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,