Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging

Get Quick Access to Cardiac MRI Techniques

high-quality images!

Williamson

• A review of the most common cardiac MR imaging planes

More than

McGee

This compact guide to cardiac magnetic resonance imaging incorporates the most common techniques with easy-tofollow step-by-step protocols. Physicians and technicians alike get quick access to the information they need at the point of exam. Features include:

200

with step-by-step protocols

imaging protocols and example cases

• A review of the basic physics of cardiac MRI, including pulse sequences and ECG gating, as well as common imaging artifacts and how to prevent them. This easy-to-use reference is the most practical guide for accessing information on all stages of the cardiac MRI exam, from graphical prescription and protocol selection to imaging troubleshooting and interpretation. ABOUT THE AUTHORS KIARAN P. McGEE is Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Biomedical Engineering and Radiologic Physics, College of Medicine, Mayo Clinic. ERIC E. WILLIAMSON is Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Radiology, College of Medicine, Mayo Clinic. PAUL R. JULSRUD is Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Professor of Radiology, College of Medicine, Mayo Clinic.

Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging

• Descriptions of the most common indications for cardiac MRI, along with typical

Julsrud

• An overview of the various physiologic events that make up the cardiac cycle

Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging

Kiaran P. McGee, PhD Eric E. Williamson, MD Paul R. Julsrud, MD MAYO CLINIC SCIENTIFIC PRESS

Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging

Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging

Editors Kiaran P. McGee, PhD Eric E. Williamson, MD Paul R. Julsrud, MD MAYO CLINIC SCIENTIFIC PRESS AND INFORMA HEALTHCARE USA, INC.

ISBN-13: 978-1-4200-8303-3 Printed in Canada The triple-shield Mayo logo and the words MAYO, MAYO CLINIC, and MAYO CLINIC SCIENTIFIC PRESS are marks of Mayo Foundation for Medical Education and Research. ©2008 Mayo Foundation for Medical Education and Research. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted, in any form by any means—electronic, mechanical, photocopying, recording, or otherwise—without the prior written consent of the copyright holder, except for brief quotations embodied in critical articles and reviews. Inquiries should be addressed to Scientific Publications, Plummer 10, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. For order inquiries, contact: Informa Healthcare, Kentucky Distribution Center, 7625 Empire Drive, Florence, KY 41042 USA. E-mail: [email protected]; Web site: www.informahealthcare.com Library of Congress Cataloging-in-Publication Data Mayo Clinic guide to cardiac magnetic resonance imaging/edited by Kiaran P. McGee, Eric E. Williamson, Paul Julsrud. p. ; cm. Includes bibliographical references and index. ISBN-13: 978-1-4200-8303-3 (pb : alk. paper) ISBN-10: 1-4200-8303-1 (pb : alk. paper) 1. Heart--Magnetic resonance imaging. I. McGee, Kiaran P. II. Williamson, Eric E. III. Julsrud, Paul. IV. Mayo Clinic. V. Title: Guide to cardiac magnetic resonance imaging. [DNLM: 1. Heart Diseases--diagnosis. 2. Magnetic Resonance Imaging--methods. WG 141.5.M2 M473 2008] RC683.5.M35M39 2008 616.1'207548--dc22

2008005368

Nothing in this publication implies that Mayo Foundation endorses any of the products mentioned in this book. Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, express or implied, with respect to the publication. This book should not be relied on apart from the advice of a qualified health care provider. The authors, editors, and publisher have exerted efforts to ensure that drug selections and dosages set forth in this text are in accordance with current recommendations and practices at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, readers are urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This precaution is particularly important when the recommended agent is a new or infrequently used drug. Some drugs and medical devices presented in this publication have U.S. Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of health care providers to ascertain the FDA status of each drug or device that they plan to use in their clinical practice.

DEDICATION Kiaran P. McGee, PhD To those profound sources of love, joy, and happiness: Nancy, Jeff, Max, Cora, & B.V.M.

Eric E. Williamson, MD To my parents, Byrn and Anita–for teaching me the value of high expectations.

Paul R. Julsrud, MD To my parents for their unconditional love; to my wife and children for their continued support and affection; and to Drs. Richard Van Pragh, Kenneth Fellows, and Ivar Enge for their mentorship and for being extraordinary role models for my career.

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FOREWORD

In 2003, magnetic resonance imaging was formally recognized as one of the most important advances in modern medicine by the awarding of the Nobel Prize in Physiology or Medicine jointly to Paul C. Lauterbur and Sir Peter Mansfield. Although this recognition was a “coming of age” for the field of MRI, in many respects cardiac MRI is still in its infancy, in part because of the unique technical challenges of acquiring an MR image of an organ that changes in size, shape, and location. Despite these difficulties, technological developments in MR scanner hardware and software, as well as postprocessing techniques, have allowed cardiac MRI to become more available and practical in nonacademic institutions such as community hospitals and outpatient imaging centers. What is needed to expand this trend is the ability to reliably and reproducibly perform cardiac MRI examinations in those settings. The Mayo Clinic Guide to Cardiac Magnetic Resonance Imaging is designed to facilitate the dissemination of cardiac MRI from academic centers into the broader MR community. The book’s content is designed to serve multiple groups: technologists, clinicians, and clinical medical physicists. Its organization is such that any institution should be able to rapidly develop their own program without having to seek out a variety of medical and technical texts. Technologists are the target audience of the first chapter, being the ones to acquire the actual cardiac MR data. In chapters 2 and 3, the text focuses on providing clinicians with suggested imaging protocols, along with clinical examples of the actual imaging indication. Finally, chapter 4 provides a more technical review of the underlying physical principles of the various imaging sequences used in cardiac MRI. Although this final section is quite technical, the authors have provided a general overview of the various concepts that encompass the physics of cardiac MRI. I highly recommend this text to experts and novices alike.

Jerome F. Breen, MD Chair, Division of Cardiac Radiology Mayo Clinic

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PREFACE

Over the course of the past decade, cardiac magnetic resonance imaging has developed from a boutique imaging modality to the gold standard for assessment of various functional and morphologic cardiac diseases. Based on the experience within our own institution in training physicians, technologists, and physicists alike, it became apparent that there was an unmet need for a practical “users’ guide” to cardiac MR imaging. We also quickly appreciated that such a text would not only be useful in training within our own walls but also could serve as a reference guide for others interested in establishing a cardiac MR imaging program. This was the motivation for creating a practical handbook for cardiac MR imaging. The handbook is intended to serve three basic purposes: 1) to develop a standard methodology to assist the user in prescribing MR sequences in the commonly used cardiac imaging planes, 2) to provide a set of imaging protocols that address the most common indications for which a cardiac MR exam would be ordered, and 3) to give the user a basic overview of the physical principles of cardiac MR imaging, including electrocardiographic gating, pulse sequence design and types, and typical imaging artifacts and strategies to correct them. In many respects, this work is incomplete in that it represents a broad snapshot of the landscape of cardiac MR in 2008 AD. However, it is our hope that the information contained within these pages will contribute to the growth and dissemination of cardiac MR imaging beyond the boundaries of academic medicine into the broader community.

Kiaran P. McGee, PhD Eric E. Williamson, MD Paul R. Julsrud, MD

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ACKNOWLEDGMENTS The Latin phrase “Quasi nanos, gigantium humeris insidentes, ut possimus plura eis et remotiora videre (We are like dwarfs on the shoulders of giants, so that we can see more than they)” aptly describes those pioneering individuals to whom we owe a debt of gratitude. Without their efforts and contributions this work would not be possible. In particular, we recognize Jerome F. Breen, MD, Joel P. Felmlee, PhD, and Richard L. Ehman, MD, whose diligence and hard work have developed a clinical practice that is the genesis of this text. We also acknowledge all of those colleagues, both internal and external to our institution, who are too numerous to identify individually but whose cumulative efforts have contributed to the growth of cardiac MR.

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PRODUCTION STAFF Mayo Clinic Section of Scientific Publications Alyssa C. Biorn, PhD Roberta Schwartz Kristin M. Nett Ann M. Ihrke

Editor Production editor Editorial assistant Copy editor/proofreader

Mayo Clinic Section of Illustration and Design Karen E. Barrie David T. Smyrk Robert R. Morreale James E. Rownd Deborah A. Veerkamp Kevin M. Youel

Art director Medical animator Medical illustrator Commercial illustrator Presentation designer Presentation designer

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AUTHOR AFFILIATIONS Philip A. Araoz, MD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Radiology, College of Medicine, Mayo Clinic Matt A. Bernstein, PhD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Professor of Radiologic Physics, College of Medicine, Mayo Clinic James F. Glockner, MD, PhD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Radiology, College of Medicine, Mayo Clinic Paul R. Julsrud, MD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Professor of Radiology, College of Medicine, Mayo Clinic Jacobo Kirsch, MD Fellow in Cardiac Imaging, Mayo School of Graduate Medical Education, and an Instructor of Radiology, College of Medicine, Mayo Clinic, Rochester, Minnesota. Present address: Radiology Institute, Cleveland Clinic, Weston, Florida. Kiaran P. McGee, PhD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Biomedical Engineering and Radiologic Physics, College of Medicine, Mayo Clinic Eric E. Williamson, MD Consultant, Department of Radiology, Mayo Clinic, Rochester, Minnesota; Assistant Professor of Radiology, College of Medicine, Mayo Clinic

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TABLE OF CONTENTS PREFACE

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ix

LIST OF ABBREVIATIONS

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xix

CHAPTER 1 Cardiac Anatomy and MR Imaging Planes

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

CHAPTER 2 Cardiac Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .29 CHAPTER 3 Clinical Indications and Sample Imaging Protocols With Case Examples

. . . . . . . . . . . .37

CHAPTER 4 Pulse Sequence Basics, ECG Gating, and MR Artifacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .107 INDEX

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .181

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ABBREVIATIONS 2D

two-dimensional

3D

three-dimensional

ARVC

arrhythmogenic right ventricular cardiomyopathy

AS

aortic stenosis

bpm

beats per minute

ECG

electrocardiography

EDV

end-diastolic volume

ESV

end-systolic volume

FOV

field of view

Gd-DTPA gadolinium diethylenetriamine penta-acetic acid

R-R

time interval between successive R-wave peaks in ECG waveform

RCA

right coronary artery

RF

radio frequency

RV

right ventricle

SE

spin echo

T1

longitudinal (spin-lattice) relaxation time

T2

transverse (spin-spin) relaxation time

TE

echo time

TI

inversion time

GRE

gradient-recalled echo

TR

pulse repetition rate

HR

heart rate

VCG

vector ECG

IR

inversion recovery

VENC

velocity encoding

LAD

left anterior descending artery

VPS

views per segment

LCX

left circumflex artery

LV

left ventricle

MDE

myocardial delayed enhancement

MR

magnetic resonance

MRI

magnetic resonance imaging

NEX

number of excitations or signal averages

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CARDIAC MR ACRONYMS MANUFACTURER IMAGING COMPONENT & TERM

Siemens Medical Solutions

GE Healthcare

Magnetization Preparation Phase contrast PC PC Chemical fat saturation Fat Sat Fat Sat, Chem Sat Tagging Tagging Tagging Flow compensation Flow comp, GMR Flow comp Inversion recovery IR IR Phase-sensitive inversion PSIR PSIR recovery Echo Formation Gradient echo Spoiled Gradient-recalled echo Spoiled GRE Fast gradient echo Fast gradient echo 3D Volume-interpreted GRE Steady state Balanced steady-state free precession Steady-state free precession–FID Steady-state free precession–echo Spin echo Gradient and spin echo

Philips Medical Systems

PC SPIR, SPAIR Tagging Flow comp IR-TSE PSIR

GRE FLASH TurboFLASH MPRAGE, 3D FLASH VIBE

GRE SPGR FGRE, FSPGR 3D FGRE, 3D FSPGR FAME, LAVA

FFE T1-FFE TFE 3D TFE

True FISP

FIESTA

BFFE

FISP

GRASS

FE

PSIF

SSFP

T2-FFE

SE

SE

SE

TurboGSE, TGSE

GRASE

GRASE

THRIVE

*Imaging terms and corresponding acronyms used by different MR scanner manufacturers.

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MANUFACTURER IMAGING COMPONENT Siemens Medical & TERM Solutions Data Acquisition Single-shot spin echo Multishot (echo train) spin echo Number of echoes in spin-echo echo train

Echo planar imaging Rapid Imaging Image based k-space based Imaging Mode Two dimensions Three dimensions Single image Multiframe image

GE Healthcare

Philips Medical Systems

HASTE TSE, RARE

SSFSE FSE

SS TSE TSE

Turbo factor

ETL

Turbo factor

EPI

EPI

EPI

mSENSE GRAPPA

ASSET ARC

SENSE

2D 3D Static Cine

2D 3D Static Cine

2D 3D Static Cine

ARC, autocalibrating reconstruction for Cartesian imaging; ASSET, array sensitivity encoded; ETL, echo train length; FAME, fast acquisition with multiple excitation; FE, field echo; FFE, fast-field echo; FID, free induction decay; FIESTA, fast imaging employing steady-state acquisition; FISP, fast imaging with steady precession; FLASH, fast low angle shot; FSE, fast spin echo; GMR, gradient moment recalled; GRAPPA, generalized autocalibrating partially parallel acquisition; GRASE, gradient and spin echo; GRASS, gradient-recalled acquisition in the steady state; HASTE, half Fourier-acquired single-shot turbo spin echo; LAVA, liver acquisition with volume acceleration; MPRAGE, magnetization prepared rapid acquired gradient echoes; mSENSE, modified sensitivity encoding; PSIF, reversed fast imaging with steady-state free precession; RARE, rapid acquisition with relaxation enhancement; SENSE, sensitivity encoding; SPAIR, special attenuation with inversion recovery; SPGR, spoiled gradient-recalled echo; SPIR, spectral attenuation with inversion recovery; TGSE, turbo gradient spin echo; THRIVE, T1 high-resolution isotropic volume estimation; TFE, turbo field echo; TSE, turbo spin echo; VIBE, volumetric interpolated breath-hold examination.

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CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Chapter 1

CARDIAC ANATOMY AND MR IMAGING PLANES Eric E. Williamson, MD Kiaran P. McGee, PhD Paul R. Julsrud, MD

Introduction The purpose of this chapter is to provide a step-by-step protocol for acquiring common cardiac magnetic resonance (MR) imaging planes. The workflow diagrams presented are not complete in that each represents only one example of a pathway that can be followed to facilitate consistent cardiac examinations. However, they do provide both a workflow that facilitates consistent visualization of the most clinically relevant cardiac anatomy and a method for completing the cardiac examination in a practical time frame for the patient and imaging department alike.

3

4

MAYO CLINIC GUIDE TO CARDIAC MRI

Left Ventricular Imaging MR imaging of the heart most commonly includes visualization of the left ventricle (LV). At least three separate imaging planes are acquired routinely, as shown in Figure 1.1; these include the sagittal localizer, a four-chamber localizer, and a series of so-called “short-axis” views. Three additional imaging planes can also be acquired to further characterize the LV in the long axis. Figure 1.1 shows the order in which these planes are typically acquired (numbers 1 through 6), as well as their temporal and spatial relationships. Each arrow describes the relationship between the image used as the prescription and the resultant imaging plane. For example, the sagittal localizer is used as a prescription image in order to acquire the four-chamber localizer view. Similarly, the four-chamber localizer acts as the prescription image for the short-axis views. Solid arrows represent standard imaging planes and dashed arrows identify optional planes.

Figure 1.1. Imaging planes used to characterize the LV of the heart. The numbers indicate the acquisition order. Solid arrows indicate typical imaging planes; dashed arrows indicate optional planes used to visualize the left heart.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

5

Sagittal localizer (1)

Four-chamber localizer (2)

Short axis (3)

Left ventricle two chamber (4)

Left ventricle three chamber (5) Left ventricle four chamber (6)

6

MAYO CLINIC GUIDE TO CARDIAC MRI

Sagittal Localizer The first step in prescribing the various imaging planes acquired during a cardiac MR examination is to obtain a series of straight sagittal images that include the entire volume of the heart (Figure 1.2). This is an essential first step because all subsequent planes are prescribed from these data. Prescribe enough slices to cover the entire heart. The graphical prescription should start roughly at the sternum and cover more than two-thirds of the left side of the patient’s thorax. The goal is to obtain slices that include the mitral valve plane and cardiac apex.

Figure 1.2. Anatomical reference showing the location of the sagittal localizer with respect to the heart and chest wall, as well as the corresponding MR imaging planes. The localizers start at the position of the sternum and progress laterally toward the apex of the heart.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Anatomical reference

Resultant sagittal localizer views

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MAYO CLINIC GUIDE TO CARDIAC MRI

Four-Chamber Localizer Acquisition of the sagittal localizer allows identification of the four chambers and great vessels of the heart. Review of these images shows the oblique orientation of the heart within the thoracic cavity, with the apex lying on top of the diaphragm at the level of the fifth intercostal space and the base of the heart posterior to the apex at the level of the third rib. Scrolling from left to right, the sagittal images traverse the left and then right sides of the heart. These images can be used to acquire a four-chamber localizer view. The resultant images are not true four-chamber views, but they serve as a reference point from which short-axis views are acquired. To obtain a four-chamber localizer image from the sagittal localizer images, perform the following steps: ■

■

■

Scroll through the sagittal images and find an image in which the apex of the LV can be clearly identified. This will not necessarily be the first slice that contains cardiac anatomy. It is most common to identify the slice in which the LV first appears and then choose the next medial slice. Continue scrolling through the images, moving medially from the left to the right side of the heart, until the mitral (bicuspid) valve plane is identified. If the mitral valve is not clearly identified, the root of the aorta can also be used. Prescribe an imaging plane that bisects both the apex and mitral valve planes identified in the two previous images.

Figure 1.3 shows the placement of the imaging plane on each sagittal image (yellow lines). Angulation of the imaging plane in this manner allows the imaging slice to approximately bisect all chambers of the heart. The orientation of the imaging plane in relation to the heart and the resultant image are also shown.

Figure 1.3. Four-chamber localizer. Anatomical reference image, MR prescription imaging planes (yellow lines), and the resultant four-chamber image are shown. The imaging plane bisects the apex of the LV and the mitral (bicuspid) valve, providing a view of all four chambers of the heart.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Mitral valve

Apex of LV

Resultant four-chamber localizer

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MAYO CLINIC GUIDE TO CARDIAC MRI

Left Ventricular Short-Axis Views Short-axis images of the heart show a view “down the barrel” of the LV, perpendicular to the long axis or septum of the heart. Figure 1.4 shows the placement of a short-axis imaging plane in relation to the heart and the resultant anatomical cross-section. Multiple short-axis images are typically acquired from the cardiac apex to the base of the heart and are distinguished from one another by the part of the LV imaged (eg, cardiac apex, mid ventricle, or base of the heart). The base image is closest to the great vessels and includes the left and right ventricles, whereas the apex image typically includes only the LV. Acquisition of the four-chamber view provides the anatomical landmarks necessary for prescribing the various left ventricular short-axis views. Depending on the type of study, three or more slices will be acquired. If only three slices are used, these should be through the apex, mid ventricle, and base of the LV. To prescribe short-axis views of the LV, perform the following steps: ■

■

■

From the four-chamber data set acquired previously, identify the image that is approximately at end diastole. This will be the image in which the heart is relaxed and the chamber is maximally dilated. Prescribe an imaging plane that is centered on the LV and is roughly perpendicular to the septum. The plane should be placed at approximately mid ventricle. If multiple slices are prescribed, the planes should track roughly parallel to the septum. A series of images slicing through the base, mid ventricle, and apex of the heart will result.

Figure 1.4 shows the placement of three imaging planes (yellow lines) perpendicular to the septum on the four-chamber view. The orientation of these planes in relation to the anatomical orientation of the heart is also shown.

Figure 1.4. Anatomical reference, MR prescription planes (yellow lines), and resultant MR images of the left ventricular short-axis view are shown. The MR imaging planes should be parallel to the septum of the heart and centered within the middle of the LV.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant left ventricular short-axis views

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MAYO CLINIC GUIDE TO CARDIAC MRI

Left Ventricular Long-Axis Views A second set of long-axis views also can be acquired by prescribing a set of imaging planes orthogonal to the short-axis images previously acquired. The three prescriptions that follow (two, three, and four chamber) can all be prescribed off a single short-axis image. If multiple slices are acquired, long-axis views are typically prescribed off the slice that corresponds most closely to the mid ventricle. Left Ventricular Two-Chamber (Vertical Long-Axis) View A two-chamber long-axis (or vertical long-axis) view bisects the LV through its anterior and inferior walls, parallel to the interventricular septum. This orientation is commonly known as a two-chamber view because two chambers (the left atrium and LV) are visualized. To prescribe a two-chamber long-axis view of the LV, perform the following steps: ■ ■

■

■

Select the short-axis slice that is approximately at the location of the mid ventricle. Select the image at this slice location that is approximately at end diastole. This will be the image in which the heart is relaxed and the chamber is maximally dilated. Prescribe an imaging plane that is parallel to the interventricular septum and bisects the LV from the base of the heart to the cardiac apex. The center of the imaging plane should be at the center of the LV.

Figure 1.5 shows the placement of the two-chamber imaging plane (yellow line). The prescribed imaging plane is approximately parallel to the interventricular septum. The orientation of this plane in relation to the anatomical orientation of the heart is also shown. Placement of the imaging plane at mid ventricle produces the resultant image.

Figure 1.5. Anatomical reference, MR prescription plane (yellow line), and resultant MR image of the left ventricular two-chamber vertical long-axis view are shown.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant left ventricular two-chamber long-axis view

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MAYO CLINIC GUIDE TO CARDIAC MRI

Left Ventricular Three-Chamber View A three-chamber long-axis view bisects the LV through the aortic root and lateral left ventricular wall at the base of the heart and should extend to the tip of the cardiac apex (to avoid foreshortening of the LV). This orientation allows visualization of the aortic outflow tract, as well as the anterior septum and inferolateral wall of the LV. To prescribe a three-chamber long-axis view of the LV, perform the following steps: ■

■

■

■ ■

Select the short-axis slice that is approximately at the location of the aortic outflow tract. Select the image at this slice location that is approximately at end diastole. This will be the image in which the heart is relaxed and the chamber is maximally dilated. Prescribe an imaging plane through the aortic root, bisecting the LV from the base of the heart to the cardiac apex. The center of the imaging plane should be at the center of the LV. This imaging plane can also be obtained by copying the prescription from the twochamber acquisition and rotating the imaging plane accordingly.

Figure 1.6 shows the placement of the three-chamber imaging plane (yellow line). The orientation of this plane in relation to the anatomical orientation of the heart is also shown. Placement of the imaging plane at mid ventricle produces the resultant image.

Figure 1.6. Anatomical reference, MR prescription plane (yellow line), and resultant MR image of the left ventricular three-chamber long-axis view are shown.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant left ventricular three-chamber view

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MAYO CLINIC GUIDE TO CARDIAC MRI

Left Ventricular Four-Chamber (Horizontal Long-Axis) View A final, four-chamber, long-axis view of the left and right ventricles can be obtained by prescribing an imaging plane that is perpendicular to the interventricular septum and centered on the LV. This is a true four-chamber view of the heart because it is perpendicular to the septum and bisects the left and right chambers of the heart along the long axis. To prescribe a true four-chamber long-axis view, perform the following steps: ■

■

■ ■ ■

Select the left ventricular short-axis slice that is approximately at the location of the mid ventricle. Select the image at this slice location that is approximately at end diastole. This will be the image in which the heart is relaxed and the chamber is maximally dilated. Prescribe an imaging plane that bisects the LV and inferior septum. The center of the imaging plane should be at the center of the LV. This imaging plane can also be obtained by copying the prescription from either the two- or three-chamber acquisition and rotating the imaging plane accordingly.

Figure 1.7 shows the placement of the four-chamber imaging plane (yellow line). The orientation of this plane in relation to the anatomical orientation of the heart is also shown. Placement of the imaging plane at mid ventricle produces the resultant image.

Figure 1.7. Anatomical reference, MR prescription plane (yellow line), and resultant MR image of the left ventricular four-chamber long-axis view are shown.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant left ventricular four-chamber view

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MAYO CLINIC GUIDE TO CARDIAC MRI

Right Ventricular Imaging Visualization and interpretation of the structure and function of the right ventricle (RV) is an integral part of a routine cardiac MR examination. Under most circumstances, adequate visualization can be achieved from the planes used for imaging the LV. Under certain circumstances, however, additional imaging planes are required. In most of these cases, the addition of a single, conventional, axial imaging plane will suffice. In other specific instances, more complex right ventricular views are required, such as for the diagnosis of arrhythmogenic right ventricular dysplasia or Ebstein anomaly. As with the previous figures illustrating visualization of the LV, solid arrows indicate commonly acquired imaging planes and dashed arrows represent optional planes. The color of the arrow symbolizes the left (red) or right (blue) side of the heart (Figure 1.8). The arrows also identify the relationship between the prescription and resultant image planes.

Figure 1.8. Imaging planes used to characterize the RV of the heart. The numbers indicate the acquisition order. Note that, to image the right side of the heart, it is necessary to first acquire several planes used to visualize the left heart.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Sagittal localizer (1)

Four-chamber localizer (2)

Conventional axial (3)

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MAYO CLINIC GUIDE TO CARDIAC MRI

Conventional Axial Right Ventricular View The sagittal localizer image set provides the anatomical landmarks necessary for prescribing the axial right ventricular cine data. Using the axial plane can facilitate tracing the RV for calculating RV volumes and ejection fraction. In general, straight axial data sets provide a more complete and easy-to-identify tricuspid valve plane. To prescribe conventional axial views, perform the following steps: ■

■

From the sagittal localizer image, identify the top of the ascending aorta cranially and the apex of the heart caudally. Prescribe a series of straight axial imaging planes that are centered roughly on the septum of the heart.

Figure 1.9 shows the placement of the axial image planes (yellow lines) on the sagittal localizer covering the ascending aorta and apex of the heart. The orientation of these planes in relation to the anatomical orientation of the heart is also shown.

Figure 1.9. Anatomical reference, MR prescription planes (yellow lines), and resultant MR images of the RV with conventional or true axial views are shown. Note that these planes are prescribed as true axial planes that are orthogonal to the sagittal imaging planes acquired initially.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant conventional axial right ventricular views

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MAYO CLINIC GUIDE TO CARDIAC MRI

Additional Right Ventricular Views If additional views of the RV are required, the flow diagram in Figure 1.10 can be followed.

Figure 1.10. Additional imaging planes used to characterize the RV of the heart. The numbers indicate the acquisition order. Solid arrows indicate typical imaging planes and dashed arrows indicate optional planes. Most of these planes are optional.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

23

Sagittal localizer (1)

Four-chamber localizer (2)

Conventional axial (3)

Right ventricle inflow tract vertical long axis (4)

Right ventricle sagittal outflow tract (5)

24

MAYO CLINIC GUIDE TO CARDIAC MRI

Right Ventricular Inflow Tract Long-Axis View Acquisition of the four-chamber localizer view provides the anatomical landmarks necessary for prescribing right ventricular inflow tract views. The right ventricular inflow tract long-axis view should be oriented parallel with the interventricular septum and centered at the midventricular point of the RV. To prescribe right ventricular inflow tract long-axis views, perform the following steps: ■

■

From the four-chamber localizer data, identify the image that is approximately at end diastole. At this point of the cardiac cycle, the heart is relaxed and largest. Prescribe an imaging plane that is centered on the RV and is parallel to the septum. The plane should be centered at approximately mid ventricle.

Figure 1.11 shows the placement of a single imaging plane (yellow line) parallel to the septum on the four-chamber localizer view and centered at the middle of the right ventricular cavity. The orientation of this plane in relation to the anatomical orientation of the heart is also shown. Placement of the imaging plane at mid ventricle produces the resultant image.

Figure 1.11. Anatomical reference, MR prescription plane (yellow line), and resultant MR image of the right ventricular inflow tract in the long-axis view are shown.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant right ventricular long-axis view

25

26

MAYO CLINIC GUIDE TO CARDIAC MRI

Right Ventricular Sagittal Outflow Tract View Acquisition of straight axial images provides the relevant anatomical landmarks necessary to prescribe a sagittal imaging plane oriented so as to bisect the outflow tract from the RV. To prescribe a right sagittal outflow tract view, perform the following step: ■

On the axial data, prescribe a sagittal imaging plane that is centered on the pulmonary semilunar valve and also bisects the main pulmonary artery. This plane will be slightly oblique to the anterior-posterior axis of the patient and as such is not a true sagittal view.

Figure 1.12 shows the placement of a single imaging plane (yellow line) on an axial image showing the main pulmonary artery. Placement of the imaging plane at mid ventricle produces the resultant image.

Figure 1.12. Anatomical reference, MR prescription plane (yellow line), and resultant MR image of the outflow tract of the RV in the sagittal view are shown.

CHAPTER 1

CARDIAC ANATOMY AND MR IMAGING PLANES

Prescription Anatomical reference

Resultant right ventricular sagittal outflow tract view

27

CHAPTER 2

CARDIAC PHYSIOLOGY

Chapter 2

CARDIAC PHYSIOLOGY Paul R. Julsrud, MD Eric E. Williamson, MD

Introduction In-depth knowledge of the physiology of the heart is essential to diagnosing and distinguishing the multitude of complex cardiac disease processes. The figures in this chapter show the relationships among pressure, electrical activity, and associated images throughout the cardiac cycle. As quantitative assessment of cardiac function becomes more important, so too will the need to understand the interrelationships among these various cardiac events.

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Events of the Cardiac Cycle (Left Heart) Figure 2.1 shows the various physiologic events of the left heart throughout the cardiac cycle. The relationships of pressure, volume, and flow to the electrical potential of the heart as a whole (as measured by electrocardiography [ECG]) are shown. The systolic and diastolic time intervals denote the portions of the cardiac cycle taken up by each phase and are defined by the intervals between the black and red, and red and blue lines, respectively, on the ECG waveform. It is important to note that the percentage values shown for the time intervals of systole (40%) and diastole (60%) are valid only for the given heart rate (HR) of 70 beats per minute. As HR increases, the systolic time interval remains relatively unchanged, while the diastolic interval decreases. This results in a percentage increase in systole and a percentage decrease in diastole. Consequently, end diastole is the most variable phase of the cardiac cycle.

Figure 2.1. Important cardiac physiologic waveforms during the cardiac cycle. The bottom 3 traces show the pressure, volume, and flow curves within the left-sided cardiac chambers throughout the cardiac cycle, correlated with the ECG waveform at the top. EDV, end-diastolic volume; ESV, end-systolic volume. (Modified from Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2006. Used with permission of Mayo Foundation for Medical Education and Research.)

Electrical potential

CHAPTER 2

Systole 40%

Diastole 60%

QRS

End diastole

P

T

120

Aortic pressure

80

Ventricular pressure

Atrial pressure 10 0

Volume (mL)

HR=70

End systole

P

Pressure (mm Hg)

CARDIAC PHYSIOLOGY

130

EDV

50

ESV

0

Aortic outflow

Mitral inflow

Flow (mL/s)

500

0

Isovolumic contraction

Isovolumic relaxation

33

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MAYO CLINIC GUIDE TO CARDIAC MRI

MR Imaging Characteristics of the Cardiac Cycle Figure 2.2 shows the relationship between the electrical activity of the heart as a whole and the corresponding magnetic resonance (MR) images acquired as part of a cine imaging series in both four-chamber long-axis and two-chamber short-axis views of the left ventricle (LV). Typical cine acquisitions acquire 20 images corresponding to fixed time points or phases of the cardiac cycle. In this figure, only 10 images for both views are reproduced, representing every even or odd phase of the cardiac cycle. Viewed as a dynamic display, these cine loops simulate real-time imaging and are used to interpret the contractility of the heart. The figure also shows enlarged views of the heart at end systole (red outline) and end diastole (blue outline). At end systole, the cavity of the LV is smallest, with maximal thickness of the myocardium; at end diastole, the LV is most relaxed, with maximal chamber volume and minimal myocardial wall thickness.

Figure 2.2. Four-chamber long-axis (top row) and twochamber short-axis (bottom row) cine series corresponding to the electrical potential trace of a cardiac cycle. Enlarged MR images at bottom are those acquired at end systole (red outline) and end diastole (blue outline).

CHAPTER 2

CARDIAC PHYSIOLOGY

R

T

P

S

U

Q

Four-chamber long axis

Two-chamber short axis

35

CHAPTER 3

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS WITH CASE EXAMPLES

Chapter 3

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS WITH CASE EXAMPLES Jacobo Kirsch, MD James F. Glockner, MD, PhD Philip A. Araoz, MD Paul R. Julsrud, MD Kiaran P. McGee, PhD Eric E. Williamson, MD

Introduction The purpose of this chapter is threefold. First, it provides recommended magnetic resonance (MR) imaging protocols for indications in which cardiac MR has been proved to be clinically useful. Second, it provides example MR images for each indication and the imaging sequences that most clearly illustrate the associated findings. Third, it provides descriptions of each disease process and specific recommendations for image interpretation and analysis. The list of indications is not complete, but it covers a broad spectrum of cardiac diseases, with specific focus on the conditions that are most likely to be encountered in clinical practice. Throughout this chapter, we refer to specific pulse sequences and provide examples to illustrate the appearance of a given disease process or abnormality. It is assumed that the reader is familiar with these cardiac MR imaging (MRI) techniques. For the interested reader, in-depth descriptions of all sequences used in this chapter are provided in Chapter 4. For those who are new to cardiac MRI, we recommend reviewing Chapter 4 before reviewing this chapter.

39

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Myocardial Perfusion and Viability Assessment of the delivery of blood to the myocardium is of utmost importance in patients with ischemic heart disease or the suspicion of it. Regional assessment of myocardial perfusion is performed by administering an exogenous gadolinium-based contrast agent, followed by pseudo–real-time imaging of the arrival of the contrast into the right and then left chambers of the heart. Assessment of myocardial perfusion is therefore based on the first pass of the contrast through the myocardium. Poorly perfused regions show decreased contrast enhancement and are typically identified as perfusion defects. Myocardial viability is assessed, following a delay after administration of the contrast agent, by using T1-weighted inversion recovery–based MRI sequences. The physiologic basis for this approach relies on the delayed wash-in and wash-out of the contrast agent in poorly perfused or ischemic myocardium. Nulling of normal myocardium is achieved by the appropriate choice of inversion time; regions with increased contrast uptake appear bright because of their contrast-enhanced T1 weighting. Figure 3.1 shows the 17 myocardial segments of the heart and their assigned coronary arteries, as defined by the American Heart Association. The 17th segment located at the apical tip can be supplied by any one of the three coronary arteries and has been identified in this figure as being supplied by the left anterior descending coronary artery.

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

CHAPTER 3

41

Infarct Distributions

Coronary Artery Territories Short axis Apical

Mid

Basal

8

Mid

1

7

13 14

Vertical long axis

12

2

6

16 15

17 9

11

LAD

5

3

10

4

RCA

LCX

Figure 3.1. Assignment of the 17 myocardial segments to the territories of the left anterior descending artery (LAD), the right coronary artery (RCA), and the left circumflex coronary artery (LCX). The image of the heart (top) shows the anatomical location of the three main coronary arteries, as well as the three parallel planes that correspond to the short-axis slices shown at bottom. (From Imaging guidelines for nuclear cardiology procedures: part 2. J Nucl Cardiol. 1999;6[2]:G47-84. Used with permission.)

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MAYO CLINIC GUIDE TO CARDIAC MRI

Imaging Protocol––Myocardial Perfusion and Viability

Series 1

Plane

Imaging sequence

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Specific parameters

≈ Time/slice (s)

Breath hold Single cardiac phase

20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

CHAPTER 3

Series 4

Plane

Vertical and horizontal long axis

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Imaging sequence

Specific parameters

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

43

≈ Time/slice (s) 10-16

Prescription should be based on midventricular short-axis view with slices bisecting the LV parallel and perpendicular to the septum.

5

Short axis

Perfusion

30-40 temporal phases

50 -70

Patient typically needs more than one breath hold to complete. Coaching is required beforehand to prevent rapid inspiration on second breath hold. Inject 20 mL gadolinium contrast at 4-5 mL/s and start sequence simultaneously. Instruct patient to hold his breath for as long as possible and then to do additional breath holds until the scan is over. After the scan has finished, may inject an additional 20 mL gadolinium contrast at 2 mL/s (to improve contrast on delayed enhancement sequence).

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MAYO CLINIC GUIDE TO CARDIAC MRI

Series 6

Plane Short axis

Imaging sequence Delayed enhancement

Specific parameters Breath hold TI = 100-300 ms

≈ Time/slice (s) 10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus. 7

Long axis

Delayed enhancement

Breath hold TI = 100-300 ms

10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus.

LV, left ventricle; NEX, number of excitations; TI, inversion time; VPS, views per segment.

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

45

Case Examples Subendocardial Myocardial Infarction

Figure 3.2. Short-axis perfusion image (left) acquired shortly after the intravenous administration of gadolinium shows a subendocardial area of low signal in the inferior segments, characteristic of a first-pass myocardial perfusion defect (arrow). A corresponding two-chamber myocardial delayed enhancement (MDE) image (right) shows persistent subendocardial hyperenhancement of the inferior wall of the LV, confirming the presence of an infarction (arrow).

Figure 3.3. Four-chamber MDE image demonstrates persistent subendocardial enhancement along the lateral wall of the LV.

The rationale behind MDE sequences is that cellular disruption occurring in the infarcted region causes an increase in vascular permeability and corresponding expansion of the extracellular space. Injected gadolinium accumulates in the area of infarcted myocardium and is cleared more slowly from this region than from normal, healthy myocardium. These two factors result in the characteristic appearance of persistent hyperenhancement in the region of a myocardial infarction.

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Transmural Myocardial Infarction

Figure 3.4. Four-chamber MDE image demonstrates full-thickness delayed enhancement, characteristic of a large LAD distribution infarction. The “dark core” of the infarction is believed to represent microvascular obstruction, meaning that the arterial occlusion was severe enough to prevent any gadolinium from reaching that area.

Figure 3.5. Short-axis balanced gradient echo (left) and MDE (right) images show thinning of the inferolateral left ventricular wall with corresponding full-thickness enhancement, characteristic of an underlying infarction in the LCX arterial territory.

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47

Figure 3.6. Three-chamber balanced gradient echo image shows focal thinning of the anterior left ventricular wall, consistent with an LAD distribution infarction.

Myocardial infarction spreads over time, like a wave front, from the endocardium to the epicardium. In infarcted myocardium, the subendocardial layer should always be affected. If an area of delayed enhancement spares the subendocardial layer or is not confined to a single vascular territory, nonischemic myocardial diseases should be considered.

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Ischemic Cardiomyopathy

Figure 3.7. Four-chamber balanced gradient echo (left) and MDE sequence (right) images show global dilatation of the left ventricular cavity. Thinning and persistent enhancement of the mid and apical segments of the LV are consistent with an ischemic dilated cardiomyopathy.

The term ischemic cardiomyopathy is commonly used to refer to congestive heart failure due to coronary artery disease and resulting myocardial infarction. After a myocardial infarction, some degree of left ventricular dysfunction is expected; it usually correlates with the extent and location of myocardial injury. The use of gadolinium-enhanced perfusion and MDE images for these patients can be important for distinguishing ischemic from nonischemic causes of dilated cardiomyopathy.

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

49

Cardiomyopathies The cardiomyopathies make up a heterogeneous group of disorders characterized by dysfunction of the cardiac myocytes. This dysfunction leads to a decrease in the ability of the heart to maintain adequate cardiac output. Depending on the type of cardiomyopathy, the imaging findings can be variable and relatively characteristic. Common forms of cardiomyopathy include dilated, hypertrophic, and restrictive cardiomyopathy. Additional disorders involving dysfunction of cardiac myocytes include arrhythmogenic right ventricular cardiomyopathy (ARVC), apical ballooning syndrome, and myocarditis.

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MAYO CLINIC GUIDE TO CARDIAC MRI

Imaging Protocol––Cardiomyopathies

Series 1

Plane

Imaging sequence

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Specific parameters

≈ Time/slice (s)

Breath hold Single cardiac phase

20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

CHAPTER 3

Series

Plane

4 Left ventricular outflow tract

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Imaging sequence

Specific parameters

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

51

≈ Time/slice (s) 10-16

Disease-specific imaging plane. See specific diseases for actual prescription.

5

Short axis

Perfusion

30-40 temporal phases

50-70 for total study

Patient typically needs more than one breath hold to complete. Coaching is required beforehand to prevent rapid inspiration on second breath hold. Inject 20 mL gadolinium contrast at 4-5 mL/s and start sequence simultaneously. Instruct patient to hold his breath for as long as possible and then to do additional breath holds until the scan is over. After the scan has finished, may inject an additional 20 mL gadolinium contrast at 2 mL/s (to improve contrast on delayed enhancement sequence).

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MAYO CLINIC GUIDE TO CARDIAC MRI

Series 6

Plane Short axis

Imaging sequence Delayed enhancement

Specific parameters Breath hold TI = 100-300 ms

≈ Time/slice (s) 10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus. 7

Long axis

Delayed enhancement

Breath hold TI = 100-300 ms

10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus.

LV, left ventricle; NEX, number of excitations; TI, inversion time; VPS, views per segment.

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

53

Case Examples Dilated Cardiomyopathy

Figure 3.8. Four-chamber long-axis (top left) and midventricular short-axis (top right) balanced gradient echo images show marked left ventricular dilatation. A twochamber long-axis MDE image (bottom) shows no evidence of myocardial infarction.

The most common form of cardiomyopathy, dilated (congestive) cardiomyopathy, is characterized by enlargement of the cardiac chambers and decreased contractile function in the absence of ischemic causes. Although most commonly idiopathic, dilated cardiomyopathy can be due to viral infection or exposure to toxic substances (eg, alcohol) or can be associated with pregnancy (peripartum cardiomyopathy).

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MAYO CLINIC GUIDE TO CARDIAC MRI

Hypertrophic Cardiomyopathy

Figure 3.9. Hypertrophic obstructive cardiomyopathy. Three-chamber long-axis (top) and midventricular short-axis (bottom) balanced gradient echo images demonstrate asymmetric septal hypertrophy, characteristic of hypertrophic obstructive cardiomyopathy. The low signal flow void seen in the left ventricular outflow tract (top) is consistent with obstructive physiology. Cine images in this case showed systolic anterior motion of the anterior leaflet of the mitral valve, which is thought to contribute to the outflow tract obstruction.

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55

Figure 3.10. Hypertrophic cardiomyopathy. Two-chamber long-axis balanced gradient echo (top) and midventricular short-axis MDE (bottom) images. Symmetric left ventricular hypertrophy with mitral regurgitation (top) is most likely due to outflow obstruction. MDE image (bottom) demonstrates characteristic small foci of hyperenhancement at the junction points between the right ventricle (RV) and the interventricular septum.

The second most common form of cardiomyopathy, hypertrophic cardiomyopathy, is characterized by thickening of the LV wall, which can be focal or diffuse and symmetric. In a subtype of the disorder, hypertrophic obstructive cardiomyopathy, the wall thickening can cause obstruction of the normal flow of blood, at either the left ventricular outflow tract (Figure 3.9) or the midventricular level. In the case of obstruction, flow dephasing can be observed using bright blood cine or phase-contrast images. When left ventricular outflow tract obstruction is present, it can be associated with systolic anterior motion of the anterior mitral leaflet (Figure 3.9), which typically results in mitral regurgitation (Figure 3.10).

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Restrictive Cardiomyopathy

Figure 3.11. Cardiac amyloidosis. Fourchamber long-axis balanced gradient echo (top left), two-chamber long-axis MDE (top right), and midventricular short-axis MDE (bottom) images of cardiac amyloidosis. Long-axis images show signs of increased cardiac filling pressures, with atrial dilatation (top left and right) and normal-thickness pericardium (top left). MDE images demonstrate heterogeneous, patchy-appearing myocardial signal with poor “nulling” regardless of the inversion time.

Restrictive cardiomyopathy is a less common form of myocardial dysfunction which can be idiopathic or can occur as a result of systemic diseases (eg, amyloidosis or sarcoidosis). The imaging findings in restrictive cardiomyopathy predominantly result from restricted filling in diastole and include decreased diastolic volume of the ventricles and dilated atria in the presence of preserved systolic function. A few causes of restriction have specific imaging findings on MRI that can be helpful in making the diagnosis (Figures 3.11 and 3.12).

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

57

Eosinophilic Cardiomyopathy

Figure 3.12. Eosinophilic cardiomyopathy. Four-chamber long-axis balanced gradient echo (top left and right) and two-chamber long-axis MDE (bottom) images of eosinophilic cardiomyopathy. Four-chamber images show signs of increased cardiac filling pressures, with atrial dilatation (top left and right) and normal-thickness pericardium (top right). The MDE image shows diffuse endocardial thickening and hyperenhancement not corresponding to a vascular distribution. Thickening of the mitral valve leaflets and obliteration of the left ventricular cavity also have been described for eosinophilic cardiomyopathy but neither is seen in these images.

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MAYO CLINIC GUIDE TO CARDIAC MRI

Arrhythmogenic Right Ventricular Cardiomyopathy

Figure 3.13. Four-chamber balanced gradient echo images of ARVC at end diastole (left) and end systole (right) demonstrate a small outpouching of the free wall of the RV during systole (paradoxical motion). The RV is mildly enlarged.

ARVC is characterized pathologically by fatty or fibrous fatty tissue replacement of the right ventricular myocardium. The most commonly affected locations include the right ventricular apex, pulmonary infundibulum, and subtricuspid region. The involved myocardium can evoke ventricular arrhythmias originating in the RV that induce syncope and that have been linked to an estimated 5% of sudden deaths in persons younger than 35 years in the United States. MRI has been considered the ideal imaging technique to detect fatty tissue infiltration in the RV among patients with typical ARVC. Other features such as trabecular disarray, wall thinning, regional akinesis/dyskinesis, and, most importantly, an increased right ventricular volume can also be fairly easily detected by MRI. However, care should be taken because many healthy patients can have focal fatty infiltration along the RV free wall or focal akinesis at the attachment site of the moderator band on the free wall of the ventricle.

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

59

Apical Ballooning Syndrome

Figure 3.14. Systolic two-chamber longaxis balanced gradient echo image (top left), and two-chamber long-axis (top right) and apical short-axis (bottom) MDE images. Long-axis images demonstrate systolic dilatation of the left ventricular apex with no evidence of delayed hyperenhancement (top right and bottom) to suggest myocardial infarction.

Apical ballooning syndrome is a potentially reversible clinical syndrome in which patients typically present with elevated troponin levels and electrocardiographic changes that can be indistinguishable from an acute coronary syndrome. The syndrome occurs most frequently among postmenopausal women and consists of transient hypokinesis, akinesis, or dyskinesis of the LV, typically involving more than one vascular distribution. The wall motion abnormalities seen in apical ballooning syndrome should resolve within days to weeks, and MDE MR images in these patients should not show delayed hyperenhancement in any phase of the disease. Cardiac MRI is therefore an excellent tool for distinguishing between apical ballooning syndrome and myocardial infarction.

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Myocarditis

Figure 3.15. Two-chamber long-axis MDE (top left), midventricular short-axis triple inversion recovery (top right), and midventricular short-axis MDE (bottom) images showing scattered focal areas of subepicardial delayed hyperenhancement (left) and edema (right) consistent with acute myocardial inflammation. Findings are characteristic of acute myocarditis. Follow-up images after treatment can show a decrease in regional edema; however, delayed hyperenhancement usually persists and is thought to represent irreversible myocardial injury.

Acute myocarditis comprises a wide variety of infectious, toxic, and autoimmune causes of myocardial inflammation, which can progress to widespread myocardial damage and even to cardiomyopathy. Unfortunately, clinical symptoms are nonspecific, and the diagnosis of myocarditis can be difficult to establish. Cardiac MRI is a powerful tool that can provide an assessment of regional inflammation and edema, cardiac function, and disease progression. Initial findings of edema and delayed hyperenhancement are believed to represent acute inflammation with myocyte injury, whereas persistence of hyperenhancement after resolution of acute symptoms suggests myocyte necrosis and subsequent fibrosis.

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61

Valvular Disease MRI is currently gaining acceptance as a noninvasive method of evaluating the cardiac valves. The high spatial resolution of MRI, along with its inherent ability to distinguish between cardiac structures and the adjacent blood pool without the need for intravenous contrast agents, makes this an excellent means of assessing cardiac valvular anatomy. Additionally, flow-sensitive techniques allow for detection of the turbulent jets typically seen with valvular stenosis and regurgitation. By combining cine images used for the determination of ventricular volumes and phase-contrast images for the quantitation of flow, cardiac MRI can be used as a comprehensive, noninvasive method for assessment of valvular disease.

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MAYO CLINIC GUIDE TO CARDIAC MRI

Imaging Protocol––Valvular Disease

Series 1

Plane

Imaging sequence

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Specific parameters

≈ Time/slice (s)

Breath hold Single cardiac phase

20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

CHAPTER 3

Series 4A

Plane

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Imaging sequence

Long axis– Bright blood cine left ventricle, (balanced gradient echo) left atrium (mitral regurgitation)

Specific parameters Breath hold 20 cardiac phases

63

≈ Time/slice (s) 10-16

Slices should be prescribed from the short-axis slice containing the base of the heart. Views should be prescribed in 45° increments about the center of the LV. These views should contain the mitral valve and regurgitant jet.

4B

Oblique long Bright blood cine axis– aortic (balanced gradient echo) outflow tract (aortic insufficiency)

Breath hold 20 cardiac phases

10-16

The slice should be prescribed from the short-axis slice containing the base of the heart. This view should show the regurgitant jet.

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MAYO CLINIC GUIDE TO CARDIAC MRI

Series 5

Plane

Imaging sequence

Oblique slice Cine phase contrast through aortic region of interest– ascending, descending

Specific parameters Breath hold 20 cardiac phases VPS = 4-8 VENC = 250-300 Flow sensitization direction = slice

≈ Time/slice (s) 10

For aorta: Slice should be through proximal ascending aorta, valve to coronary ostia, and perpendicular to the aorta for accurate flow measurements. Set VENC to 500-600 if patient has history of or evidence for AS (ie, systolic jet in aorta on three-chamber cine). FOV should be as small as possible to maximize number of pixels within aorta. An additional in-plane slice is useful for measuring peak velocities in AS and should be prescribed oblique to the long axis of the aorta. Most useful flow-encoding direction is along the slice-encoding axis. 6

Valve plane

Bright blood cine (balanced or spoiled gradient echo)

Breath hold 20 cardiac phases

10

Imaging plane bisects the valve plane. Good for aortic outflow tract and aortic valve views; regurgitant jets are often visualized more clearly with spoiled gradient echo sequence, although image quality is poor compared with balanced steady-state acquisition. In general, there also is less turbulent flow artifact. To increase conspicuity of the flow jet, reduce imaging bandwidth. AS, aortic stenosis; FOV, field of view; LV, left ventricle; NEX, number of excitations; TI, inversion time; VENC, velocity encoding; VPS, views per segment.

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CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

65

Case Examples Aortic Stenosis, Aortic Insufficiency

Figure 3.16. Aortic insufficiency. Three-chamber balanced gradient echo cine image in diastole (left) shows a dark jet of aortic insufficiency extending from the aortic valve toward the anterior mitral valve leaflet. Transverse diastolic balanced gradient echo cine image through the aortic valve plane (right) shows a small central regurgitant orifice.

Figure 3.17. Aortic stenosis. Coronal oblique balanced gradient echo cine image (left) reveals a dark stenotic jet extending from the aortic valve into the proximal aorta. The corresponding valve plane image (right), also obtained in systole, reveals a bicuspid aortic valve with a very narrow opening.

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Aortic insufficiency can be caused by primary valve disease or aortic root dilatation. The most common cause is idiopathic degeneration of a normal valve, with additional causes including Marfan syndrome, aortic aneurysm, bicuspid aortic valve, rheumatic heart disease, and endocarditis. Combined aortic insufficiency and stenosis is common. Patients are often asymptomatic despite severe left ventricular volume overload and may have irreversible LV dysfunction by the time symptoms appear, which limits the value of valve replacement. For this reason, close monitoring of patients with significant aortic insufficiency is recommended. MRI can be a valuable tool for evaluating patients with aortic insufficiency. It provides accurate measurements of left ventricular size and function, as well as visualization of abnormal valve morphology. Qualitative estimation of the severity of aortic insufficiency by MRI agrees fairly well with that obtained by echocardiography, and quantitative evaluation can be performed using cine phase-contrast flow measurement techniques or by noting the difference in stroke volume between the RV and LV.

QUANTIFYING AORTIC INSUFFICIENCY Regurgitant volume Mild Moderate Moderate/severe Severe

<30 mL/beat 30-45 mL/beat 46-60 mL/beat >60 mL/beat

Regurgitant fraction Mild Moderate Severe

15%-20% 21%-40% >40%

Aortic stenosis most commonly occurs with idiopathic degeneration of a normal valve but can also be caused by degeneration of a bicuspid valve (typically occurring at a younger age) or by rheumatic heart disease. Supravalvular and subvalvular stenosis usually are congenital lesions, but subvalvular functional stenosis also occurs with hypertrophic obstructive cardiomyopathy. Classic symptoms include dyspnea on exertion, exertional syncope, and angina. After symptoms occur, the clinical course usually deteriorates rapidly unless the valve is replaced. Left ventricular hypertrophy is the primary compensatory mechanism. MRI can directly demonstrate hypertrophy of the LV and provide accurate measurements of ventricular mass and function. Stenosis can be qualitatively estimated by visualizing flow jets; quantitative measurements can be obtained either by direct planimetry of the valve or by applying cine phase-contrast techniques to measure peak velocities across the valve, which can be used to estimate pressure gradients.

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67

QUANTIFYING AORTIC STENOSIS Aortic valve area Normal Mild AS Moderate AS Severe AS

Peak systolic velocity cm2

2.0-4.0 1.1-1.9 cm2 0.75-1.0 cm2 <0.75 cm2

Normal Mild AS Moderate AS Severe AS

1-2.4 m/s 2.5-2.9 m/s 3.0-4.0 m/s >4 m/s

Analysis of aortic insufficiency and stenosis by MRI: Useful cardiac MRI–derived metrics include: ■ Regurgitant volume per beat ■ Regurgitant fraction: regurgitant volume or regurgitant flow divided by positive volume or flow ■ Ejection fraction ■ Cardiac output ■ End-systolic and end-diastolic volumes, as well as short-axis LV diameter at end systole and end diastole at the midventricular level (to duplicate standard echocardiographic measurement) ■ Flow though the pulmonary artery. (Note: in normal patients this should be identical to cardiac output; with aortic insufficiency, the cardiac output is increased because of the regurgitant volume.) In patients with aortic stenosis: Peak pressure gradient = 4(Vmax)2 where Vmax is the maximal velocity of the stenotic jet in the proximal aorta. Mean pressure gradient = (4 ∑[Vmax]2dt)/Δt where dt is the time interval for the phase-contrast cine image in which Vmax is measured and Δt the interval over which these velocities are summed (typically one R-R interval).

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This is the time average of Vmax over systole. For this measurement, it is best to choose a small region of interest that encompasses the highest velocity portion of the flow jet (this is somewhat arbitrary). Aortic valve area = AOT(VOT)/Vmax where AOT is the outflow tract area, VOT the outflow tract maximum velocity, and Vmax the maximum velocity of the stenotic jet in the proximal aorta. This measurement can also be performed directly if good cine images have been made through the stenotic valve. Alternative measurement of regurgitant volume: ■ Phase-contrast based = stroke volume in aorta – stroke volume in main pulmonary artery OR = stroke volume in aorta – mitral valve inflow ■

Short-axis balanced gradient echo based = LV stroke volume – RV stroke volume

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Mitral Stenosis, Mitral Regurgitation

Figure 3.18. Mitral stenosis. Short-axis balanced gradient echo cine image at base of heart during diastole (left) and three-chamber cine image (right) show stenotic mitral valve (arrows) with reduced area and thickened leaflets.

Figure 3.19. Mitral valve prolapse and regurgitation. Diastolic (left) and systolic (right) images from three-chamber bright blood cine sequence reveal prolapsing mitral valve leaflets and a small jet of mitral regurgitation (arrow).

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Mitral stenosis is most often a result of rheumatic heart disease. Symptoms typically include shortness of breath and fatigue, which are often exacerbated by exercise. A substantial percentage of patients with moderate or severe mitral stenosis eventually have development of atrial fibrillation, which complicates evaluation with MRI. Elevated left atrial pressure leads to atrial dilatation, pulmonary edema, and signs of pulmonary artery hypertension. MRI can visualize stenotic flow jets across the mitral valve, and mitral valve area can be estimated by planimetry. Peak velocities can be measured with cine phase-contrast sequences to estimate pressure gradients. Left atrial size, as well as right ventricular size and function, can be determined. Mitral regurgitation has many causes, including ischemia and papillary muscle rupture, infective endocarditis, mitral valve prolapse, hypertrophic obstructive cardiomyopathy, rheumatic disease, and idiopathic valvular degeneration. Patients with acute mitral regurgitation may present with pulmonary edema and low cardiac output, whereas those with chronic mitral regurgitation may have symptoms of fatigue and weakness. With significant mitral regurgitation, both the left atrium and LV become dilated. MRI can visualize jets of mitral regurgitation in the left atrium, which can be qualitatively evaluated. Quantitative measurement of mitral regurgitant volumes may be obtained by measuring the difference in left and right ventricular stroke volume, or by the difference in left ventricular stroke volume and forward flow in the aorta (using cine phase-contrast sequences). MRI also provides accurate assessment of left ventricular size and function, as well as left atrial size.

QUANTIFYING MITRAL REGURGITATION Grade Grade I/IV Grade II/IV Grade III/IV Grade IV/IV

Regurgitant volume Mild Moderate Moderately severe Severe

<30 mL 30-44 mL 45-59 mL ≥60 mL

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Cine flow analysis of mitral stenosis and regurgitation: Useful cardiac MRI–derived metrics include: ■ Regurgitant volume per beat––can be calculated by: 1. The difference between flow in the proximal main pulmonary artery and proximal aorta. 2. Measurement of left ventricular stroke volume by tracing end-systolic and end-diastolic short-axis images and subtracting flow in the proximal aorta as measured by phase-contrast flow sequence. 3. Direct phase-contrast flow measurement of regurgitant jet in left atrium: for accurate quantitation it is important that the VENC is set high enough and that the slice is oriented perpendicular to the direction of flow. 4. Inflow through the mitral valve plane minus left ventricular stroke volume, as calculated from phase-contrast images through the proximal aorta. 5. Left ventricular minus right ventricular stroke volumes, as measured from short-axis cine bright blood images. ■ Ejection fraction ■ Cardiac output ■ Left atrial diameter ■ End-systolic and end-diastolic volumes, as well as short-axis left ventricular diameter at the midventricular level at end systole and end diastole (to duplicate standard echocardiographic measurement) ■ Reversal of flow in pulmonary veins. (This is useful to note, but it is unclear whether quantitation is important.)

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Tricuspid Stenosis, Tricuspid Regurgitation

Figure 3.20. End-diastolic (left) and end-systolic (right) frames from four-chamber balanced gradient echo cine sequence show dilatation of the RV in a patient with pulmonary hypertension. A small jet of tricuspid regurgitation is seen in the right atrium (right).

Tricuspid stenosis is almost always related to rheumatic heart disease and is rarely an isolated finding; the aortic and mitral valves also are usually involved. Other causes of tricuspid stenosis include congenital atresia and carcinoid syndrome. Patients typically present with signs and symptoms of right heart failure: fatigue, abdominal pain, and lower-extremity swelling. Tricuspid regurgitation is most commonly a result of dilatation of the RV and tricuspid annulus rather than a result of intrinsic valvular disease. This is also the most common valvular lesion among intravenous drug abusers with infectious endocarditis, since leftsided valves are protected by the lungs, which act as a filter.

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150

150

100

100

50 0 -50 -100 -150

Velocity (cm/s)

Velocity (cm/s)

Pulmonary Stenosis, Pulmonary Regurgitation

50 0 -50 -100 -150

Figure 3.21. Pulmonary regurgitation. Frames from a 3D representation of cine phase-contrast blood flow data across the pulmonary valve during systole (left) and diastole (right) in a patient with severe pulmonary regurgitation. Note the near-complete flow reversal in diastole.

Figure 3.22. Pulmonary stenosis. Systolic frame from balanced gradient echo cine sequence oriented through the right ventricular outflow tract shows incomplete opening of the pulmonary valve leaflets with slight doming.

Pulmonary stenosis is almost always due to congenital deformity of the valve. A pressure gradient develops across the valve, eventually resulting in right heart failure. Pulmonary regurgitation is most commonly caused by dilatation of the valve ring secondary to pulmonary hypertension. Infective endocarditis is the second leading cause of pulmonary regurgitation.

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Cardiac Masses The pathology and etiology of a cardiac mass can be determined by following the cardiac mass imaging decision tree at right. Examples of various masses, identified according to the decision tree schema, are given in this section. Characteristic imaging features are presented for each type of mass.

Cardiac Mass

hypertrophy of the interatrial septum (fat in the interatrial septum, spares fossa ovalis)

Thrombus

Neoplasm

• Typical

location (near area of dyskinesis, especially the apex or left atrial appendage)

• No

enhancement

• Pericardial

sleeve recess (low density inferior and/or posterior to right pulmonary vein)

Extension from mediastinum? • Primary

lung cancer

Extension from inferior vena cava? • Renal

cell carcinoma

• Metastases

• Hepatocellular

carcinoma

• Thymoma

• Adrenocortical

carcinoma

or other mediastinal mass

• Lymphoma

• Trabeculation/papillary

muscle

Diagnosis suggested by clinical history? • Known primary – Metastases (variable appearance) • Tuberous sclerosis – Rhabdomyoma (multiple masses, may be low density) • Hypertension – Pheochromocytoma (very vascular, often along coronaries) • Immunocompromise – Lymphoma (variable appearance)

Aggressive features present? (Invasive, heterogeneous, associated pericardial effusion) • Primary cardiac sarcoma (variable appearance) • Metastases (variable appearance)

Nonaggressive features present? (Circumscribed, noninvasive, homogeneous) • Hemangioma (homogeneous, marked enhancement) • Myxoma without characteristic narrow stalk (broad base of attachment, well-circumscribed, may be heterogeneous)

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Definitive diagnosis from imaging appearance? • Metastases – Visualized masses elsewhere • Myxoma – Narrow stalk (especially if attached to interatrial septum) • Lipoma – Homogeneous fatty mass • Angiosarcoma – Hemorrhagic, vascular, aggressive mass in pericardium or right atrium • Fibroma – Large, nonenhancing mass in myocardium, especially with calcification

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Normal Variant • Lipomatous

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Invading from outside the heart

Arising from inside the heart

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Imaging Protocol––Cardiac Masses

Series 1

Plane

Imaging sequence

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Specific parameters

≈ Time/slice (s)

Breath hold Single cardiac phase

20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

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Series 4

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Plane

Oblique based on mass location

Imaging sequence Black blood inversion recovery

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Specific parameters

≈ Time/slice (s)

Breath hold

10-16

Inversion recovery sequence to show cardiac morphology. There is no fat suppression in this sequence, so nonflowing fluids and lipids will both have high signal. Short-axis views are typically used to prescribe these imaging planes. Location is patient specific. 5

Oblique based on mass location

Black blood inversion recovery with fat suppression

Breath hold

10-16

Inversion recovery sequence with fat suppression. Acquisition of identical imaging planes as in series 4 provides a differential method for determining the likely histologic composition of the mass. Location is patient specific.

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Series 6

Plane Short axis

Imaging sequence Perfusion

Specific parameters 30-40 temporal phases

≈ Time/slice (s) 50-70 entire volume

Patient typically needs more than one breath hold to complete. Advise patient to avoid rapid inspiration on second breath hold. Inject 20 mL gadolinium contrast at 4-5 mL/s and start sequence simultaneously. Instruct patient to hold his breath for as long as possible and then to do additional breath holds until the scan is over. After the scan has finished, may inject an additional 20 mL gadolinium contrast at 2 mL/s (to improve contrast on delayed enhancement sequence). 7

Short axis

Delayed enhancement

TI = 100-300 ms

10-16

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus. 8

Long axis

Delayed enhancement

TI = 100-300 ms

10-16

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus.

LV, left ventricle; NEX, number of excitations; TI, inversion time; VPS, views per segment.

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Case Examples Thrombus

Figure 3.23. Four-chamber balanced gradient echo images in diastole (top left) and systole (top right) show a large area of dyskinesis at the apex. Within this region can be seen a mass with a broad attachment to the myocardium (arrows) which is well circumscribed and shows no discernable invasion. An MDE image (bottom) shows that the mass does not enhance.

This combination of features allows for a confident imaging diagnosis of a thrombus.

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Myxoma

Figure 3.24. Axial balanced gradient echo image (top left) shows a large mass in the left atrium (arrow). In an MDE image (top right), the mass (arrow) shows heterogeneous enhancement, indicating that the mass is a neoplasm. In this large mass, no definite attachment to the wall is visualized; this suggests that it could be a myxoma, which typically attaches by a narrow stalk. However, for confident diagnosis of a myxoma, direct visualization of a narrow stalk is required. A computed tomographic image from a different patient (bottom) depicts the narrow stalk (arrow). (From Araoz PA, et al. CT and MR imaging of benign primary cardiac neoplasms with echocardiographic correlation. Radiographics. 2000;20:1303-19. Used with permission.)

Myxomas most frequently arise from the atria, attached to the fossa ovalis, but may occur anywhere in the heart. Visualization of mobile tumor with a narrow stalk allows a confident diagnosis of myxoma.

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Figure 3.25. Oblique sagittal double inversion recovery image (left) from a different patient shows a large, circumscribed mass in the right ventricular outflow tract. The mass has a large base of attachment. An MDE image (right) shows that the mass has a central enhancing region. These imaging features suggest a benign neoplasm, most likely a hemangioma or a myxoma without the typical stalk.

This case was a pathologically proven cardiac myxoma that, atypically, had a broad base of attachment.

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Metastasis

Figure 3.26. Short-axis MDE image shows a large mass in the lateral wall (arrow). The mass has a broad attachment, shows no gross invasion of the underlying myocardium, and enhances.

The imaging characteristics of the mass itself do not allow for a confident diagnosis, but inspection of the liver on this image showed a mass that was a metastasis from a known carcinoid. The presence of an indeterminate mass with a known primary elsewhere is strongly suggestive of cardiac metastasis, the most common type of neoplasm in the heart.

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Hemangioma

Figure 3.27. Short-axis balanced gradient echo image (top) shows a well-circumscribed mass near the apex. The corresponding MDE image (bottom) shows that the mass has homogeneous bright enhancement, is well circumscribed, and does not appear to grossly invade the myocardium. These imaging features suggest a benign neoplasm, most likely a hemangioma or a myxoma without the typical stalk.

This case was a pathologically proven cardiac hemangioma.

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Lipoma

Figure 3.28. Four-chamber double inversion recovery MR image (top) shows a wellcircumscribed mass (arrow) in the apex of the RV, with diffuse increased signal. The wellcircumscribed appearance suggests it is benign. However, performing triple inversion recovery (bottom) provides fat saturation.

The signal in the mass decreases uniformly with fat saturation, meaning it is a homogeneous fatty mass and therefore a benign lipoma.

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Lipomatous Hypertrophy

Figure 3.29. Axial double inversion recovery image (top left) shows a lobulated mass in the interatrial septum with homogeneous increased signal. An image from the same series at a slightly lower level (top right) shows that the mass spares the fossa ovalis, which is characteristic of lipomatous hypertrophy of the interatrial septum. A triple inversion recovery image (bottom) at the same level as in the top left panel shows that the mass has homogeneously suppressed signal and is therefore made of fat.

These findings indicate lipomatous hypertrophy of the interatrial septum, which is not encapsulated, is not a mass or a neoplasm, and is a benign finding.

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Angiosarcoma

Figure 3.30. Axial double inversion recovery image (left) shows a large, lobulated, invasive mass centered on the right atrioventricular groove. A triple inversion recovery image (right) at a lower level with contrast shows that the mass enhances diffusely, clearly invades into the right atrium, and has an associated pericardial effusion.

The presence of enhancement and invasion into a chamber alone indicate that this is a malignant neoplasm, and, without a patient history of a primary neoplasm elsewhere, should represent a primary cardiac neoplasm. However, the location in the right atrium, bright enhancement, and presence of pericardial effusion are all typical features of angiosarcoma, the most common primary malignant cardiac neoplasm.

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Pericardial Disease The pericardium is a flask-shaped sac composed of two virtually inelastic layers, with a small amount of fluid between them, surrounding the heart. Its functions are to anchor the heart in the mediastinum, prevent the heart from dilating to an extreme degree in acute settings, and potentially act as a barrier to the spread of disease from contiguous organs. Pathologic changes in the stiffness of the pericardium or in the amount of fluid in it can alter normal heart function.

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Imaging Protocol––Pericardial Disease

Series 1

Plane

Imaging sequence

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Specific parameters

≈ Time/slice (s)

Breath hold Single cardiac phase

20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Black blood inversion recovery

Single cardiac phase

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. There is no fat suppression in this sequence, so nonflowing fluids and lipids will both have high signal.

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Series 4

Plane Short axis

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Imaging sequence Black blood inversion recovery with fat suppression

Specific parameters Single cardiac phase

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≈ Time/slice (s) 10-16

Inversion recovery sequence with fat suppression. Acquisition of identical imaging planes as in series 3 provides a differential method for diagnosis.

5

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

6

Horizontal long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

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Series 7

Plane Short axis

Imaging sequence Perfusion

Specific parameters 30-40 temporal phases

≈ Time/slice (s) 50-70 for entire volume

Patient typically needs more than one breath hold to complete. Coaching is required beforehand to prevent rapid inspiration on second breath hold. Inject 20 mL gadolinium contrast at 4-5 mL/s and start sequence simultaneously. Instruct patient to hold his breath for as long as possible and then to do additional breath holds until the scan is over. After the scan has finished, may inject an additional 20 mL gadolinium contrast at 2 mL/s. 8

Short axis

Delayed enhancement

Breath hold TI = 100-300 ms

10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus. 9

Long axis

Delayed enhancement

Breath hold TI = 100-300 ms

10-20

TI chosen to null normal myocardium. If imaging sequence does not provide recommended TIs (phase-sensitive inversion recovery), a prior multi-inversion time sequence must be run to determine this value. Imaging performed approximately 10 minutes after administration of first contrast bolus.

LV, left ventricle; NEX, number of excitations; TI, inversion time; VPS, views per segment.

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Case Examples Pericardial Effusion

Figure 3.31. Short-axis balanced gradient echo image near the mid ventricle (notice the papillary muscles) demonstrates increased pericardial fluid layering in the most dependent region of the pericardial sac.

The normal pericardium contains only 15 to 50 mL of pericardial fluid. Imaging of pericardial effusion is usually done to assess its severity and to determine the causative insult. The effusion can be secondary to an inflammatory process such as pericarditis (see next section) or can be noninflammatory in nature (eg, due to congestive heart failure, hypothyroidism, or cirrhosis).

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Pericarditis

Figure 3.32. Axial double inversion recovery image (top left) and three-chamber (top right) and short-axis (bottom) MDE images demonstrate circumferential pericardial thickening with persistent enhancement. This constellation of findings is consistent with active pericardial inflammation.

Pericarditis is the most common pericardial pathology. It refers to inflammation of the pericardial layers and can have multiple causes––infectious, postradiation, drug-induced, or post–myocardial infarction––or can be a manifestation of a systemic disorder. However, most commonly it is considered to be idiopathic and no cause can be found. In most cases, some amount of pericardial fluid is present.

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Pericardial Constriction

Figure 3.33. Four-chamber balanced gradient echo image (left) and short-axis double inversion recovery image (right) demonstrate circumferentially thickened pericardium with a trace amount of a pericardial effusion. The interventricular septum in the image at left is sigmoid shaped, reflecting increased right ventricular pressures.

Figure 3.34. Four-chamber balanced gradient echo image showing thickened pericardium and a sigmoid-shaped interventricular septum. Prominent biatrial enlargement is also seen.

The main characteristic of pericardial constriction is an impairment of the normal cardiac filling physiology. It is important to distinguish it from a restrictive cardiomyopathy because the treatments are different. Imaging findings that can help with the diagnosis are those of pericardial thickening, effusion, inflammation, calcification (best seen on computed tomography), and findings secondary to the abnormal filling pressures, such as septal bounce, a D-shaped LV, increased atrial size, and large coronary sinus or inferior vena cava.

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Pericardial Cyst

Figure 3.35. Axial double inversion recovery (top left) and coronal triple inversion recovery (top right) images demonstrate a large lobulated cystic structure at the right cardiophrenic angle in close association with the pericardium. The bottom image shows the axial balanced gradient echo image for reference.

These pericardial cysts are usually incidental findings, and the vast majority of them are located in the cardiophrenic angle, most often on the right side. They do not communicate with the pericardial sac.

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Congenital Disease Compared with other noninvasive imaging modalities, MRI has unique capabilities that are of great benefit for evaluating patients with congenital heart disease. This is especially true for older patients who have undergone attempts at surgical correction. Unlike echocardiography, which may have difficulty gaining adequate “acoustic windows” to optimally evaluate these patients, cardiac MRI provides unlimited freedom for selecting the ideal imaging planes to display the relevant anatomic and physiologic abnormalities in these often-complex situations. In addition, compared with most other imaging modalites, MRI’s unique ability to both quantitate flow and characterize tissue makes it an ideal technique to evaluate patients with congenital heart disease.

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Imaging Protocol––Congenital Disease

Series 1

Plane

Imaging sequence

Specific parameters

Sagittal

Bright blood static (balanced or spoiled gradient echo)

Breath hold Single cardiac phase

≈ Time/slice (s) 20

Localizer scan to identify imaging volume. Prescribe enough slices to include entire heart. Typical left-to-right range, ≈200 mm depending on body habitus (≈120 mm left to 80 mm right of midline). 2

Four chamber long axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Single slice through left ventricular apex and mitral valve. Adjust VPS based on heart rate and breath-hold duration; minimize breath-hold time for patient comfort.

3

Short axis

Bright blood cine (balanced gradient echo)

Breath hold 20 cardiac phases

10-16

Center each slice on the center of the LV. Ensure that slices cover the entire ventricle from apex to base. Adjust imaging parameters (VPS, imaging matrix, NEX) based on breathhold duration and patient compliance.

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Series 4

Plane Imaging plane dependent on pathology

CLINICAL INDICATIONS AND SAMPLE IMAGING PROTOCOLS

Imaging sequence Black blood inversion recovery

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Specific parameters

≈ Time/slice (s)

Breath hold

10-16

Black blood imaging sequence without fat suppression. For coarctation, prescribe a sagittal ‘candy cane’ view of the aorta. 5

Oblique 3D volume

3D MR angiography

Breath hold

60-80

Angiography sequence with gadolinium contrast administration for visualizing disease-specific pathology. A test scan should be run before administration of contrast agent to verify that the prescription includes the relevant anatomy.

6

Imaging plane dependent on pathology

Cine phase contrast

Breath hold 20 cardiac phases Flow direction sensitization = slice VENC = 200

10-16

Imaging plane should bisect the anatomical region of interest. Optional flow quantitation through collateral vessels. Field of view as small as possible without wraparound artifact superimposing the area of interest. Plane must be perpendicular to the vessel. Collateral vessels with flow directed below coarctation indicates physiologically significant coarctation. LV, left ventricle; NEX, number of excitations; TI, inversion time; VENC, velocity encoding; VPS, views per segment.

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Case Examples Tetralogy of Fallot

*

Figure 3.36. MR images in a patient with tetralogy of Fallot. Short-axis balanced gradient echo image (top left) at the level of the the left ventricular papillary muscles demonstrates marked dilatation of the right ventricular outflow tract (*). (See discussion regarding calculations of ventricular volumes and regurgitant fractions on page 66.) Transaxial magnitude image (top right) of a phase-contrast study at the level of the right pulmonary valve. Phasecontrast images, also at the level of the right pulmonary valve, acquired during systole (bottom left; note that cephalad flow is dark and caudal flow is bright) and during diastole (bottom right). In the image at diastole (bottom right), the bright signal in the main pulmonary artery just above the pulmonary valve is due to retrograde (caudal) flow caused by pulmonary valve regurgitation.

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Figure 3.37. Gadolinium-enhanced MR angiography performed postoperatively in a patient with tetralogy of Fallot who underwent attempted left pulmonary artery angioplasty. Note the severe residual stenosis (7 mm) and poststenotic dilatation at the origin of the left pulmonary artery.

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Transposition Complexes

a

p

Figure 3.38. MR images from a patient with D-transposition of the great arteries after an intraatrial baffle procedure (Mustard operation). Balanced gradient echo MR image in the transaxial plane at the level of the atrioventricular valves (top; note marked narrowing in the mid portion of the pulmonary venous pathway [arrow]). Balanced gradient echo MR image in the sagittal plane (bottom) through the stenotic pulmonary venous pathway (arrow) demonstrates the anterior (a) and posterior (p) compartments of the surgically created pulmonary venous atrium.

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Figure 3.39. Axial balanced gradient echo pulse image at the level just above the aortic valve in a patient with D-transposition of the great arteries after an “arterial switch” procedure, which included placing the pulmonary arteries anterior to the aorta (Lecompte maneuver). Note mild narrowing of both proximal left and right pulmonary arteries.

*

a p

r

Figure 3.40. Balanced gradient echo MR images from a patient with congenitally corrected transposition of the great arteries. Oblique sagittal view (left) shows the aorta located anterior to and originating from the RV (r). Note the left atrium (arrow) connecting with the RV and the dilated main pulmonary artery (*), which resulted from pulmonary valve stenosis. Axial view (right) at the level of the bifurcation of the main pulmonary artery (p); note the aorta (a) anterior and slightly to the left of the pulmonary artery.

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Partial Anomalous Pulmonary Venous Connections

Figure 3.41. Maximum-intensity projection image from gadolinium-enhanced MR angiography. Data set demonstrates partial anomalous pulmonary venous connections of the left upper lobe pulmonary veins to a left vertical vein (arrow).

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*

Figure 3.42. Balanced gradient echo pulse sequence in the coronal plane at the level of the superior vena cava. Image shows partial anomalous pulmonary venous connections of the right upper (arrow) and right middle (arrowhead) lobe pulmonary veins to the superior vena cava. This patient also had a sinus venosus atrial septal defect (*).

Figure 3.43. Opposing views of gadolinium-enhanced MR angiography with volume rendering demonstrate infracardiac partial anomalous pulmonary venous connections of all the right pulmonary veins. Additional images for this patient (not shown) demonstrated that the anomalous connection was into the inferior vena cava.

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Coarctation

Figure 3.44. Gadolinium-enhanced MR angiography with volume rendering demonstrates severe coarctation at the juxtaductal location. Note the enlarged intercostal and internal mammary arteries due to collateral blood flow.

The minimum imaging requirements include a scout sequence and 3D MR angiography. Balanced steady-state sequences are useful for demonstrating left ventricular hypertrophy or dysfunction, as well as a bicuspid aortic valve. A phase-contrast sequence is also valuable to document flow reversal in collateral vessels.

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Ebstein Anomaly

a r

Figure 3.45. Balanced gradient echo images in a patient with Ebstein anomaly. Axial view (top) at the level of the atrioventricular valves shows displacement of the tricuspid valve toward the right ventricular apex (arrow). Oblique sagittal view (bottom) through the right atrium and RV shows the large “sail-like” anterior leaflet (arrow) of the apically displaced abnormal tricuspid valve. a, atrialized right ventricle; r, residual trabeculated portion of the right ventricle; arrowhead, right atrioventricular groove.

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Ventricular Noncompaction

Figure 3.46. Balanced gradient echo images in a patient with myocardial noncompaction. Short-axis view (top) near the apex demonstrates the thickened left ventricular wall, which is composed primarily of trabeculated myocardium containing numerous sinusoidal spaces. Four-chamber view (bottom) demonstrates noncompaction of the left ventricular myocardium.

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PULSE SEQUENCE BASICS, ECG GATING, AND MR ARTIFACTS Kiaran P. McGee, PhD Matt A. Bernstein, PhD

Introduction The purpose of this chapter is to provide an overview of some of the more technical aspects of cardiac magnetic resonance (MR) imaging. To this end, three broad topics are covered: pulse sequence basics, electrocardiographic (ECG) gating, and common imaging artifacts. Cardiac pulse sequences are described by grouping individual imaging options into five broad categories: magnetization preparation, echo formation, data acquisition, rapid imaging, and imaging mode, with the resultant image being described by the blood pool signal. Using this nomenclature, individual pulse sequences are described, and sequence-specific variables, recommended values, and example images are provided. Pulse sequences are also distinguished according to their application—imaging of morphology or function. The sections on ECG gating include information on the biophysical origin of the ECG signal, strategies for successful gating in MR imaging (MRI), and a list of ECG artifacts encountered in the MR environment and recommendations to reduce or eliminate them. Finally, examples of several commonly seen imaging artifacts are provided, along with a discussion of their sources and preventive or corrective measures.

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Anatomy of a Cardiac MRI Pulse Sequence Conceptually, a cardiac MRI pulse sequence can be broken down into five constituent categories (boxes 1-5 below). Each category contains multiple components that can be combined in various ways to provide the full range of image contrasts and applications (eg, studies of function or morphology). The scheme below shows these five categories and the resultant image (box 6), as defined by the blood pool signal. This section describes each category and gives a list of components that make up each one.

1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

Magnetization Preparation Magnetization preparation involves the application of radio frequency (RF) and gradient pulses to prepare the MR signal and, hence, image contrast before data acquisition. Saturation Recovery — Application of a series of 90˚ RF pulses to convert longitudinal into transverse magnetization. Recovery of the longitudinal magnetization will occur as a result of spin-lattice (ie, T1) relaxation effects. By choosing the appropriate delay between the RF pulses (ie, the pulse repetition rate [TR]), suppression of specific tissues can be achieved. Inversion Recovery — Application of a 180˚ RF pulse, followed by a delay time. Tissue suppression is achieved by selection of the delay between the 180˚ pulse and the commencement of the imaging sequence, such that the signal of the tissue to be suppressed is zero because of T1 recovery. Fat Saturation — Application of an RF pulse spectrally tuned to the resonant frequency of lipids, followed by gradient-induced spoiling. This RF pulse only dephases the magnetization of lipids, unless the main magnetic field is very inhomogeneous. Fat saturation can also be achieved by application of multiple inversion pulses as part of the magnetization preparation phase of the imaging sequence.

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Tagging — Application of an RF pulse to create transverse magnetization, followed by gradient-induced spatial modulation and a second RF pulse of equal amplitude but opposite flip angle. This creates a modulation of the MR signal that is spatially dependent, which can then be used to track motion by following the banding pattern in the images. Phase Contrast (Flow Encoding) — Application of gradient waveforms before data acquisition to encode the velocity (ie, speed and direction) of moving tissues into the phase of the MR image. This is typically used for quantifying blood flow but also can be used to track bulk motion, such as in the heart. A specific range of velocities is mapped to the minimum and maximum values of the phase (–180˚ to +180˚). Unlike the other entries for magnetization preparation listed here, flow encoding is applied after the RF excitation pulse, so it affects transverse rather than longitudinal magnetization.

Echo Formation Echo formation refers to the method by which the MR signal is generated. With application of appropriate spatial encoding gradients, these echoes encode the spatial frequency or k-space representation of the MR image. Fourier transformation of these data produce the final MR image. Spin Echo — Formation of the k-space signal by application of two RF pulses (90˚ and 180˚). The formation of the signal (echo) occurs at a time equal to twice the interval between the two pulses. For a standard spin echo, each TR consists of a single 90˚–180˚ RF pulse pair. Multiecho spin echoes are formed by repetition of the 180˚ pulse. Gradient Echo — Formation of an echo signal and subsequent image by application of an RF pulse with a flip angle typically much less than 90˚ (<45˚). Immediately after the RF pulse, the transverse magnetization is dephased by application of a negative-polarity gradient along the readout direction, followed by a contiguous positive-polarity gradient that reverses the effect of the negative gradient and results in the formation of the image echo. Additional gradient fields are added for slice selection and phase encoding, necessary to complete the image acquisition sequence. Short image echo times, on the order of 1 millisecond, can be achieved with high-performance gradient systems on most high-field imaging systems. Gradient echo imaging sequences are typically used for fast imaging applications such as MR angiography or cine imaging sequences. In all types of gradient echo imaging, the longitudinal component of the magnetization reaches a dynamic equilibrium as a result of the trade-off between magnetization loss

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from the application of RF pulses and gain from T1 recovery. The two most commonly used types of gradient echoes in cardiac imaging are spoiled and balanced, which will be the focus in this chapter. Other types of gradient echo imaging include coherent gradientrecalled echo and reversed steady-state free precession. Spoiled — Residual transverse magnetization is eliminated (spoiled) by either varying the phase of the RF pulses or applying additional gradient lobes. A spoiled gradient echo is typically T1 weighted but can show bright blood signal as a result of inflow. Balanced — Residual transverse magnetization is maintained and strongly contributes to the net signal. As shown in Figure 4.1, the net gradient area on each axis is nulled (balanced) in each TR interval. Maintaining zero net phase accumulation along all spatial encoding axes provides a steady-state balanced gradient echo. For these types of sequences, the phase of the RF pulses follows a simple pattern (like sign alternation) from one TR to the next. A steady-state balanced gradient echo produces contrast that is proportional to the ratio of T2 (transverse relaxation) to T1 (T2/T1), with fat and fluid being bright. This type of gradient echo is highly susceptible to gradient balancing errors and magnetic field inhomogeneities. These effects are manifested as banding (bright to dark transitions) within the image.

Data Acquisition Data acquisition refers to the method by which echoes, either spin or gradient, are collected as part of the process of acquiring the k-space data necessary for image reconstruction. Single Echo — Acquisition of a single line of data per repetition (TR) of the imaging sequence. The total imaging time for a single-echo imaging sequence is equal to the product of the TR and the number of phase-encoding steps performed by the sequence, unless rapid imaging techniques are used. Echo Train — Acquisition of more than one image echo or line of data per TR by the application of additional RF (eg, fast or turbo spin-echo sequences) or gradients (for multi-echo gradient echo–based sequences). The total imaging time is equal to the product of the TR and the phase-encoding steps, divided by the number of lines of data acquired per TR (echo train length). The acquisition time of echo train methods can be further shortened with use of rapid imaging techniques. Single Shot — Extension of the echo train concept, whereby all of the lines of data are acquired within a single TR or “shot.” (Note that certain gradient-echo sequences [balanced steady-state free precession] are sometimes classified as single-shot sequences but

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180°

Spin Echo

90° RF pulse

Slice-selection gradient waveform Phase-encoding gradient waveform Frequency-encoding gradient waveform MR signal

Spoiled Gradient Echo RF pulse Slice-selection gradient waveform Phase-encoding gradient waveform Frequency-encoding gradient waveform MR signal

Balanced Gradient Echo RF pulse Slice-selection gradient waveform Phase-encoding gradient waveform Frequency-encoding gradient waveform MR signal

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apply an RF pulse for each echo or line of data. Image data are acquired sequentially and thus considered as from a single shot.) Multishot — An echo train that requires more than one repetition (shot) to acquire all of the raw data for an image. The number of shots required per image is equal to the number of lines of data divided by the number of lines in each echo train. Segmented Data Acquisition — The acquisition of a limited number of lines (views) of image data at a given phase (segment) of the cardiac cycle. Acquisition of the total number of views of a single image occurs over multiple cardiac cycles. Acquisition of a limited number of views reduces the temporal footprint or width (≈tens of milliseconds) of the data acquisition window within the cardiac cycle, resulting in a “static” image at each cardiac phase. Repetition of the acquisition process at differing segments results in a multiphase or cine data set, allowing visualization of the motion of the heart. The number of image echoes (lines) acquired per segment is known as the views per segment (VPS). The VPS is adjusted on the basis of heart rate to maintain sufficient temporal resolution of each image in the cine series. View Sharing — Lines of k-space are shared between images representing adjacent phases of the cardiac cycle, thereby reducing the number of R-R intervals over which the data are collected but reducing temporal resolution of the image. Most commonly used in cine cardiac sequences.

Rapid Imaging Rapid imaging comprises a group of imaging techniques designed to reduce the total acquisition time by undersampling of the k-space data, followed by image reconstruction. Image-Based Parallel Imaging (SENSE) — Decreasing the number of phase encodings acquired in a standard acquisition to intentionally induce aliasing (wrap) in the phaseencoded direction, followed by unwrapping (unaliasing) to produce an image with an effectively larger field of view (FOV). (In a three-dimensional [3D] acquisition, decreasing the number of phase encodings along the two phase-encoding directions sometimes is Figure 4.1. Pulse sequence diagrams for the three basic pulse sequence types used in cardiac MRI: spin echo, spoiled gradient echo, and balanced gradient echo. Each sequence shows the RF pulse(s) and spatial encoding gradients used to create a single image echo. Repetition of this sequence generates the k-space data necessary for image reconstruction. Multiple gradient waveforms are shown on the phase-encoding axis.

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possible for further acceleration.) Differences in spatial sensitivity of the elements of a phased-array coil are used to mathematically map the unwrapping. Reduction in imaging time is equal to the fractional reduction in phase encodings. Calibration data are also required to map the spatial coil sensitivities and can be performed as part of the imaging sequence or as a separate scan. K-Space–Based Parallel Imaging (SMASH and GRAPPA) — Undersampling of the k-space data in the phase-encoding direction, followed by reconstruction of the missing data using the elements of a phased-array coil and the harmonic nature of the phaseencoding process. Hybrid (Spatial-Temporal) —Techniques to improve the speed of a time series (cine) data set. UNFOLD is a method of decreasing aliasing artifacts by identification of temporal harmonics of the image data. kt-BLAST and TRICKS are additional rapid imaging techniques that apply related concepts. Partial Fourier — Not all of the lines of k-space are acquired, thereby decreasing the number of TRs and, hence, total imaging time. The missing data can be synthesized by applying a homodyne reconstruction technique or simply setting those data to zero (zero filling). Rectangular-Phase FOV — The spacing between k-space lines is inversely proportional to the FOV. Decreasing the FOV increases the spacing between k-space lines; consequently, fewer lines are required to cover the same k-space range in the phase-encoding direction. Acquisition of fewer k-space lines means fewer TRs and, hence, shorter acquisition times.

Imaging Mode Imaging mode defines the type of data set acquired. Single Frame — Acquisition of a single imaging plane, set of slices, or volume at a single time point, without any temporal information. Cine — Acquisition of multiple images of the same anatomical location (prescription) but over a given time interval. For the large majority of cardiac acquisitions, the time interval over which a cine series is acquired is the ECG R-R interval, or multiples thereof. 2D — A plane of data whose orientation can be defined by any three points in physical space. A matrix of data points (pixels) fills the plane. The size of the two-dimensional (2D) image equals the number of frequency encodings and phase encodings plus any zero filling of the data (eg, 256 × 192 OR 256 × [192 + 64], where 64 lines are zero filled). These can be thought of as the number of rows and columns, respectively, in the image matrix (or columns and rows, depending on the orientation of the image). Multiple 2D

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planes can be acquired with or without gaps to cover an imaging volume. 3D — A volume of data with any arbitrary orientation in physical space. The 3D volume can be considered as consisting of a series of contiguous (zero or negative gap) 2D imaging planes. The term “3D” is reserved for acquisitions in which the imaging volume is excited with a single RF pulse; typically the data are phase encoded in two different directions. Matrix sizes are defined by the number of rows and columns of each plane and the number of planes that define the third dimension of the volume.

Blood Pool Blood pool refers to the intensity of the blood pool signal in the final MR image. Bright–Exogenous Contrast Agent — Blood pool has the highest signal in the image and arises from the use of T1-shortening gadolinium-based contrast agents. Most commonly used in conjunction with short echo time (TE) and TR gradient echo pulse sequences. Bright — Blood pool provides the highest signal in an image. For cardiac applications, high blood pool signal (ie, bright blood) is most commonly achieved with gradient echo sequences (spoiled and balanced). Dark — Blood pool is suppressed and has intensity approximately equal to the background signal (zero). Blood pool signal suppression is typically achieved by application of an inversion pulse, followed by a spin echo or a gradient echo imaging sequence.

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Pulse Sequences for Imaging Cardiac Morphology Balanced Gradient Echo (Balanced Steady-State Free Precession) Cine This method is the most common sequence used for assessment of cardiac function. Image contrast is roughly proportional to the ratio of the two relaxation parameters (T2/T1), and as such, fluid is bright despite the short TE and TR values used. This sequence provides high blood pool–to-myocardial contrast. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

Sequence-Specific Variables Views per segment The number of lines of k-space sampled per cardiac phase; it determines the temporal resolution of each cardiac phase of the cine sequence. VPS is based on the patient’s heart

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rate (in beats per minute [bpm]). A decrease in the VPS will increase imaging time. Thus, a compromise is often struck between sufficient temporal resolution and breath-hold duration. To keep imaging times within normal breath-hold times (<20 seconds) for low VPS values, several strategies can be used, including decreasing the number of phaseencoding steps, partial-phase FOV, or parallel imaging techniques.

T YPICAL VPS VERSUS HEART RATE Heart Rate (bpm)

VPS

≤60 61-95 96-125 126-155 ≥156

10-12 8-10 6-8 4-6 <4

Cardiac phases The number of images reconstructed across the cardiac cycle. Each image is at a specific time point or phase of the cardiac cycle. The larger the number of cardiac phases the higher the temporal resolution of the cine series. Twenty cardiac phases are most commonly reconstructed for cine sequences. Balanced gradient echo short-axis view

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Spoiled Gradient Echo Cine This has a lower signal than a balanced gradient echo sequence, but it also is less susceptible to magnetic field inhomogeneity artifacts. Fluid is dark, except for blood that flows into the slice or has contrast agent on board. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

Sequence-Specific Variables Views per segment The number of lines of k-space sampled per cardiac phase; it determines the temporal resolution of each cardiac phase of the cine sequence. VPS is based on the patient’s heart rate. A decrease in the VPS will increase imaging time. Thus, a compromise is often struck

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between sufficient temporal resolution and breath-hold duration. To keep imaging times within normal breath-hold times (<20 seconds) for low VPS values, several strategies can be used, including decreasing the number of phase-encoding steps, partial-phase FOV, or parallel imaging techniques.

T YPICAL VPS VERSUS HEART RATE Heart Rate (bpm)

VPS

≤60 61-95 96-125 126-155 ≥156

10-12 8-10 6-8 4-6 <4

Cardiac phases The number of images reconstructed across the cardiac cycle. Each image is at a specific time point or phase of the cardiac cycle. The larger the number of cardiac phases the higher the temporal resolution of the cine series. Twenty cardiac phases are most commonly reconstructed for cine sequences. Spoiled gradient echo short-axis view

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Myocardial Delayed Enhancement This method comprises inversion recovery, single-shot, or multishot spoiled gradient echo. Myocardium inversion time (TImyo) is chosen so that signal from normal myocardium is suppressed and the signal from gadolinium contrast-enhanced infarcted myocardium is maximized. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables Myocardium inversion time The delay time from the application of the RF inversion pulse to data acquisition. TImyo is chosen so that the longitudinal magnetization of normal myocardium is zero at the time of data collection. The choice of TImyo is based on the delay between administration of contrast agent and initiation of delayed enhancement imaging, as well as the wash-in and wash-out kinetics of the contrast agent within the myocardium. For single-shot and multishot sequences that acquire multiple lines of data for a single inversion pulse, TImyo is the time delay from the RF inversion pulse to the acquisition of the center of the data acquisition window. Typical TImyo = 100-300 milliseconds Example images

Images show myocardial delayed enhancement images of normal (left) and infarcted (right) myocardium. The blood pool is bright, identifying a high concentration of contrast agent, whereas the signal from normal myocardium is suppressed and appears dark. Regions of infarction are bright due to delayed uptake of the contrast agent.

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Double Inversion Recovery This is an inversion recovery pulse sequence that applies an inversion pulse to the entire imaging volume, a slice-selective reverse inversion pulse, and a spin echo, echo train imaging sequence. The time between the first inversion pulse and the spin echo readout is known as the blood inversion time (TIblood) and is chosen so that the blood signal is nulled at the time of the imaging sequence. This is not a fat-suppressed imaging sequence. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

2D, cine Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables Blood inversion time The time delay between the RF inversion pulse and data acquisition. A non–slice-selective (hard) RF pulse is applied in order to invert the MR signal from all of the blood within the imaging volume. It is important to note that this value is field strength dependent. Typical TIblood = 650 milliseconds at 1.5T field strength and HR = 60 bpm (For more information, see Simonetti et al in Selected References.) Double inversion recovery image (short-axis view)

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Triple Inversion Recovery This is an inversion recovery with three inversion pulses, followed by an echo train spin echo imaging sequence. This sequence is very similar to the double inversion recovery sequence but with the addition of the third inversion pulse before the echo train spin echo imaging sequence to suppress fat signal. The time between the imaging sequence and the third RF pulse is known as the fat inversion time (TIfat). Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables Blood inversion time The time delay between the RF inversion pulse and data acquisition. A non–slice-selective (hard) RF pulse is applied in order to invert the MR signal from all of the blood within the imaging volume. This value is field strength dependent. Fat inversion time Time delay between the application of a spatially selecive RF pulse and data acquisition. This inversion time is shorter than TIblood and is placed after the RF pulse and before data acquisition. Inclusion of both inversion pulses allows complete suppression of signal from blood and lipids (fat). Note that both TIblood and TIfat values vary with field strength. When imaging at higher field strengths (3.0T) it is advisable to check these values. Typical TIblood = 650 milliseconds at 1.5T field strength and HR = 60 bpm Typical TIfat = 150 milliseconds at 1.5T field strength (For more information, see Simonetti et al in Selected References.) Triple inversion recovery image (short-axis view)

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Spin Echo T1-Weighted This involves a fast spin echo, with TE chosen to allow blood within the imaging slice to flow out of the volume before data collection begins. This effectively eliminates any signal from the blood pool. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables TE/2 Time between the 90˚ and 180˚ RF pulses. This value must be large enough to allow for blood to flow out of the imaging slice (or volume), thereby not contributing to the signal within the image. TR Time between successive repetitions of the 90˚ RF pulse or lines of data. Typical TE = as short as possible and should not exceed 50 milliseconds Typical TR = one R-R interval and should not exceed 800 milliseconds Note that slow-flowing blood can be mistaken for pathologies within the cardiac chambers because the blood does not wash out of the imaging volume during the time TE/2 and therefore contributes to signal within the chambers in the slice of interest.

T1-Weighted axial image

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Pulse Sequences for Imaging Cardiac Function Gradient Echo (Balanced and Spoiled) Cine See previous section (pages 118-121) for a complete description. 3D MR Angiography This uses a 3D spoiled gradient echo sequence. The sequence uses an ultrashort TR (≈5 ms) and TE (≈1 ms) to produce a T1-weighted imaging sequence. T1-shortening contrast agent (eg, a gadolinium chelate such as Gd-DTPA) is administered before initiation of the imaging sequence to provide maximum contrast between the blood pool and background tissue. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables Centric view order encoding K-space views are acquired based on their radial distance from the center of k-space, starting from the center or the outer limits (reverse centric) of k-space. Data acquisition is typically initiated upon arrival of the bolus peak within the imaging volume. Sequential view order encoding K-space views are acquired in a rectilinear, sequential order. Example images

Maximum-intensity projection images from four different perspectives (rotation angles) of the imaging volume.

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Cine Phase Contrast This involves gradient-recalled echo (coherent or spoiled), with motion-sensitizing gradients added between RF excitation and acquisition of the image data. The velocity of flowing blood is encoded into the phase of the MR signal and is measured by the velocity encoding (VENC) parameter.

Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

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Sequence-Specific Variables Velocity encoding The maximum velocity that is mapped to the highest phase value in the image (180˚ or π=3.14159 radians).

Measurement Vessel Internal and common carotid artery

Typical VENC Values (cm/s)

<120

Thorax Ascending aorta Descending aorta Vena cava

<175 (range, 100-250) <175 (range, 100-250) <40

Abdomen Aorta

<100

Pathologies Aortic valve stenosis Valvular insufficiency

<800 (range, 200-800) <400 (range, 200-400)

Carotids Prestenotic Intrastenotic

<50 (range, 5-50) <500 (range, 100-500)

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Flow-encoding direction Direction that is sensitized to flow; often described as along the three imaging axes (frequency, phase, and slice). To obtain the three components of the flow vector, the imaging sequence must be repeated three separate times. It is most common to choose the flow direction along the slice-encoding direction. Encoding along all directions requires separate acquisitions or a reduction in temporal resolution for interleaved acquisitions. Reconstruction type Phase or complex difference; method by which the phase (velocity) data are reconstructed. Phase difference calculates the difference in the phase of the two data sets acquired in the cine phase contrast sequence; complex difference uses magnitude and phase information. Views per segment The number of lines of k-space sampled per cardiac phase; it determines the temporal resolution of each cardiac phase of the cine sequence. VPS is based on the patient’s heart rate. A decrease in the VPS increases imaging time. Thus, a compromise is often struck between sufficient temporal resolution and breath-hold duration. To keep imaging times within normal breath-hold times (<20 seconds) for low VPS values, several strategies can be used, including decreasing the number of phase encoding steps, partial-phase FOV, or parallel imaging techniques.

T YPICAL VPS VERSUS HEART RATE Heart Rate (bpm)

VPS

≤60 61-95 96-125 126-155 ≥156

10-12 8-10 6-8 4-6 <4

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Cardiac phases The number of images reconstructed across the cardiac cycle. Each image is at a specific time point or phase of the cardiac cycle. The larger the number of cardiac phases, the higher the temporal resolution of the cine series. Most commonly, 20 cardiac phases are reconstructed for cine sequences. Example images

Phase (top) and magnitude (bottom) images of the ascending and descending aorta. The two directions of flow in the phase image are represented by the bright and dark signal within the vessel lumen.

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Perfusion This uses a saturation recovery preparation pulse, followed by a spoiled or balanced gradient echo readout. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single Echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

Sequence-Specific Variables Phases per slice The number of samples (images) over which the perfusion bolus wash-in and wash-out are measured. Each image represents a separate time point. Total imaging time is proportional to this value, which can be between 20 and 40 seconds (typically 30-40). For larger phases (≈40), total imaging time can be >1 minute.

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Example images

Images show a perfusion sequence at time delays of 0, 5, 13, 20, and 31 seconds, respectively, after administration of a gadolinium-based contrast agent. A bright blood pool indicates the presence of the contrast agent, with the filling of the right ventricle followed by the left ventricle. Overall contrast diminishes over time as the contrast is diluted into the blood pool.

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Tagging This method involves a tagging preparation sequence before initiation of a spoiled gradient echo imaging sequence. Imaging Components 1

2

3

4

5

6

Magnetization preparation

Echo formation

Data acquisition

Rapid imaging

Imaging mode

Blood pool

2D, cine

Single shot

SENSE, SMASH, hybrid, partial k-space, fractional phase FOV

Phase contrast

Inversion recovery

Spin echo

Inversion recovery, fat saturation

Balanced gradient echo

Multishot

Saturation recovery

Spoiled gradient echo

Single echo, segmented

Bright– contrast agent

2D, static Bright

3D, cine Dark Full acquisition 3D, static Tagging

Sequence-Specific Variables Tag spacing The spacing between the individual tag lines. This parameter is typically stated in millimeters, ranges between 5 and 10 mm, and is dependent on gradient performance. Tag type Tags can be defined as a series of lines (1D displacement) or grids (2D displacement).

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Views per segment The number of lines of k-space that are sampled per cardiac phase; it determines the temporal resolution of each cardiac phase of the cine sequence. VPS is based on the patient’s heart rate. A decrease in the VPS will increase imaging time. Thus, a compromise is often struck between sufficient temporal resolution and breath-hold duration. To keep imaging times within normal breath-hold times (<20 seconds) for low VPS values, several strategies can be used, including decreasing the number of phase-encoding steps, partial-phase FOV, or parallel imaging techniques.

T YPICAL VPS VERSUS HEART RATE Heart Rate (bpm)

VPS

≤60 61-95 96-125 126-155 ≥156

10-12 8-10 6-8 4-6 <4

Cardiac phases The number of images reconstructed across the cardiac cycle. Each image is at a specific time point or phase of the cardiac cycle. The larger the number of cardiac phases the higher the temporal resolution of the cine series. Most commonly, 20 cardiac phases are reconstructed for cine sequences. Example images

Tagged short-axis images at systole, mid diastole, and late diastole showing tag fading over time.

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ECG Gating The Einthoven Lead Arrangement The heart’s electrical activity was first measured in 1889 by Augustus Desiré Waller, who measured the electrical potential difference (voltage) across electrode pairs placed at five separate anatomical locations (two on the arms, two on the legs, and one at the mouth). Waller’s method of measuring the time-varying voltage signals across various electrode pairs (lead combinations) is commonly referred to as the electrocardiogram (ECG). The original configuration suggested by Waller was modified by Willem Einthoven in 1908. The so-called “Einthoven configuration” or “Einthoven’s triangle” required placement of electrodes at three locations: the left and right arms and the left leg (Figure 4.2). The differences in electrical potential between electrodes are known as limb leads I (potential difference between left and right arms), II (potential difference between right arm and left leg), and III (potential difference between left arm and left leg).

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VI =

L

141

R

Lead I R

L

R

L

p

Lead II Lead III

VII =

F

R

VIII =

F

L

F

F

Figure 4.2. Three-lead ECG configuration and Einthoven’s triangle. (From Malmivuo J, Plonsey R. Bioelectromagnetism: principles and applications of bioelectric and biomagnetic fields. New York: Oxford University Press; 1995. Used with permission.)

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The Einthoven diagram also shows the electrical model of the heart—a dipole (positive and negative charge separated in space) whose magnitude and orientation vary throughout the cardiac cycle. This model is also known as the vector ECG (VCG). Measurement of the time-varying voltage of leads I, II, or III is the mathematical equivalent of the projection of the VCG onto the respective lead. This projection produces the characteristic ECG waveform (Figure 4.3). This complex waveform can be decomposed into separate waveforms that describe the various phases of the cardiac cycle. Key components of the ECG waveform include the P wave, which signifies the onset of atrial depolarization, the QRS complex, which represents ventricular depolarization, and the T wave, which indicates ventricular repolarization.

R

T

P

R

R-R interval

S

U

Q

Ventricular Atrial repolarization depolarization Ventricular depolarization

T

P Q

S

PR interval ST segment

Figure 4.3. ECG and components of the cardiac cycle. (From Bernstein MA, et al. Handbook of MRI pulse sequences. Amsterdam: Elsevier Academic Press; 2004. Used with permission.)

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ECG Gating in MRI ECG gating is a fundamental part of a cardiac MRI examination. We next describe the important aspects of ECG gating in the MRI environment along with recommendations for reproducible and reliable gating. Why Gate in MRI? ■ To enable consistent temporal sampling of data throughout the cardiac cycle, which is necessary for cine acquisitions. ■ To allow acquisition of static images at a given phase of the cardiac cycle. ■ For correct sorting of static and dynamic k-space data obtained over multiple R-R intervals using segmented acquisition schemes. Patient Preparation Reliable, trouble-free ECG gating in MRI involves identification of the appropriate anatomical locations for placement of the ECG electrodes, followed by adequate preparation of the patient’s skin surface. Identification of the appropriate lead locations is described in more detail below, but three rules should be observed: 1) Lead locations should be placed farther from rather than closer to the sternum, particularly if the patient has had prior chest surgery and sternal wires are present. 2) For women with large, pendulous breasts, an alternative location along the chest wall inferior to the breast should be identified. Large amounts of breast tissue can attenuate the ECG signal. 3) Leads should be placed on the anterior chest surface as opposed to the posterior. The heart is generally located closer to the anterior chest wall, and the ECG voltage is generally greater there. After identification of the appropriate lead locations, the patient’s skin surface should be prepared. For males, this typically requires shaving the chest around the region of the electrodes. Caution should be exercised if this procedure is performed in the MR scan room because most disposable razors use steel blades and can represent a projectile hazard if brought too close to the MR scanner. Commercial abrasive gels are available to remove keratinized skin from the epidermis, thereby creating a better electrical contact between the skin and electrode. Fine-grit sandpaper also can be used but is generally not recommended. The use of a gel has the added advantage of cleaning the skin’s surface of oil and dirt.

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When the appropriate electrode locations are identified and the skin has been prepared, the electrodes can be applied. MR-compatible electrodes should be used at all times. The vendor of the MR scanner provides the appropriate type of electrode either directly or through a third-party supplier. These electrodes usually have a small amount of conducting gel on their tips to further improve conductivity. ECG Lead Placement A major contributor to a prolonged cardiac examination is the amount of time spent attempting to optimize lead placement either immediately before or during the cardiac MR examination. The Division of Cardiac Radiology, Mayo Clinic Rochester, has developed several lead placement configurations (“the Mayo configuration”) that hold the most promise for gating success. A second lead placement set is also recommended when the MR scanner is equipped with VCG gating. Mayo Configuration Figure 4.4 describes the four lead placement configurations used at Mayo Clinic. The Mayo lead placements are variations of the precordial locations used in 12-lead ECG. The locations have been modified on the basis of those arrangements that have proved successful for the ensemble average of the entire patient population at Mayo Clinic.

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Configuration 1

Configuration 2

Configuration 3

Configuration 4

145

Figure 4.4. The Mayo Configuration. The recommended ECG lead placement for male and female patients. Electrode locations are variations of the precordial locations used in a 12-lead ECG. Lead color coding: black, left arm; green, right leg; red, left leg; white, right arm.

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VCG Configuration VCG gating involves measurement of the ECG dipole projected onto two orthogonal axes. It has been shown that when the ECG waveform is measured in this way, T-wave swelling as a result of the magnetohydrodynamic effect can be isolated from the QRST complex waveform. T-wave swelling can be so large that the amplitude of the T wave is greater than that of the R wave, resulting in incorrect triggering of the MRI sequence. Most MR scanners offer a modified form of the original VCG concept. Lead placement for VCG gating is similar to that for the Mayo configuration, except that lead pairs are used to measure voltages that are orthogonal to one another. Each MR manufacturer provides general guidelines for lead placement. However, the general lead placement for VCG gating is shown in Figure 4.5.

Configuration 1

Configuration 2

Figure 4.5. VCG lead placement. The lead placement is based on measurement of the ECG dipole projected onto two orthogonal axes. Black and white electrodes replace the previous colored electrodes. The black electrodes are equal to the left arm (black) and right leg (green), and the white electrodes are equivalent to the right arm (white) and left leg (red) electrodes of the Mayo configuration.

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Peripheral Photo-Pulse Sensor Under certain circumstances, it may not be technically feasible to use an ECG waveform for gated cardiac acquisitions. For example, irregular heart rates or low ECG voltages can render the ECG waveform unusable. In other circumstances, a “quick and dirty” waveform for a gated MR angiography sequence may be sufficient. Under these conditions, a peripheral photo-pulse waveform can be used as an ECG substitute. Blood flowing in the capillaries of peripheral tissues (fingers or toes) can be measured by photoplethysmography. This technology involves applying a light beam (typically within the infrared region of the electromagnetic spectrum) and detecting the light reflected or backscattered from the beam as it passes through the epidermal and dermal layers of the skin. Changes in blood flow in the capillaries modify the optical path length and, hence, the amount of backscattered light. Typical photo-pulse sensors use independent transmitting and receiving detectors separated by a small distance, which allows simultaneous transmission and detection of the beam. Because the electrical activity of the heart precedes the flow of blood outside of the left ventricle, the waveform has an inherent delay from the peak of the R wave of the QRS complex to the peak of the flow profile. For this reason, peripheral photo-pulse triggering is used less commonly than ECG-based methods. However, this form of triggering is extremely reliable and, as such, is a standard feature on all high-performance cardiac MR scanners. Often, a second peak also can be seen on the photo-pulse waveform, which corresponds to the left atrial contraction following left ventricular contraction. Figure 4.6 shows a typical photo-pulse waveform.

Reflected light

Left ventricular contraction

Left atrial contraction

Time Figure 4.6. Schematic representation of a pulse profile from a peripheral photo-pulse sensor on the finger.

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MR-Induced ECG Artifacts Figure 4.7 shows an ECG waveform of a healthy volunteer. The QRS complex and T wave are easily distinguished, with the T-wave amplitude being substantially less than the R-wave peak. Unfortunately, the MR environment is particularly hostile for ECG measurement. Table 4.1 lists some of the more common sources of interference that exist in a typical MR environment, along with their amplitude and frequency ranges. The table also includes, as a reference, a typical ECG waveform.

6,000

ECG signal (relative units)

5,000 4,000 3,000 2,000 1,000 0 -1,000 0

500

1,000

1,500

2,000

Time (ms) Figure 4.7. ECG waveform from lead II from a normal (healthy) volunteer.

2,500

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TABLE 4.1. SOURCES OF ECG NOISE IN MRI Source

ECG reference signal

Induced Electrical Voltage (typical range)

Frequency Spectrum (typical range)

0.2-3 mV

0.05-100 Hz

Magnetohydrodynamic effect

Several mV; can be greater than the ECG waveform

<100 Hz

Triboelectric effect: lead and electrode motion due to respiration or other motion

Several mV

Several Hz

RF body coil switching

40-700 mV depending on RF pulse type, body coil design, and location within magnet bore (isocenter smallest)

2-70 kHz

Gradient switching

100-600 mV depending on location within MR scanner (ie, gradient amplitude)

32-125 kHz

Note: The frequencies of induced electric fields from RF pulses are multiple orders of magnitude greater than those of the ECG waveform and do not contribute substantially to the noise spectrum. (Resonant frequency of scanner is ≈64 MHz at 1.5T.)

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Magnetohydrodynamic Effect Blood is composed of formed elements (45% by volume) and plasma. Plasma is composed of approximately 90% solvent and 10% solute. The solvent is water and the solute is composed of salts (sodium, potassium, calcium, magnesium, chloride, and bicarbonate), plasma proteins (albumin, fibrinogen, and globulins), and other substances (nutrients, waste products, respiratory gases, and hormones). Blood is a conductive medium—positive and negative charges exist and allow current flow. When moving blood is exposed to a magnetic field, charge separation occurs, inducing a time-varying electrical dipole signal that is a function of the magnitude and direction of flow within the field of the MR scanner. This dipole is detected as a time-varying electrical signal superimposed onto the ECG waveform. This second electrical signal precedes ventricular contraction and consequently is detected after the QRS complex of the ECG waveform. Ventricular repolarization, as described by the ST segment, is detected at approximately the same time as the flow of blood through the aorta and, hence, is often superimposed onto the T wave of the ECG. This is most commonly known as “T-wave swelling” (or “T-wave elevation”) and can cause the T wave to be of even greater amplitude than the R wave. T-wave swelling often results in unreliable triggering and poor image quality. Figure 4.8 shows a normal ECG waveform of a volunteer in the absence of an external magnetic field (ie, non-MR environment) and in the presence of a large external magnetic field (ie, inside an MR scanner). Effect on ECG Waveform Increase in amplitude of the ST segment of the QRST complex, also known as T-wave swelling. Effect on MR Data Acquisition If ECG triggering is based on the peak voltage of the waveform, the scanner could trigger off the T wave or switch between the R-wave and T-wave peaks. Detection-peak switching can result in a miscalculation of the patient’s heart rate. If some form of arrhythmia detection is used in the ECG gating algorithm, data collection will not occur during that R-R interval, thereby resulting in an increase in data acquisition time. Increases in scan time are unacceptable, particularly for some breath-hold scans. Trigger detection based on the slope of the QRST complex can decrease false triggering but cannot eliminate it entirely. Triggering off the T wave also results in imaging at inconsistent phases of the cardiac cycle.

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Miscalculation of the R-R interval resulting from false ECG triggers degrades the image quality because data are collected at a different phase of the cardiac cycle than expected. This is particularly true for segmented cine data acquisition schemes.

— Inside MR scanner — Outside MR scanner

6,000

ECG signal (relative units)

5,000 4,000 3,000 2,000 1,000 0 -1,000 0

400

800

1,200

1,600

2,000

2,400

Time (ms) Figure 4.8. ECG waveform from a healthy volunteer, as measured outside (red) and inside (black) the MR scanner before imaging. The magnetohydrodynamic effect introduces distortion of the ECG waveform, most notably T-wave swelling.

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Triboelectric Effect The triboelectric effect is the build-up of static charge due to the rubbing of two different materials against each other (for example, an ungrounded conductor and the insulator of the ECG cable). Effect on ECG Waveform Introduces a slowly varying change in the baseline voltage (baseline drift) of the ECG signal (Figure 4.9). Effect on MR Data Acquisition Baseline drift results in either positive or negative change of the mean ECG signal. If a threshold value is used to detect the trigger point, noise spikes can be detected if the drift is positive, or the R wave can be missed if the drift is negative. Miscalculation of the R-R interval resulting from false ECG triggers results in degraded image quality because data are collected at a different phase of the cardiac cycle than expected.

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— Inside MR scanner — Outside MR scanner

ECG signal (relative units)

2,000

1,500

1,000

500

0

-500

-1,000 0

500

1,000

1,500

2,000

2,500

3,000

Time (ms) Figure 4.9. ECG waveform from a healthy volunteer, as measured outside (red) and inside (black) the MR scanner before imaging. The triboelectric effect introduces a drift in the baseline signal. Respiratory motion also induces a similar baseline drift.

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RF Body Coil Switching The RF body coil functions in one of two states. An “on” state allows RF current to flow into the coil, thereby irradiating the patient with RF energy necessary to create a detectable MR signal. A second or “off” state effectively detunes or decouples the RF body coil from the RF circuit, thereby allowing other, more sensitive (eg, surface) coils to be used for MR signal detection. Switching of the body coil is typically performed by applying oppositepolarity (±) voltages on the order of several hundred volts to pin diodes within the body coil circuit. Degradation Source On/off switching of the RF body coil before and after RF pulse generation. Effect on ECG Waveform All imaging sequences require that RF energy be transmitted into the patient. The RF body coil is the largest and most commonly used coil for this purpose. For cardiac imaging, it is used almost exclusively in transmit-only mode. The enabling and disabling of the RF body coil before and after generation of the RF pulse induces a voltage that is superimposed onto the ECG signal. When an RF pulse is generated, a time-varying electric field (current) can also be generated along the ECG cable at the same frequency as the resonant magnetic field. However, because the frequency of the electric field is in the megahertz range (64 MHz at 1.5T), this component can be effectively filtered out of the ECG waveform because the ECG signal only covers a frequency range of approximately 0 to 100 Hz. Effect on MR Data Acquisition Introduction of noise spikes that can cause false ECG triggers (Figure 4.10).

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— Imaging — No imaging 2,000

ECG signal (relative units)

Body coil switching 1,500

1,000

500

0

-500

-1,000 0

250

500

750

1,000

1,250

1,500

1,750

2,000

Time (ms) Figure 4.10. Noise spikes in the ECG waveform caused by on/off switching of the body coil.

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Gradient Switching Image formation in MR is achieved, in part, by applying gradient magnetic fields with amplitudes that vary linearly with spatial position. These fields are zero at the isocenter of the magnet and greatest near the bore wall or the ends of the magnet. Acquisition of a single image requires these magnetic fields or gradients to be rapidly turned off and on throughout the imaging sequence. Exposure of the ECG circuit (patient, electrodes, and cable) to a time-varying magnetic field induces a time-varying electrical voltage in the ECG circuit. This induced voltage is greatest when the rate of change of the magnetic field is also at its maximum. This occurs when the polarity of the gradients is switched and generally increases as the speed of the imaging sequence increases. Effect on ECG Waveform Superposition of additional waveforms (noise) onto the ECG signal. Gradient switching noise amplitudes can, under certain circumstances, be many times larger than the ECG voltage (Figure 4.11). Effect on MR Data Acquisition Gradient switching–induced noise can cause false trigger detection and prolongation of the scan time or scan failure due to timing out of the data acquisition window.

Figure 4.11. Examples of gradient switching interference in ECG waveforms from two separate pulse sequences. The black waveform was acquired during a gradient-intense imaging sequence, and the red waveform was acquired with imaging gradients turned off. The top waveform pair is from a gradient echo perfusion sequence; the bottom image is from a balanced steady-state sequence.

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— Imaging gradients ON — Imaging gradients OFF

600

ECG signal (relative units)

500 400 300 200 100 0 -100 -200 -300 0

500

1,000

1,500

2,000

2,500

3,000

Time (ms)

16,000

ECG signal (relative units)

14,000 12,000 10,000 8,000 6,000 4,000 2,000 0 -2,000 0

200

400

600

Time (ms)

800

1,000

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Sternal Wires or Clips Sternal wires used to close the chest cavity after thoracic surgery create conducting loops that can induce additional electric fields that are superimposed onto the ECG signal during imaging. Effect on ECG Waveform The electrical dipole resulting from the time-varying magnetic field through a sternal wire loop acts as another noise source. Effect on MR Data Acquisition Unless noise from the wires is successfully filtered, the result is false triggering and corrupt data collection. To minimize this effect, electrodes should be moved away from the sternum. This is most commonly achieved by placing the electrodes along the lateral chest wall of the patient.

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Gating During Chemical Stress Gating during a chemically induced stress MRI examination can be particularly problematic because of changing heart rate and increased artifacts from physiologic and other effects. In general, adequate patient preparation and monitoring of the ECG signal throughout the cardiac examination are sufficient to ensure that the MR scanner can detect and trigger off the peak of the R wave in the QRS complex. If gating off a particular ECG lead begins to fail, it is advisable to review the signal from the remaining leads. Another option is to switch to the peripheral photo-pulse waveform. Therefore, it is a good idea to place the pulse unit on the finger of the patient before beginning the examination. Because the electrical activity of the heart precedes the flow of blood into the system, the peripheral photo-pulse gating trigger point does not correspond to the peak of the ECG R wave. Thus, this method of gating should be considered a fallback rather than the default option.

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Common Artifacts in Cardiac MR Artifacts are unavoidable in MRI. Even when the MR scanner is functioning correctly, specific imaging parameter choices will produce artifacts. This section describes the artifacts seen most commonly in cardiac MRI and proposes solutions for their reduction or removal.

Gradient Decay or Fall-Off Source This artifact occurs as a result of excitation and reception of signal from tissue in the falloff zone of the spatial encoding gradients, particularly in the superior-inferior direction. Spatial encoding gradient fields decay from their maximum amplitude to zero outside the physical dimensions of the gradient coil. RF excitation and reception of signal from tissue within the fall-off zone of these gradient fields results in tissue at an incorrect physical location being mapped onto the reconstructed image. This can also occur when the RF coil used for excitation is larger than the physical extent of the gradient encoding fields (Figure 4.12). Solutions ■ Use receive-only coils that do not extend beyond the anatomical region of interest. ■ If anatomical coverage is large and multicoil element surface coils are used, only those coils that cover the region of interest should be selected. ■ Place saturation bands over those regions in the fall-off zone of the gradient fields. ■ Use transmit-receive RF coils. For cardiac applications this is usually not practical because the body RF coil typically must be used for transmission and provides images with lower signal-to-noise ratio when used as a transmit-receive coil. ■ For dual gradient systems, switch to the larger FOV gradient set. ■ Apply any of the solutions listed to solve “aliasing” as described in the next section.

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Figure 4.12. Images show the effect of choice of RF coil. The image at left shows the gradient fall-off artifact resulting from signal reception by the surface coil in the region where the gradient amplitude is decaying to zero. The image at right shows the effect of selecting a smaller surface coil whose physical coverage does not include the fall-off region of the gradient fields.

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Aliasing Source Aliasing occurs when the FOV in the phase-encoding direction is smaller than the anatomy being imaged. The data are undersampled and the image appears to be wrapped from one side to the other along this direction (Figure 4.13). This can occur in two directions when 3D data are acquired, but it does not occur along the frequency-encoding direction. Solutions ■ Increase the FOV along the phase-encoding axes. This will solve this problem but at the expense of decreased spatial resolution. ■ Increase the phase FOV percentage or enable the no-phase-wrap feature. ■ Swap the readout and phase-encoding directions, unless this increases flow artifacts to an unacceptable degree. ■ Apply parallel imaging techniques to “unwrap” the artifact. This will solve the problem but can decrease signal-to-noise ratio in the image. ■ Reposition the center of the FOV so that the aliased data are not included in the anatomy of interest. Signal-to-noise ratio and resolution are not decreased, but several attempts may be required to position the aliased tissue outside of the region of interest.

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Figure 4.13. Reduced-phase FOV in a four-chamber image of the heart (top) demonstrating aliasing of chest wall and arms into the anatomical region of interest. Full-phase FOV image of the heart (bottom) with phase- and frequency-encoding directions swapped.

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RF Zipper Source An RF zipper results when RF energy from a source other than the patient is detected by the RF coil used for imaging. The signal is not spatially encoded and appears as a line whose intensity varies from bright to dark along the phase-encoding direction (Figure 4.14). The typical source of this noise is (but is not restricted to) a pump or other electromechanical device in the room. Also, any conducting cable that enters the room can act as an antenna, propagating noise from outside into the scan room. Finally, a leak in the RF shield of the MR scan room can allow external RF noise to enter. These RF leaks occur most commonly around doors and windows. Note that zipper-type artifacts that occur along the frequency-encoding axis arise from sources internal to the MR scanner such as stimulated echoes and pulse sequence timing errors. Solutions ■ Identify and remove all noise sources within the room. ■ Have a qualified service engineer check for leaks in the RF shield of the scan room.

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Figure 4.14. Four-chamber balanced gradient echo (top), perfusion (bottom left), and delayed enhancement (bottom right) images showing RF zipper propagating along the phaseencoding direction. The noise source that produced this artifact was an infusion pump inside the MR scan room. For imaging sequences with low signal-to-noise ratio, such as myocardial delayed enhancement imaging, the artifact can be particularly prominent.

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ECG Gating Mistriggers Source A poor quality (low-voltage) ECG waveform or an irregular heart rate can degrade cardiac MR image quality. When the voltage of the QRS complex is nearly the same value as that of the noise, triggering on noise spikes instead of the R-wave peak causes data to be collected at incorrect phases of the cardiac cycle. The random nature of the noise results in mixing of data from multiple cardiac phases into a single phase and produces motion blurring and signal loss. ECG-gated MR sequences typically use some type of arrhythmia rejection to ensure that all data are collected at the correct cardiac phase. Arrhythmia rejection prolongs the data-acquisition period, which results in longer breath-holds for the patient. If arrhythmia-induced heart rate changes are too great, the scanner may time out, resulting in no data being acquired. Note that poor ECG gating does not produce respiratoryinduced motion artifacts. If breath-holding throughout the data-collection process is adequate but ECG gating is poor, the heart alone will show motion-induced artifacts and the chest wall will appear static (Figure 4.15). Solutions ■ Check all lead voltage waveforms for optimal ECG signal. ■ Recheck the placement of electrodes. Check for adequate electrical contact between the electrode and skin surface by using appropriate skin preparation (eg, abrasive gel). ■ Decrease the tolerance for ECG arrhythmias. This reduces the range of heart rates over which data are collected, eliminating the effect of collecting data at different phases of the cardiac cycle because of irregular heart rates or false ECG triggers. This can increase the image acquisition time because of the extra time required to complete data acquisition. ■ Increase the VPS and, if necessary, decrease the number of cardiac phases, which will decrease the number of R-R intervals over which data are collected and potentially the amount of mistriggered data. ■ Check to ensure that the ECG cable travels as closely as possible to the center of the MR scanner bore as it exits. ■ Choose peripheral photo-pulse gating.

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Figure 4.15. Four-chamber view of heart. Gating mistriggers are shown at top; mixing of different cardiac views from across the cardiac cycle produces motion blurring of the heart only. Correctly gated four-chamber view is shown at bottom.

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Respiratory Motion Artifact Source Respiratory motion artifacts occur if patients are unable to hold their breath or resume breathing during the data-acquisition process. Movement of the heart through the imaging plane due to diaphragm motion induces blurring, ghosting (Figure 4.16), and volume averaging of the heart. These effects can affect image quality and quantitative measures such as ejection fraction and myocardial mass. This motion is distinguishable from ECG gating artifacts because of the presence of chest wall motion–induced ghosting. Solutions ■ If possible, decrease the imaging time so that the patient can achieve a breath-hold throughout the imaging sequence. Parallel imaging techniques are useful in this regard. Another approach is to decrease the number of phase-encoding steps of the imaging sequence. If a perfusion sequence is being used, decreasing the number of phases will also decrease imaging time. ■ In some instances, the use of navigator echoes or respiratory bellows, which allow free breathing during data acquisition, may be appropriate, particularly for non-cine sequences such as T1-weighted black blood imaging. ■ Use single-shot techniques so that the patient can free breathe during data acquisition. ■ Coach the patient before the breath-hold acquisition.

Figure 4.16. Short-axis images of the heart during a free-breathing (top) and a breath-hold (bottom) ECG gated acquisition. Although the imaging sequence was able to successfully gate the ECG of the volunteer, respiratory motion severely degraded image quality. Movement of the diaphragm results in movement of the cardiac anatomy through the imaging slice, producing blurring and ghosting of the cardiac anatomy.

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Flow-Related Artifacts Source Blood flow into and out of the imaging volume during data acquisition results in modulation of the magnetization of the blood throughout the imaging sequence. This modulation produces replication and blurring of the signal along the phase-encoding direction of the image (Figure 4.17). This effect is most apparent for balanced steady-state sequences and is exacerbated at increased TR and higher field strength (3.0T). Longer TR allows more time for the blood to flow out of the volume and accumulate phase, and higher field strength increases the susceptibility variation, as measured in hertz. Solutions ■ Use the shortest possible TR for balanced gradient echo sequences. ■ Swap the phase- and frequency-encoding directions to change the direction of artifact propagation. ■ Choose a spoiled rather than balanced gradient echo sequence. ■ Image at a lower field strength (1.5T vs 3.0T) ■ For non-cine acquisitions, choose a more quiescent portion of the cardiac cycle for data collection (diastole vs systole).

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Figure 4.17. Fully magnetized blood in the aorta is shown entering the imaging slice during a balanced steady-state gradient echo imaging sequence (top). Same slice is shown during late diastole when flow is at a minimum (bottom).

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Susceptibility-Induced Signal Loss Source Differences in magnetic susceptibility of tissues or implanted materials (metals such as sternal wires or stents) distort the magnetic field around the tissue interface or object, thereby producing image distortion and signal loss (Figure 4.18). Solutions ■ Use linear or higher-order shimming of the volume around the region of differing tissue susceptibilities; this can improve the main magnetic field homogeneity and sometimes decrease the artifact. ■ Increase the receiver bandwidth of the imaging sequences or choose spin echo–based sequences for imaging around metal implants when appropriate. ■ Decrease the TR in balanced steady-state free precession pulse sequences. ■ Decrease the voxel size (ie, increase the spatial resolution). ■ Image at lower field strength (ie, 1.5T instead of 3.0T).

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Figure 4.18. Multiple short-axis views of the heart showing signal loss and distortion around sternal wires (arrows).

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Banding on Balanced Steady-State Free Precession Images Source Balanced steady-state free precession imaging requires that the net area on each gradient axis be zero during any TR interval. Spatially varying magnetic field inhomogeneities introduce net phase accrual and violate this condition. This results in varying bright and dark bands across the image (Figure 4.19). The source of this inhomogeneity can be due to the physical design limitations of the main magnetic field or susceptibility-induced field variations from different tissue interfaces (eg, lung to liver to heart) or implanted devices (eg, stents). Solutions ■ The spatial period of the banding is proportional to the inhomogeneity of the main magnetic field and the inverse of the TR of the imaging sequence. Decreasing the TR will increase the separation of the bands. However, decreasing the TR may not be possible if the TR is already at a minimum. Improving the homogeneity of the main magnetic field by linear or higher-order shimming over the localized volume of the heart can decrease the artifact. ■ Switch to another type of pulse sequence such as a spoiled gradient echo; however, signal-to-noise ratio may decrease. ■ The bands can be shifted by changing the resonant frequency of the receiver, thereby shifting the banding artifact so that the region of signal loss is outside of the critical anatomical region of interest. ■ Decrease the field strength (ie, 1.5T instead of 3.0T).

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Figure 4.19. Balanced steady-state gradient echo images (left) demonstrating banding and signal loss due to magnetic field inhomogeneities (arrows). Spoiled gradient echo images are shown at right.

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Parallel-Imaging Reconstruction Artifact Source For image-based parallel-imaging algorithms (eg, SENSE), it is possible that the RF coil sensitivity map may not cover the anatomical region being imaged. Because the sensitivity map is used to define the spatial coil maps for the various coil elements, it does not include the volume over which the data are collected, and the reconstruction algorithm is unable to unwrap those regions within the image (Figure 4.20). Regions of low signal such as the background or lungs produce similar artifacts. Solutions ■ Rescan the calibration volume to include the imaging volume. This will reduce this artifact for subsequent parallel-imaging sequences. So-called “autocalibration” sequences such as GRAPPA or ARC that acquire the calibration scan as part of the data collection process can also decrease this error, at the expense of increased scan time of the parallel-imaging technique. ■ Reduce the acceleration factor to improve the signal-to-noise ratio of the reconstruction process. ■ Acquire a fully sampled MR data set.

Figure 4.20. Short-axis spoiled gradient echo images acquired with parallel-imaging (SENSE) techniques (left) and full-acquisition short-axis views (right) for two separate volunteers. Insufficient coverage of the imaging volume by the calibration scan results in reconstruction errors in the parallel images (arrows).

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SELECTED REFERENCES Anatomy, Physiology, and Biophysics Hobbie RK, Roth BJ. Intermediate physics for medicine and biology. 4th ed. New York: Springer; c2007. Malmivuo J, Plonsey R. Bioelectromagnetism: principles and applications of bioelectric and biomagnetic fields. New York: Oxford University Press; c1995. Marieb EN. Essentials of human anatomy & physiology. 7th ed. San Francisco: Benjamin Cummings; c2003. Cardiac MRI Bogaert J, et al. Clinical cardiac MRI: with interactive CD-ROM. Berlin: Springer; c2005. Lee VS. Cardiovascular MRI: physical principles to practical protocols. Philadelphia: Lippincott Williams & Wilkins; c2006. Miscellaneous Cerqueira MD, et al, American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002;105(4):539-42. MR Acronyms Boyle GE, et al. An interactive taxonomy of MR imaging sequences. Radiographics. 2006;26(6):e24. Brown MA, Semelka RC. MR imaging abbreviations, definitions, and descriptions: a review. Radiology. 1999;213(3):647-62. Nitz WR. MR imaging: acronyms and clinical applications. Eur Radiol. 1999;9(5):979-97. Sprung K. Basic techniques of cardiac MR. Eur Radiol. 2005;15 Suppl 2:B10-6. MR Physics and Pulse Sequences Bernstein MA, et al. Handbook of MRI pulse sequences. Burlington (MA): Elsevier Academic Press; c2004. Haacke EM, et al. Magnetic resonance imaging: physical principles and sequence design. New York: Wiley-Liss; c1999. Simonetti OP, et al. “Black blood” T2-weighted inversion-recovery MR imaging of the heart. Radiology. 1996;199(1):49-57. Vector ECG Gating Chia JM, et al. Performance of QRS detection for cardiac magnetic resonance imaging with a novel vectorcardiographic triggering method. J Magn Reson Imaging. 2000;12(5):678-88. Fischer SE, et al. Novel real-time R-wave detection algorithm based on the vectorcardiogram for accurate gated magnetic resonance acquisitions. Magn Reson Med. 1999;42(2):361-70.

INDEX

INDEX

MRI analysis, 67–68 quantifying, 67 Apex, four-chamber view, 9 Apical ballooning syndrome, 49, 59 Apical short-axis MDE, apical ballooning syndrome, 59 Arrhythmogenic right ventricular cardiomyopathy (ARVC), 49, 58 Arrhythmogenic right ventricular dysplasia, 18 Atrial pressure, 33 Autoimmune myocarditis, 60 Axial balanced gradient echo myxoma, 80 transposition complexes, 100, 101 Axial double inversion recovery angiosarcoma, 86 lipomatous hypertrophy, 85 pericardial cyst, 94 pericarditis, 92

A Acquisition protocol, cardiac magnetic resonance (MR) imaging, 3 Aliasing artifact, 162, 163 intentional, 115 Anatomical reference LV four-chamber localizer, 9 LV four-chamber long-axis, 17 LV sagittal localizer, 7 LV short-axis, 11 LV three-chamber long-axis, 15 LV two-chamber long-axis, 13 RV conventional axial, 21 RV inflow tract vertical long-axis, 25 Angiosarcoma, axial double inversion recovery image, 86 Aortic insufficiency causes, 66 MRI analysis, 67–68 oblique long axis/aortic outflow tract, 63 quantifying, 66 three-chamber balanced gradient echo cine, 65 Aortic pressure, 33 Aortic stenosis causes, 66 coronal oblique balanced gradient echo cine, 65

B Balanced gradient echo cine, 118–119 Balanced gradient echo signal, 113, 114 Balanced gradient echo MR Ebstein anomaly, 105 partial anomalous venous connections, 103 183

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perfusion, 136 transmural myocardial infarction, 46, 47 transposition complexes, 100, 101 ventricular noncompaction, 106 Balanced steady-state free precession cine, 118 Balanced steady-state free precession images, banding, 174, 175 Black blood inversion recovery cardiac masses, 77 congenital disease, 97 pericardial disease, 88, 89 Blood flow-related artifacts, 170, 171 Blood inversion time (TIblood), 124 double inversion recovery, 125 Blood pool definition, 117 signal, 109 Breath-hold cardiac masses, 76–77 cardiomyopathies, 50–51 congenital disease, 96, 97 ECG gated acquisition, 169 myocardial perfusion and viability, 42–43 normal, 119, 121, 139 pericardial disease, 88, 89, 90 valvular disease, 62, 63, 64 Bright blood balanced gradient echo, 118 cardiac masses, 76 cardiomyopathies, 50, 51 cine phase contrast, 132 myocardial perfusion and viability, 42–44 spoiled gradient echo, 120 tagging, 138 valvular disease, 62, 63, 64 Bright blood pool signal, 117

Bright-exogenous contrast agent blood pool signal, 117 myocardial delayed enhancement, 122 perfusion MR, 136 3D MR angiography, 130

C Cardiac amyloidosis, 56 Cardiac cycle, 32, 33 ECG waveforms, 142 Cardiac magnetic resonance (MR) cardiac cycle characteristics, 34, 35 cardiomyopathies, 49–60 congenital disease, 95–106 ECG artifacts, 109, 148–159 ECG gating, 109, 140–147 imaging artifacts, 109, 160–177 left ventricular imaging, 4–17 masses, 74–86 myocardial perfusion and viability, 40–48 pericardial disease, 87–94 pulse sequence components, 111–117 pulse sequences for function, 130–139 pulse sequences for morphology, 118–129 right ventricular imaging, 18–25 valvular disease, 61–73 workflow, 3 Cardiac masses decision tree, 75 MRI examples, 79–86 MRI protocols, 76–78 Cardiac phases balanced gradient echo, 119 cardiomyopathies, 50–51 cine phase contrast, 135 congenital disease, 96, 97

INDEX

masses, 76 myocardial perfusion and viability, 42–43 pericardial disease, 88, 89 spoiled gradient echo cine, 121 tagging, 139 valvular disease, 62, 63, 64 Cardiac physiology, 31–35 Cardiomyopathies MRI examples, 53–60 MRI protocols, 50–52 Centric view order encoding, 3D MR angiography, 131 Chemical stress, ECG effects, 159 Cine imaging, definition, 116 Cine phase contrast MR, 132–135 congenital disease, 97 Coarctation, gadolinium-enhanced MR angiography, 104 Congenital disease MRI examples, 98–106 MRI protocols, 96–97 Congestive heart failure pericardial effusion MRI, 91 resulting from myocardial infarction, 48 Conventional axial RV view acquisition, 20, 21 planes, 19 Coronal oblique balanced gradient echo, aortic stenosis, 65 Coronary artery territories, 41

D D-transposition great arteries, MR images, 100, 101 Dark blood pool signal, 117 double inversion recovery, 124 spin echo T1-weighted, 128 triple inversion recovery, 126

185

Data acquisition gradient switching ECG waveform effect, 156, 157 image reconstruction, 113, 115 magnetohydrodynamic ECG waveform effect, 150, 151 RF body coil switching ECG waveform effect, 154, 155 sternal wires/clips ECG waveform effect, 158 triboelectric ECG waveform effect, 152, 153 Diastole, 33 Dilated cardiomyopathy, 53 Double inversion recovery, 124–125

E Ebstein anomaly, 18 balanced gradient echo images, 105 ECG (electrocardiographic) gating, 109, 143 artifacts, 109, 148–159 chemical stress, 159 lead placement, 144 Mayo configuration, 145 mistriggers, 166, 167 MR interference, 148, 149 patient preparation, 143–144 VCG configuration, 146 ECG waveform, 142 gradient switching effect, 156, 157 magnetohydrodynamic effect, 150, 151 RF body coil switching effect, 154, 155 sternal wires/clips effect, 158 triboelectric effect, 152, 153 Echo formation, 112–113 Echo train, 113 Einthoven lead triangle, 140, 141 Einthoven, Willem, 140

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End-diastolic volume (EDV), 33 End-systolic volume (ESV), 33 Eosinophilic cardiomyopathy, 57

F Fat inversion time (TIfat), 126 triple inversion recovery, 127 Fat saturation, 111 myocardial delayed enhancement, 122 triple inversion recovery, 126 Fatty tissue infiltration, RV, 58 Flow encoding, 112 Flow-encoding direction, cine phase contrast, 134 Four-chamber balanced gradient echo ARVC, 58 ischemic cardiomyopathy, 48 pericardial constriction, 93 RF zipper, 165 thrombus, 79 tricuspid stenosis and regurgitation, 72 ventricular noncompaction, 106 Four-chamber double inversion recovery, lipoma, 84 Four-chamber horizontal long-axis view (LV), 16, 17 Four-chamber imaging plane left ventricle, 5 right ventricle, 19 Four-chamber localizer (LV), acquisition, 8, 9 Four-chamber long-axis balanced gradient echo, eosinophilic cardiomyopathy, 57 Four-chamber long-axis plane cardiac masses, 76 cardiomyopathies, 50 congenital disease, 96

dilated cardiomyopathy, 53 LV cardiac cycle correlation, 34, 35 myocardial perfusion and viability, 42 pericardial disease, 88, 90 valvular disease, 62 Four-chamber myocardial delayed enhancement (MDE) ischemic cardiomyopathy, 48 subendocardial myocardial infarction, 45 transmural myocardial infarction, 46 Four-chamber view, ECG gating mistrigger, 167 FOV (field of view) enlarging, 115 and k-space, 116 phase-encoding direction, 162, 163 Free-breathing ECG gated acquisition, 169 Function, pulse sequences for, 130–139

G Gadolinium-based contrast agent, 40, 51 Gadolinium-enhanced MR angiography coarctation, 104 partial anomalous venous connections, 102, 103 tetralogy of Fallot, 99 Gradient decay/fall-off, artifact, 160, 161 Gradient echo signal, 112–113 Gradient switching effect, 156, 157 GRAPPA (k-space-based parallel imaging), 116 autocalibration, 176

H Hemangioma, short-axis balanced gradient echo image, 83 Horizontal long-axis, pericardial disease, 89 Hypertrophic cardiomyopathy, 54–55

INDEX

I Image ghosting, 168, 169 Image-based parallel imaging (SENSE), 115 reconstruction artifacts, 176, 177 Imaging artifacts, 109, 160–177 Imaging modes, 116–117 Imaging protocols and sequences cardiomyopathies, 50–52 myocardial perfusion and viability, 42–44 Infarct distributions, 41 Infectious myocarditis, 60 Inversion recovery, 111 cardiac masses, 77 double, 124 myocardial delayed enhancement, 122 triple, 126 Inversion time (TI) cardiac masses, 78 cardiomyopathies, 52 myocardial perfusion and viability, 44 pericardial disease, 90 Ischemic cardiomyopathy, 48 Ischemic heart disease, 40

187

four-chamber localizer, 8, 9 long-axis view, 12, 13 planes, 4, 5 sagittal localizer, 6, 7 short-axis view, 10, 11 three-chamber view, 14, 15 two-chamber vertical long-axis view, 12, 13 Left ventricular imaging, 4–17 Left ventricular outflow tract, cardiomyopathies, 51 Limb leads I, II, and III, 140, 141 Lipoma, four-chamber double inversion recovery image, 84 Lipomatous hypertrophy, axial double inversion recovery image, 85 Long axis left ventricle, 12, 13 left ventricle/left atrium, mitral regurgitation, 63 right ventricle, 23 Long-axis delayed enhancement cardiac masses, 77 cardiomyopathies, 52 myocardial perfusion and viability, 44 pericardial disease, 90

K K-space, 115 and FOV, 116 K-space-based parallel imaging, 116 kt-BLAST rapid imaging, 116

L Left anterior descending artery (LAD), 41 Left circumflex coronary artery (LCX), 41 Left heart, cardiac cycle, 32, 33 Left ventricle (LV) four-chamber horizontal long-axis view, 16, 17

M Magnetization preparation, 111–112 Magnetohydrodynamic effect, 150–151 Mayo lead placement configuration, 144, 145 Mediastinum extension, 75 Metastasis, short-axis delayed enhancement, 82 Midventricular short-axis balanced gradient echo, hypertrophic obstructive cardiomyopathy, 54 Midventricular short-axis MDE

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MAYO CLINIC GUIDE TO CARDIAC MRI

cardiac amyloidosis, 56 hypertrophic cardiomyopathy, 55 myocarditis, 60 Mitral regurgitation causes, 70 cine flow analysis, 71 long-axis left ventricle/left atrium, 63 quantifying, 70 Mitral stenosis causes, 70 cine flow analysis, 71 short-axis balanced gradient echo, 69 Mitral valve four-chamber view, 9 prolapse and regurgitation, threechamber bright blood cine, 69 Morphology, pulse sequences for, 118–129 Multishot double inversion recovery, 124 echo train, 115 myocardial delayed enhancement, 122 3D MR angiography, 130 triple inversion recovery, 126 Mustard operation, postsurgical MR images, 100 Myocardial delayed enhancement (MDE), 122–123 hemangioma, 83 myxoma, 80, 81 pericarditis, 92 RF zipper, 165 subendocardial myocardial infarction, 45 thrombus, 79 transmural myocardial infarction, 46 Myocardial heart segments, AHA, 40, 41 Myocardial infarction, MRI examples, 45–48 Myocardial perfusion and viability MRI examples, 45–48 MRI protocols, 42–44

Myocarditis, acute, 60 Myocardium inversion time (TImyo), 122, 123 Myxoma, MRI, 80, 81

N Neoplasm, 75 Noise sources ECG in MRI, 149 RF zipper, 164 Normal variant masses, 75

O Oblique based on mass location, cardiac masses, 77 Oblique long axis/aortic outflow tract, aortic insufficiency, 63 Oblique sagittal double inversion recovery image, myxoma, 81 Oblique slice aortic region of interest, valvular disease, 64 Oblique 3D volume, congenital disease, 97

P P wave, atrial depolarization, 142 Partial anomalous venous connections, MR images, 102, 103 Partial Fourier rapid imaging, 116 Partial-phase FOV, 119, 121 Pathology-dependent imaging plane, congenital disease, 97 Perfusion MR, 136–137 RF zipper, 165 Pericardial constriction, four-chamber balanced gradient echo image, 93 Pericardial cyst, axial double inversion recovery image, 94

INDEX

Pericardial disease MRI examples, 91–94 MRI protocols, 88–90 Pericardial effusion, short-axis balanced gradient echo image, 91 Pericarditis, axial double inversion recovery image, 92 Peripartum cardiomyopathy, 53 Peripheral photo-pulse sensor, 147, 159 Phase contrast, 112 cine phase contrast MR, 132 Phases per slice, perfusion MR, 136, 137 Photoplethysmography, 147 Prescription images inflow tract vertical long-axis, 25 LV four-chamber localizer, 9 LV four-chamber long-axis, 17 LV planes, 4, 5 LV sagittal localizer, 7 LV short-axis, 11 LV three-chamber, 15 LV two-chamber long-axis, 13 RV conventional axial, 21 Pulmonary regurgitation, cine phasecontrast blood flow data, 73 Pulmonary stenosis, balanced gradient echo cine, 73 Pulse sequence, 109 components, 111–117 Pulse sequences clinical correlation, 39 for function, 130–139 for morphology, 118–129

Q QRS complex healthy example, 148 ventricular depolarization, 142

189

R Radio frequency (RF) body coil switching effect, 154, 155 MR signal, 111 zipper-type artifacts, 164, 165 Rapid imaging, 115–116 Reconstruction artifact, parallel imaging, 176, 177 Reconstruction type, cine phase contrast, 134 Rectangular-phase FOV rapid imaging, 116 Respiratory motion artifacts, 168, 169 Restrictive cardiomyopathy, 56–57 Resultant image, as blood pool signal, 111 Resultant views inflow tract vertical long-axis, 25 LV four-chamber localizer, 9 LV four-chamber long-axis, 17 LV sagittal localizer, 7 LV short-axis, 11 LV three-chamber, 15 LV two-chamber long-axis, 13 RV conventional axial, 21 Rheumatic heart disease aortic insufficiency, 66 mitral stenosis, 70 tricuspid stenosis, 72 Right coronary artery (RCA), 41 Right ventricle (RV) conventional axial views, 19, 20, 21 four-chamber localizer, 19, 23 inflow tract vertical long-axis view, 23, 24, 25 outflow tract view, 23 planes, 18, 20, 23 sagittal localizer, 19, 23 Right ventricular imaging, 18–25

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S Sagittal plane cardiac masses, 76 cardiomyopathies, 50 congenital disease, 96 LV acquisition, 6, 7 LV localizer, 4, 5 myocardial perfusion and viability, 42 pericardial disease, 88 RV localizer, 19 valvular disease, 62 Saturation recovery, 111 perfusion MR, 136 3D MR angiography, 130 Segmented data acquisition, 115 balanced gradient echo, 118 cine phase contrast, 132 myocardial delayed enhancement, 122 spoiled gradient echo cine, 120 SENSE (image-based parallel imaging), 115 balanced gradient echo, 118 cine phase contrast, 132 double inversion recovery, 124 myocardial delayed enhancement, 122 perfusion MR, 136 reconstruction artifact, 176, 177 spin echo T1-weighted, 128 spoiled gradient echo cine, 120 tagging, 138 3D MR angiography, 130 triple inversion recovery, 126 Septum, short-axis view, 10, 11 Sequential view order encoding, 3D MR angiography, 131 Short-axis balanced gradient echo hemangioma, 83 mitral stenosis, 69 pericardial effusion, 91 tetralogy of Fallot, 98 transmural myocardial infarction, 46

ventricular noncompaction, 106 Short-axis delayed enhancement cardiac masses, 77 cardiomyopathies, 52 metastasis, 82 myocardial perfusion and viability, 44 pericardial disease, 90 Short-axis double inversion recovery, pericardial constriction, 93 Short-axis plane cardiac masses, 76 cardiomyopathies, 50, 52 congenital disease, 96 coronary artery territories, 41 left ventricle, 4, 5, 10, 11 myocardial perfusion and viability, 42 perfusion, 43, 51, 78 pericardial disease, 88 subendocardial myocardial infarction, 45 tissue susceptibility signal loss, 173 valvular disease, 62 Signal loss/distortion, tissue magnetic susceptibility, 172, 173 Single echo imaging, 113 Single frame image, 116 Single shot image echo, 113, 115 myocardial delayed enhancement, 122 perfusion MR, 136 spin echo T1-weighted, 128 SMASH (image-based parallel imaging) balanced gradient echo, 118 cine phase contrast, 132 double inversion recovery, 124 k-space-based parallel imaging, 116 myocardial delayed enhancement, 122 perfusion MR, 136 spin echo T1-weighted, 128 spoiled gradient echo cine, 120 tagging, 138

INDEX

3D MR angiography, 130 triple inversion recovery, 126 Spatial relationship, LV images, 4, 5 Spin echo imaging double inversion recovery, 124 T1-weighted, 128 tagging, 138 triple inversion recovery, 126 Spin echo signal, 112, 114 Spin echo T1-weighted, 128–129 Spoiled gradient echo cine, 120–121 Spoiled gradient echo MR cine phase contrast, 132 myocardial delayed enhancement, 122 perfusion, 136 tagging, 138 3D MR angiography, 130 Spoiled gradient echo, signal, 113, 114 Standard imaging planes, 4, 5 Sternal wires/clips ECG effects, 158 tissue susceptibility signal loss, 172–173 Subendocardial myocardial infarction, 45 Systole, 33

T T wave healthy example, 148 ventricular repolarization, 142 Tagging, 112 Tagging MR, 138–139 spoiled gradient echo imaging, 138 TE/2 (echo time), spin echo T1-weighted, 128–129 Temporal relationship, LV images, 4, 5 Tetralogy of Fallot, MR images, 98, 99 Three-chamber balanced gradient echo aortic insufficiency, 65 transmural myocardial infarction, 47

191

Three-chamber bright blood cine, mitral valve prolapse and regurgitation, 69 Three-chamber imaging plane, LV, 5 Three-chamber long-axis hypertrophic obstructive cardiomyopathy, 54 left ventricle, 14, 15 3D imaging, 117 3D MR angiography, 130–132 congenital disease, 97 3D static myocardial delayed enhancement, 122 3D MR angiography, 130 Thrombus, 75 four-chamber balanced gradient echo, 79 Tissue magnetic susceptibility signal loss, 172, 173 Tissue suppression, 111 Toxic myocarditis, 60 Toxic substance, cardiomyopathy, 53 TR (repetition time), spin echo T1weighted, 128-129 Transmural myocardial infarction, 46, 47 Transposition complexes, MR images, 100, 101 Transverse diastolic balanced gradient echo, aortic insufficiency, 65 Triboelectric effect, 152, 153 TRICKS rapid imaging, 116 Tricuspid stenosis and regurgitation, four-chamber balanced gradient echo cine, 72 Triple inversion recovery, 126–127 Two-chamber imaging plane, LV, 5 Two-chamber long-axis balanced gradient echo apical ballooning syndrome, 59 hypertrophic cardiomyopathy, 55 Two-chamber long-axis MDE

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apical ballooning syndrome, 59 cardiac amyloidosis, 56 cardiomyopathy, 53 eosinophilic cardiomyopathy, 57 myocarditis, 60 Two-chamber myocardial delayed enhancement (MDE), subendocardial myocardial infarction, 45 Two-chamber short-axis, LV cardiac cycle correlation, 34, 35 Two-chamber vertical long-axis, LV, 12, 13 2D cine balanced gradient echo, 118 cine phase contrast, 132 perfusion MR, 136 spoiled gradient echo cine, 120 tagging, 138 2D imaging, 116–117 2D static double inversion recovery, 124 myocardial delayed enhancement, 122 spin echo T1-weighted, 128 triple inversion recovery, 126

UNFOLD rapid imaging, 116

MRI evaluation, 61 MRI examples, 65–73 MRI protocols, 62–64 Vector ECG (VCG), 142 lead placement configuration, 146 Velocity encoding (VENC) values, cine phase contrast, 64, 97, 132, 133. Ventricular noncompaction, balanced gradient MR, 106 Ventricular pressure, 33 Vertical and horizontal long-axis, myocardial perfusion and viability, 43 Vertical long-axis, coronary artery territories, 41 View sharing, k-space lines, 115 Views per segment (VPS) balanced gradient echo, 119 cardiac masses, 78 cardiomyopathies, 50 cine phase contrast, 134 congenital disease, 96 definition, 115 myocardial perfusion and viability, 42 spoiled gradient echo cine, 120–121 tagging, 139 Viral infection cardiomyopathy, 53

V

W

Valve plane, valvular disease, 64 Valvular disease

Waller, Augustus Desiré, 140 Waveforms, cardiac cycle, 32, 33

U

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