of aortic valve homografts.[157] [164] [165] Both these valves types offer the advantages of improved hemodynamics compared with conventional valves, the absence of the need for chronic anticoagulation, and the hope of increased durability. Some centers also have reported success with the pulmonic valve autograft procedure in young adults, as well as adolescent patients.[166] [167] [168] In this procedure, the patient's stenotic aortic valve is replaced with his or her own native pulmonic valve. A homograft then is used in the pulmonic position. Potential advantages of this procedure include optimal hemodynamics and low thrombogenicity. In addition, tissue viability of the pulmonic autograft provides the possibility of tissue growth and repair, which are particularly important features in adolescent patients. In one series including patients up to age 35 years, event-free survival rate after the pulmonic autograft procedure was 90% at 7 years.[166] Events included reoperation for either aortic or pulmonic valve dysfunction, significant aortic regurgitation, and death. More recently, echocardiographic follow-up of 100 patients undergoing the pulmonic valve autograft procedure was reported.[169] The reintervention rate was 2% at a mean follow-up period of 33 months, with a range of 6 months to 7

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years. A unique complication of the pulmonic autograft procedure is the development of homograft failure, either from stenosis or regurgitation. With homograft stenosis, patients typically develop progressive dyspnea approximately 3 to 6 months following surgery, at a time when continued physical recovery from the surgical procedure would be expected. Tissue from these failed explanted homografts show a prominent inflammatory cell infiltrate and therapy has thus focused on suppressing the heightened immune response with oral steroids. When a course of oral steroids fails to control the disease process, reoperation may be required. Since stentless tissue valve, homografts, and pulmonic autografts appear similar to a native aortic valve on echocardiographic examination,[160] [165] it is important that details about the surgical procedure be available at the time of the echocardiographic examination. Doppler findings for these valves also are similar to findings in native valves except that antegrade velocities may be slightly higher. Pulmonic autografts tend to have some degree of regurgitation early postoperatively, which typically decreases over the next several months, presumably due to collagen synthesis and increased structural stability of the valve in response to the increased mechanical stress on the valve leaflets. Other Hemodynamic Changes Postoperatively If left ventricular end-diastolic pressure has been chronically elevated preoperatively, as the ventricle remodels and filling pressures normalize, there may be a corresponding decrease in pulmonary artery pressures. If pulmonary pressures are elevated because of coexisting lung disease, little change is expected postoperatively. Moderate pulmonary hypertension (pulmonary artery pressures of 31 to 50 mm Hg) occurs in approximatly 50% of patients evaluated preoperatively with right heart catheterization.[170] However, the presence and magnitude of pulmonary hypertension do not appear to be related to the severity of aortic stenosis. It remains unclear whether preoperative pulmonary hypertension is related to postoperative survival, because studies have yielded conflicting results. [171] The effect of aortic valve replacement on coexisting mitral regurgitation remains controversial. In theory, mitral regurgitant severity should decrease given the "afterload reducing effect" of aortic valve replacement.[172] However, the magnitude of this effect may be small, particularly if there is anatomic abnormality of the mitral valve apparatus.[173] When significant mitral regurgitation accompanies severe aortic stenosis, it is prudent to consider a surgical intervention to reducing mitral regurgitant severity at

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the time of aortic valve replacement. Intracavity gradients due to dynamic obstruction at the midventricular level are seen in one quarter to one half of aortic stenosis patients in the early postoperative period.[174] [175] The severity of obstruction varies from trivial to severe, and clinical evidence of hemodynamic compromise may be seen in some patients. Patients with small hypertrophied and hyperdynamic ventricles at baseline are more likely to have obstruction postoperatively. [176] Typically, obstruction is manifested as a late-peaking systolic velocity curve, which is similar to the pattern seen in hypertrophic obstructive cardiomyopathy. However, the level of obstruction is at the midventricular or papillary muscle level, rather than subaortic, and systolic anterior motion of the mitral valve is not seen. Obstruction is dynamic in that the presence and severity of obstruction varies from day to day (peaking at the third postoperative day) and in that obstruction can be provoked or increased 495

by maneuvers that decrease left ventricular preload or increase contractility. Echocardiographic recognition of midcavity ventricular obstruction in the postoperative period affects clinical management, since intravascular volume loading and avoidance of agents that increase contractility or reduce afterload can result in significant clinical improvement. The echocardiographic finding of dynamic obstruction after aortic valve replacement also has significant prognostic implications. Patients with obstruction have more frequent postoperative complications (hypotension, arrhythmias), a longer hospital stay, and a higher mortality rate than those without obstruction.[175] [176] [177] The Effect of Valve Replacement on the Left Ventricle When left ventricular systolic function is depressed because of valvular aortic stenosis, improvement is seen early in the postoperative period. Predictors of improvement in the ejection fraction include female gender and less severe coexisting coronary artery disease.[103] When measured by quantitative angiography, left ventricular mass and wall thickness decrease substantially in the postoperative period. By 10 months postoperatively, left ventricular mass has decreased by about 30% as compared with the preoperative left ventricular mass, with a further decrease in left ventricular mass observed at studies performed 8 years

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postoperatively. Left ventricular mass may remain elevated in some patients, particularly if the prosthetic valve has suboptimal hemodynamics. Despite the apparent improvement in left ventricular geometry and systolic function seen in most patients, irreversible (or only very slowly reversible) changes in myocardial structure persist late postoperatively, with a relative increase in myocardial interstitial fibrosis as compared with normal and persistent diastolic dysfunction.[178] These myocardial changes, in combination with the mild pressure overload of the prosthetic valve, can result in persistent systolic overload at the myofibrillar level.[93]

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Future Directions Echocardiographic evaluation of aortic stenosis is an established and effective clinical tool. However, to explain the relationship between hemodynamic severity and symptom onset, a flow-independent measure of stenosis severity still is needed. At this point, the most promising research approach to a flow-independent measure of stenosis severity is to determine the change in the degree of valve narrowing measured at two different volume flow rates rather than utilizing data obtained only at rest. Continuity equation valve area and the slope of the maximum velocity/maximum volume flow rate relationship both are potentially useful approaches to this problem. A plausible hypothesis is that early in the disease course of "degenerative" aortic stenosis, increases in volume flowrate result in increased opening of the valve leaflets. As leaflet stiffness increases, this increase in leaflet motion diminishes until, eventually, increases in left ventricular ejection force no longer result in increased leaflet motion. We propose that symptom onset correlates with a stiff and rigid valve that limits the patient's ability to increase cardiac output with exercise. Other investigators have proposed a similar approach measuring stenosis severity at different flow-rates using exercise or dobutamine.[50] [78] [87] Further studies are needed to assess the potential prognostic value of this approach. As studies using Doppler approaches provide additional insight into the natural history of this disease, these data will allow prediction of disease progression in individual patients. In addition, these data will allow sample size calculation and appropriate risk stratification for interventional trials. In the future, these techniques will be used as end points in clinical trials of interventions to prevent or delay progression of "degenerative" valvular aortic stenosis.

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501

Chapter 23 - Fluid Dynamics of Prosthetic Valves Ajit P. Yoganathan PhD Brandon R. Travis PhD

Doppler echocardiography has made noninvasive examination of prosthetic heart valve function a clinical reality. Unfortunately, there are still many imperfections in echocardiographic examinations, including acoustic shadowing, reflections caused by implanted valves, and limitations in ultrasound technology. Despite these limitations, a number of important parameters can be calculated or estimated to aid in the assessment of prosthetic heart valve function and performance. Once a valve has been implanted, its function is governed primarily by its hemodynamic characteristics. In order to understand the hemodynamic performance of prosthetic heart valves, it is necessary to have a solid background in the physical laws that govern their function; therefore, the purpose of this chapter is to introduce cardiologists to the governing principles of fluid dynamics, relevant formulations used in prosthetic valve assessment, and fluid mechanical characteristics of specific prosthetic heart valves.

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Fluid Dynamics With few exceptions, a material can be characterized as a fluid if it deforms continuously under the action of shear stress.[1] Shear stress is defined as a force per unit area applied tangentially to a surface. Viscosity is related to the amount of deformation that a fluid experiences when a shear stress is imposed on it. A constant viscosity fluid, called a Newtonian fluid, is one in which the relationship between viscous shear stress and strain rate is linear, as shown in Equation 1: where µ is the viscosity, usually defined in centipoise (grams/cm·s). The coefficient in this linear relationship is the dynamic viscosity. Equation 1 states the relationship between viscous shear stress (τ), viscosity (µ), and strain rate for flow in the x-direction with the derivative taken in the ydirection, perpendicular to the direction of flow. Blood behaves as a Newtonian fluid in regions of high strain rate. For flow in large arteries, 3.5 cp is often used as a viscosity estimate for blood.[2] Conservation of Mass Conservation of mass governs all materials, and it is the logical starting point for an introduction to fluid motion. Consider an imaginary volume, a control volume, enclosed by a surface through which fluid can flow, as shown in Figure 23-1 . It is not necessary for this control volume to coincide with any physical boundaries; it is purely a tool for the analysis of physical systems. Conservation of mass, or continuity, states that the change in mass within this control volume is equal to the mass of fluid that enters the volume, minus the mass that exits. [3] A very good assumption for cardiovascular applications is that 502

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Figure 23-1 Control volume for the conservation of mass. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 . ρ, fluid density.

blood is incompressible, meaning its density does not vary. Assuming that there are only two surfaces across which fluid flows, surfaces 1 and 2, the velocities (v) and areas (A) can be related by conservation of mass, as shown in Equation 2.

pρv1 (t)A1 = ρv2 (t)A2 (2) Conservation of Momentum The principle of conservation of momentum was initially formulated as Newton's second law of motion—mass times the acceleration of an object is equal to the sum of the forces acting on that object. For application to fluid mechanics, it is more convenient to define this in terms of the fluid momentum. The momentum of a fluid is a measure of the mechanical force it is able to transfer and is equal to the product of fluid mass and fluid velocity. A change in momentum of a fluid can only be accomplished by the application of a force. The general form of the principle of conservation of momentum for an incompressible Newtonian fluid is called the NavierStokes equations.[3] The forces that merit consideration within the cardiovascular system are pressure, gravity, viscous shear stresses, and turbulent stresses. Conservation of Energy Consider the conservation of energy statement, again using the control volume approach. The change in energy within a control volume is equal to the net rate of energy crossing the surface of the control volume plus the net rate of energy generated within the control volume. Energy loss occurs when the net rate of energy generated within the control volume is negative. In cardiovascular applications, energy loss usually occurs because the viscosity of the fluid converts its kinetic energy to heat. The general equation for energy conservation is difficult to apply to cardiac blood flow; however, with a number of simplifying assumptions a useful relation can be obtained. The Bernoulli equation,[4] as shown in Equation 3, is used

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extensively in noninvasive cardiology:

where p is the static pressure and v is the velocity, along the streamline, h is the vertical distance above some reference point, and s is the distance between points one and two along the streamline. This equation can be derived from either the conservation of energy or the conservation of momentum. Each term in Equation 3 has a physical definition that aids in comprehension and application of the Bernoulli equation. The left side of the equation represents the difference in pressure acting on the fluid between the positions one and two. The first term on the right side is called the inertial term and represents the change in fluid acceleration owing to temporal changes in the applied force. The second term on the right side is the kinetic energy associated with the fluid at each location. This term can also be considered the convective acceleration term, which is associated with a change in the velocity of a fluid as it travels from one location to another. The classic example of convective acceleration is the steady flow of fluid through a converging nozzle, such as a funnel. Because of continuity, the velocity is higher at the exit of the funnel than at the entrance, and acceleration occurs even though the flow is steady. The third term on the right side of the equation is the hydrostatic pressure difference, owing to the difference in elevation between the two points. The final term on the right side of the equation is the irreversible loss of mechanical energy or momentum owing to viscous effects. The limitations that arise when using Equation 3 are important to understand. Initially, Bernoulli's equation was derived for inviscid flow, in which there are no viscous effects. Because it is not physically possible to obtain such a flow, the term on the far right was added to account for losses caused by viscous effects. Equation 3 must also be applied between two points that lie along a streamline within a flow field. Streamlines are imaginary lines in a flow field to which the velocity vector is always parallel. In steady flow situations, streamlines can be traced by placing a particle or dye into the fluid and following their motion throughout the flow field. If the flow is unsteady, however, streamlines change from one time to another, and the particle paths no longer coincide with streamlines. Because of the difficulty in defining streamlines, rigorous application of Equation 3 is not possible in cardiovascular flows.

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Dimensionless Quantities The structures of cardiovascular flows are governed by chamber geometry and two dimensionless quantities. The first of these quantities, the Reynolds number, is defined as follows: where v is the velocity, µ is the viscosity, ρ is the fluid density, and d is a length representative of the flow regime 503

in question. For flow in a pipe, d is the pipe diameter, whereas for jet flows, it is the diameter of the orifice through which the jet exits. Physically, the Reynolds number represents the ratio of the fluid inertia to the viscous forces acting on a fluid. The other important dimensionless quantity in cardiovascular flows, the Womersley number (α), represents the ratio of the local acceleration a fluid experiences to the viscous forces acting on it. The Womersley number is defined as follows:

where ω is the frequency (heart rate) and all other variables are the same for those used in the definition of the Reynolds number. These dimensionless numbers can be used to define a transition regime to turbulence common to all cardiovascular flows occurring in a similar geometry. Turbulence Consider a car traversing a winding road. As long as the car stays below a certain speed, the frictional force between its tires and the road enable the car to follow the path in which its front wheels are aligned. When the car surpasses a certain speed and passes around a large curve, however, the inertia of the car overcomes the frictional force holding the tires to the road. Similarly, flows with large inertia relative to the frictional, or viscous, forces acting on them become turbulent. Under these conditions, a small instability in the flow field (e.g., surface roughness within a pipe) can initiate fluctuations in fluid motion. When these fluctuations propagate to the point where fluid motion can only be described as random fluctuations about a mean velocity, the flow is said to be turbulent.

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In steady flows, the tendency of a flow to be turbulent is governed only by the Reynolds number and the chamber geometry. Two geometries that have been studied extensively and have direct applications to cardiovascular fluid mechanics are flow through a straight pipe and flow through a small, circular orifice. Flow through a straight pipe transitions to turbulence at Reynolds numbers of approximately 2000.[5] Flow through small, circular orifices create a phenomenon known as a free jet. For steady free jet flows, which are inherently more unstable than pipe flows, the critical Reynolds number is approximately 1000, with fully turbulent flow occurring at Reynolds numbers greater than 3000.[6] [7] In pulsatile flow, the transition to turbulence depends on the Womersley number and the shape of the flow waveform as well as the Reynolds number and chamber geometry.[8] [9] The critical Reynolds numbers for the transition to turbulence in pulsatile flow is much higher than the corresponding numbers in steady flow. Estimates of transition to turbulence in the ascending aorta by Yoganathan et al[4] (based on work by Nerem and Seed[10] ) indicated that the critical Reynolds number for transition is approximately 8000. It is also important to note that in pulsatile flow, turbulence may not be present during the entire cycle. Because flow acceleration is inherently more stable than flow deceleration, turbulence is more often observed during the deceleration phase of pulsatile flow. [9] Shear Stress Both viscous and turbulent shear stresses, if large enough, can potentially lyse or activate cells of the blood[11] [12] [13] [14] however, the origin, and consequently the scale, of viscous and turbulent shear stresses is different. Viscous shear stresses act on a molecular scale; they arise from the tendency of one molecule to remain near its neighbors. This tendency is quantified in fluids by their viscosity. Because viscous stresses act on a scale much smaller than the diameter of a blood cell, blood cells always experience a viscous shear stress if such a stress is present. In contrast, turbulent shear stresses arise from the inertia contained within the fluctuations of turbulent flow. Turbulent shear stresses act on a scale comparable to the length of the smallest turbulent fluctuations, often much larger than the diameter of a blood cell. Even if a turbulent shear stress is present, a blood cell may not experience this stress if the cell diameter is much smaller than the length scale of the smallest turbulent fluctuations. Boundary Layer Separation

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Due to viscosity, when a flowing fluid contacts a solid body, because of viscosity, the fluid that is immediately adjacent to the body must be the same velocity as the body. For this reason, a boundary layer is formed. The boundary layer is a region in which the velocity changes from zero at the wall to that of the free stream value. Boundary layers are extremely thin but very important, for it is only in this region of the flow that viscous effects are significant. As a fluid moves downstream, viscous diffusion occurs and the viscous effects are felt farther from the wall, and the boundary layer grows. When a fluid flows over a solid body, it must change direction to pass around the body. A pressure gradient is required for this to occur. When an adverse pressure gradient (i.e., a pressure gradient against the flow direction, tending to decrease fluid velocity) is applied, if the magnitude of the pressure gradient is large enough, the fluid within the boundary layer reverses and boundary layer separation occurs. Downstream of the separation point, a region exists in which there may be reversed, turbulent, or disturbed flow. Recirculating or vortical flows are characteristic of this region; they can lead to high particle residence times and oscillatory shear stresses, both of which can have a wide variety of clinical implications, including atherosclerosis.[15] [16] In pulsatile flows, separation can be generated by a geometric adverse pressure gradient or by temporal changes in the driving pressure. Geometric adverse pressure gradients are present behind all prosthetic heart valves because of the small orifice area. As the area increases downstream of a prosthetic heart valve, the velocity decreases, in accordance with the continuity equation. The decrease in velocity is caused by an adverse pressure gradient. Because of the contractile nature of the heart, 504

the blood that flows through it also experiences both acceleration and deceleration during a cardiac cycle. It is during the deceleration phase of a particular flow, when an adverse pressure gradient is present, that boundary layer separation is most likely to occur. Thus, in regions in which there are both geometric and temporal adverse pressure gradients, separation is even more likely. Cavitation Cavitation is the formation of vaporous bubbles resulting from a sudden

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drop in local pressure below the vapor pressure of the fluid. The abrupt closure of a mechanical prosthesis has been shown to induce cavitation in in vitro flow circuits,[17] [18] [19] and a few works have linked cavitation with mechanical valve closure in vivo as well.[20] , [21] The formation and subsequent collapse of cavitation bubbles releases a tremendous amount of energy within a very localized area; cavitation has been known to crack steel turbomachinery. Cavitation during the mechanical valve closure event is thought by some to be responsible for pitting on mechanical prosthesis surfaces[22] and the blood damage induced by mechanical prostheses.[18] The sharp drops in local pressure created by mechanical prosthesis closure lasts less than 2 ms,[18] [19] [20] [21] so the resulting cavitation bubbles collapse soon after they are created. Vaporous cavitation bubbles could act as nucleation sites, however, drawing in blood gasses such as nitrogen and carbon dioxide. The resulting gaseous emboli could last much longer than the cavitation event. Indeed, gaseous emboli have been detected in the circulation of patients with mechanical prostheses by transcranial Doppler. [23] Such emboli have been dubbed with the acronym HITS (high intensity transient signals). Pressure Recovery Consider steady flow of fluid through a pipe with a restrictive orifice placed downstream of the pipe entrance. Because of continuity, as the fluid enters the restriction, it accelerates. Assuming that the flow is streamlined when the particle enters the restriction, the velocity increases and the static pressure decreases, according to the Bernoulli equation. Once it exits the restriction and the cross-sectional area increases, the particle's velocity decreases and the pressure increases. The increase in pressure distal to a restrictive orifice is called pressure recovery. If there are no viscous energy losses, the pressure recovers to the value it had at the entrance to the restriction; however, viscous losses always occur, pressure does not recover completely, and irreversible mechanical energy losses occur.[3] Consider two similar steady flow situations. The first geometry is that of a Venturi flow meter, as shown in Figure 23-2 . The second case involves flow through an orifice meter, in which a restrictive orifice is placed in the center of a straight pipe (see Fig. 23-2A) . In the first case, because of the smooth contraction before the Venturi throat and the gradual area expansion downstream, there is no separation and very little energy loss. Most of

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Figure 23-2 A, Orifice meter with pressure drop. B, Venturi meter with pressure drop.

the velocity at the Venturi throat is converted back to pressure. For the same flow through the orifice meter, the velocity at the orifice would be approximately the same as the velocity at the Venturi throat. Because of the very rapid area contraction and expansion surrounding the orifice, however, a large separation region forms downstream and energy is lost. Pressure measurements at the location of the greatest contraction within each model would yield approximately the same value, which could lead one to believe that the energy losses in both models are identical. If the pressure is measured further downstream, however, it is evident that the Venturi meter has a much smaller energy consumption than the orifice meter, owing to downstream recovery of pressure. The same concepts may hold true for stenoses within the cardiovascular system. In the Venturi model, the peak velocity and the smallest pressure occur at or very near to the throat of the model, whereas in the orifice meter, because fluids cannot turn sharp corners, the peak velocity occurs slightly downstream of the orifice. The location at which this occurs is called the vena contracta because the area that the fluid passes through is less than the orifice area. Therefore, according to the Bernoulli and continuity equations, the maximum pressure drop across a prosthetic valve occurs at the location of the vena contracta and not at the valve orifice.

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Application of Fluid Mechanics to Prosthetic Heart Valves Pressure Drop The pressure drop (∆P) across a prosthetic valve is related to the energy losses caused by its presence. Pressure 505

drops across natural valves can be measured with invasive catheter techniques; however, it is both difficult and dangerous to pass a catheter through a prosthetic valve. Fortunately, the Bernoulli equation can provide a noninvasive estimate of the pressure drop across prosthetic or natural valves. Neglecting the viscous effects and applying Equation 3 at mean conditions, so that the integral term vanishes, yields Equation 4: Point 1 is proximal to the valve and point 2 is at the orifice. If the velocity upstream of the valve is much smaller than at the valve, v1 can be neglected and Equation 5 is obtained:

If the velocity is measured with continuous wave Doppler ultrasound (in meters per second), the pressure drop can be obtained from this equation in millimeters of mercury. When measuring pressure distal to prosthetic valves, it is important to note whether or not the recovered pressure is measured. It is especially important when using continuous wave Doppler ultrasound to evaluate prosthetic heart valves. Continuous wave Doppler ultrasound measures the highest velocity, which occurs at the vena contracta. Consequently, the Doppler-derived pressure drops are always based on the pressure at the vena contracta, before pressure recovery occurs. Thus, one is likely to

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overestimate the transvalvular pressure drop because pressure recovery is not considered. Although Doppler ultrasound may overestimate transvalvular pressure drops, however, they are extremely useful in patient diagnosis. A study by Marcus et al[24] has shown that Doppler-derived pressure drops measured across small-diameter prosthetic mechanical valves (Medtronic-Hall and St. Jude) correlate just as strongly with fluid mechanical energy losses as the recovered pressure drops measured by catheterization. Pressure drop and recovery through prosthetic valves can be significant factors affecting the pressure within the left ventricle. A larger pressure drop across a prosthetic valve requires a larger systolic pressure in the left ventricle to drive flow through the circulation. Because it has been shown that left ventricular pressure is the primary determinant of myocardial oxygen consumption,[25] it is imperative that the pressure in the left ventricle is minimized when dealing with prosthetic valves. Numerous studies detailing the effects of recovery on pressure drop measurements for both natural and prosthetic heart valves have been published, and this topic continues to be an area of active research.[26] [27] [28] [29] [30] [31] [32] [33] [34] [35] Valve Area Cardiologists have used a variety of methods to determine the forward flow area of a valve. Because of acoustic anomalies caused by prosthetic valves and the limited spatial resolution of echocardiography, it is often impossible Figure 23-3 Control volume in the left ventricle for determining aortic valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 .

to measure the valve area directly. Applying a control volume analysis to a prosthetic valve in the aortic position (Fig. 23-3) and rewriting Equation 1, however, allows for estimation of the mean area over which fluid flows, as shown in Equation 6: The integral is taken with respect to time over the systolic flow period, v1 is

the velocity upstream of the aortic valve, and v2 is the velocity at the vena

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contracta. A2 is the area of the vena contracta or the effective valve area and A1 is the area at the upstream face of the control volume, measured by

echocardiography. Inherent to Equation 6 is the assumption that the spatial velocity profile is uniform over the entire orifice area; however, because the velocity profile is nonuniform in mechanical prostheses, it is difficult to apply Equation 6 accurately. By extending the control volume from the left ventricular outflow tract to encompass the entire left ventricle (Fig. 23-4) , it is possible to use this technique to determine the mean mitral valve area. The time-velocity integral of both the mitral and the left ventricular outflow tract positions must be calculated over the entire cardiac cycle. It is only necessary to integrate the velocity at the mitral valve during diastole and that of the aortic valve during systole, because these are the only times in which there is flow through the valves. If regurgitation is not present in either valve, Equation 6 can be applied and the effective area of the mitral valve can be obtained. When aortic regurgitation is present, the velocity and area at the light ventricular outflow tract can be used instead for calculation of effective mitral orifice area. Another method for determining valve area can be 506

Figure 23-4 Control volume in the left ventricle for determining mitral valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2

derived using the Bernoulli equation and conservation of mass. A contraction coefficient (Cd ) can be defined as the area of the vena contracta

divided by the area of the valve orifice (Ao ).[3] The continuity equation for flow through an orifice, including the contraction coefficient, appears in Equation 7, where Q is the flow rate and v is the velocity at the vena contracta: Q = Ao vCd (7) Substituting Equation 5 into Equation 7 and solving for velocity yields an

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equation that can be used to determine the effective orifice area of a cardiac valve:

The constant was determined by using the density of blood (ρ = 1050 kg/m3 ) and converting the units to those convenient for biomedical use.

The effective area will be square centimeters, if the root mean square systolic or diastolic flow rate (Qrms ) is in cubic centimeters and the mean systolic or diastolic pressure drop (∆P) is measured in millimeters of mercury.

Another method that has been developed involves measuring the pressure half-time of an orifice to estimate the orifice area. The pressure half-time (Pt/2 ) is the time required for left ventricular pressure to decrease to half of its peak value. An empiric relation between the pressure half-time and the area of the mitral valve (Amv ) has also been established. It was based on observations that changes in the mitral pressure drop with time were constant for a particular orifice area[36] [37]

The constant 220 was empirically determined,[38] but this equation has been shown to be dependent on a number of factors other than the valve area, including the severity of aortic regurgitation and ventricular wall properties. This equation is ineffective for prosthetic heart valves, limiting its application.[39] [40] Regurgitant Flow Rate Because mechanical prosthetic valves are fairly rigid, they are unable to form tight seals when closed. Consequently, regurgitant jets are present in prosthetic valves under normal conditions, although the amount of regurgitation is usually small. Normal regurgitant flow is characterized by a closing volume during valve closure and leakage after closure (see Figure 23-11) . Regurgitant flow is often characterized by the regurgitant volume. The regurgitant volume is the total volume of fluid through the valve per beat owing to the retrograde flow. It is equal to the sum of the closing volume and the leakage volume. The closing volume is the volume of fluid flowing retrograde through the valve during valve closure. Any fluid volume accumulation after valve closure is caused by leakage and is

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referred to as the leakage volume. These quantities are dependent on valve size, increasing with increasing valve diameter. Typically, the regurgitant volume is higher for mechanical valves than for bioprosthetic valves; however, prosthetic valves can exhibit substantial regurgitation when they malfunction. To distinguish normal from abnormal valve function, it is important to differentiate between normal regurgitant volume and additional regurgitation owing to disease. Fluid mechanical analysis of this problem has provided two different techniques that at least partially fulfill this requirement. Turbulent Jet Theory

Using free turbulent jet theory, Cape et al[41] [42] [43] (and later Sugawara et al [44] ) were able to derive relations for the regurgitant flow rate based solely on Doppler ultrasound measurements. Turbulent jets have a number of unique characteristics. Upon entering a chamber they spread radially, pulling or entraining stationary fluid with them. Initially, though, the jet has a core of fluid that is not affected by the stationary fluid. This potential core has the same velocity as the jet at the orifice and persists for a few orifice diameters downstream, as shown in Figure 23-5 . Once the core vanishes, the jet reaches a state that is amenable to theoretical analysis. It is important to recognize, however, the assumptions inherent in this theoretical analysis. Unsteady flow effects are neglected, and the analysis assumes that the jet enters a stationary fluid and does not impinge on solid boundaries. In the heart, regurgitant jets are unsteady, often impinge on the walls of the heart, and always encounter incoming forward flow. Additional work has been performed that treats jets in confined and impinging geometries; these geometries more closely resemble the chambers of the left heart. Burleson et al [45] [46] constructed a dimensional analysis model of valvular regurgitation based on the center line velocity decay of the jet and the width and length of the receiving chamber. Their equation has been shown to 507

Figure 23-5 Free jet center line velocity decay showing jet velocity (v) plotted versus distance (x).

be accurate for a number of in vitro geometries and conditions.[45] [47]

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Proximal Flow Convergence

The principle of conservation of mass was also applied in the region proximal to the valvular orifice to measure regurgitant volume.[48] [49] [50] [51] When fluid enters a regurgitant orifice it must accelerate to reach a peak velocity at the throat of the orifice. If the orifice is circular, this acceleration region should be axisymmetric about the center of the orifice. Thus, upstream of the regurgitant orifice, a series of concentric isovelocity contours hemispherical in shape can be defined within the flow field. This physical argument is the basis for the proximal flow convergence method of quantifying regurgitant flow rate. If a control volume is constructed to coincide with a hemispherical contour and the regurgitant orifice, as shown in Figure 23-6 , the same amount of fluid that enters the volume from an isovelocity contour exits the control volume through the regurgitant orifice. The control volume statement is represented mathematically in Equation 9. Qo = (2πr2 )Vr (9) The term within parentheses is the surface area of the hemispherical control surface. Vr is the velocity measured with color Doppler echocardiography

and r is the distance at which the velocity is measured. Qo is the flow rate at the regurgitant orifice.

Because of its simplicity and ease of application, this technique has received a great deal of attention, especially for mitral regurgitation. The effects of regurgitant orifice motion,[52] orifice geometry variation,[53] [54] [55] [56] and ultrasound machine settings[53] have all been addressed with both in vitro and in vivo investigations. In addition, its application to prosthetic valve regurgitation has also been considered.[57] Studies in our laboratory have found that isovelocity contours from regurgitant orifices can be described better by a hemielliptical shape than by a hemispherical shape, yielding more accurate estimations of regurgitant flow rate in vitro.[58] [59] Unfortunately, rigorous in vivo validation of the proximal flow convergence technique is difficult.

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Hemodynamic Characteristics of Native Valves In order to effectively analyze flow through prosthetic heart valves in the mitral or aortic positions, it is important to understand the conditions under which natural valves function. Figure 23-7 illustrates typical pressure and flow waveforms for healthy individuals at both the aortic and the mitral valves. During systole, the pressure difference required to drive the blood through the aortic valve is on the order of a few millimeters of mercury. Diastolic pressure differences across the aortic valve are much larger than systolic, the pressure usually being about 80 mm Hg. The valve closes near the end of the deceleration phase of systole with very little reverse flow. The blood flow through the mitral valve is biphasic during diastole, as shown in Figure 23-4 . The first peak, the E wave, is due to ventricular relaxation, whereas the second peak, the A wave, is caused by contraction of the left atrium; therefore, all valves in the mitral position open and close twice during each cardiac cycle. It is also evident that all cardiac valves are closed during both isovolumic contraction and isovolumic relaxation. Measurements of the velocity profile just distal to the aortic valve have been performed with Doppler echocardiography in normal subjects.[60] The peak systolic velocity is Qo = (2πr2 )Vr . (12) Figure 23-6 Proximal isovelocity surface area schematic. Vr is the velocity on a hemispheric shell defined by the radius (r) with surface area A1 . A2 is the regurgitant orifice area and Vo is the peak regurgitant jet velocity.

508

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Figure 23-7 Pressure and flow waveforms for the left heart.

1.35 ± 0.35 m per second and the velocity profile at the level of the aortic valve annulus is relatively flat; however, there is usually a slight skew toward the septal wall (<10% of the center line velocity) caused by the orientation of the aortic valve relative to the long axis of the left ventricle. This skew in the velocity profile has been shown by many experimental techniques, including hot film anemometry,[61] [62] Doppler ultrasound,[60] and magnetic resonance imaging.[63] The flow patterns distal to the aortic valve also play an important role in proper valve function. During systole, vortices form behind each leaflet in the sinus region. In vitro studies have attempted to relate these vortices to effective valve closure.[64] [65] It has been shown that the ventricular vortices are unnecessary for valve closure; however, they do ensure that the valve closes quickly, reducing leakage.[66] The velocity profile at the mitral valve has been determined in detail in pigs and should be comparable to the velocity profile in humans because of the similarity in cardiac anatomy.[67] Again there is a slight skew to the profile, but there does not seem to be a preferred orientation. It is dependent on the particular geometry of the mitral valve, the diastolic flow patterns within the left ventricle and the location at which the pulsed Doppler sample volume is placed.[67] When the sample volume was placed at the mitral annulus, the peak early diastolic velocity was 63.6 ± 16.1 cm per second, whereas the late diastolic peak velocity was 53.7 ± 10.8 cm per second.[67] When the sample volume was at the tip of the mitral valve leaflets, the peak early diastolic velocity was 82.9 ± 30.8 cm per second and the peak late diastolic velocity was 39.6 ± 14.2 cm per second. Vortices develop in the left ventricle during diastole as blood enters through the mitral valve. Bellhouse[68] proposed that the vortices helped to close the mitral valve at the end of diastole. Later work has shown that the vortices play a role in early closing of the mitral valve, but late closure is dominated by left ventricular pressure.[69] Because of the restrictive area of prosthetic valves, the peak velocities are usually higher, and the spatial velocity profiles are dramatically different from those in natural valves. The shear stresses in prosthetic valves also are

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much larger because of the higher velocities and turbulence. The magnitude of the shear stress varies greatly depending on the type of prosthetic valves. It is important to note the differences and similarities between valve types in terms of shear stress magnitudes, peak velocities, and flow patterns so that an effective assessment of prosthetic valve function can be performed.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Fluid Mechanics of Specific Prosthetic Valve Designs Prosthetic heart valves have been successfully used in heart valve replacement over the past 40 years. Currently, heart valve prostheses can be classified into two primary categories, mechanical and biologic. Mechanical valves in current clinical use are composed of three basic designs or classifications: ball-and-cage, tilting disc, and bileaflet. The biologic valves can be further classified into three categories: stented, unstented, and homograft valves. Although significant progress has been made in the development of better prostheses through new materials and more physiologic valve designs, several problems associated with prosthetic valves have not been eliminated. Existing problems that can be related to the valve hemodynamics or local fluid mechanics are (1) thrombosis and thromboembolism, (2) hemolysis, (3) tissue overgrowth, (4) damage to endothelial lining, and (5) regurgitation. The presence of high shear stresses can lead to damage of formed blood elements, platelet activation, and initiation of biochemical processes affecting coagulation. Lethal damage to red cells can occur with fluid shear stresses as low as 1500 dyn/cm2 .[11] These levels can be significantly lower (10 to 100 dyn/cm2 ) in the presence of foreign surfaces, such as those presented by a valve prosthesis.[12] [13] Sublethal damage can occur in stress fields as low as 500 dyn/cm2 .[14] In addition, platelet activation and damage have been shown to occur in shear stresses ranging from 100 to 500 dyn/cm2 .[70] The residence time of the cell in the damaging fluid environment is a significant factor in determining lethal stress levels that further complicates the mechanism for damage. Additionally, regions of flow separation and stagnation form local environments suitable for accumulation and growth of thrombi and fibrous or pannus tissue.[71] The fluid mechanic performance of prosthetic heart valves is often assessed

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through in vitro testing to determine transvalvular pressure drops, regurgitant volumes (closure and leakage), distal and proximal velocity fields, 509

and the locations and levels of turbulent stresses. The relationship between valve fluid mechanics and the development of problematic function have been studied by numerous investigators over the past two decades. In vitro studies have concentrated on quantifying local fluid stress levels through state-of-the-art flow measurement techniques such as laser Doppler anemometry,[72] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [91] hot film anemometry,[92] [93] [94] and ultrasound velocimetry.[95] The fluid mechanics of the various prosthetic valve designs are discussed in this section. Comparisons between the many valve designs within each classification of prostheses are left to the many references dealing with the assessment of individual valves. Antegrade and retrograde flow fields are described, including turbulence levels, regurgitation, and pressure drop characteristics for the different valve designs. All flow characteristics are referenced from in vitro experiments conducted in our laboratory unless otherwise specified. In most citations, the data are representative of 25- or 27-mm aortic prostheses tested under physiologic pulsatile flow conditions providing a cardiac output (CO) of 5.0 to 6.0 L per minute and a heart rate (HR) of 70 bpm. Exact test conditions (valve size, CO, HR, pressures) are noted for each citation. The measurement of pressure drop is intrinsically related to the distal flow fields of valves. The effect of pressure recovery depends strongly on flow structure and the vessel geometry in which the flow is entering. Stewart et al[29] have assessed the differences in determining transvalvular pressure drops across aortic valves owing to pressure recovery effects, when using standard in vivo techniques such as Doppler ultrasound or cardiac catheterization. Doppler-measured pressure drops are not equal to cathetermeasured drops, unless the catheter is placed at the same location where the peak velocity is measured by Doppler, typically the vena contracta of the jet. Pressure recovery is very dependent on valve type, size, orientation, and position (i.e., aortic or mitral), and it is particularly likely with mechanical valves, which exhibit complex jet flow patterns with more than one jet, and in smaller aortic valves at higher flow rates. In general, the Doppler technique measured higher pressure drops in mechanical aortic valves,

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especially in the larger sizes, than did the catheterization technique. In addition, some valve designs such as the Medtronic Freestyle unstented bioprosthesis and larger size bileaflet and tilting disc mechanical valves require that the upstream approach velocity (i.e., the term v1 in Equation 4) be measured and used in the modified Bernoulli equation, owing to small pressure drops. When pressure drops are expected to be small, neglecting the approach velocity in the calculations can lead to significant overestimation in the pressure drop. Clinicians should be aware of these effects when interpreting pressure drop data in diagnostic exams. Mechanical Valves The three major mechanical valve designs or classes are the tilting disc, bileaflet, and ball-and-cage. These valves differ primarily in the type and function of the occluder. Although these different designs influence the valvular Figure 23-8 Schematic showing the geometry of commonly used mechanical valve prostheses.

fluid mechanics, all three share common flow structures such as welldefined jet flows, wakes with some degree of flow reversal, and turbulent shear layers. The antegrade flow, regurgitant flow, and pressure drop characteristics for each valve design are discussed separately in the following sections. Because the design of a valve can strongly influence the local fluid dynamics, a brief discussion of the pertinent design features of each class of valve is provided. Figure 23-8 illustrates the design features of the three classes of mechanical valve prostheses. Tilting Disc Valves

The tilting disc valve has one occluder (disc) generally of a circular cross section. The disc is often mounted such that it is free to rotate about a pivot axis, typically displaced from the disc diameter. Metal struts are used to secure the disc within the valve housing and control its range of motion. Numerous design variations on the tilting disc valve exist. These different designs vary in the pivot mechanism or strut design, the range of disc motion allowed, or in the geometry of the disc, which can range from flat to curved. Typically, the occluder opens to angles between 60 and 80 degrees with respect to the valve annulus.

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The tilting disc valve is characterized by two orifices separated by the occluder. The major orifice is the larger open area formed between the disc pivot axis and the housing, as the disc swings distally to the open position. This orifice is free of blockage owing to mounting struts and causes little resistance to transvalvular flow. As the disc opens, the remaining part of the disc, on the other side of the pivot axis, swings in the proximal direction to form the minor orifice. Mounting struts, which can vary from one to two depending on valve design, typically span the minor orifice. Because of the upstream protrusion of the disc into the minor orifice tract and the presence of the mounting struts, a slight obstruction of flow is encountered. Antegrade Flow.

Figure 23-9 and Figure 23-10 illustrate the antegrade flow patterns of the Björk-Shiley monostrut and Medtronic-Hall tilting disc valves. The antegrade flow is characterized by a major orifice jet and a minor orifice jet. The major orifice jet is spatially larger than the minor orifice jet. It is semicircular in cross section with 510

Figure 23-9 Velocity and turbulent shear stress profiles downstream of a 27-mm Björk-Shiley monostrut tilting disc valve at peak systole. A and C, Profile through the major and minor orifices at 11 mm downstream. B and D, Center line profile 17 mm downstream across the major and minor orifices (major orifice to the right).

peak systolic velocities of approximately 2 m per second in the aortic position. Under comparable flow conditions, most tilting disc valves exhibit similar major orifice jet structures and peak velocity magnitudes. The spatial structure of the minor jet varies depending on the number of struts used to secure the disc. In single-strut designs such as the BjörkShiley monostrut and the Medtronic-Hall tilting disc, the minor orifice jet appears as two jets separated by a well-defined wake behind the strut. The flow on each side of the strut is nearly symmetric with similar spatial structure and velocity magnitude. Valves with two struts display a minor orifice jet structure consisting of a strong central jet bounded by two weaker jets. The adjacent weaker jets are separated from the central jets by the wakes of the struts. Their velocity magnitude is roughly 30% to 40% of the velocity magnitude of the central jet. The peak velocities of the minor orifice jet are typically of the same magnitude or slightly less than the peak

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velocity in the major orifice jet in nearly all tilting disc designs. Wake regions are observed behind the valve struts and disc. These wake regions are areas of flow separation with significant velocity defect and nearly stagnant flow. Wake regions persist for 10 to 20 mm downstream of the valve annulus. Owing to the opening angle of the disc, the major and minor orifice jets are directed toward the wall on the major orifice side of the valve, following the occluder. In the aortic position, this results in a region of separated flow in the sinuses located below or near the minor jet at peak systole. Because of the strong major orifice jet and the orientation of the disc with respect to the flow, strong secondary flow structures are encountered downstream of the valve. These secondary flows form a pair of counter-rotating vortices or helical motions. The vortices are generated by the high-momentum fluid in the major jet wrapping around the sides of the disc and flowing into the low-momentum, separated flow regions immediately behind the disc. Flow over the disc generates vortex shedding similar to that observed with flow over a delta wing airfoil. Turbulent stresses associated with the titling disc design are located in the jet shear layers and in the wakes of the discs and struts. The turbulent shear stress profiles for the monostrut and Medtronic-Hall valves are shown in Figure 23-9 511

Figure 23-10 Velocity and turbulent shear stress profiles downstream of a 27-mm Medtronic-Hall tilting disc valve at peak systole. A and C, Center line profile 15 mm downstream across the major and minor orifices (major orifice to the right). B and D, Profile through the major and minor orifices at 13 mm downstream.

and Figure 23-10 . Peak turbulent shear stresses, in the aortic position, can range from 1500 to 3500 dyn/cm2 depending on the particular tilting disc design. These stress levels were measured 10 to 15 mm downstream of the valve housing and may be even higher closer to the valve. Large stresses persist almost into the aorta, indicating that a significant volume of the fluid is occupied by the turbulent shear layers, which may be relevant in that sufficiently long residence times may exist for formed blood elements exposed to turbulent stresses. Table 23-1 summarizes the peak velocity and turbulent shear stress levels for many of the 27-mm aortic valves in clinical use.

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Normal Regurgitant Flow.

The tilting disc design shows slightly lower regurgitant volumes than the bileaflet design, owing to reduced closing and leakage volumes (Fig. 2311) . Ranges for the regurgitant volume of the tilting disc valve vary from approximately 5.5 mL per beat for 19- and 20-mm valves to 9 mL per beat for 29-mm valves. Table 23-2 and Table 23-3 list the regurgitant volumes for several prosthetic valve designs. The leakage flow in mechanical valves is often in the form of small-scale regurgitant jets. In the tilting disc design these jets emanate from small gaps around the perimeter of the valve between the disc and the valve housing. [76] [96] [97] , Baldwin et al[96] measured the gap width of a Björk-Shiley monostrut valve with Delrin rings and obtained widths of approximately 75 µm, which varied nonuniformly around the valve perimeter. These leakage jets were believed to be advantageous because of the potential for washing of the perimeter of the valve housing 512

TABLE 23-1 -- Peak Systolic Velocity and Turbulent Shear Stress Levels for Common 27-mm Aortic Valve Prostheses †

Valve Type Valve Ball-and-cage Starr-Edwards 1260 Tilting disc

Björk-Shiley convexo-concave

Björk-Shiley Monostrut

Medtronic-Hall

Peak Turbulent Shear Peak Measurement Velocity Stress Location (cm/s) (dyn/cm2 ) 12 mm 220 1850 downstream 7 mm 200 3400 downstream 11 mm 200 1800 downstream 8 mm 200 1250 downstream 11 mm 200 800 downstream 13 mm 200 1500

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downstream Omnicarbon 14 mm downstream Bileaflet St. Jude Medical 13 mm Standard downstream Duramedics 13 mm downstream Carbomedics 12 mm downstream Stented Carpentier-Edwards 15 mm bioprostheses Porcine 2625 downstream Carpentier-Edwards 15 mm Porcine 2650 downstream Carpentier-Edwards 17 mm Pericardial 2900 downstream Hancock MO Porcine 10 mm 250 downstream Hancock II Porcine 18 mm 410 downstream Ionescu-Shiley 27 mm Standard Pericardial downstream Hancock Pericardial 18 mm downstream Nonstented Medtronic Freestyle * Leaflet tips bioprostheses 10 mm from tips St. Jude Medical Leaflet tips * TSPV 10 mm from tips

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225

2000

210

1500

210

2300

228

1520

370

4500

200

2000

180

1000

330

2900

260

2500

230

2500

170

2100

125 100 150 125

†Data obtained at 5 L/min CO, 70 bpm HR, and 120/80 mm Hg aortic pressure. *Data obtained from in vitro Doppler ultrasound measurements.

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during closure. Other studies have shown that the regurgitant jets are of a significant velocity magnitude, ranging from 2 to 5 m per second, and turbulent stresses are several times greater than in the antegrade flow field. Measurements in the regurgitant jets of the Björk-Shiley valve indicate that peak turbulent shear stresses are as high as 10,000 dyn/cm2 .[96] Turbulent scales in these jets are estimated to be of the same order of magnitude as the size of red cells and may result in higher rates of hemolysis than in the antegrade turbulent fields. Pressure Drop Characteristics.

To minimize the workload on the heart, a prosthetic valve should not impose resistance to forward flow. In general, prosthetic Figure 23-11 Regurgitant, closing, and leakage volumes of a valve in the aortic position.

valves impose more forward flow resistance than do natural valves. Prosthetic valves are often characterized by their pressure drop or through their effective orifice areas (Equation 8), which can be used to estimate the resistance a valve imposes on forward flow across it. The effective orifice area (Aeff ) is an index of how well a valve design uses its primary or internal orifice area. Another measure of a valve's resistance to forward flow is the performance index (PI), the ratio of Aeff to the valve sewing ring area. The PI provides a measure of how well a valve design uses its total mounting area, the area the flow would see without the valve. Although the Aeff is a function of the valve size, the PI attempts to normalize for valve size, providing a more uniform measure of a valve's resistance characteristics independent of the size and nearly independent of the flow rate. The tilting disc design presents a relatively streamlined configuration to the flow and thus shows relatively low gradients. Tilting disc valves typically show a PI ranging from 0.4 to 0.65. Aeff and PI for several prosthetic valve designs in clinical use today are provided in Table 23-2 and Table 23-3 . Orientation.

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The orientation of the tilting disc valve in the mitral position has been studied in vivo by Jones et al.[98] These authors made comparisons of the orientations of the major orifice jet of tilting disc valves with respect to the left ventricular geometry. The studies indicated that the preferred orientation for tilting disc valves in the mitral position is with the major orifice oriented toward the left ventricular free wall, as opposed to the septum. Greater intraventricular turbulence was observed with a septal orientation of the major orifice than with a free wall orientation. Orientation of the major orifice toward the septal wall produced large areas of velocity reversal, directed against the minor orifice. In contrast, 513

TABLE 23-2 -- In Vitro Hemodynamic Data for Common Aortic Valve Prostheses *

Valve Type Ball-and-cage

Tilting disc

Regurgitant Size Volume Valve (mm) (mL/beat) Starr-Edwards 1260 27 5.5 25 4.3 21 2.5 Björk-Shiley convexo27 8.5 concave 25 7.3 21 5.5 Björk-Shiley Monostrut 27 9.2 25 7.6 23 6.9 21 5.9 19 5.5 Medtronic-Hall 27 9.6 25 8.4 23 7.3 20 6.2

EOA †

(cm2 ) 1.75 1.62 1.23 2.59

PI 0.30 0.33 0.36 0.45

2.37 1.54 3.34 2.62 2.00 1.45 1.07 3.64 3.07 2.26 1.74

0.48 0.45 0.58 0.53 0.48 0.42 0.38 0.64 0.62 0.54 0.51

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Bileaflet

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St. Jude Medical Standard

St. Jude Medical Regent

Carbomedics

Sorin Bicarbon ‡

Stented bioprostheses

Carpentier-Edwards Porcine 2625

Carpentier-Edwards Porcine 2650

27

10.8 4.09 0.71

25 23 21 19 29

9.9 8.3 6.8 6.8 13.5

27 25 23 21 19 17 27 25 23 21 19 27 25 23 21 19 27

12.3 11.2 10.3 9.0 7.6 6.3 7.5 6.1 6.5 3.4 3.0

3.23 2.24 1.81 1.21 4.98

0.66 0.54 0.52 0.43 0.75

4.40 3.97 3.47 2.81 2.06 1.56 3.75 3.14 2.28 1.66 1.12 3.06 2.39 2.07 1.54 0.97 <3 1.95

0.77 0.81 0.83 0.81 0.73 0.69 0.65 0.64 0.55 0.48 0.40 0.71 0.69 0.73 0.67 0.55 0.34

25 21 27

<2 1.52 0.31 <2 1.28 0.37 <2 2.74 0.48

25

<2 2.36 0.48

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Carpentier-Edwards Pericardial 2900

Hancock Porcine 242

Hancock MO Porcine 250

Hancock II Porcine 410

Ionescu-Shiley Standard Pericardial Mosaic Porcine

Mitroflow Pericardial

21 19 27

<2 1.38 0.40 <2 1.17 0.41 <3 3.70 0.64

25 21 19 27 25 23 21 19 25

<2 <2 <2 <3 <2 <2 <2 <2 <2

3.25 1.88 1.56 2.14 1.93 1.73 1.31 1.15 2.16

0.66 0.54 0.55 0.37 0.39 0.42 0.38 0.41 0.44

23 21 19 27 25 23 21 27

<2 <2 <2 <2 <2 <2 <2 <3

1.94 1.43 1.22 2.36 2.10 1.81 1.48 2.35

0.47 0.41 0.43 0.41 0.43 0.44 0.43 0.41

29 27 25 23 21 29 23 19

<3 <2 <2 <2 <1 <4 <3 <2

3.15 2.81 2.11 1.74 1.54 3.71 2.12 1.34

0.48 0.49 0.43 0.42 0.44 0.56 0.51 0.47

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Nonstented bioprostheses

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Medtronic Freestyle Porcine

27

25 23 21 19 EOA, effective orifice area; PI, performance index.

<4 3.75 0.65 <4 <3 <2 <2

3.41 2.69 2.17 1.84

0.69 0.65 0.63 0.65

*5 L/min CO typical, 70 bmp HR, 120/80 mm Hg aortic pressure. †EOA Computed from Equation 8. ‡Values from Badano L, Mocchegiani R, Bertoli G, et al: J Am Soc Echocardiogr 1997; 10:632–643.

514

TABLE 23-3 -- In Vitro Hemodynamic Data for Common Mitral Valve Prostheses *

Valve Type Ball-and-cage

Valve Starr-Edwards 1260

Tilting disc

Björk-Shiley Standard

Björk-Shiley convexoconcave

Medtronic-Hall

Regurgitant EOA † Size Volume (mm) (mL/beat) (cm2 ) PI 30 1.99 0.28 28 1.66 0.27 26 1.56 0.29 31 3.40 0.45 29 6.7 2.79 0.42 25 2.15 0.44 29 10.1 2.96 0.45 27 25 31

8.3 2.28 0.40 2.03 0.41 10.0 3.53 0.47

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Bileaflet

Stented bioprostheses

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St. Jude Medical Standard

Hancock Porcine 342

Hancock II Porcine

Carpentier-Edwards Porcine 6650 Carpentier-Edwards Porcine 6900 Carpentier-Edwards Porcine 6625 Ionescu-Shiley Standard Pericardial

Mosaic Porcine

29 27 25 31

10.0 8.9 7.2 13.1

3.53 2.73 2.23 3.67

0.53 0.47 0.45 0.48

29 27 35

10.9 3.40 0.51 9.7 2.81 0.49 <4 2.72 0.28

33 31 29 27 25 33 31 29 27 25 27

<4 <4 <4 <2 <2 <4 <3 <3 <2 <2 <2

2.54 2.36 2.11 1.77 1.63 2.66 2.29 2.05 1.78 1.59 2.03

27

<2

2.68 0.47

31

<4

2.58 0.39

31

<5

3.00 0.40

27 25 33 31 29

<2 <2 <4 <3 <3

1.77 1.61 2.38 2.26 2.02

0.30 0.31 0.32 0.31 0.33 0.31 0.30 0.31 0.31 0.32 0.35

0.31 0.33 0.28 0.30 0.31

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Nonstented bioprostheses

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Mitral Valve Allograft ‡

27 25 25

23 EOA, effective orifice area; PI, performance index.

<2 <2

1.71 0.30 1.55 0.32 3.38 0.69 1.80 0.43

*5 L/min CO typical, 70 bpm HR. †EOA computed from Equation 8. ‡In vitro measurements at 5 L/min CO.

free wall orientation of the major orifice produced more physiologic left ventricular flow patterns. These results have been corroborated in in vitro flow visualization studies conducted in our laboratory, under physiologic flow conditions in an anatomically correct left ventricular model.[99] Studies by Travis et al[100] and Kleine et al[101] have examined the effects of valve orientation on forward flow hemodynamics through mechanical prostheses in the aortic position. Travis et al studied the effects of valve orientation on fluid mechanical energy loss and transvalvular pressure drop in angled in vitro models of the aortic inflow tract. Their study showed that orientation of the disc so that it is parallel to the proximal flow direction when the valve is in the open position minimizes energy loss and pressure drop for the tilting disc valve. Kleine et al used an in vivo pig model to examine the effects of prosthesis orientation on turbulent stresses. These researchers found a minimum in turbulent stress magnitude with orientation of the major orifice to the right posterior aortic wall, which is the area of highest velocities during ejection. Bileaflet Valves

The bileaflet design is characterized by two semicircular leaflets typically made of pyrolytic carbon that are hinged to the valve housing. The leaflets divide the flow into three regions, two lateral orifices and a central orifice. The primary differences between the many bileaflet valves are in the hinge design, the leaflet opening angle, and curvature of the leaflets. Hinge design variations are employed to control opening angle and influence the local fluid mechanics, washout, and flow patterns generated in the hinge, which may affect leaflet function and pressure

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515

drop. Leaflet opening angles vary from 75 to 90 degrees in the bileaflet designs in current clinical use. The bileaflet valves tend to show better bulk flow hemodynamics than the tilting disc or ball-and-cage designs. The characteristic geometry of the bileaflet design is illustrated in Figure 23-8 . Antegrade Flow.

The antegrade flow fields of bileaflet designs are characterized by three jets. Two jets emanate from the lateral orifices and one from the central orifice, as illustrated in Figure 23-12 . All three jets tend to show similar peak velocity magnitudes, independent of valve design. Greater forward flow emerges from the lateral orifices, however, than from the central orifice. The cross section of the lateral jets tends to be of a crescent shape, whereas the central jet is nearly planar in cross section. Wakes generated from the leaflets separate the three jets and persist for several centimeters downstream. The triple jet pattern is also discernible in two-dimensional color flow maps, using color Doppler ultrasound techniques as Figure 23-12 Velocity and turbulent shear stress profiles 13 mm downstream of a 27-mm St. Jude Medical bileaflet valve at peak systole. A and C, Center line profile through lateral and central orifices. B and D, Profile through the central orifice only.

illustrated in Figure 23-13 . This color Doppler flow map was obtained in pulsatile flow in vitro studies of a 31-mm St. Jude Medical bileaflet valve in the mitral position. The central jet loses its coherence after 2 or 3 cm as the lateral jets grow and merge into the central flow region. The lateral jets do maintain their coherence and relatively high velocity magnitude over a greater distance. The flow is initially well ordered during the early acceleration phase and becomes turbulent before peak systole. Separated regions with flow reversal are generally observed around the perimeter of the housing. The separated regions tend to be asymmetric around the valve with larger spatial dimensions near the hinges than adjacent to the lateral jets. This asymmetric behavior may be related to the increased thrombogenecity of the bileaflet design that occurs in the hinge regions.

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Turbulent stresses are concentrated in the leaflet wakes and in the shear layers alongside the three jets. The bileaflet design exhibits lower turbulent stresses than the 516

Figure 23-13 (color plate.) Two-dimensional color Doppler flow mapping of the downstream triple jet flow fields of a bileaflet valve design under physiologic pulsatile flow conditions.

tilting disc and ball-and-cage designs, with peak aortic values ranging from 1000 to 1500 dyn/cm.2 Peak stresses in the mitral position are less because of the lower peak diastolic transvalvular velocities. Three-component turbulent stress measurements have shown that the turbulent stress distribution is similar to that of local two-dimensional jets and wakes.[102] The onset of turbulence can be related to a Reynolds number based on the local flow properties of the jets and wakes and not on a Reynolds number based on global geometry, such as the size of the annulus or the diameter of the aorta. Understanding this turbulence structure may also provide potential leaflet design changes to minimize stress levels. As a result of this similarity with jet and wake structures, computational techniques may be able to use low Reynolds number turbulence models developed for jet and wakes. Peak aortic velocity and turbulent stress levels for clinically used 27-mm bileaflet valves are provided in Table 23-1 . Normal Regurgitant Flow.

Retrograde flow characteristics for the bileaflet design are similar to those for the tilting disc valve. Regurgitant volume characteristics are summarized in Table 23-2 and Table 23-3 . The bileaflet design shows slightly larger regurgitant volumes than the tilting disc valve. Leakage flow through the bileaflet valve design occurs primarily through the pivots. In addition, leakage is also observed around the periphery and from the gap between the two leaflets. Figure 23-14 illustrates typical two-dimensional color Doppler flow mapping images of these regurgitant jets. Velocity and turbulence measurements, obtained both within the pivots and 1 mm upstream of the valve housing in the aortic position, indicate that the major jets persist through nearly all of diastole. The mean velocity magnitudes in the jets are on the order of 2 or 3 m per second with turbulent shear stress

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levels exceeding 3000 dyn/cm.2 These high turbulent stresses, when coupled with a relatively stagnant adjacent flow regime, could lead to thrombus formation. Such a region of stagnation was noted in the pivots of the Medtronic Parallel valve. This design was voluntarily withdrawn from the market after a high incidence of thrombosis was noted in clinical trials. Explant data revealed that this thrombus was located preferentially within the inflow region of the valve pivots. Ellis et al,[103] Gross et al,[104] and Healy et al[105] subsequently performed extensive laser Doppler velocimetry measurements, computational simulations, and flow visualization studies that linked the thrombus formation within the Medtronic Parallel pivot to a persistent stagnation region at the same location. In contrast, in studies of bileaflet prostheses that have clinically acceptable rates of thrombosis, such as the St. Jude Medical Standard and Regent valve designs, no persistent regions of stagnation were found within the pivots.[106] [107] Pressure Drop Characteristics.

The bileaflet design in general has lower pressure drops than do any of the three mechanical valve designs, although the pressure drop of the Medtronic-Hall tilting disc valve is comparable to that of the St. Jude Medical Standard valve. [82] Recent bileaflet prosthesis designs, such as the St. Jude Medical Regent valve, have incorporated narrower sewing cuffs and a thinner, reinforced valve orifice to increase the Aeff and PI for a given valve size. These values as well as data from other bileaflet valve designs are tabulated in Table 23-2 and Table 23-3 . Orientation.

The bileaflet valve is mounted in one of two orientations in the mitral position. The first position is the anatomic position, with the leaflet hinge plane of the valve oriented in a direction perpendicular to the plane of the aortic outflow and mitral inflow tracts. The leaflets pivot in a similar plane as that of the native mitral valve leaflets. The second position is the antianatomic position, with the valve mounted such that the leaflet hinge plane is rotated 90 degrees from the anatomic position. The orientation of the St. Jude Medical bileaflet valve in the mitral position has been studied in in vitro flow visualization experiments conducted in our laboratory. The results of these studies indicate that the antianatomic Figure 23-14 (color plate.) Two-dimensional color Doppler flow mapping of the regurgitant jet flow field of a bileaflet valve design

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under physiologic pulsatile flow conditions.

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position provides better flow patterns along the posterior wall of the ventricle. Potentially better lateral flow expansion in the plane perpendicular to the plane of the aortic outflow and mitral inflow tracts is also observed. The anatomic position, however, provides adequate flow patterns within the left ventricle with slightly narrower lateral expansion of the inflow jets. Van Rijk-Zwikker et al[108] investigated the effects of orientation of the Carbomedics bileaflet valve in in vivo pig studies. Two-dimensional echocardiographic and color Doppler measurements were analyzed to determine the influence of valve orientation on valve function and the transvalvular flow patterns within the left ventricle. The 90-degree, antianatomic orientation was found to be superior to the anatomic orientation of the valve. The anatomic orientation resulted in diastolic backflow directed toward the valve, which may lead to asymmetric motion of the valve leaflets. The antianatomic position produced diastolic backflow patterns that enter the left ventricular outflow tract. Minimal interference with the function of the leaflets is expected from these flow patterns. The studies of Travis et al[100] and Kleine et al[101] examined the effects of aortic bileaflet valve orientation as well as tilting disc valve orientation on forward flow hemodynamics. Travis et al found that orienting the leaflets of the open valve parallel to the proximal flow direction resulted in decreases in energy losses and pressure drops in vitro. Kleine et al found that turbulence created by bileaflet valves was minimal when one of the lateral orifices faces the right posterior wall of the aorta. Ball-and-Cage Valve The ball-and-cage valve is characterized by a silicone ball mounted into a wire cage, as illustrated in Figure 23-8 . The Figure 23-15 Center line velocity and turbulent shear stress profiles 30 mm downstream of a 27-mm Starr-Edwards ball-and-cage valve at peak systole.

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only ball-and-cage valve in use today is the Starr-Edwards 1260. The cage is constructed from three wire struts separated by 120 degrees. The struts emanate from the valve housing and converge at the distal end of the valve, the apex of the cage. The ball is free to travel along the cage, typically over a 1- to 2-cm distance. Antegrade Flow.

The flow fields of these valves consist of annular jets that emerge from around the occluder or poppet. In the aortic position, the jets are initially directed toward the wall of the aorta where they impact and then follow the contour of the aortic wall. Peak systolic velocities in the aorta are comparable to those encountered in the other valve designs, approximately 2 m per second at peak systole. The annular jets show rapid development early in systole during the acceleration phase of flow. A gradual divergence and growth of the jet is observed with increasing displacement downstream, where the jet maintains its structure over a considerable axial distance. Velocity profiles at peak systole are shown in Figure 23-15 , 30 mm downstream of the valve. Large mean velocity gradients are observed alongside the annular jet, with values exceeding 1500 L per second. The flow field in the mitral position is similar to the jet structure in the aortic position; however, the jet peak velocities are lower, the jet decays more rapidly, and greater lateral expansion of the jet occurs in the ventricle. The ball generates a large wake in the central part of the flow field that starts in early systole and grows into a region of reverse flow lasting from peak to end-systole. The lateral extent of this region of reverse flow is on the order of 8 to 10 mm distal to the apex of the cage. Peak reverse velocities can be as high as 20 to 25 cm per second. These regions of large separation are responsible for the thrombogenecity of these valves.[109] The ball in these types of valves is often observed to fluctuate at the apex, which is most likely caused by flow instabilities within the wake or vortex shedding from the ball. This 518

phenomenon increases the lateral extent of the wake and produces an increase in the relative velocity between the ball and the model wall and an increase in pressure drop across the prosthesis. The turbulent stresses are concentrated in the large velocity gradients associated with the annular jets of these valves. Turbulent shear stresses as

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high as 1900 dyn/cm2 have been measured downstream of these valves in the aortic position. High turbulent stresses are observed through most of systole over a significant length downstream of the valve. The rapid turbulent stress generation indicates a quick temporal development of the jet and prolonged perseverance of the jet structure. Immediately adjacent to the ball, peak turbulent shear stresses are estimated to be as high as 3500 dyn/cm2 . The large wall shear stresses associated with the ball valve could cause damage to the endothelial lining of the aorta. The turbulent stresses measured in the annular jets are more than sufficient to cause lethal damage to red blood cells, as well as platelet damage and activation. Coupled with the large separated region behind the ball, thrombus formation on the apex of the cage is likely and has been documented in the medical literature. Normal Regurgitant Flow.

The normal regurgitant flow of the ball-and-cage design is composed mainly of the closing volume flow. The seating of the ball valve is generally very good with little or no leakage flow. Typical values of the regurgitant volume are roughly 5 mL per beat for the 25- and 27-mm valve sizes. These values are also provided in Table 23-2 and Table 23-3 . Pressure Drop Characteristics.

These valves typically show larger pressure drops than do the tilting disc and bileaflet designs. The PI and Aeff of the Starr-Edwards valve range from 0.36 and 1.62 cm2 for 25-mm size valves to 0.3 and 1.71 cm2 for the 27-mm valve. Typical values of the Aeff and PI are tabulated in Table 23-2 and Table 23-3 . The large wake region is principally responsible for the large pressure drop across the valve. Figure 23-16 Center line velocity and turbulent shear stress profiles 17 mm downstream of a 27-mm Carpentier-Edwards pericardial valve at peak systole.

Bioprostheses The most common bioprosthetic valves are composed of three biologic leaflets made from the porcine aortic valve or bovine pericardium. They are

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constructed similarly to the natural aortic valve. The annular ring is cloth covered and molded to function similarly to the aortic annulus. Metal or polymeric stents provide support to the leaflets at their commissures in the stented design, whereas the leaflet commissures in nonstented aortic valves must be attached to the native aorta for support. The clinically available designs vary mainly in the support structure and in the leaflet material and construction. All trileaflet bioprostheses, however, open to a centrally located orifice with respect to the valve annulus and mimic the open geometry of the normal aortic valve but with a smaller orifice area. Tissue valves are less thrombogenic than mechanical valves and thus do not require anticoagulant treatment; however, tissue valves exhibit higher pressure gradients than do most commonly used mechanical valves, particularly in the small sizes that exhibit stenotic characteristics. These valves also suffer from calcification of the leaflets, material fatigue leading to valve failure because of leaflet rupture or tearing, or both. Calcification of the tissue is often a precursor to leaflet rupture and tearing, as these are often observed adjacent to calcified lesions. Stented Valves Antegrade Flow.

All stented bioprosthetic valves have central jet type flow fields as illustrated in Figure 23-16 and Figure 23-17 . The newer generation porcine valves and most pericardial valves create flatter velocity profiles than do the earlier porcine valve designs. Flatter velocity profiles 519

Figure 23-17 Center line velocity and turbulent shear stress profiles 15 mm downstream of a 27-mm Carpentier-Edwards 2625 porcine valve at peak systole.

result in more evenly distributed downstream flow fields and lower turbulent shear stress levels. Early designs, such as the Carpentier-Edwards porcine model 2625 and the Hancock I porcine valves, generated asymmetric jet profiles. The jets were directed slightly away from the stent in a plane that bisected one leaflet and the stent opposite that leaflet, as illustrated in Figure 23-17 . Peak aortic velocities exceed 3 m per second at peak systole for normal flow conditions.

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The newer porcine designs, such as the Carpentier-Edwards porcine 2650, and the pericardial valves produce jets that are wider and have more blunted profiles. These jets exhibit a more axisymmetric velocity profile with large mean velocity gradients (viscous stresses) alongside the jets. Peak velocities range from 2 to 3 m per second under normal flow conditions in the aortic position. These jets still show a slight laterally directed motion similar to the older porcine valve designs, but it is not as pronounced. In in vitro experiments, stagnant flow can be observed throughout systole between the outflow surfaces of the valve leaflets and the flow model wall. In earlier valve designs, these stagnation regions were larger and exhibited regions of flow reversal. Stented bioprosthesis stagnant regions can be amplified in conditions of low cardiac output, in which one of the three leaflets may fail to open fully. Flow stasis can lead to deposition of thrombogenic elements on the outflow surfaces of the leaflets. In all stented valve designs, the turbulent shear stresses are confined to narrow regions in the shear layers of the central jets. Peak turbulent shear stresses in the aorta ranged from greater than 2000 dyn/cm2 to greater than 4500 dyn/cm2 in the early valve designs. The pericardial and newer porcine aortic valve designs exhibit lower stress levels, in the range of 1000 to 2500 dyn/cm.2 Additionally, turbulent shear stresses show a more confined spatial structure along the jet shear layers in the newer valve designs, as shown in Figure 23-15 . Turbulent shear stress levels are high enough to cause hemolysis and platelet activation. Considering the location of peak stresses adjacent to the regions of reverse flow, it may be speculated that the tissue valve would also be prone to thrombogenic events or tissue overgrowth of the sewing ring. Normal Regurgitant Flow.

All tissue valves exhibit some degree of regurgitant flow in the closing volume. Leakage volume is essentially zero in properly functioning valves. The closing volumes, however, are generally lower in bioprostheses than in the mechanical prostheses. The lower closing volumes are caused by more rapid closure of the valve leaflets for tissue valves compared with the occluders of the mechanical valve designs. Regurgitant volumes are on the order of 1 mL per beat for most tissue valves. The Ionescu-Shiley pericardial valve, however, has closing volumes ranging from 2.5 to 6.5 mL per beat, depending on valve size and position (aortic or mitral). Typical values of the regurgitant volumes for several bioprosthetic valves are given in Table 23-2 and Table 23-3 . Regurgitant jets are normally nonexistent

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and the presence of such a jet indicates valve incompetence. Pressure Drop Characteristics.

All stented porcine tissue valves are mildly stenotic compared with the natural valve in large sizes, and they are moderately to severely stenotic in the small sizes. Porcine valves in small sizes exhibit a higher degree of stenosis than do comparably sized mechanical valves. As a result, the PI of common stented porcine tissue valves ranges from 0.3 to 0.4, compared with values around 0.6 to 0.7 for similarly sized mechanical valves. This stenotic behavior is due in part to the construction of the leaflets, the stiffness of the fixed tissue, and the man-made commissures. The stents also act to restrict the motion of the leaflets somewhat during opening. Typical Aeff ranges from 1.3 to 2.5 cm2 for 21- to 27-mm porcine aortic valves, respectively.[110] The new generation of stented pericardial valves (e.g., Carpentier-Edwards, MitroFlow), however, have pressure drop characteristics comparable to the St. Jude Medical Standard and MedtronicHall mechanical valve designs in all sizes. For example, the CarpentierEdwards aortic pericardial valves (sizes 27 to 19 mm) have Aeff values ranging from 3.7 to 1.56 cm2 . The Aeff and PI values for several tissue 520

valves, both porcine and pericardial, are listed in Table 23-2 and Table 233. Nonstented Valves

Nonstented aortic valve prostheses are composed of a natural porcine valve and usually some length of the intact aorta. The original right and left coronary arteries are also ligated with short remnants to aid in reimplantation of the patient's coronaries. In vitro testing of nonstented aortic bioprostheses requires a compliant test chamber capable of simulating the human aortic root. Hemodynamic data show that aortic nonstented valves have pressure drops comparable to mechanical prostheses. [111] [112] [113] During the past few years, several investigators have begun testing and using mitral valve heterografts.[114] These mitral heterografts typically use fixed valves with or without intact papillary muscles. These new mitral replacements can be considered to be nonstented bioprostheses. Currently,

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quantitative in vitro testing of the flow fields of these valve designs is limited; however, our laboratory has begun assessing the hemodynamic characteristics of these mitral replacements. A study by Jensen et al[115] has shown that the fixation of porcine mitral heterografts in glutaraldehyde reduces orifice area and increases total regurgitation in these valves. Although no mitral valve replacements are currently approved in the United States, one design is in clinical trials in Europe. This valve, the St. Jude Medical Quattro valve, is fashioned from pericardium and offers reasonable hemodynamics. Mitral heterografts have the potential for better hemodynamic performance, reduced thrombogenesis, and improved left ventricular function. Antegrade Flow.

Currently, quantitative data on the antegrade flow fields for both aortic and mitral nonstented tissue valves are under study. Ultrasound Doppler results for a 27-mm Medtronic Freestyle valve[111] indicate that the flow accelerates uniformly through the valve with an apparent uniform and flat profile downstream of the valve. Doppler-measured peak velocities at the leaflet tips ranged from 75 to 125 cm per second at cardiac outputs from 3.0 to 5.0 L per minute. The peak velocities decreased to a range of 60 to 100 cm per second at 5 to 10 mm from the leaflet tips over the same range of cardiac outputs. There is no appearance of a jet with steep velocity gradients, as is observed in stented bioprostheses. Similar results were obtained from ultrasound Doppler measurements conducted with a 29-mm St. Jude Medical TSPV valve design. Normal Regurgitant Flow.

The nonstented aortic valves exhibit regurgitant volumes that are comparable to closing volumes of valves exhibiting similar Aeff . Good coaptation is observed with little or no leakage. Nonstented mitral valve heterografts tested in our laboratory exhibited comparable closing volumes to unfixed natural valves tested in the same flow loop. Good coaptation was observed with no leakage. The function of mitral heterografts is strongly dependent on the implantation technique, which is expected when considering the complicated function of the mitral complex compared with the aortic valve. Pressure Drop Characteristics.

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The unstented Medtronic Freestyle valve has a lower pulsatile pressure drop than comparably sized stented valves. In the 25 and 27 mm size Freestyle valves, Aeff was comparable to the St. Jude Medical Standard bileaflet valve, whereas in smaller sizes it was comparable to the St. Jude Medical Regent valve. The Medtronic Freestyle and Mosaic porcine valves use the exact same tissue, treated with the same processes. The Aeff of a 23mm Medtronic Freestyle stentless valves, however, was found to be similar to that of a 27-mm stented Mosaic valve. Thus, removal of bioprosthetic valve stents definitely creates less forward flow obstruction and significantly improves overall hemodynamic performance. The Aeff for several sizes of the Medtronic Freestyle porcine valve are listed in Table 23-2 and Table 23-3 . Because of the added complexity of the unstented design and the increased factors governing selection and style, optimal flow performance of these valves both in vitro and in vivo depends on the type of valve configuration used for a particular patient geometry and on the proper sizing of the valve. Improper selection of style and size can compromise hemodynamic performance of the valve. In vitro tests of the Medtronic Freestyle valve indicate that the Aeff can be optimized by using a valve one size larger than the size of the simulated aorta. Thus, a 23-mm valve should be used in a 21-mm aorta. Total root or an inclusion cylinder valve geometry technique showed better Aeff results than partially or fully scalloped valve configurations. Pressure drops for mitral valve heterografts are generally higher than normal mitral valves, owing to stiffening of the valve tissue resulting from fixation. Homograft Valves

Homograft valves are cryopreserved human valves, and they have been used for more than two decades in the aortic position. With the advent of improvements in surgical techniques and viable mitral heterografts, a mitral homograft is also a possibility. Aortic homografts are typically implanted as a complete valve, annulus, and aortic section. As a result, the effective annulus area is reduced from the original aortic valve annulus before replacement. Mitral homografts consist of intact mitral valves with annulus, papillary muscles, and chordae tendineae. Antegrade Flow.

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The flow field characteristics of the homograft aortic valves are similar to those of the natural valve, although peak velocities are slightly higher because of a reduced Aeff resulting from the smaller area of the outflow tract. Peak velocities, however, are smaller in homograft valves than those observed in other prosthetic designs for comparably sized valves. The aortic homograft shows excellent hemodynamics over the entire size range in contrast to the stented bioprostheses, which show increased stenosis in the smaller valve sizes. Studies conducted in our lab indicate that sheep allograft mitral valves and untreated normal mitral valves have excellent hemodynamics compared with that of stented valves.[115] The unfixed mitral valves exhibit both qualitatively and quantitatively similar forward flow characteristics to those observed clinically for normal human mitral 521

Figure 23-18 Planar two-dimensional transmitral flow patterns in the left ventricle during diastole. Images were obtained from in vitro planar flow visualization experiments of natural, untreated mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.)

valves. The qualitative left ventricular flow fields during diastole are illustrated in Figure 23-18 . This figure shows the in vitro flow patterns for the natural mitral valve using a two-dimensional planar flow visualization technique outlined in Lefebvre.[99] These experiments were conducted in an anatomically correct left ventricular model constructed of polished transparent acrylic. The models were manufactured so that the native mitral valve complex, including papillary muscles and chordae tendineae, could be implanted and tested under normal physiologic conditions. Figure 23-19 illustrates the model and relationship of a native valve mounted in the model. Normal Regurgitant Flow.

As with other bioprosthetic valves, the homograft valves exhibit small closing volumes. Properly functioning homograft valves should exhibit little or no regurgitation caused by leakage. The mitral homografts show the same dependency of implantation technique on overall hemodynamics. Proper implantation of the valve complex including proper alignment of the

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papillary muscles with the valve annulus results in superior function with no regurgitation other than normal closing volume. Pressure Drop Characteristics.

The homograft valves show low pressure drops with large Aeff compared with mechanical and stented valves. Vetter et al[116] conducted in vitro tests of 23- and 25-mm mitral homograft valves at physiologic conditions of 5 L per minute CO and 70 bpm HR to measure the pressure drop and Aeff characteristics of these valves. Measured pressure drops ranged from 10.4 to 3.4 mm Hg for the 23- and 25-mm valves, respectively. The corresponding Aeff ranged from 1.8 to 3.4 cm2 . These values are comparable to 25- and 27-mm Hancock 342 and Hancock II bioprostheses, indicating a significant improvement in hemodynamics for similar valve size. Typical values for the Aeff and PI of homograft valves are listed in Table 23-2 and Table 23-3 .

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Future Directions We foresee that the future direction of prosthetic valve research will follow several courses: tissue-engineered bioprosthetic valves; invention of novel tissue fixation techniques; improved mechanical valve design; improved in vitro, computational, and animal testing protocols; and development of noninvasive diagnostic capabilities. Conceptually, tissue-engineered valves would hold the most promise for a near-perfect valve replacement. The goal of this research is to grow living human aortic valves in the laboratory, preferably using the patient's own tissue. Potential advantages involve total acceptance of the living tissue, with hemodynamic and cellular function similar to the normal human aortic valve, resulting in a lifetime equal to that of native valves. Tissue xenografts are currently fixed in glutaraldehyde, which stiffens the compliance of the valve material and hinders hemodynamic performance. [115] Other fixative techniques may improve hemodynamic performance or increase the functional lifetime of xenografts. For mechanical valves, the focus will be on reducing their thrombogenic properties. This goal could possibly be achieved by development of biocompatible surface coatings and materials, or by changing valve geometry to improve closure and leakage flow through these valves. [117] A first step in this research should be to improve understanding of blood element damage, thromboembolic events, and thrombus formation. As we enrich our understanding of these topics, in vitro evaluation techniques and in vivo diagnostic capabilities should also improve.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Acknowledgments The work reported from our laboratory has been supported by grants from the Food and Drug Administration, Figure 23-19 The anatomically correct left ventricular in vitro model used in the testing of nonstented and homograft mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.)

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the American Heart Association, the heart valve industry, and generous gifts from Tom and Shirley Gurley and the Lilla Boz Foundation.

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525

Chapter 24 - Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction Miguel Zabalgoitia MD

After more than 3 decades of clinical experience, the search for the "ideal" artificial heart valve continues with increasing interest. Thirty years ago, prosthetic valves were limited to the ball-and-cage mechanism; since then, single and double tilting discs and several stented and nonstented biologic devices have been introduced. Each of these valves is accompanied by individual ultrasonic and hemodynamic characteristics (see Chapter 23) , making the roles of the echocardiographer and sonographer understandably more complex. The optimal management of patients with prosthetic valves requires serial assessment of valve function and left ventricular performance. Symptoms of fatigue, dyspnea, and exercise intolerance may be caused by valve dysfunction or a variety of comorbid conditions. Doppler echocardiography is the imaging modality of choice in evaluating patients with known or suspected prosthetic valve dysfunction because it provides information regarding valve structure, hemodynamics, native valve status, and left ventricular function.[1] [2] [3] Since its clinical introduction more than a decade ago, transesophageal echocardiography (TEE) has been widely

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accepted as a tool that allows superior anatomic and functional assessment of native and prosthetic valves.[4] [5] [6] TEE now is a routine diagnostic procedure in assessing prosthetic heart valves. Three-dimensional (3D) echocardiography is an evolving new technology with a wide range of potential clinical applications, and evaluation of prosthetic heart valves, particularly tissue valves, may be one of them. Other available methods for assessing prosthetic valves include cardiac catheterization with angiography for both hemodynamic and structural information. Cardiac catheterization also provides the opportunity to perform fluoroscopy in the case of metallic valves. The potential use of magnetic resonance imaging in assessing prosthetic valve function has been suggested by a comparative study detecting pathologic prosthetic regurgitation.[7] Further studies are needed to determine the most appropriate clinical setting for this imaging modality. Nowadays, it is impossible to ignore the impact that economics has on our daily practice. Evaluation of cost and effectiveness of diagnostic testing is complex; it involves the test itself and the treatment strategies that follow. [8] In this regard, one must answer the following questions: Do the test results affect the decision-making process?; Do the test results lead to the treatment of choice?; What is accuracy of the testing?; What is the cost?; and What is the morbidity due to the test? Although a detailed ultrasound cost analysis of prosthetic heart valves is lacking, the subject offers a useful frame of thought, and the answer to each of the above-mentioned questions is clearly favorable. In fact, the perception of most clinicians is that Doppler echocardiography in patients with prosthetic heart valves is a highly cost-effective tool.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Prosthetic Heart Valve Classification Several types of prosthetic heart valves, divided into mechanical and biologic categories based on their primary 526

TABLE 24-1 -- Classification of Prosthetic Heart Valves Mechanical Ball-and-cage (Starr-Edwards) Single tilting disc (Medtronic-Hall, OmniScience) Double tilting disc (St. Jude Medical, Carbomedics) Biologic Heterograft stented (Hancock, Carpentier-Edwards) Heterograft nonstented for aortic valve (Toronto SPV, Medtronic Freestyle, and CryoLife-O'Brien) Heterograft nonstented for pulmonic valve (CryoLife-Ross) Homografts (aortic, pulmonic, and mitral) manufacturing material, are available for implantation. Table 24-1 lists the most common prosthetic heart valves currently used in clinical practice. Mechanical Valves Ball-and-Cage.

The first successful valve replacement used a ball-and-cage design, [9] [10] and after several modifications, only the Starr-Edwards valve has endured with an estimated usage of more than 200,000. It consists of a Silastic ball

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with a circular sewing ring and a cage formed by metal arches located around the sewing ring (Fig. 24-1) . The silicone rubber ball retracts toward the apex of the cage as antegrade blood flows through the valve orifice and between the ball and the stents. [11] Single Tilting Disc.

A single disc tilting valve consists of a circular sewing ring with a circular disc eccentrically attached by lateral or central metal struts. MedtronicHall, Figure 24-1 Mechanical heart valves. Starr-Edwards (S-E), MedtronicHall (M-H), OmniScienct (Omni), and St. Jude Medical (SJM).

Björk-Shiley, and OmniScience are representatives of this group. The first successful low-profile design was the Björk-Shiley, introduced in 1969,[12] with an estimated usage of 360,000. The Björk-Shiley valve has been discontinued from the United States market. When the pyrolytic carbon disc opens, blood flows through two unequal (major and minor) orifices and the disc opens with an angle ranging from 60 to 80 degrees, which favors closure by a backflow mechanism (see Fig. 24-1) . This angle results in resistance to flow around the disc and stagnated flow behind the disc, a site of potential thrombus formation. Double Tilting Disc.

Bileaflet valves have two semicircular pyrolytic carbon discs attached to the valve ring by two small midline hinges. St. Jude Medical and Carbomedics are the prototypes of this group (see Fig. 24-1) . The bileaflet design was introduced by St. Jude Medical in 1977 and has been used over 600,000 times. Mechanical valves are extremely durable with overall actuarial survival rates ranging from 94% ± 2% at 10 years for the St. Jude Mechanical valve to between 60% and 70% at 10 years for the Starr-Edwards valve.[13] [14] [15] Primary structural abnormalities are very rare,[16] [17] [18] and most valve malfunctions are caused by perivalvular leak, endocarditis, and thrombosis. Chronic anticoagulation is required in all patients with mechanical valves to prevent valve thrombosis and embolic events. With adequate

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anticoagulation, the rate of thrombosis is 0.6% to 1.8% per patient-year for bileaflet valves.[13] [19] [20] Biologic (Tissue) Valves Stented Bioprostheses.

Porcine valves currently in use are the Hancock and Carpentier-Edwards. The leaflets are treated with glutaraldehyde to reduce antigenicity, but they are less pliable than normal human valves.[21] The Carpentier-Edwards porcine valve has a stent made from a single piece of wire and the three leaflets are mounted above the sewing ring, allowing a larger orifice area and a better hemodynamic profile. Both porcine bioprostheses have a similar macroscopic appearance, but they are easily distinguishable by their radiographic appearance; Hancock appears as a circular ring whereas Carpentier-Edwards appears as a crown. The Ionescu-Shiley bioprosthesis from bovine pericardial tissue was discontinued after 10 years of use because of dehiscence.[22] The Carpentier-Edwards pericardial (Perimount) valve is currently available, but unlike the Ionescu-Shiley, which used retention sutures to attach the leaflets, the Perimount valve is mounted within the stent to maximize cusp opening and to reduce abrasion between tissue and stent. The long-term results with this valve are very encouraging. A major advantage of bioprosthetic valves is the low rate of thromboembolism (1.6% per patient-year) in the absence of chronic anticoagulation[23] however, stented heterograft valves are subject to progressive calcific degeneration and failure typically after 6 to 8 years of implantation.[24] [25] [26] [27] [28] [29] Calcific degeneration is faster in children, young adults, and patients with abnormal calcium metabolism.[30] [31] In several large series, the rate of degeneration for porcine valves was 3.3% per patient-year and a freedom 527

from valve failure rate for aortic valves was 78% ± 2% and for mitral valves was 69% ± 2%.[23] [32] [33] After 10 years, the rate of deterioration accelerates abruptly with freedom from valve failure rates of 49% ± 4% for aortic and 32% ± 4% for mitral prostheses.[32] Using the porcine bioprosthesis in patients over 70 years of age, a 90% freedom from valve replacement at 12 to 15 years has been reported.[33] [34] This finding may be related to a decreased rate of degeneration in elderly patients or an increased rate of death from other than valve-related causes in the group of

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patients who did not outlive their prostheses. Nonstented Bioprostheses.

Nonstented heterografts are expected to improve hemodynamics and longterm durability while retaining the fundamental advantages of tissue valves. The goals are to return the patients to their own baseline conditions as is feasible, prolong survival, and improve quality of life. The absence of the stent and sewing cuff make it possible to implant a larger valve for a given annular size, resulting in a greater effective orifice area. A nonstented bioprosthesis uses the patient's aortic root as the valve stent, absorbing the motion stress induced during the cardiac cycle and leading to better hemodynamic performance. Nonstented bioprostheses include the Toronto SPV,[35] [36] Medtronic Freestyle,[37] [38] [39] [40] and CryoLife-O'Brien.[41] [42] [43] There are several variations within the same valve, depending on the patient's needs and the surgeon's preference. These variations include the full root technique with reimplantation of the coronary arteries, the root inclusion technique with preservation of the native coronary arteries, or the subcoronary technique. Figure 24-2 depicts a subcoronary implantation. Removal of the stent appears to eliminate much of the stress that promotes calcification and valve deterioration. Nonstented bioprostheses typically are manufactured from intact porcine aortic valves processed at very low fixation pressures. Moreover, some valves (i.e., Medtronic Freestyle) are treated with the anticalcificant amino-oleic acid, which may further decrease calcific deposits. The addition of a layer of polyester fabric around the graft adds support and aids implantation.[44] [45] Nonstented valves have been used primarily in the aortic position in men older than 60 years of age. The reported operative mortality rate for patients with nonstented valves is 3% to 6%,[46] [47] but these figures are probably affected by patient selection. Postoperative complications at 12 months appear to be low, with endocarditis reported at 1% to 2%, thromboembolism at 2% to 3%, and hemorrhage at 1.5%.[44] [46] [47] There have been no reports of primary structural failure, and the reported survival rates have been as high as 91% ± 4% at 6 years.[44] [47] [48] The CryoLife-Ross valve is a pulmonary nonstented bioprosthesis made of three noncoronary porcine cusps used to correct congenital defects involving the pulmonic valve, and they can also be used during the Ross procedure as described later.

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Homografts.

Homografts are antibiotic-sterilized, cryogenically-preserved valves harvested from cadaveric human hearts.[49] Their major advantages are relative resistance to infection, lack of need for chronic anticoagulation, and excellent hemodynamic profile, most notably in Figure 24-2 Drawing of a nonstented aortic valve (Toronto SPV) at the subcoronary position. (Courtesy of St. Jude Medical, Inc., St. Paul, Minn. All rights reserved. Copyright © 2001 St. Jude Medical, Inc. Toronto SPV is a registered trademark of St. Jude Medical, Inc.)

smaller aortic root sizes.[50] [51] As illustrated in Figure 24-3 (Figure Not Available) , homografts have been developed for the aortic, pulmonic, and even for mitral valves. The technical aspects of homograft preparation and the meticulous and highly skilled freehand surgical technique required for implantation in some cases have limited their use on a routine basis. Typically, homografts are inserted without a stent, using the patient's natural fibrous annular tissue for support. Ross Procedure.

The pulmonic autograft (or Ross procedure), first described in 1967,[52] consists of replacing the abnormal aortic valve with the native pulmonic valve of the same patient, then placing a nonstented homograft or porcine bioprosthesis in the pulmonic position. The operation is technically demanding; the pulmonic valve is removed with healthy tissue above and below the valve insertion. This procedure requires some reconstruction of the right ventricular outflow tract. In addition, the coronary arteries are reimplanted into the pulmonary artery trunk that serves as the new aortic root. Although the Ross procedure involves two valve operations (aortic valve autograft and pulmonic valve nonstented allograft) to correct one diseased valve, it provides optimal hemodynamics and echocardiographic performance and low valve-related complication rates.[53] The main longterm problem with this operation has been degeneration and failure of the right-sided valve caused by obstruction in the distal segment of the homograft conduit.[54] [55] Early 528

Figure 24-3 (Figure Not Available) Drawing of cardiac anatomy depicting the

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availability of homografts for the pulmonary, aortic, and mitral valves. (Courtesy of CryoLife, Kennesaw, Ga.)

autograft failure (<6 months) most often is due to technical errors or persistent endocarditis, and late failures generally are due to aortic annulus dilation, endocarditis, or valve degeneration.[56] [57]

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Fundamental Principles Pertaining to Prostheses Modified Bernoulli Equation Blood flow velocity through a narrow orifice is related to the pressure difference between two chambers as described by the Bernoulli principle used to convert flow velocity (m/sec) to pressure gradient (mm Hg). The modified Bernoulli equation used in prosthetic valves is the same as that used in native valves: Pressure gradient = 4(VMAX )2 where VMAX is the maximal (peak) velocity across the valve orifice. It is

important to recognize that the modified Bernoulli equation neglects the effects of acceleration and viscous losses, and yet it has proved to be remarkably accurate when compared with catheter-derived pressure gradients when both are obtained simultaneously.[58] [59] [60] [61] [62] [63] When the left ventricular outflow tract velocity (V1 ) is greater than 1 m per

second, such as in patients with concomitant aortic regurgitation, V1 should

be subtracted from VMAX . Maximal instantaneous and mean gradients

should be calculated for aortic valves, and mean gradient should be calculated for mitral valves. A high gradient in the setting of anemia, tachycardia, or sepsis does not necessarily indicate stenosis; conversely, an upper normal limits gradient in the setting of severe left ventricular dysfunction may indicate significant stenosis. Pressure Recovery Recording valve gradients that appear to be an "overestimation" when compared with those at catheterization may result from distal pressure recovery, which refers to the conversion of kinetic energy present at the

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valve level to pressure energy distal to the valve.[64] [65] When flow passes through the prosthesis, components of velocity and momentum are directed centrally, causing the flow stream to contract distally for a short distance. This point of maximal constriction is called vena contracta and occurs downstream distally from the anatomic location of the prosthesis. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure or pressure recovery. Under these circumstances, when the aortic pressure is measured in the upper ascending aorta (distal to the vena contracta), the pressure difference between the left ventricle and the aorta is less than the aortic pressure measured at the vena contracta. The degree of pressure recovery may be as high as a mean of 10 mm Hg in small St. Jude Medical valves challenged under physiologic flow rates. The magnitude of pressure recovery is greater with larger valve areas and with smaller aortic roots; therefore, patients with severe prosthetic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and normal aortic root diameter. Pressure recovery and vena contracta are important concepts to keep in mind when Doppler- and catheter-derived pressure gradients are being compared. Because continuous wave Doppler measures velocity at the level of the vena contracta (physiologic variable) and catheterization measures the difference between left ventricle and the fully recovered static pressure in the aorta, catheter-derived data must be interpreted with caution. Failure of the invasive technique to record the gradient at the vena contracta level may explain some of the reported discrepancies.[66] Continuity Equation An important limitation of Doppler velocities (and pressure gradients derived thereof) is that they are flow volume rate dependent. When transvalvular flow is decreased, such as in patients with significant left ventricular systolic dysfunction, Doppler velocities may only be moderately elevated despite severe obstruction. Thus, comparisons may be confounded by interval changes in flow volume rate. For these reasons, estimation of valve areas, in addition to mean pressure gradients, should be routinely calculated. The equation of continuity can be used to estimate aortic and mitral valve areas. Figure 24-4 illustrates how to apply the continuity equation in aortic prostheses:

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AVA = (ALVOT × VTILVOT )/VTITRANSPROSTHESIS

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Figure 24-4 Effective orifice area (EOA) calculation for an aortic valve prosthesis. The left panel corresponds to the outflow tract (subvalvular) velocity, also known as V1 . The middle panel corresponds to the prosthesis velocity, also known as V2 . The right panel corresponds to the parasternal long-axis view, showing the outflow tract diameter (arrows). Ac, aortic closure; AO, aorta; Ao, aortic opening; LA, left atrium; LV, left ventricle; RV, right ventricle; subvalve, subvalvular; vel. int., velocity integral.

where ALVOT is the cross-sectional area of the outflow tract at end-systole measured just underneath the prosthesis from the parasternal long-axis view. VTILVOT is the velocity time integral proximal to the valve as seen

from an apical view using pulsed wave Doppler. One must be careful placing the sample volume immediately adjacent to the aortic prosthesis from the apical five-chamber view while avoiding the region of subvalvular acceleration. The Doppler wave form should be smooth with minimal spectral broadening and a well-defined peak. VTITRANSPROSTHESIS is the

velocity time integral across the prosthesis using continuous wave Doppler. Because the direction of the jet may be eccentric, all acoustic aortic windows (apical, suprasternal, and right parasternal) should be carefully examined to detect the highest velocity signal. Continuity equation valve areas have been compared with invasively obtained data for bioprosthetic[67] [68] [69] and mechanical valves.[70] [71] The largest source of variability is the accurate and reliable measurement of the left ventricular outflow tract. When this diameter is difficult to obtain from the precordial window, TEE offers an excellent alternative for calculation of aortic valve area.[72] For mitral valve area (MVA), the continuity equation is as follows: MVA = (AVA × VTIAORTIC )/VTITRANSPROSTHESIS where AVA is the cross-sectional aortic valve area as measured from the

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parasternal long-axis view, VTIAORTIC is the velocity time integral across the native aortic valve, and VTITRANSPROSTHESIS is the velocity time

integral across the mitral prosthesis.[73] Because the continuity equation is based on the principle of conservation of mass, it assumes that flow across the mitral prosthesis and that across the second valve are equal. Thus, in patients with greater than mild mitral regurgitation, the preferred method to estimate valve area is the pressure half-time. In the presence of aortic regurgitation, the pulmonic valve area and flow can be used in lieu of the aortic valve. The limiting step in using the pulmonic valve is the accurate and reproducible measurement of the right ventricular outflow tract diameter from the precordial approach. An important advantage of the continuity equation is its relative independence from valvular gradient and chamber compliance.[74] Data acquisition for the continuity equation, however, is more cumbersome than the pressure half-time. Doppler Velocity Index The Doppler velocity index (DVI) is a dimensionless ratio of the left ventricular outflow tract to prosthesis velocities: DVI = VLVOT /VTRANSPROSTHESIS Because it is independent of valve size, this index can be particularly helpful when the cross-sectional area of the outflow tract cannot be obtained. Because the velocity proximal to the valve is subtracted from that across the prosthesis, the patient serves as his or her own control, 530

with flow being the main dependent factor. The higher the index, the larger the area; the lower the index, the smaller the area. Index values calculated from 25 patients with normally functioning St. Jude Medical aortic valves were 0.39 ± 0.07, range 0.28 to 0.55. In a small group of patients with severe stenosis of St. Jude Medical aortic valves requiring reoperation, the DVI was 0.19 ± 0.05, range 0.12 to 0.27, which was significantly different from normal values at the 0.05 level.[75] Valve Resistance Resistance is the quotient of gradient and flow (R = ∆P/Q). This

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hemodynamic parameter suggested by Ford et al[76] is an alternative to the Gorlin formula in assessing severity of native aortic stenosis. It can be calculated from echo-Doppler data as follows: Resistance = 1.33 ∆P (ET/SV) where ∆P is the mean pressure gradient in mm Hg, ET is the ejection time in seconds, and SV is the stroke volume in mL per minute. The ratio of mm Hg to mL per minute is converted to dyne-sec-cm5 when multiplied by 1.33. In conditions characterized by variation of flow, valve resistance remained more constant than the Gorlin estimated area. In considering valve resistance, however, one must recognize that most data have been derived from native valve stenosis, not from prostheses; no information is available during changing flow conditions, such as exercise; and there is virtually no clinical data in prosthetic mitral valves. Saad et al[75] studied two groups of patients with prosthetic aortic malfunction (predominant stenosis versus predominant regurgitation) and compared them with a control group. Effective orifice area (continuity equation), Doppler velocity index, and valve resistance were all very helpful in separating the groups. It is unclear, however, whether valve resistance per se added clinically significant information beyond that derived by valve area and Doppler velocity index. An important role of valve resistance in artificial valves may be in patients with small aortic valve areas, relatively low flow velocities, and severe left ventricular systolic dysfunction, to differentiate severe prosthetic valve stenosis from a low cardiac output state, which has been shown to be useful in patients with native aortic stenosis.[77] Pressure Half-Time The pressure half-time is the time required for the peak velocity to decline by a factor of 1 divided by the square root of 2, and it can be helpful in separating normal from obstructed prostheses. The pressure half-time is dependent on several factors, including atrial and ventricular compliance, ventricular stiffness, and, of course, the actual effective orifice area (EOA). Pressure half-time is used to calculate the EOA of mitral and tricuspid valve prostheses based on the inverse relationship between pressure halftime and valve area[78] EOA (cm2 ) = 220 / pressure half-time (msec)

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Validation of this method with invasive data has showed good correlation. Kapur et al[79] compared mitral valve areas derived by pressure half-time with those derived by the Gorlin formula in 32 patients with mitral valve prosthesis and found correlations of 0.94 and 0.79 for bioprosthetic and mechanical valves, respectively. In contrast, Wilkins et al,[59] using simultaneous catheterization and Doppler techniques in 11 patients with mitral prosthesis, found poor correlation. This method relies on the constant, 220, which was originally derived for native rheumatic mitral stenosis. Application of this constant to the wide variety of valve types and sizes cannot be expected to yield predictable results.[3] The continuity equation is an excellent alternative to the pressure half-time to calculate mitral valve area. [80] Leakage Backflow Prosthetic mechanical valves have a normal regurgitant volume known as leakage backflow that occurs when the valve occluder has already been seated and blood leaks into the proximal chamber between and around the occluder assembly. In theory, this "built-in" regurgitation prevents stasis and thrombus formation by a "washing" mechanism. The jets of leakage backflow are characterized by being short in duration, narrow, symmetrical (bileaflet valves), and having low velocities (nonaliasing) encoded in a homogeneous color—red or blue, depending on the transducer location (assuming Nyquist limit >0.53 m/sec). [81] [82] The normal regurgitant jets in the Carbomedics valve are larger than those of the St. Jude Medical. Abnormal jets, on the other hand, are longer in duration, wider, larger, asymmetrical across the valve midline, frequently eccentric ("hugging the wall"), extending far into the receiving chamber, and display a mosaic pattern reflecting high-velocity, turbulent flow. A jet with an unusual angle (i.e., one anteriorly directed toward the atrial appendage) is also typical of a paravalvular leak. Figure 24-5 depicts the typical appearance of a normal backflow in a bileaflet mitral valve (see Fig. 24-5A) . In contrast, a larger, wider, eccentric jet "hugging" the left atrial lateral wall characteristic of severe perivalvular regurgitation is seen (see Fig. 25-5B) . Table 24-2 highlights the differences between physiologic leakage backflow and pathologic regurgitant jets. TABLE 24-2 -- Physiologic Leakage versus Pathologic Regurgitation of

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Mechanical Prosthesis Jet Feature Size Symmetry Aliasing Eccentric

Physiologic Leakage Short and narrow Symmetrical (bileaflet valves) No (low velocity) No

Pathologic Regurgitation Large and wide Asymmetrical Yes (high velocity) Yes

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Figure 24-5 (color plate.) TEE longitudinal views of a normal CarboMedics valve in the mitral position (A). Two symmetrical regurgitant backflow jets are seen within the left atrium (LA). These jets are low velocity, nonaliased, and encoded in red. In contrast, a pathologic periprosthetic leak is seen in an abnormal valve (B). The jet is high velocity, mosaic in color, and eccentric, and it encircles the left atrial wall (open arrow). The normal regurgitant backflow jets (solid arrows) are also seen. See Table 24-2 for differentiation of physiologic versus pathologic jets.

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MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement

Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography of Normal Prosthetic Valve Function In general, the same principles used in native valves are applicable to artificial valves. Echocardiography has some limitations related to reverberations and shadowing from the interface between ultrasound and the foreign material composing the valve.[83] Intense reverberations projected behind the prosthesis can mask normal structures or instead create artifacts, leading to a misdiagnosis. Table 24-3 describes common limitations and technical errors or "pitfalls" as well as suggestions on how to overcome or minimize their impact. A complete examination should include estimation of pressure gradients and valve area, degree of normal or TABLE 24-3 -- Echocardiography of Prosthetic Valves: Pitfalls Technical Limitations or Pitfalls Suggestions Acoustic shadowing Use window in which ROI is not obscured by the valve's artifact. Consider TEE. Failure to detect peak Image from multiple windows. velocity Under- or Include proximal velocity in continuity equation if overestimation of it is >1 m/sec. valve gradient or effective orifice area Consider pressure recovery. Use mean valve gradient, not "peak-to-peak" or maximal instantaneous gradient. Unexpectedly high Consider high cardiac output setting, i.e., valve gradient or small tachycardia, anemia, sepsis.

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effective orifice area Calculate DVI and valve resistance. Compare to previous echo study. Consider prosthesis-patient mismatch. Consider valve thrombosis (TEE?). Consider pannus formation (TEE?). DVI, Doppler velocity index; ROI, region of interest; TEE, transesophageal echo. abnormal regurgitation, left ventricular size and function, native valve structure and function, and calculation of the pulmonary artery systolic pressure. M-mode recording may assist in evaluating disc or leaflet excursion, whereas color M-mode recording may assist in timing regurgitant jets. Two-dimensional (2D) imaging should begin by identifying the sewing ring, the occluder mechanism, and the surrounding area. The ball or disc is often indistinctly imaged because of echo reverberations. The leaflets of normal tissue valves should be thin with an unrestricted motion. A very helpful and frequently overlooked parameter for evaluation of prosthetic valves is comparison with prior studies. The importance of a timely baseline postoperative study cannot be overemphasized. In our institution we routinely perform an ultrasound examination prior to hospital discharge, or in the patient's first clinic visit. This initial study establishes the baseline gradients and area, the postoperative ventricular systolic function, and the systolic pulmonary artery pressure for that particular patient, at that particular time. This anatomic and hemodynamic profile is subsequently used whenever prosthetic dysfunction becomes a concern. How often "routine" echocardiographic follow-up studies should be performed is a controversial topic. Table 24-4 lists the recommended schedule for early and long-term follow-up of prosthetic heart valve evaluation. Follow-up for nonstented bioprostheses and homografts clearly should be different from stented bioprostheses, because nonstented bioprothesis deterioration rates are lower. The effective orifice area is not the sewing ring orifice; it is the remaining area not occupied by the valve occluder assembly. Normally functioning mechanical and stented bioprostheses, therefore, have higher velocities than native valves. The smaller the size of the bioprosthesis, the smaller the

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effective orifice area, and the higher the flow velocities. For homografts and the newest nonstented bioprostheses, the hemodynamic profile is near normal. Table 24-5 and Table 24-6 provide the normal range of in vivo velocities for mechanical and bioprosthetic valves in the aortic and mitral positions, respectively.

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TABLE 24-4 -- Recommended Doppler Echocardiography Follow-up in Patients with Prosthetic Heart Valves Patient Category EARLY POSTOPERATIVE Any type of valve LONG-TERM FOLLOW-UP Stented Bioprosthesis Clinically normal

Recommendation Baseline study in all patients

Every 2 years for the first 6 years, then every year for 4 years, then every 6 months Patient-prosthesis mismatch Once a year Chronic renal failure Once a year Nonstented Bioprosthesis and Homografts Clinically normal Every 2 or 3 years Mechanical Valves Clinically normal Every 2 or 3 years Patient-prosthesis mismatch Once a year

Echocardiographic Features by Valve Type Ball-and-Cage.

The Silastic ball produces multiple echoes from its leading edge, obscuring other aspects of its structure. Flow through a normally functioning ball-andcage valve is characterized by turbulence created by the high-profile ball in the center of the blood stream and by the eddies created as flow circulates retrogradely (Fig. 24-6) . Consequently, when compared with single and

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double tilting disc valves, the hemodynamic performance of the ball-andcage valve is less, with higher pressure gradients. This hemodynamic profile increases its intrinsic thrombogenicity because of blood cell damage.[15] Color flow in a normal ball-and-cage valve includes lowvelocity closure backflow (2 to 5 mL per beat).[11] [84] Single Tilting Disc.

Figure 24-7 illustrates a single tilting disc valve in the mitral position. The left panel illustrates the typical antegrade flow through the major and minor orifices in the correct orientation (major orifice toward the lateral aspect, away from the outflow tract) as opposed to the incorrect orientation seen on the right panel. Typical flow velocity of a single tilting disc valve is TABLE 24-5 -- Normal Doppler Values for Aortic Prostheses ‡

Type Starr-Edwards Björk-Shiley St. Jude Medical Medtronic-Hall OmniScience Hancock CarpentierEdwards Aortic Homograft Toronto SPV † Freestyle † O'Brien †

Peak Velocity (m/sec) 3.1 ± 0.5 2.5 ± 0.6 3.0 ± 0.8 2.6 ± 0.3 2.8 ± 0.4 2.4 ± 0.4 2.4 ± 0.5

Mean Area Mean Gradient (mm Hg) (cm2 ) * 24 ± 4 * 14 ± 5 * 11 ± 6 * 12 ± 3 * 14 ± 3 11 ± 2 1.8 14 ± 6 1.8

Area Range (cm2 ) * * * * *

1.4–2.3 1.2–3.1

1.8 ± 0.4

7±3

2.2

1.7–3.1

2.2 ± 0.4 2.2 ± 0.4 2.2 ± 0.4

3±4 3±4 3±4

2.2 2.2 2.2

2.0–2.8 2.0–2.8 2.0–2.8

‡Data from references [5] [11] [14] [18] [19] [23] [38] [40] [41] [46] [51] [58] [67] [68] [69] [75] [88] [90] [95] and [103] . *Insufficient data available. †Nonstented bioprostheses.

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Figure 24-6 A, Normal diastolic intracavitary flow pattern. B, Disturbed antegrade flow across a ball-and-cage valve. Note the high-profile ball located in the center of the blood stream, creating turbulence and eddying as flow changes direction.

around 2 m per second. Flow through the minor orifice consists of two jets separated by a well-defined wake behind the tilting disc but with a velocity similar to the major orifice. The appearance of the disc is characterized by echoes produced by its motion. Color flow in these valves includes a small amount of normal backflow (5 to 9 mL per beat), originated from small gaps around the perimeter of the valve. [85] [86] Hixson et al[81] have reported that the Medtronic-Hall valve has a large central regurgitant backflow that can extend back into the left atrium with aliasing, whereas the peripheral jets are nonaliasing, low-velocity flow. Double Tilting Disc.

Figure 24-8 illustrates the anatomic orientation of a bileaflet valve in the mitral position during diastole and normal mitral inflow. The blood flow is near-laminar with a path similar to the laminar flow of the native valve. In the opening position, the hemidiscs appear as parallel lines with a short angle between them. Imaging of the normal valve includes the sewing ring and two distinct echoes in the opening position and a wide obtuse angle in the closing position. Identification of the two hemidiscs may be problematic with the standard approach of transthoracic echocardiography (TTE), particularly in the aortic position. However, multiplane TEE at the upper and midesophageal level can better visualize the hemidiscs for aortic and mitral positions.

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TABLE 24-6 -- Normal Doppler Values for Mitral Prostheses *

Type Starr-Edwards Björk-Shiley

Peak Velocity (m/sec) 1.8 ± 0.4 1.6 ± 0.3

Mean Gradient (mm Hg) 4.6 ± 2.4 5.0 ± 2.0

Area Mean (cm2 ) 2.1 2.4

Area Range (cm2 ) 1.2–2.5 1.6–3.7

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1.6 ± 0.3 1.7 ± 0.3 1.8 ± 0.3 1.5 ± 0.3 1.8 ± 0.2

5.0 ± 2.0 3.1 ± 0.9 3.3 ± 0.9 4.3 ± 2.1 6.5 ± 2.1

2.9 2.4 1.9 1.7 2.5

1.8–4.4 1.5–3.9 1.6–3.1 1.3–2.7 1.6–3.5

1.8 ± 0.4

6.4 + 3.0

2.2

1.9–2.9

*Data from references [5] [14] [58] [59] [69] [73] [80] [88] and [103] .

In normally functioning bileaflet valves, color demonstrates a small amount of normal backflow (5 to 10 mL per beat) designed to decrease the risk of thrombosis by a "wash out" mechanism. TEE visualization of the bileaflet valve depends on the image orientation in the parallel or perpendicular position of the discs in relation to the sound beam. In the parallel position, the discs appear in profile as two lines. Color may reveal up to three distinct jets: two at the edges of the valve directed upward and outward; one centrally located and directed straight up. In the perpendicular position, the leaflets reflect dense reverberations into the ventricular cavity and color reveals a semicircular flare on the atrial aspect. As the probe is pulled or advanced, the central flare becomes narrower. [81] [82] The Carbomedics is a newer version of bileaflet mechanism with recessed pivots that may result in larger regurgitant jets.[87] Stented Bioprostheses.

The cross-sectional appearance of porcine valves is that of three cusps and three struts with an echogenic sewing ring. Normal flow pattern is a bellshaped central flow with a relatively flat velocity profile. Peak flow velocities commonly found in the aortic position are around 2.5 m per second, and in the mitral position are around 1.7 m per second. Mild backflow in normally functioning bioprostheses is less common than in mechanical valves, and it has been reported in up to 10% of the cases.[88] Nonstented Bioprostheses.

Careful measurement of the patient's outflow tract or the sinotubular junction is

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Figure 24-7 Single tilting disc mitral prosthesis. A, Correct anatomic disc orientation, allowing the major orifice flow to be directed away from the left ventricular (LV) outflow tract. B, Incorrect anatomic disc orientation, in which the major orifice flow is directed toward the LV outflow tract, creating turbulence.

an important contribution of ultrasound in determining nonstented valve size.[89] After implantation, the appearance is of a normal trileaflet valve, with increased echogenicity in the annular region from the layer of fabric supporting the graft. [90] Reported hemodynamics are very encouraging with nearly-natural transvalvular gradients resulting in significant reduction in afterload and wall stress.[46] [47] [48] Ventricular remodeling through regression of cardiac hypertrophy may be an important predictor of survival after valve replacement, and hypertrophy regression as early as 6 months after valve replacement has been reported with nonstented valves.[91] Homografts.

Preoperative or intraoperative TEE measurement of the aortic annulus has been used to select the correct homograft size.[51] The 2D imaging of the nonstented homograft is similar to the native aortic valve, with increased echoes at the level of the annulus resulting from the retaining sutures as the only hint that a new valve has replaced the native valve. Homograft failure commonly results from progressive aortic insufficiency; valve stenosis is rare.[92] [93] Long-term outcome with homograft valves is complicated by differences in harvesting, sterilization, and preservation, as well as differences in the surgical techniques applied. In the Ross procedure, TEE plays an important role in providing accurate measurement of the right ventricular outflow tract for choosing the homograft size. In addition, color flow Doppler within the left and right ventricular outflow tracts provides essential information regarding aortic and pulmonic regurgitation, respectively. For Figure 24-8 Double tilting disc mitral valve. A, Normal mitral inflow. B, Mitral inflow across a double tilting disc valve, with flow passing through three separate orifices, creating a near-normal flow pattern.

534

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these reasons, in our institution intraoperative TEE is routinely performed during the Ross procedure. Valved Conduits and Composite Grafts.

Valved conduits have been used most often in the repair of congenital heart disease. Reestablishing flow from the right heart to the pulmonary artery is often performed with a bioprosthesis. The echocardiographic evaluation should include definition of the anatomic relation of the valve conduit to the heart and the flow velocity through the proximal and distal aspects of the conduit. Careful Doppler evaluation of the entire conduit is necessary because stenosis can occur at either end or anywhere along the conduit. The extracardiac course of the conduit can result in variable angles and directions of flow; therefore, color Doppler may be helpful in defining the location of high-velocity flow. Additional windows from the subcostal, subclavian, and right parasternal windows may be necessary to align the Doppler beam. Composite grafts for left-sided valves are most commonly seen in patients with aortic valve and aortic root diseases such as connective tissue disorders (e.g., Marfan's syndrome), leading to aortic aneurysm or dissection. Complications include pseudoaneurysm of the ascending aorta caused by dehiscence, which can occur at the annulus, at the distal anastomosis with the native aorta, or at the coronary artery reimplantation site.[94] TTE is essential for serial follow-up. TEE can provide additional views of the aortic valve and ascending aorta and should be considered in the evaluation of symptomatic patients or in those in whom the precordial imaging suggests an aneurysm or pseudoaneurysm formation. Echocardiographic Features by Valve Position Aortic.

Gradients and areas should be measured and averaged from at least three (sinus rhythm) to five (atrial fibrillation) beats. A clear understanding of the differences among peak gradient, maximal instantaneous gradient, peak-topeak gradient, and mean gradient is essential to avoid confusion when they are compared to those derived by catheterization. The peak gradient obtained by Doppler closely correlates with the maximal instantaneous gradient derived by catheterization. The mean gradient obtained with either technique correlates very closely with each other. When Doppler and fluidfilled pressure gradients are recorded at the same time in the catheterization

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suite, the degree of concordance is superb.[58] [59] [79] For example, Burstow et al[58] found excellent correlation for the mean gradient (tissue valves, r = 0.93; mechanical valves, r = 0.96) when data were recorded simultaneously; however, when they were not simultaneous, the correlations fell slightly (tissue valves, r = 0.85; mechanical valves, r = 0.87). Values derived with the continuity equation have correlated well with prosthesis size.[95] [96] Peak velocities as high as 3.5 to 4.0 m per second have been recorded in normally functioning prosthetic mechanical aortic valves. These high-flow velocities exist briefly at valve opening; however, the mean gradient usually falls within the normal range. The mean pressure gradient, therefore, and not the peak pressure gradient, Figure 24-9 (Figure Not Available) Simultaneous catheterization and Doppler recordings in a Starr-Edwards prosthesis (A) and a Braunwald-Cutter prosthesis (B) in the mitral position. Note the excellent pressure gradient correlations. (From Burstow DJ, Nishimura RA, Bailey KR, et al: Circulation 1989;80:504–514.)

should be used in making clinical decisions, and it is the one to be reported for subsequent comparative studies on the same patient. If the mean pressure gradient is abnormally elevated, prosthetic valve stenosis should be suspected and TEE (or fluoroscopy) should be considered. Mitral.

Echocardiographic assessment of mitral prostheses includes calculation of the mean pressure gradient and the effective orifice area. Similar to aortic prostheses, the mitral mean pressure gradient correlates very well with the mean gradient derived at the time of catheterization when both data are recorded simultaneously. As illustrated in Figure 24-9 (Figure Not Available) , the mean pressure gradient is the average of multiple gradient calculations across the Doppler spectral envelope. Assessment of mitral regurgitation is often difficult because reverberations shadow the left atrium. The parasternal long-axis view may be helpful in eccentric jets; however, for accurate determination of mitral regurgitation, multiplanar TEE is the method of choice. This approach is ideally suited for assessing the mitral valve because of its close proximity to the left atrium and the use of high-frequency transducers. The exact appearance of the mitral

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535

valve depends on the valve's orientation and the degree of left atrial enlargement. During the examination, the valve sewing ring should be carefully searched at the midesophageal and transgastric levels. The left atrium and its appendage should be searched for spontaneous echo contrast and thrombus because they may be present in patients with prosthetic mitral valves even if they are in sinus rhythm and have normal left ventricular function.[97] Evaluation of pulmonary venous flow may be important in assessing severity of regurgitation. Tricuspid.

Data with tricuspid valve prostheses are far more limited than data with left-sided valves. In many respects Doppler evaluation is similar to mitral prostheses. The prosthesis should be imaged from all available views (parasternal short-axis, parasternal right ventricular inflow, apical fourchamber, and subcostal views). Bioprostheses are preferred over mechanical valves because of their high thrombogenic potential in this position. Because flow across the right-sided chambers increases with inspiration, one should expect mild variations in the peak E wave velocity; therefore, three (sinus rhythm) to five (atrial fibrillation) beats should be taken for an average. Severe tricuspid regurgitation is frequently caused by dilation of the native annulus; therefore, annular rings are nowadays preferred over prosthetic valves to correct hemodynamically significant tricuspid regurgitation. TEE plays an important role in these cases by confirming annular dilation as the origin of the regurgitation and not an intrinsic leaflet abnormality. Pulmonic.

Prostheses in this position are relatively uncommon in part because percutaneous balloon valvuloplasty Figure 24-10 Step-by-step recommended approach for evaluating a patient with suspected prosthetic valve dysfunction. Note that auscultation and TTE examination are the initial steps. TEE and cinefluoroscopy are intermediate steps; cardiac catheterization is the last.

is an effective tool in hemodynamically significant stenosis.[98] When a surgical intervention is needed, valvotomy is frequently used to palliate the

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valve, and later in life a bioprosthesis can be used. As with the native pulmonic valve, the bioprosthesis is best seen from the parasternal shortaxis and subcostal views. The more commonly used TEE views include the basal short-axis and the longitudinal views, which may be helpful in choosing the appropriate homograft size. Color flow Doppler examination within the right ventricular outflow tract is essential to document any residual regurgitation.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Echocardiography of Prosthetic Valve Dysfunction Figure 24-10 illustrates the recommended step-by-step approach in patients with suspected prosthetic valve dysfunction. A careful clinical examination has no substitute. TTE should always be included in the initial assessment. If a high gradient is detected, additional tests may be needed, including TEE and cinefluoroscopy. Cardiac catheterization and angiography provides important hemodynamic and pathologic confirmation in many cases; however, its use should be restricted to patients in whom TEE and cinefluoroscopy have not provided a definitive diagnosis.[5] For mechanical valves, cinefluoroscopy renders a better means to evaluate the actual valve opening and closing motion. It is clearly indicated whenever valve thrombosis is suspected. One needs to determine the valve's rotational 536

Figure 24-11 Radiographic side view of a bileaflet valve. In the opening position (A), the two discs form a 10-degree angle, whereas in the closing position (B), they form a 120-degree (<25 mm) or 130-degree (>27 mm) angle, depending on valve size. C, Photograph of a bileaflet mechanical valve in the opening position.

orientation by positioning the imaging intensifier in a view perpendicular to the valve plane. The right anterior oblique cranial view is frequently used for this purpose, although occasionally a left anterior oblique caudal view may be needed. Depending on the valve type and radiographic characteristics (i.e., radiolucency, radiopacity), the discs appear as dense lines inside the circle formed by the valve housing mechanism. The fluoroscopic side view renders important information in determining the closing angle degree. To achieve the side view, the image intensifier

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should be moved longitudinally 90 degrees and rotated transversely to a position in line with the valve leaflets. For the St. Jude Medical valve, the opening angle between the two parallel lines should be 10 degrees (Fig. 2411A) . In the closing position, the two lines form a wide obtuse angle in the form of a "V" (see Fig. 24-11B) ; for valves less than 25 mm the angle should be 120 degrees, and for valves greater than 27 mm it should be 130 degrees. A complete cinefluoroscopic examination can be performed in 15 minutes or less. Figure 24-12 Radiographic representation of a bileaflet valve in the opening position. A, A "frozen" leaflet. By cinefluoroscopy, only one leaflet moves during the cardiac cycle. B, Normal appearance as rotated 90 degrees.

In the typical case of thrombosis of a double tilting disc prosthesis, only one leaflet may be moving, indicating leaflet entrapment. Figure 24-12 shows still frames recorded during cinefluoroscopy in a patient with valve thrombosis and entrapment. The opening (A) and closing (B) positions of a St. Jude Medical valve clearly indicate that the right-sided leaflet (near the patient's spine) remains "frozen" during the entire cardiac cycle, indicative of leaflet entrapment by the thrombus. Primary Mechanical Failure Dysfunction from an intrinsic valve problem is known as primary mechanical failure. This complication is rare in the use of current mechanical valves. The Starr-Edwards valve had a rare intrinsic problem called ball variance, in which changes of the ball resulted in emboli either from ball material or thrombi formed on the irregular or cracked ball.[99] [100] Figure 24-13 illustrates a classic example of ball variance with a crack seen across the 537

Figure 24-13 Pathologic specimen showing ball variance in a StarrEdwards valve. Notice the crack seen across the midportion of the ball and a large thrombus entrapped between the ball and the cage.

midportion of the ball and a large thrombus trapped between the ball and

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the cage. Disc embolization from single or double tilting disc valves is rare. The older version of the Björk-Shiley valve had several reported cases of fractured struts resulting in disc embolization. The Björk-Shiley valve is no longer available in the United States, but this valve was implanted in thousands of patients who continue to require follow-up. Monostrut (available in Europe), a new Björk-Shiley valve, is designed so the inflow and outflow struts are machined from a single piece of alloy.[18] Disc fracture has been reported in 3 Medtronic-Hall and in 10 St. Jude valves.[18] Stented bioprostheses on the other hand, may undergo primary failure called calcific degeneration. This type of valve failure is characterized by restricted cusp motion leading to stenosis or cusp tears, which then leads to regurgitation and different degrees of mixed lesions.[101] [102] Flail cusp owing to leaflet tears is associated with severe regurgitation; therefore, the echocardiographic detection of a flail cusp has important therapeutic implications. Figure 24-14A illustrates the TEE image at the midesophageal level of a patient with a flail cusp in a stented bioprosthesis. Figure 24-14B shows the explanted bioprosthesis depicting the flailed cusp. A musical or "cooing" sound has been reported with pulsed Doppler in patients with perforated or torn leaflets, which result in a striated, "shuddering" appearance to the signal, referred to as harmonics. [103] [104] [105] Leaflet thickening in the absence of endocarditis most likely represents milder degrees of calcific degeneration; however, a thickened and often irregular appearance can also be seen in endocarditis. In patients with "fibrocalcific" changes on their cusps, the differentiation between calcific degeneration and endocarditis should be based on the clinical context.[103] [106]

Thrombosis Thrombosis occurs almost exclusively in mechanical valves, leading to predominant stenosis with or without some regurgitation. Figure 24-15 illustrates a thrombosed Beall valve (disc-in-cage) in the mitral position in a patient presenting in pulmonary edema; in addition, a large left atrial thrombus is sitting in the posterior aspect of the left atrium. The onset of symptoms may be gradual or sudden, and its incidence does not vary significantly Figure 24-14 TEE, horizontal four-chamber view, demonstrating a flail cusp (FC) in a mitral stented bioprosthesis (A). The patient presented to the

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hospital with progressive dyspnea on exertion, orthopnea, and fatigue. Ten years earlier, his mitral valve was replaced with a Hancock bioprosthesis. B, The excised valve with one of the cusps flailed and the other two with signs of degeneration. LA, left atrium; LV, left ventricle; RA, right atrium.

538

Figure 24-15 Prosthetic valve thrombosis in a Beall valve. A, Parasternal long-axis view from a patient with a disc-in-cage prosthesis (c) in the mitral position. A large thrombus (th) is noted in the posterior left atrial (LA) wall. B, The excised valve with a large thrombus obstructing the disc motion. AO, aorta; RV, right ventricle.

among different mechanical valves, except when the valve is in the tricuspid position. The low flow rate through the right-sided chambers is the most likely predisposing factor for the thrombosis rate as high as 20%, [107] limiting the use of mechanical valves in this position. Echocardiography should focus on determining the range of occluder motion. Several views should be used to determine the plane of maximal excursion. Bileaflet valves present a unique problem because thrombosis can affect only one hemidisc (see Fig. 24-12) . TEE is a sensitive and accurate tool for diagnosing prosthetic valve thrombosis and for evaluating the efficacy of thrombolytic therapy in the emergency room.[107] [108] [109] [110] Although reoperation is frequently recommended in these patients, thrombolysis has been used many times in critically ill patients who are not otherwise candidates for reoperation. Emergent surgery for acute valve thrombosis has a perioperative mortality of 30% to 40%, with the risk linked to the preoperative New York functional class, status of the left ventricular systolic function by echocardiography, urgency of operation, and concomitant coronary artery disease.[111] [112] [113] Thrombolytic therapy is a logical alternative to surgery in these high-risk patients. Numerous reports of the use of thrombolytics in acutely thrombosed mechanical valves have been published mostly in the form of case reports. [107] [109] [110] Table 24-7 includes the four largest series, representing nearly 90% of the total patients so far reported.[114] [115] [116] [117] As can be appreciated, the success rate is 81%; however, there are unavoidable complications including systemic emboli in 18% and an overall mortality rate of about 15%. In clinically stable patients with stuck leaflets and no

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high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence.[117] The best thrombolytic regimen is yet to be established, but streptokinase has been the most commonly used. For patients with high-risk (i.e., large) thrombus, valve replacement is clearly indicated unless the surgical risk is prohibitive. Thromboembolism Despite the routine use of anticoagulants in patients with mechanical valves, thromboembolism remains a major cause of morbidity and mortality. The incidence of thromboembolic episodes, however, has been significantly reduced with anticoagulation to between 1% and 4% per patient per year, and the risk of serious bleeding on anticoagulation is between 1% and 5% per patient per year.[118] [119] [120] According to the two largest trials, there is no difference in embolization with stented bioprosthetic versus adequately anticoagulated mechanical valves.[118] [120] In the decision of valve replacement, one must consider underlying risk factors such as prior thromboembolism, atrial fibrillation, significant left ventricular dysfunction, left atrial enlargement, left atrial appendage thrombus, and hypertension. The single most attractive advantage of bioprostheses is that in most cases anticoagulation is not needed. The increased risk of reoperation noted with stented bioprostheses, however, is a high price to pay for the reduced risk of bleeding through avoiding anticoagulation. Newer tissue valves such as nonstented bioprostheses and homografts may prove to be durable and yet enjoy the benefit of avoiding anticoagulation. An interesting observation described with TEE is fibrin strands. [121] Fibrin strands are commonly located on the atrial aspect of mitral prostheses or on the ventricular aspect of aortic prostheses. As illustrated in Figure 24-16 , their appearance is that of thin structures a few millimeters in length moving independently from the leaflets. Fibrin strands should be distinguished from vegetations or thrombi by their chaotic movement in and out of the imaging plane. They are more commonly seen on mechanical valves, but they also have been reported on tissue valves, and they have been associated with a higher incidence of embolic events.[122] [123] In a study by Isada et al,[122] 539

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TABLE 24-7 -- Combined Data for Patients with Left-Sided Prosthetic V Thrombosis Undergoing Thrombolytic Therapy Complications

Deaths

No. of Valve Clinical Reference Patients Location Success EMB HEM SURG TOTAL SURG TH Witchitz 12 8M/4A 69% 0 2 5 3 2 [114] et al Lorient 26 15M/11A 89% 5 0 4 4 2 Roudaut et al[115] 12 12M 83% 4 3 2 0 1 Shapira et [116] al Özkan et 89% 1 3 0 1 0 36 * 28M/8A [117] al Total 86 63M/23A 82% 10 8 11 8 5 A, aortic; Emb, embolic; Hem, hemorrhagic; M, mitral; Surg, surgical; th thombotic or thromboembolic. *36 episodes in 32 patients.

fibrin strands were found in 15 (18%) of 83 prosthetic mitral valve patients, and of those 15 patients, 8 (53%) had embolic events compared with 12 (18%) of 68 patients without strands. In contrast, fibrin strands have also Figure 24-16 (color plate.) TEE, horizontal four-chamber view, demonstrating fibrin strands (arrows) on the atrial side of a St. Jude Medical prosthesis (A). Chaotic movement of these structures in and out of the imaging plane characterizes real-time imaging. LA, left atrium; RA, right atrium; RV, right ventricle. Mild mitral regurgitation is noted in the medial aspect of the prosthesis.

been detected in otherwise normal prosthetic valves.[121] Further studies are needed to determine the clinical significance of fibrin strands before clinical decisions are made based solely on their presence. Endocarditis

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Prosthetic valves are at a high risk for endocarditis because of their foreign material and abnormal flows. Prosthetic valve endocarditis carries a significant morbidity and mortality. Older series reported a mortality rate as high as 75% with early endocarditis (<60 days) and 45% with late endocarditis (>60 days). In a more recent study evaluating echocardiographic findings and their relation to morbidity and mortality,[124] the presence of an infected prosthetic valve was a major risk factor for death. Five of 11 deaths related to endocarditis occurred in patients with prosthetic valves. The annual rate for late prosthetic endocarditis is estimated at 0.5% per year. [13] [19] , [118] , [120] According to the Veterans Cooperative[118] and the Edinburgh study,[120] there is no significant difference of endocarditis between mechanical and stented bioprosthetic valves; however, when compared with native valves, prosthetic valve endocarditis is more likely to be associated with ring abscess, conduction abnormalities, and a more grave prognosis. [125] Vegetations typically appear as irregular masses of echoes attached to the valve components commonly moving with the blood path. On tissue valves vegetations usually result in leaflet destruction, whereas on mechanical valves they may interfere with the occluder mechanism, resulting in stenosis, regurgitation, or both. Large vegetations (>10 mm) are associated with increased embolic complications.[126] , [127] Figure 24-17 shows a TEE at the midesophageal level in a septic patient with a stented bioprosthesis in the aortic position. The large echodense mass seen within the left ventricular outflow tract is consistent with a vegetation. Differentiation of vegetation from thrombus may be difficult and often impossible. An important hint is that endocarditis more commonly is associated with regurgitant lesions, whereas thrombosis more commonly is associated with stenotic lesions. Either condition, however, can be seen as mobile echodense masses. Thus, such separation primarily should be based on the clinical presentation and bacteriologic results. Rarely, both complications 540

Figure 24-17 TEE at the midesophageal level from the transverse (T) and longitudinal (L) views in a septic patient with a stented bioprosthesis in the aortic position. A large echodense mass in the left ventricular outflow tract is clearly seen (arrows). LA, left atrium; LV, left ventricle; RA, right atrium, RVOT, right ventricular outflow tract.

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may be present in the same valve. Figure 24-18 corresponds to a midesophageal view in a septic patient with a St. Jude Medical valve in the mitral position and a bioprosthesis in the tricuspid position. A large vegetation and a thrombus can be seen on the atrial aspect of the mitral valve. Early and accurate identification of septic complications TABLE 24-8 -- Sensitivity (Sens) and Specificity (Spec) of TTE versus TEE for the Diagnosis of Vegetations and Associated Abscesses in Patients with Endocarditis TTE

Reference Mugge et al (1989)[127] * Taams et al (1990)

No. of Patients Studied 105

No. of Patients with PVE 25

SENS (%) 58

33

12

36

118

34

28

TEE

SPEC SENS SPEC (%) (%) (%) ‡ 90 ‡ 100 100 100

[128] *

Daniel et al (1991)

99

87

95

[129] †

PVE, prosthetic valve endocarditis; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *Identification of vegetations. ‡Insufficient data available, but smaller studies have reported specificity of TEE at 100%. †Identification of abscesses.

Figure 24-18 TEE at the midesophageal level from the transverse view in a septic patient with a St. Jude Medical valve in the mitral position and a stented bioprosthesis in the tricuspid position. A large vegetation (veg) and a thrombus (th) are clearly identified within the left atrium. LV, left ventricle; RA, right atrium; RV, right ventricle.

in patients with prosthetic valves have a significant impact on the decisionmaking process. TEE has dramatically improved the diagnostic accuracy in detecting vegetations, abscesses, and other complications associated with

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prosthetic valve endocarditis. [127] [128] [129] [130] Studies comparing TTE and TEE have included both native and prosthetic valves in their analysis. Table 24-8 lists studies comparing the two modalities in which patients with prosthetic valves were included. Although prosthetic valves are not analyzed separately, the data clearly favors TEE as a superior imaging modality; therefore, TEE should be performed routinely in patients with suspected prosthetic valve endocarditis, most notably in patients who fail to improve on therapy. Development of a perivalvular abscess is associated with a grave prognosis and indicates the need for aggressive medical and surgical therapies.[131] [132] Clinical findings suggestive of an abscess include persistent sepsis despite appropriate antibiotics, new or worsening heart failure symptoms, and development of first-degree atrioventricular block or incomplete right bundle branch block. Figure 24-19 illustrates a range of possible outcomes of a prosthetic valve abscess. Rupture may occur into adjacent structures, including the pericardial sac creating cardiac 541

Figure 24-19 A to D, Clinical, electrocardiographic, and echocardiographic characteristics in septic complications of mechanical valves. AV, atrioventricular; CHF, congestive heart failure; RBBB, right bundle branch block.

tamponade; however, a rather common outcome is the development of perivalvular dehiscence with a tunnel communicating the aorta with the left ventricular outflow tract and consequently severe perivalvular regurgitation. Emergent surgical treatment may be a lifesaving procedure in these acutely ill patients. Echocardiographic findings of perivalvular abscess include valve rocking, periaortic root thickening, or perivalvular echolucency.[133] As noted in Table 24-8 , identification of an abscess is very difficult from TTE; therefore, TEE is mandatory when this complication is clinically suspected. In addition, fistulous tracts connecting the perivalvular space with adjacent structures can be imaged and tracked down with color flow. Figure 24-20 represents the mid- and upper esophageal images in a septic, critically ill patient with a St. Jude Medical aortic prosthesis who presented to the emergency room with acute aortic insufficiency and pulmonary edema; a large perivalvular abscess is clearly noted.

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Patient-Prosthesis Mismatch The term patient-prosthesis mismatch refers to the clinical setting in which the prosthesis is structurally normal but the hemodynamic data are consistent with a greater stenosis than expected for the valve type and size. [134] [135] The mismatch occurs because the valve area is relatively insufficient to fit the patient's body surface area. A given valve area perfectly acceptable for a small relatively inactive subject may be inadequate for a larger physically active individual. This problem is usually seen in patients with small aortic annulus sizes and in whom the valve replacement was performed because of native valve stenosis rather than regurgitation.[134] From the clinical point of view, the patient fails to improve or may even be symptomatically worse. The long-term implications of this condition are not known. After successful aortic valve replacement, regression of cardiac hypertrophy is commonly detected. Failure to regress 6 months after surgery may be a subtle indication that residual aortic stenosis is present and that the hemodynamic burden persists.[136] [137] In some patients inadequate hemodynamics may be apparent only at higher cardiac output stages (i.e., during exercise). For patients with exertional symptoms suggesting high valve resistances without evidence of a primary valve dysfunction, stress echocardiography (see later) should be considered. The diagnosis of patient-prosthesis mismatch requires exclusion of an intrinsic valve dysfunction, which further emphasizes the need for a baseline postoperative study. Prosthetic Aortic Stenosis The initial suspicion of prosthetic valve stenosis may be the incidental finding of abnormally high flow velocities detected during a routine examination. This finding should prompt careful inspection from the parasternal long- and short-axis views to determine possible causes. In addition to thrombus formation, obstruction also can occur from gradual ingrowth of fibrous tissue called pannus formation. An encapsulated perivalvular abscess may reduce the outflow tract area leading to stenosis. Figure 24-21 shows images from a patient with a homograft and a sterile perivalvular cavity reducing the effective orifice area. In the absence of symptoms and if there is normal valve motion otherwise, close follow-up is probably appropriate. Alternatively, stress echocardiography may be necessary to unmask a truly symptomatic stenosis or to address the patient's or referral physician's concerns. If the valve area calculated from TTE data

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is markedly reduced, 542

Figure 24-20 TEE in a septic patient with a St. Jude Medical aortic valve. A, Partial dehiscence and a large abscess cavity (arrow). B, Cross-sectional view of the same pathology. The abscess cavity is composed of echodense and echolucent material (arrow). AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium.

we commonly reassess the aortic valve area (continuity equation) by combining the diameter of the left ventricular outflow tract accurately determined by TEE at the upper-midesophageal level with the transthoracic velocity time integrals obtained during the same setting. Prosthetic Mitral Stenosis Valve area should be routinely calculated from the pressure half-time or the continuity equation (or both) in patients with suspected prosthetic mitral stenosis. Although an E wave velocity greater than 2 m per second may be indicative of prosthesis stenosis, increased velocities in the absence of a prolonged pressure half-time may be a result of prosthetic regurgitation.[2] Color flow can aid in aligning the Doppler beam parallel to the mitral inflow in obtaining the most representative Doppler signal. Mean valve gradient should be combined with pressure half-time or flow volume determination to differentiate prosthesis stenosis from increased transvalvular volume. As noted earlier, TEE is a very useful tool for detecting thrombosed mitral prosthesis and guiding thrombolytic therapy; thus, TEE should always be performed in patients in whom stenosis is suspected. Prosthetic Aortic Regurgitation The approach to grading prosthetic regurgitation is similar to that of native valves and involves evaluation of several echo-Doppler indices. As with native valve regurgitation, ventricular size and function are important clues to the severity of regurgitation. Normal left ventricular internal dimensions is incompatible with severe chronic Figure 24-21 TTE of a patient with stenosis of an aortic homograft. A, Parasternal long-axis view showing an encapsulated antibiotic-sterilized

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cavity (C), which reduces the outflow tract diameter (LVOT) in half (arrows). B, Continuous wave Doppler from the five-chamber view in the same patient with elevated velocities up to 4.0 m/sec, maximal gradient of 64 mm Hg, and a mean gradient of 34 mm Hg. The continuity equation valve area was estimated at 0.7 cm2 . LA, left atrium.

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aortic regurgitation. Jet height and area from the short-axis view have been compared with angiographic grading in native valve regurgitation with excellent correlations of 0.93 and 0.91, respectively.[138] [139] In our laboratory we have found the parasternal long-axis view a more useful view to assess the jet area in relation to the left ventricular outflow tract area. Eccentric valvular or perivalvular jets may overestimate the severity of prosthetic regurgitation because they may be directed perpendicular to the outflow tract, occupying a larger portion of the ventricular outflow tract area. The apical five-chamber view should also be used to determine jet characteristics. The pressure-half time can be helpful in differentiating chronic from acute regurgitation. In general, acute (commonly severe) aortic regurgitation has a rapid slope decay indicative of acute elevation of left ventricular pressures at end-diastole. Although highly specific, this finding is poorly sensitive because the decay slope may be altered by changes in diastolic function, particularly ventricular compliance, heart rate, and rhythm. Thus, patients with severe chronic aortic regurgitation and a compliant left ventricle may have an aortic-ventricular diastolic pressure slope similar to patients with milder degrees of aortic regurgitation. Consequently, in many patients the Doppler diastolic slope decay helps in differentiating acute from chronic regurgitation, but not severe from moderate regurgitation. The intensity of the continuous wave Doppler signal may help in assessing severity of regurgitation. In patients with severe regurgitation, the signal intensity of the forward and regurgitant flows are similar. Unfortunately, such estimation is subject to wide interobserver variations. In addition, signal intensity depends highly on the specific gain settings on different ultrasound systems and even in the same machine. Thus, in our laboratory an intense Doppler signal of aortic insufficiency is a hint that the severity of regurgitation is more than mild. The amount of flow reversal in the descending thoracic aorta also has been correlated with severity. Normal flow reversal in the ascending aorta is confined to the early part of diastole,

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whereas flow reversal that persists throughout diastole is seen in patients with severe regurgitation.[3] [81] TEE may provide important etiologic information such as primary mechanical failure (i.e., flail cusp), ring dehiscence, vegetations, or abscess formation with a paravalvular fistula (see Fig. 24-19D) . Additionally, TEE offers an excellent visualization of the ventricular outflow tract area for severity assessment based on the relation of jet area and ventricular outflow tract area. Finally, evaluation of the ascending aorta for aneurysmal dilation or dissection should be part of the TEE examination in these patients. Prosthetic Mitral Regurgitation Assessment of mitral regurgitation by TTE is problematic because reverberations from the metallic material of the prosthesis commonly obscure the left atrium. This problem is less noticeable with bioprostheses. Nevertheless, the common practice in our laboratory is to turn to TEE every time there is clinical or TTE suspicion of pathologic mitral regurgitation, regardless of the type of prosthesis. Color Doppler demonstrating flow convergence or a clearly visible proximal isovelocity surface area on the ventricular aspect of the valve is suggestive of severe regurgitation. The maximal area of the acceleration signal has been used to assess severity of mitral regurgitation.[140] Similar to aortic insufficiency, the intensity of the continuous wave Doppler signal is related to severity; the more intense the signal, the more severe the regurgitation.[71] Significant regurgitation has a density similar to the antegrade flow signal.[141] A recent evaluation of TTE for evaluating prosthetic mitral regurgitation compared proximal isovelocity surface area, intensity of the Doppler signal, and color Doppler jet within the left atrium.[142] Flow convergence was more sensitive but less specific for predicting significant prosthetic mitral regurgitation. Doppler indices used for severe native valve regurgitation also may be helpful in prosthesis regurgitation, such as increased E wave velocity (>2 m/sec), increased mean gradient (>5 to 7 mm Hg), short pressure half-time (<100 m/sec), and increased time velocity integral (>40 cm).[6] [142] [143] Unexplained, worsening, or new pulmonary hypertension may be indicative of significant regurgitation. TEE has substantially improved the diagnostic accuracy of the jet characteristics for determining severity and etiology of prosthetic regurgitation. [4] [144] Remember that color Doppler is a measure of velocity and not of volume, and although the jet area may be relatively small,

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eccentric jets may result from severe regurgitation, particularly when they wrap around ("hug") the left atrial wall (Fig. 24-22) . An eccentric jet of severe mitral regurgitation loses momentum and velocity as it contacts the atrial wall despite a large volume, a phenomenon known as the Coanda effect.[145] In our laboratory, we use an eccentric jet as an evidence of severity. In fact, most cases of eccentric regurgitation hugging the lateral wall of the left atrium Figure 24-22 (color plate.) TEE from the transverse plane (0 degrees) illustrating a large, eccentric jet of severe mitral regurgitation.

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enter into one of the pulmonary veins or into the left atrial appendage, confirming severe mitral regurgitation. Prosthetic valve dehiscence, that is, a separation of the prosthetic sewing ring from the native fibrous ring, is caused by detachment of the retaining sutures. Careful TEE evaluation of the annulus at the midesophageal and transgastric levels can reveal a dropout of echoes; when color Doppler is applied, an eccentric jet may become obvious. Detection of valve dehiscence is important because it usually means severe regurgitation requiring surgical repair or replacement. Figure 24-23 is a set of TEE images illustrating a patient with a Hancock bioprosthesis in the mitral position with dehiscence and severe eccentric regurgitation. The morphology of the pulmonary vein Doppler waveform is dependent on both volume of regurgitation and left atrial properties. Pulmonary vein flow characteristics have been useful in assessing severity of native mitral valve regurgitation. Typically, there is loss of the systolic wave amplitude and eventually reversal of systolic flow as the Figure 24-23 (color plate.) TEE showing dehiscence in a stented mitral bioprosthesis with perivalvular regurgitation. A and C, The dehiscent site (arrows) is seen as a dropout of echoes at the annular attachment. B and D, Eccentric severe paravalvular regurgitation is seen through the dehiscence. LA, left atrium; LAA, left atrial appendage; LV, left ventricle; RA, right atrium; RV, right ventricle.

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severity of regurgitation increases from moderate to severe. These changes should not be interpreted as an absolute measure of regurgitant severity, however. In vivo models suggest that pulmonary venous flow reversal is more likely in acute versus chronic mitral regurgitation because the atrium is less compliant and has a smaller initial volume.[146] In addition, characterization of the pulmonary vein flow in prosthetic mitral regurgitation is lacking, and extrapolation of the data from native to prosthetic valves has not been documented.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Stress Echocardiography in Assessing Prosthetic Valve Function In patients with suspected prosthetic valve dysfunction, one may encounter symptomatic patients in whom the 2D and Doppler imaging indicates normal valve function at rest. Under these circumstances, exercise echocardiography may elicit abnormal hemodynamics indicating valve 545

TABLE 24-9 -- Prosthetic Valve Exercise Doppler Hemodynamics No. of Patients Aortic Position CarpentierEdwards MedtronicHall MedtronicHall St. Jude Medical Mitral Position Björk-Shiley

Valve Sizes (mm)

Mean Gradient (mm Hg) * EXERCISE INCREASE † REST (%)

4 21

15 ± 3

21 ± 3

70

14 21

15 ± 4

24 ± 6

80

14 21–27

9±4

15 ± 6

83

17 21–27

11 ± 4

18 ± 7

81

11 25–31

4.9 ± 1.8

10.3 ± 2.9

100

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6 28–32

4.6 ± 12.6 ± 130 1.2 4.1 St. Jude 17 26–32 2.5 ± 5.1 ± 3.5 102 Medical 1.4 Medtronic15 26–32 3.0 ± 7.0 ± 2.9 116 Hall 1.1 Data from Tatineni et al,[147] Wiseth et al,[148] and Halbe et al.[150]

*Mean ± SD. †Exercise protocols used were symptom-limited treadmill and upright or supine bicycle.

dysfunction or patient-prosthesis mismatch. In our laboratory, we prefer supine bicycle ergometry over treadmill because serial hemodynamic data can be obtained at different exercise stages. Normal hemodynamics with stress in these patients excludes valve dysfunction as the cause of the patient's symptoms. Valve gradient, valve area, degree of regurgitation, and systolic pulmonary artery pressure can all be calculated at rest and at peak stress (or immediately afterward). Despite its clinical potential, relatively few stress echocardiographic studies in patients with suspected prosthetic valve dysfunction have been published.[61] [147] [148] [149] [150] Table 24-9 summarizes data available regarding valve gradients at rest and with exercise. Dobutamine provides an excellent alternative for evaluating valve hemodynamics when the patient is unable or unwilling to undergo treadmill exercise or bicycle ergometry.[151] In our laboratory we use a protocol similar to that for ischemic heart disease; that is, we attempt to reach at least 85%, or ideally 90%, of the maximal predicted heart rate according to the patients' age and gender. We start with IV administration of dobutamine at 10 µg/kg per minute and increase sequentially every 3 minutes to 20, 30, and 40 µg/kg per minute. If the Doppler signal intensity of tricuspid regurgitation is weak because of trivial or mild regurgitation, we routinely add a small amount of diluted Optison to enhance signal intensity, allowing calculation of systolic pulmonary artery pressure. In patients with single tilting disc prostheses in the aortic position, peak and mean gradients are higher with the dobutamine stress echocardiography compared with symptom-limited treadmill exercise.[152]

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Evaluation of the patient with decreased left ventricular systolic function and possible prosthetic aortic stenosis is problematic. In 24 adults with native aortic valve stenosis (area ≤ 0.5 cm2 /m2 ), mean gradient less than 30 mm Hg, and ventricular dysfunction (ejection fraction ≤ 0.45), deFilippi et al[153] performed echocardiography at baseline and at peak dobutamine stress to distinguish severe fixed aortic stenosis from flow-dependent (relative) aortic stenosis. Three hemodynamic subsets were identified: (1) fixed aortic stenosis with increased cardiac output and transvalvular gradient and no change in valve area; (2) relative aortic stenosis with increased valve area but no change in gradient; and (3) lack of contractile reserve with indeterminate stenosis because of inability to increase cardiac output.[153] Theoretically, a similar study may be applicable, although not yet proved, in patients with severe ventricular dysfunction and prosthetic stenosis of undetermined severity.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Three-Dimensional Echocardiography in Assessing Prosthetic Valve Function Current echocardiographic approaches to determination of effective orifice area are based on flow characteristics. Flow characteristics, however, also depend on several factors in addition to the actual orifice area, including ventricular compliance, systolic function, and loading conditions. A classic dilemma is the patient with a mechanical aortic valve with high flow velocities detected in a routine Doppler examination. Is this a normal finding? Is it consistent with pannus formation and therefore with some stenosis? Is this a patient-prosthesis mismatch? An echocardiographic technique that actually allows us to visualize the orifice size would likely improve our diagnostic abilities. Three-dimensional echocardiography involves the acquisition and display of cardiac structures in three spatial dimensions allowing their visualization and analysis as they move in time and space. Figure 24-24 illustrates a commonly used rotational scanning mechanism in which the transducer is rotated at 3-degree increments up to 180 degrees. Dynamic 3D imaging may provide a more realistic representation of prosthetic morphology than 2D images. Recent advances in ultrasound equipment, digital storage, and display techniques have made 3D clinically feasible; however, the clinical potential of 3D imaging has just begun to be recognized, and there are no published data on the use of 3D technology in assessing prosthetic valve function. Figure 24-25 depicts a 3D reconstruction of a St. Jude Medical valve performed in our laboratory. The two hemicircular lateral orifices and the central rectangular orifice are clearly indicated. Mitral annular rings have been reconstructed with 3D 546

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Figure 24-24 Left, The rotational mechanism for acquisition of two-dimensional images at 3-degree intervals from 0 to 180 degrees. Right, The twodimensional images are piled up one after another, gated by the electrocardiogram. Figure 24-25 Three-dimensional reconstruction of a St. Judge Medical valve in the mitral position as seen from the left atrium or "surgeon's view." The semicircular orifices (curved arrows) and the rectangular orifice (straight arrow) are seen.

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technology.[153] Dall'Agata et al[154] used TEE to analyze mitral valve rings in 19 consecutive patients who underwent annuloplasty because of severe regurgitation. Fifteen patients received a Cosgrove-Edwards (flexible) ring and four received a Carpentier (rigid) ring. Imaging acquisition used the rotational technique immediately after the operation and was considered to be adequate in 17 of 19 patients. The authors were able to differentiate values from end-systolic to end-diastolic orifice areas (4.2 ± 1.5 cm2 versus 4.8 ± 1.5 cm2 ; P < .0001) in the Cosgrove-Edwards ring, and no significant change in the Carpentier ring.[154]

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551

Chapter 25 - Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves William A. Zoghbi MD

The surgical approach to treating diseases of the aorta and cardiac valves has evolved dramatically over the past two decades. Concurrent with these developments, echocardiography and particularly Doppler techniques have been refined, allowing a better definition of cardiac structures and flow dynamics. Furthermore, transesophageal echocardiography (TEE) has improved the diagnostic capabilities of sonographic techniques by providing superior imaging of the aorta and cardiac structures, thus increasing the diagnostic impact of echocardiography in patients with diseases of the aorta and cardiac valves. A variety of complications, however, may occur in patients undergoing surgery on the great vessels and cardiac valves. These complications may occur early or late in the postoperative period and include infection, thrombosis, obstruction or dehiscence of prosthetic material, and progression of the underlying disease disorder, particularly in diseases of the aorta. Recognition of diseases of the aorta and of the infectious complications and dysfunction of prosthetic valves has been addressed elsewhere in detail ( see Chapter 23 and Chapter 24 ). This chapter focuses

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on unusual complications following surgery on the aorta and cardiac valves and the role of echocardiographic techniques in assessing these complications.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Unusual Complications Following Surgery on the Aorta Pseudoaneurysms of Composite Aortic Grafts Clinical Setting

In patients with aortic aneurysm or those with dissection of the aortic root involving the aortic sinuses and aortic valve, which are not amenable to repair, replacement of the aortic root with a composite graft is now widely accepted. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] First reported, in 1968, by Bentall and De Bono,[1] and more recently modified since then, [5] , [6] [10] [11] [12] [13] this surgical procedure has significantly prolonged the life expectancy of patients affected with annuloaortic ectasia.[5] [9] [14] Knowledge of this procedure, its variations, and complications is crucial for the echocardiographer, particularly because echocardiography with Doppler has emerged as a powerful diagnostic modality in assessing the function and complications of composite aortic grafts. The original Bentall procedure consists of replacing the aortic root and valve with a composite aortic graft 552

(ascending aortic graft and prosthetic aortic valve). The coronary arteries are reimplanted onto the graft, and the aorta is wrapped around the graft to improve hemostasis.[1] [2] [3] [4] [15] Among the complications of composite aortic grafts is the development of a pseudoaneurysm of the ascending aorta. This pseudoaneurysm occurs secondarily to dehiscence of the suture line at the aortic annulus, the coronary ostia, or the distal graft anastomosis. In patients with composite grafts who underwent the original Bentall procedure, this potentially lethal complication was reported to occur at a rate of 7% to 25%. [3] [16] [17] [18] [19] Modifications of the original method have since been proposed to decrease the incidence of pseudoaneurysm

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formation.[2] [5] [6] [11] [12] [13] In 1981, Cabrol et al[2] modified the operation by introducing a second tube graft connecting the coronary ostia and the main ascending aortic graft (Fig. 25-1) . In 1991, Kouchoukos and co-workers[5] showed that the "open," or "button," technique for reimplantation of the coronary arteries led to a lower incidence of pseudoaneurysms. With the present modifications, the incidence of pseudoaneurysm formation has decreased to less than 6%.[5] [7] [8] [9] [12] [19] [20] [21] [22] The clinical symptoms associated with pseudoaneurysm formation vary. Whereas some patients have nonspecific symptoms or may be completely asymptomatic, other patients may be severely limited by dyspnea and fatigue. Given the possibility of aortic rupture, early diagnosis of aortic pseudoaneurysm is therefore essential. Echocardiography with Doppler and, more recently, TEE have had a significant impact on the detection of pseudoaneurysms and the evaluation of patients with composite grafts.[18] [23] [24] [25] [26] [27] [28] [29] [30]

Figure 25-1 (color plate.) Diagram of the surgical reconstruction of the aortic root in a patient with ruptured aortic dissection, using a composite aortic graft (modified Cabrol technique). The native aortic root is excised and replaced with a composite graft. A tube graft connects the aortic graft to the left main coronary artery. A vein graft (dark blue) was used in this case to bypass a stenosed right coronary artery. (Courtesy of Dr. Hazim J. Safi.) Echocardiographic and Doppler Findings

A normal composite aortic graft is visualized with echocardiography as an echo-dense ascending aortic root, with a prosthetic valve in the aortic position. The maximal diameter of the composite graft depends on the size of the graft. In 27 patients with normal composite grafts evaluated in the author's institution, the diameter of the ascending aorta ranged from 3.2 to 5 cm (mean of 4.2 cm).[18] In patients whose native aorta wrapped the graft, a small echo-free space between the graft and the wall of the aorta was seen in most patients (80%) and usually was small, ranging from 0 to 1.4 cm (mean 0.6 cm).[18] In all cases of normal composite graft, Doppler examination showed no evidence of flow in this small echo-free space and the presence of only trivial aortic insufficiency. Echocardiography can provide important diagnostic information about the presence of the pseudoaneurysm and the site of dehiscence of the surgical anastomosis.[18] [31] [32] [33] The identification of an enlarged ascending aorta with an echo-free space around the aortic graft should prompt investigation

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for the presence of a pseudoaneurysm. Other considerations include a hematoma without pseudoaneurysm or, depending on the clinical setting, the presence of graft infection with abscess formation. The space around the graft may contain varying amounts of echo-dense debris or thrombus. A pseudoaneurysm is diagnosed as an enlarged ascending aorta with an echofree space between the aortic graft and the wall of the aorta, along with the demonstration of flow into the echo-free space (Fig. 25-2) .[18] [31] [32] In a series of patients with pseudoaneurysms diagnosed in the author's institution, [18] 553

Figure 25-2 (color plate.) Echocardiographic and Doppler findings using transthoracic echocardiography in a patient with a large pseudoaneurysm of the ascending aorta complicating a composite graft. The dehiscence was at the aortic annulus anastomosis. A and C show the extent of the pseudoaneurysm as delineated by the arrows in short-axis (A) and long-axis (C) views. The origin and extent of the systolic jet into the pseudoaneurysm are shown in B and D in the same image planes as in A and C. During diastole (E), blood converges from the pseudoaneurysm toward the aortic annulus and enters the left ventricle (arrow) through the dehiscence, mimicking aortic insufficiency. The corresponding angiographic findings are shown in Figure 25-9 . GR, aortic graft; LA, left atrium; LV, left ventricle; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

the maximal diameter of the ascending aorta ranged from 6 to 14 cm. The maximal echo-free space between the aortic graft and the wall of the ascending aorta ranged from 2 to 7 cm. This space may be eccentric or concentric around the graft. Although most cases of pseudoaneurysms report more than 2 cm of echo-free space surrounding the graft, the demonstration of flow into the space outside the graft is essential for the diagnosis, irrespective of the size of the echo-free space. Once a pseudoaneurysm is suspected, special attention is directed to imaging the ascending aorta, aortic root, the plane of the prosthetic valve, and the coronary ostia from the left and right parasternal and suprasternal windows. In cases of pseudoaneurysms, color-flow Doppler imaging frequently demonstrates evidence of a pulsatile flow jet into the echo-free space between the graft and the wall of the ascending aorta (see Fig. 2) . This finding confirms the entity of pseudoaneurysm, as opposed to the mere presence of blood or fluid collected around the graft (Fig. 25-3) . In

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the author's experience, however, transthoracic color-flow examination may not identify flow in the echo-free space in some patients. In these cases, transesophageal examination clearly demonstrates flow into the pseudoaneurysm (Fig. 25-4) . This limitation is the result of the lower resolution and sensitivity of surface echocardiography combined with posterior shadowing from the graft and aortic prosthesis. Transthoracic and transesophageal echocardiography do provide complementary information regarding the status of a composite aortic graft. If any suspicion arises about the presence of a pseudoaneurysm, a TEE is clearly indicated for further evaluation of the abnormality. Following is a description of Doppler echocardiographic findings observed with composite graft pseudoaneurysms.

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Figure 25-3 Transesophageal horizontal plane demonstrating a large hematoma (arrows) surrounding a composite aortic graft (G) in a patient early after operation. There was no flow detected around the graft by Doppler echocardiography at any level. Th, Thrombus. The hematoma was secondary to postoperative bleeding complications. Aortic Annulus Dehiscence

In cases of dehiscence at the aortic annulus anastomosis, with ensuing communication between the left ventricle and the pseudoaneurysm, colorflow Doppler identifies a systolic jet arising from the paraprosthetic valve area, directed cranially into the pseudoaneurysm ( see Fig. 25-2 and Fig. 25-4 ). Because the jet frequently is eccentric, the imaging plane showing the flow jet in the long axis of the aortic root usually is lateral or medial to the plane showing the aortic graft. Thus, the flow jet and aortic graft may not be seen in the same longitudinal plane (see Fig. 25-2) . The short-axis view at the level of the prosthetic aortic valve demonstrates the jet arising in the Figure 25-4 (color plate.) Transesophageal echocardiographic frames and corresponding color Doppler systolic frames in a patient with composite graft pseudoaneurysm. The transthoracic examination in this patient did not demonstrate flow in the pseudoaneurysm. The upper panels are at the level of the ascending aorta; the lower panels are at the prosthetic aortic valve level. The dehiscence at the aortic annulus is depicted by a

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straight arrow. Color flow Doppler demonstrates flow into the pseudoaneurysm. GR, aortic graft; LA, left atrium; LV, left ventricle; PrV, prosthetic valve; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

paravalvular area and oriented into the pseudoaneurysm. Short-axis views from a more cranial angle demonstrate the orientation of the jet in the pseudoaneurysm in relation to the aortic graft. These considerations apply for both transthoracic and TEE imaging ( see Fig. 25-2 and Fig. 25-4 ). Generally, detection of the dehiscence and flow into the pseudoaneurysm is much easier with TEE than with the transthoracic approach. In most cases of dehiscence at the aortic annulus, continuous-wave Doppler views from the apical window demonstrate two distinct systolic jets: one coursing through the prosthetic valve and another coursing through the left ventricular-pseudoaneurysm communication (Fig. 25-5) . In the author's experience, the maximal velocity and derived pressure gradient through the communication have been higher than those through the prosthesis.[18] The systolic jet through the dehiscence frequently starts before the opening click of the prosthetic valve, and its duration is usually longer than the ejection time through the valve (see Fig. 25-5) . In all cases of dehiscence of the aortic annulus, a diastolic jet is seen in the left ventricular outflow, simulating valvular aortic insufficiency. In these cases, concomitant aortic insufficiency arising from within the valve usually cannot be excluded with confidence; however, with TEE, the mechanism of regurgitation can be much better defined. Continuous-wave Doppler recording of these diastolic jets also shows a short pressure half-time, mimicking severe aortic insufficiency. In some cases, an abrupt termination of diastolic flow before the prosthetic aortic-valve click at the onset of early systolic flow through the communication supports the conclusion that this regurgitation is not occurring through the aortic valve (see Fig. 25-5) . Coronary Artery Dehiscence

Coronary artery dehiscence is diagnosed by color-flow Doppler as a jet arising from the level of the coronary ostia or coronary anastomosis and directed into the pseudoaneurysm. Dehiscence 555

Figure 25-5 Continuous wave Doppler from the apical window of the

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patient with aortic annulus dehiscence shown in Figure 25-2 . Recordings are obtained from the same position on the chest wall, with minor change in angulation. Compared with the systolic jet velocity through the prosthetic aortic valve, the systolic jet through the ventricular-pseudoaneurysm communication has a higher maximal velocity (Vmax), is of longer duration, and starts (oblique arrow) before the first click of the prosthetic valve (horizontal arrow). The diastolic regurgitant jet into the left ventricle has a steep deceleration slope and ends before the first systolic aortic valve click (upper panel, straight arrow) at the time of onset of systolic flow into the pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

usually is easier to define in patients in whom the pseudoaneurysm is large because of the more defined spatial distribution of the jet. Various flow patterns may be recorded, as shown in Figure 25-6 . Whether the flow is predominantly systolic into the pseudoaneurysm or systolic and diastolic depends on factors such as the compliance of the pseudoaneurysm and whether a communication exists between the pseudoaneurysm and the left ventricle. Compression of the Composite Graft or Adjacent Structures

Compression of the graft may result from hematoma or pseudoaneurysm formation[27] and is most commonly observed with aortic annulus dehiscence. With two-dimensional echocardiography, pulsatile compression of the graft can be seen during systole (Fig. 25-7) , most likely because of the high pressure surrounding the graft and possibly a Venturi phenomenon occurring within the graft. Using continuous-wave Doppler, a high-velocity systolic jet can be recorded, a finding similar to that seen in an obstructed prosthetic aortic valve. Differentiation of the two entities may be difficult; however, visualization of the pulsatile compression of the graft provides a good assessment of the underlying condition. If the pseudoaneurysm is extensive, it may compress adjacent structures. Compression of the pulmonary artery with resultant pulmonary arterial stenosis was recently reported as a complication of a large pseudoaneurysm.[33] Role of Transesophageal Echocardiography

The use of TEE clearly is advantageous in the overall definition of complications of composite aortic grafts.[18] , [27] [30] [31] [32] [33] [34] For delineation of pseudoaneurysms, the aortic suture ring is clearly visualized with TEE, thereby enhancing the evaluation of dehiscence at this level with both echocardiography and Doppler techniques. Furthermore, the

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anastomosis of the coronary arteries to the aortic graft is better assessed. Evaluation of flow in the potential space between the graft and native wrapped aorta or fibrous tissue (in the case of excision of the native aorta) is improved. Dehiscence at the distal anastomosis of the aortic graft to the aortic arch remains difficult to assess because of limitations of imaging in this area; however, this type of dehiscence is the least frequent and rarely occurs alone. In cases of pseudoaneurysm formation secondary to endocarditis, TEE may detect vegetations that can further substantiate the diagnosis (Fig. 25-8) . In the absence of such a finding, however, exclusion of an infected graft based on echocardiographic examination, or based on any structural imaging alone, is difficult. Because of anterior 556

Figure 25-6 (color plate.) Examples of different velocity patterns observed by continuous wave Doppler in two patients with coronary artery dehiscence. In A, the color jet arising from the left main dehiscence is depicted in the parasternal long- (A1 ) and short- (A2 ) axes by a large arrow. In this patient with concomitant aortic annulus dehiscence, continuous wave Doppler (A3 ) shows increased systolic and diastolic velocities directed from the graft into the pseudoaneurysm. The patient in B has a sole dehiscence at the right coronary anastomosis depicted in short axis (B1 and B2 ). Continuous wave Doppler recording (B3 ) shows flow directed from the graft into the pseudoaneurysm in systole and flow reversal from the pseudoaneurysm into the graft in diastole (small arrows). GR, graft; LV, left ventricle; PA, pulmonary artery; PSA, pseudoaneurysm; RV, right ventricle. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

shadowing produced from the prosthetic valve and graft, an optimum assessment of the aortic root in composite grafts involves combined transthoracic and transesophageal studies. In cases of suspected pseudoaneurysm formation in which a collection of blood and thrombus is seen around the graft, and without demonstration of flow by transthoracic echocardiography or other imaging modalities, a transesophageal study is crucial in providing the diagnosis.[18] Other Imaging Modalities

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Several modalities have been suggested as diagnostic screens for the development of pseudoaneurysm after Figure 25-7 Right parasternal transthoracic echocardiographic images of composite graft pseudoaneurysm demonstrating systolic compression of the graft by the pseudoaneurysm. Gr, graft; PSA, pseudoaneurysm.

composite graft surgery, including chest radiography, computed tomography (CT), digital subtraction angiography, and more recently, magnetic resonance imaging (MRI).[3] [17] [35] , [36] Although chest radiography may warn of the possibility, its sensitivity and specificity for the diagnosis of pseudoaneurysm are poor. Computed tomography and MRI are currently recommended as diagnostic imaging modalities for the serial evaluation of composite grafts and progression of the underlying disease to other segments of the aorta. [10] As for diagnosing pseudoaneurysm, although CT scanning or MRI can provide the diagnosis of blood or fluid collection around the graft, whether this finding represents a mere collection of fluid around the graft or is the result of communication with the ventricle, coronary arteries, or aorta may not be adequately differentiated. Until recently, aortography was the most widely used method for diagnosis of pseudoaneurysms and was the primary diagnostic modality for further evaluation of fluid collection around the composite graft.[36] Aortography still is an excellent modality for diagnosing dehiscence of the composite graft at the coronary artery anastomosis and distal graft (Fig. 25-9) ; however, in cases of isolated dehiscence of the graft at the aortic annulus anastomosis, aortography has been found to completely miss the diagnosis of pseudoaneurysm.[18] [27] This is explained by the fact that in these cases, the pseudoaneurysm communicates only with the left ventricle; a contrast injection in the aortic root would therefore not opacify the left ventricle or the pseudoaneurysm. An example of such a case is 557

Figure 25-8 (color plate.) Transesophageal echocardiographic frames (left) and corresponding color Doppler systolic frames (right) in a patient with endocarditis and composite graft pseudoaneurysm secondary to aortic annulus dehiscence. The upper panels are at the level of the prosthetic valve; the lower panels are at the level of the left main coronary artery. Two large vegetations are depicted (top, arrows) near the site of dehiscence.

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Systolic flow into the pseudoaneurysm is shown, and the limits of the pseudoaneurysm are indicated (bottom, arrows). Gr, graft; LA, left atrium; LVO, left ventricular outflow; P, pseudoaneurysm; RV, right ventricle; Veg, vegetations. Figure 25-9 Aortograms of the thoracic aorta in two patients with pseudoaneurysm complicating composite aortic graft. A, The pseudoaneurysm around the ascending graft is opacified (arrows). B, Aortogram of the patient whose echocardiographic images are in Figure 252 . In this case with single aortic annulus dehiscence, the large pseudoaneurysm is not opacified. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.)

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presented in Figure 25-2 and Figure 25-9 . Echocardiography in these cases is superior to aortography in the detection of pseudoaneurysms. Because in most of these cases the prosthetic aortic valve is not crossed at catheterization, opacification of the pseudoaneurysm necessitates a left ventriculogram using the transseptal technique or the levo phase of a pulmonary angiogram. In cases with concomitant dehiscence at the coronary or distal graft anastomoses, or in those with coexisting aortic insufficiency, the pseudoaneurysm may be opacified with aortography. [18] Complications of Aortic Allografts for Replacement of the Aortic Valve and Aortic Root Clinical Setting

Allograft or homograft replacement of the aortic root also has provided an effective therapy for diseases of the aortic root and the aortic valve. [37] [38] [39] [40] Three general techniques for insertion have been used: subcoronary valve implantation, a mini- or inclusion-root implantation, and an aorticroot replacement. Compared with composite graft replacement of the aortic root, the use of an allograft is particularly helpful in recurrent complications of the aortic root, especially in the presence of infection. Aortic allografts, therefore, have been performed predominantly in patients with destruction of the aortic root resulting from endocarditis, in patients with congenitally narrowed or hypoplastic aortic roots, in patients with complications involving previous root replacement such as heavy calcifications, and in those for whom anticoagulation is contraindicated.

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Among the most commonly reported complications of aortic allografts are calcifications of the root, aortic regurgitation, and infectious complications occurring primarily in patients whose underlying indication for aortic root replacement was endocarditis. Similar to composite aortic grafts, reports of unusual complications include problems with anastomotic sites (dehiscence with pseudoaneurysm formation), problems with coronary artery anastomosis, and possible compression of the graft. [38] [40] [41] [42] Figure 25-10 (color plate.) Transesophageal echocardiographic findings in a patient with systolic compression of aortic homograft secondary to dehiscence at the aortic annulus anastomosis. The upper panels display the dynamic compression of the homograft in short axis. Color M-mode echocardiography at the same level shows the systolic compression of the graft (white arrows) and systolic flow in both the pseudoaneurysm (above the arrows) and the homograft. Continuous wave Doppler recording from the transgastric view depicts the high gradient through the obstruction. The aortic valve was normal. Gr, gradient; H, aortic homograft; LA, left atrium; RV, right ventricle. (From Nagueh SF, Bozkurt B, Li GA, et al: Am Heart J 1996;132(5):1070–1073, with permission.) Echocardiographic and Doppler Findings

Data are scarce on the echocardiographic findings in aortic root allografts. [42] [43] A normal aortic root allograft, especially early after surgery, may be difficult to differentiate from a native aortic root. Late after surgery, however, calcifications of the homograft are common and are detected by echocardiography as increased echogenicity in the aortic root. If leaflet degeneration occurs, varying degrees of aortic insufficiency, with or without aortic stenosis, may be present. In a recent study, paravalvular aortic insufficiency and eccentric jets were more common in patients with subcoronary aortic allograft implantation (41%) than in those with root replacement (11%).[43] Some unusual complications may affect the allograft, but these complications have occurred early in the postoperative period and can be detected with intraoperative TEE. Recently, cases have been reported with complications related to anastomosis of the coronary arteries with the allograft.[41] Aliasing by color flow was detected along with ischemia in the distribution of the involved anastomosis (left main or right coronary artery). Other reported complications included dehiscence of the homograft with resultant pseudoaneurysm formation. Compression of the graft by the pseudoaneurysm may occur, simulating valve stenosis (Fig. 2510) .[42] With more extensive experience in cardiac imaging of these patients, the spectrum of complications and the role of echocardiography and other imaging modalities in patients undergoing aortic allograft surgery

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will be better defined. Replacement of the Aorta with an "Elephant-Trunk" Procedure In patients with extensive aortic aneurysmal disease or in dissection involving the ascending aorta, arch, and descending aorta, replacement of the aortic arch and varied lengths of the aorta can be a major undertaking. In 1983, Borst et al[44] described a dual-stage technique whereby the ascending aorta and arch are replaced first, leaving a segment of the distal tubular graft in the descending 559

Figure 25-11 (color plate.) Transesophageal imaging of the descending aorta (Desc Ao) (longitudinal plane) in a patient with aortic aneurysm involving the arch and descending aorta following a successful first stage of an "elephant trunk" procedure. The free distal end of the tubular graft is seen in the descending thoracic aneurysm. Color flow Doppler shows flow into the descending aorta arising from the distal end of the graft (Gr).

thoracic aorta. Borst coined the name "elephant-trunk" technique for this procedure. [44] At a second stage, the distal aorta is repaired beyond the subclavian artery. Since its original description, few modifications have been applied to the technique.[6] [45] [46] After the first stage of the operation, TEE imaging of the descending aorta shows the free position of the distal tubular graft in the descending aneurysm, with blood flow detected in the graft emptying into the aneurysm (Fig. 25-11) . This finding at this stage is normal and should not be mistaken for dehiscence of the graft. Following a successful first stage of the procedure, the most serious and usually fatal complication is rupture of the remaining descending thoracic aneurysm while awaiting the second stage of the surgery. The author has observed an unusual interim complication of severe hemolytic anemia following the first stage, which resolved after the second stage of the repair. The intravascular hemolysis was caused by insertion of the distal graft into the false lumen during the first operation. Because insertion of the graft into the descending aorta during the first stage is performed blind, some surgeons in the author's institution currently use intraoperative TEE to assess the position of the inserted graft in the descending aorta. Other Complications Progression of aortic disease with further aneurysm formation or dissection

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in additional segments of the aorta is the most common cause for reoperating on patients with diseases of the aorta.[19] [47] [48] [49] Monitoring the progression of aortic disease after the initial surgery affects prognosis and is crucial in the overall management of these patients. In addition to the complications mentioned earlier, rupture of the great vessels with fistula formation, although infrequent, can occur as a complication of aortic dissection or aneurysm. Communication between the aorta and pulmonary artery is clinically suspected by the findings of a continuous murmur, similar to patent ductus arteriosus or the presence of heart failure. Echocardiographic findings depend on the size of the shunt and may include volume overload of the left ventricle and elevated pulmonary pressures. Doppler echocardiographic findings are those of continuous flow into the pulmonary artery from the aorta.

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Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company

Unusual Complications Following Valve Surgery Left Ventricular Pseudoaneurysm After Mitral Valve Replacement Clinical Setting

Rupture of the left ventricle with pseudoaneurysm formation is a rare but serious complication following mitral valve replacement. Overall, the incidence appears to range from 0.5% to 2% in isolated or combined mitral valve procedures. [50] [51] [52] [53] [54] Rupture of the left ventricle may occur immediately after surgery, presenting with hemodynamic collapse, or may present in the delayed postoperative period as a false aneurysm of the left ventricle. Anatomic characteristics and other factors have been described as predisposing to rupture of the ventricle such as heavy mitral or annular calcifications, the operative procedure itself, the number of surgical procedures previously undergone, or other hemodynamic considerations; however, often no clear cause for the pseudoaneurysm formation can be found.[55] The clinical presentation of pseudoaneurysm formation is variable. In the early postoperative period, it can present as poor postoperative progress, chest pain, heart failure, or as the development of a new murmur.[51] [52] [56] Late postoperative presentation may be similar or may be totally asymptomatic. In unusual cases, the pseudoaneurysm can compress the coronary arteries, leading to ischemia or myocardial hibernation.[57] Echocardiographic and Doppler Findings

Echocardiographic techniques play a significant role in the diagnosis of left ventricular pseudoaneurysm.[58] [59] A pseudoaneurysm, in contrast to a true aneurysm, is visualized as a saccular or globular chamber communicating with the left ventricle through a narrow and abrupt discontinuity in the ventricular myocardium. Over the past few years, the important role of Doppler echocardiography in the diagnosis of pseudoaneurysms has been increasingly appreciated. The demonstration of flow into the

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pseudoaneurysm by pulsed- and color-flow Doppler substantiates the diagnosis and may at times be the only clue for its presence in cases where the origin of the pseudoaneurysm cannot be visualized.[60] [61] [62] Doppler echocardiography is crucial in differentiating a pseudoaneurysm from other entities such as pericardial cysts, loculated pericardial effusion, or hematoma, especially in cases in which communication of the cavity with the left ventricle is not seen. As with true left ventricular aneurysm, a pseudoaneurysm demonstrates akinesis or dyskinesis during ventricular systole. Characteristic Doppler patterns can be seen with systolic filling and diastolic emptying of the pseudoaneurysm.[63] In patients with sinus rhythm, filling of the pseudoaneurysm during atrial contraction 560

can also be seen. With the availability of intravenous contrast echo agents that can cross the pulmonary circulation,[64] the administration of contrast can be of important diagnostic value in these situations by identifying whether such a communication exists with the left ventricle and by localizing its site. The use of contrast is particularly helpful when the communication with the ventricle is rather large and blood velocity in the cavity is too low to be clearly detected with Doppler. The location of the pseudoaneurysm can vary in relation to the prosthetic valve. Transthoracic echocardiography can demonstrate its presence and characteristic features; however, because of technical difficulties and imaging in the far field, the pseudoaneurysm may be frequently missed with the transthoracic approach. TEE is currently the echocardiographic method of choice in evaluating patients with suspected left ventricular pseudoaneurysm complicating mitral valve replacement.[63] [65] [66] [67] An example of a pseudoaneurysm complicating mitral valve replacement demonstrated by TEE and missed by transthoracic imaging is shown in Figure 25-12 . Other Imaging Modalities

Nonsurgical detection of pseudoaneurysm previously has depended on left ventriculography. Angiography is still important in the diagnosis of pseudoaneurysms in patients in whom the transthoracic examination may be difficult and also provides a spatial distribution of the Figure 25-12 (color plate.) Transverse transesophageal

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echocardiography planes at four levels (A to D) are shown along with contrast left ventriculography in the right oblique view, demonstrating opacification of a left ventricular pseudoaneurysm complicating mitral valve replacement. The approximate locations of the transverse echo planes are schematically shown on the angiogram. A1 and A2 show the maximal extent of the pseudoaneurysm and respective color flow demonstrating flow in the cavity. B and C show the neck of the pseudoaneurysm by color Doppler and its proximity and impingement on the proximal circumflex artery (C, arrows). The most caudal plane (D) is at the level of the prosthetic valve (PrV), which is normal. Ao, aorta; LA, left atrium; LV, left ventricle; PsAN, pseudoaneurysm; RV, right ventricle. (From Baker WB, Klein MS, Zoghbi WA: J Am Soc Echocardiogr 1993;6:548–552.)

pseudoaneurysm (see Fig. 25-12) ; however, because of its tomographic nature, TEE can further add to left ventricular angiography in pinpointing the site of origin of the pseudoaneurysm and its relation to adjacent structures for later surgical correction. The intraoperative use of TEE in surgical repair of these lesions can also be crucial when the repair involves areas close to the coronaries, in the assessment of ventricular function immediately postoperatively, and to indirectly detect whether injury occurred in the area of the coronary vessels with the evaluation of regional myocardial function.[63] It is generally agreed that management of patients with pseudoaneurysm formation of the left ventricle necessitates surgical intervention because of the risk of rupture and potential sudden death. Although surgical correction has been carried out almost uniformly in highrisk patients, some authors have advocated continued TEE follow-up in asymptomatic patients.[67] Left Atrial Dissection after Mitral Valve Replacement Clinical Setting

Dissection of the left atrium with resultant pseudoaneurysm formation is a rare complication of mitral valve replacement.[68] [69] [70] [71] [72] Predisposing factors for this unusual complication are similar to those for left ventricular pseudoaneurysms and include mitral annulus calcifications, 561

Figure 25-13 Dissection of the left atrium demonstrated with intraoperative transesophageal echocardiography after mitral valve surgery. A, horizontal view; B, 73-degree view. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (From Genoni M, Jenni R, Schmid ER, et al: Ann Thorac Surg 1999;68:1394–1396.)

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external cardiac massage, friable atrial wall tissue, preexisting pericardial adhesions, and technical considerations during surgery. Clinical presentation varies from detection in the operating room with TEE, to the presence of a systolic murmur of mitral regurgitation, heart failure, or an asymptomatic state. Surgical correction is recommended for symptomatic cases or those with severe left atrial compression. Spontaneous healing has been reported in only one case.[70] Internal drainage of the false lumen into the right atrium has been recently proposed in cases where the dehiscence at the mitral annulus is small.[71] Echocardiographic and Doppler Findings

On echocardiography, a cavity formation is seen within the left atrium, with a linear echo density consisting of the dissection of the atrial wall. This is best delineated with TEE (Fig. 25-13) .[71] [72] Paraprosthetic valve regurgitation is usually seen, with flow by Doppler entering into the false lumen through the communication.[72] Recording of the jet with continuouswave Doppler provides various degrees of velocity and duration of flow, depending on the size of the communication, and compliance of the false lumen. Pseudoaneurysm of the Ascending Aorta After Aortic Valve Replacement Clinical Setting

False aneurysm of the ascending aorta is a rare but serious complication of aortic valve replacement. Potential factors contributing to this complication include leaking aortotomy suture lines, needle punctures for air-evacuation procedures after surgery, postoperative endocarditis, or friability of the aortic wall.[73] [74] [75] [76] Clinical presentation is variable, including an asymptomatic, incidental finding on chest radiography or echocardiography, symptoms of atypical chest discomfort or dyspnea, and the finding of a continuous murmur because of fistula formation with adjacent cardiac chambers.[73] [74] [75] [76] Surgical repair generally is recommended because these pseudoaneurysms have a high propensity for rupture. Echocardiographic and Doppler Findings

Echocardiography shows a typical pseudoaneurysmal cavity arising from the ascending aorta in the vicinity of the prosthetic aortic valve. Usually the aorta is of normal size, and the neck of the pseudoaneurysm is small and

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may be difficult to appreciate on transthoracic echocardiography. TEE enhances imaging and definition of the pseudoaneurysm, which could be lined with thrombus. Color Doppler identifies flow into the cavity in systole, emptying in diastole (Fig. 25-14) . In a typical aortic pseudoaneurysm, there is no associated aortic insufficiency or flow in the cavity. In case of further complications of the pseudoaneurysm, however, continuous flow can be detected at the site of rupture into the right atrium or right ventricle.[75] [76] Similar to other pseudoaneurysms of the aorta, aortography, CT, or MRI also can delineate the pseudoaneurysm 562

Figure 25-14 (color plate.) Echocardiographic and Doppler images of an aortic pseudoaneurysm obtained with transesophageal echocardiography in the 30-degree and 90-degree planes. Flow is seen entering the pseudoaneurysm in systole and emptying in diastole. The corresponding aortogram delineates the extent of the pseudoaneurysm. Ao, aorta; An, pseudoaneurysm; LA, left atrium.

(see Fig. 25-14) . In these cases, Doppler echocardiography and aortography can aid surgical correction by more accurately pinpointing the site of rupture and flow into the pseudoaneurysm. Pseudoaneurysm of the Mitral-Aortic Intervalvular Fibrosa Clinical Setting

The region of the mitral-aortic continuity or mitral-aortic intervalvular fibrosa (MAIVF) contains mostly fibrous, relatively avascular tissue. Because of its composition, the MAIVF is the weakest segment of the aortic ring,[77] is prone to infection, and is more sensitive to trauma. The roof of the MAIVF is formed of pericardium, and its ventricular side is the posterior portion of the left ventricular outflow tract. Dehiscence in the MAIVF region, secondary to infection, trauma, or even surgical manipulation may result in the formation of an abscess or a pouch between the medial wall of the left atrium and the aorta. An intervalvular pseudoaneurysm ensues when the abscess or pouch communicates with the left ventricular outflow tract.[78] [79] [80] [81] An example of an MAIVF pseudoaneurysm is shown in Figure 25-15 . Most pseudoaneurysms in the MAIVF region occur secondarily to infection and are more common in

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patients with prosthetic valves.[82] Other causes include trauma, surgical trauma, and congenital pseudoaneurysms.[82] [83] [84] Detecting these pseudoaneurysms is important because of their potential complications, which may include rupture into the left atrium or aorta, resulting in mitral or aortic regurgitation, respectively, or even rupture into the pericardial space, with ensuing cardiac tamponade and death.[78] [81] [83] Determining the incidence of MAIVF pseudoaneurysms is difficult. Prior to the use of TEE, the few reports available surfaced at pathology or during angiography. With the advent of TEE, the most sensitive technique for evaluating these lesions, MAIVF pseudoaneurysms were detected in 9% of patients undergoing TEE for suspected aortic valve or ring disease.[82] The clinical presentation varies but is most commonly that of endocarditis, congestive heart failure, valvular regurgitation, or it may be asymptomatic, without a history of endocarditis. Because the pseudoaneurysm is located between the left atrium and aorta, and its origin is in the left ventricular outflow, it is not readily identified at surgery and may be missed. Thus, accurate detection, delineation, and differentiation of MAIVF pseudoaneurysms from ring abscesses is important in overall patient management and in the guidance of surgical correction. Echocardiographic and Doppler Findings

Transthoracic echocardiography has been used for the diagnosis of aortic root complications.[85] [86] Its sensitivity, however, recently has been shown to be limited in the evaluation of posterior lesions, particularly in the presence of prosthetic aortic valves; by contrast TEE substantially improves the diagnosis of such lesions.[87] [88] In a series from the author's institution, transthoracic echocardiography detected 43% of a total of 23 lesions affecting the aortic root, whereas TEE identified 90% of the lesions.[82] The importance of the transthoracic approach in detecting anterior ring abscesses cannot be ignored, however, particularly in the presence of prosthetic aortic valves, where TEE may have significant limitations because of shadowing of the prosthesis in the region of the anterior aortic ring. Combining transthoracic and transesophageal imaging, therefore, would allow a comprehensive evaluation of the aortic root and is strongly recommended. In contrast to aortic ring abscesses, intervalvular pseudoaneurysms exhibit a characteristic dynamic feature during the cardiac cycle. Marked pulsatility is observed in most MAIVF pseudoaneurysms, with expansion during early systole and collapse in diastole (see Fig. 25-15) . [82] This

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feature is explained by the fact that the pressure in the pseudoaneurysm reflects left ventricular pressure and 563

that a large portion of the pseudoaneurysm is surrounded by the left atrium. Thus, when left atrial pressure exceeds left ventricular pressure in diastole, the pseudoaneurysm collapses, whereas it expands in systole. This dynamic behavior during the echocardiographic examination is indeed the first clue to the presence of an MAIVF pseudoaneurysm. In contrast, aortic ring abscesses located anteriorly or posteriorly in the aortic root do not exhibit this marked pulsatility, which may be explained by several factors. In walled-off abscesses without detectable flow, pulsatility is not expected. In ring abscesses with systolic and diastolic flow owing to paraprosthetic aortic regurgitation, the pressure remains high throughout the cardiac cycle in these cavities compared with adjacent chambers so that pulsatility is not seen. Although collapsibility provides indirect evidence for the presence of an MAIVF pseudoaneurysm, confirmation of this diagnosis requires visualization of the neck of the pseudoaneurysm in the left ventricular outflow. This communication rarely can be seen by transthoracic echocardiography[82] however, it is usually well visualized with the transesophageal approach. In the author's experience, the size of the neck has ranged from 0.5 to 2.1 cm in diameter. In cases where there is still doubt about whether the cavity communicates with the aorta or left ventricle, the administration Figure 25-15 (See also color plate.) Echocardiographic and color Doppler frames from the transverse plane during transesophageal echocardiography showing a typical simple mitral-aortic intervalvular fibrosa pseudoaneurysm with its location, pulsatility, and flow patterns during the cardiac cycle. Top, Pseudoaneurysm (straight arrow) and communication with the left ventricular outflow (curved arrow) are shown. The pseudoaneurysm begins to expand during early systole, remains distended in late systole, and collapses during diastole. Bottom, Magnified color Doppler views of the area within the box seen in the top middle panel. During early systole, the pseudoaneurysm fills, showing high, aliased velocities. Low, nonaliased velocities are seen during the remainder of systole while the pseudoaneurysm remains expanded (middle). During diastole, the pseudoaneurysm empties and collapses. LA, left atrium; LV, left ventricle.

of intravenous contrast agents that cross the pulmonary circulation can help resolve this issue.

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Color Doppler imaging is crucial in the evaluation of MAIVF pseudoaneurysms. Its application helps to assess whether rupture of this cavity into adjacent chambers has occurred and define its communication. The following are characteristic Doppler features in unruptured and ruptured MAIVF pseudoaneurysms. In the case of unruptured pseudoaneurysms, Doppler evaluation usually is less impressive. Only a brief duration of flow into the pseudoaneurysm occurs during early systole (20–60 msec), at which time pressure between the pseudoaneurysm and left ventricle is equalized, and no further flow is detected by Doppler (see Fig. 25-15) .[82] During diastole, a brief period of flow exiting from the pseudoaneurysm may be seen but frequently can be missed because of its low velocity. In contrast, in pseudoaneurysms that have ruptured, into either the left atrium or aorta, an intense color-flow signal can be seen during the cardiac cycle. In cases of rupture into the left atrium, color Doppler shows holosystolic, intense flow signal in the pseudoaneurysm and eccentric "mitral" regurgitation through the perforation of the pseudoaneurysm, the latter acting as a conduit for blood flow from the left ventricle to the left atrium (Fig. 25-16) . The use of color Doppler actually facilitates 564

Figure 25-16 (See also color plate.) Two-dimensional and color flow transesophageal echocardiography images of a complicated mitralaortic intervalvular fibrosa pseudoaneurysm with rupture into the left atrium in the setting of endocarditis after mitral valve annuloplasty and aortic valve replacement. The pseudoaneurysm (slender arrow) and its neck (large arrow) are shown. The pseudoaneurysm is septate, has mobile vegetations, and expands significantly in systole. An intense color flow jet in systole is seen through the pseudoaneurysm with subsequent, eccentric regurgitation into the left atrium. Ao, aorta; LA, left atrium; LV, left ventricle.

the identification of the rupture site of the pseudoaneurysm by tracking the origin of the regurgitant jet. The ruptured site is rarely seen by transthoracic echocardiography but can be suspected by the presence of eccentric mitral regurgitation arising close to the aortic root. Similar to unruptured pseudoaneurysms, those pseudoaneurysms communicating with the left atrium show systolic expansion and diastolic collapse (see Fig. 25-16) . In cases where rupture of the pseudoaneurysm occurs into the aorta, with or without concomitant dehiscence of the prosthetic aortic valve, aortic insufficiency is detected (Fig. 25-17) . In systole, color Doppler shows

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antegrade flow from the ventricle through both the pseudoaneurysm and the prosthetic aortic valve. In diastole, retrograde flow of "aortic" insufficiency is seen, directed from the aortic root into the pseudoaneurysm and into the ventricle. Other Imaging Modalities

Until recently, cineangiography has been the standard for diagnosing aortic root lesions.[89] With the advent of echocardiography with Doppler, and more recently TEE, however, these techniques have rivaled the invasive diagnostic modality. Few cases of MAIVF pseudoaneurysms have been described with angiography.[80] [90] [91] The pulsatility described earlier is also seen on angiography (Fig. 25-18) . In a case series in which patients underwent both diagnostic modalities, MAIVF pseudoaneurysms were more frequently detected by TEE than by aortography.[82] Only 2 of 9 pseudoaneurysms were identified by aortography, both of which had associated aortic insufficiency (Fig. 25-19) . The direct communication between the left ventricular outflow tract and pseudoaneurysm explains the need for a ventricular injection of dye to detect this abnormality. This finding is similar to that described earlier for pseudoaneurysms of composite aortic grafts with a single dehiscence at the aortic annulus anastomosis. Thus, in patients without aortic insufficiency, demonstration of the pseudoaneurysm with angiography requires left ventriculography. Compared with angiography, TEE more clearly delineates the origin of the intervalvular pseudoaneurysms and their communication elucidating 565

Figure 25-17 (See also color plate.) Two-dimensional and color Doppler frames during omniplane transesophageal examination at an angulation of 120 degrees, showing a ruptured mitral-aortic intervalvular fibrosa pseudoaneurysm into the aorta. During systole, blood flows into the pseudoaneurysm and from the pseudoaneurysm into the aorta through small fenestrations (white arrow). Normal flow direction through the prosthesis (black arrow) is also shown. During diastole, blood regurgitates into the left ventricle through the pseudoaneurysm (black arrows). An, pseudoaneurysm; Ao, aorta; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.)

the origin of concomitant mitral regurgitation or aortic insufficiency and, therefore, assisting in planning surgical repair.[82]

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Patients with cavitary lesions complicating aortic valve disease, particularly prosthetic valves, require extensive surgical intervention, including in some cases aortic root replacement. Because of the risk of rupture into the pericardium, surgical correction of MAIVF pseudoaneurysm is warranted in most cases. Although the natural history of uncomplicated pseudoaneurysm is unclear, surgical repair was performed in th