M AYO C L I N I C G U I D E T O C A R D I AC

M AG N E T I C R E S O N A N C E I M AG I N G

SECOND EDIT ION

MAYO CLINIC SCIENTIFIC PRESS

Mayo Clinic Atlas of Regional Anesthesia and Ultrasound-Guided Nerve Blockade

Edited by James R. Hebl, MD, and Robert L. Lennon, DO

Mayo Clinic Preventive Medicine and Public Health Board Review

Edited by Prathibha Varkey, MBBS, MPH, MHPE

Mayo Clinic Challenging Images for Pulmonary Board Review

Edited by Edward C. Rosenow III, MD

Mayo Clinic Infectious Diseases Board Review

Edited by Zelalem Temesgen, MD

Mayo Clinic Antimicrobial Handbook: Quick Guide, Second Edition

Edited by John W. Wilson, MD, and Lynn L. Estes, PharmD

Just Enough Physiology

By James R. Munis, MD, PhD

Mayo Clinic Cardiology: Concise Textbook, Fourth Edition

Edited by Joseph G. Murphy, MD, and Margaret A. Lloyd, MD

Mayo Clinic Internal Medicine Board Review, Tenth Edition

Edited by Robert D. Ficalora, MD

Mayo Clinic Internal Medicine Board Review: Questions and Answers

Edited by Robert D. Ficalora, MD

Mayo Clinic Electrophysiology Manual

Edited by Samuel J. Asirvatham, MD

Mayo Clinic Gastrointestinal Imaging Review, Second Edition

By C. Daniel Johnson, MD

Arrhythmias in Women: Diagnosis and Management

Edited by Yong-Mei Cha, MD, Margaret A. Lloyd, MD, and Ulrika M. Birgersdotter-Green, MD

Mayo Clinic Body MRI Case Review

By Christine U. Lee, MD, PhD, and James F. Glockner, MD, PhD

Mayo Clinic Gastroenterology and Hepatology Board Review, Fifth Edition

Edited by Stephen C. Hauser, MD
 M AYO CLI NIC GUIDE TO
CA R DI AC M AGNETIC
R ESONA NCE I M AGI NG
SECOND EDITION

Editors
Kiaran P. McGee, PhD Eric E. Williamson, MD
C O N S U LTA N T, D E PA RT M E N T O F R A D I O L O G Y CH A I R , DI V I S ION OF C A R DIOVA S C U L A R R A DIOL O G Y

M AY O C L I N I C , R O C H E S T E R , M I N N E S O TA M AY O C L I N I C , R O C H E S T E R , M I N N E S O TA

A S S O C I AT E P R O F E S S O R O F M E D I C A L P H Y S I C S A N D ASSOCIATE PROFESSOR OF R ADIOLOGY

A S S I S TA N T P R O F E S S O R O F B I O M E D I C A L E N G I N E E R I N G M AY O C L I N I C C O L L E G E O F M E D I C I N E

M AY O C L I N I C C O L L E G E O F M E D I C I N E

Matthew W. Martinez, MD
D I R E C T O R , S P O RT S C A R D I O L O G Y & H Y P E RT R O P H I C C A R D I O M Y O PAT H Y P R O G R A M S A N D C A R D I O VA S C U L A R

I M A G I N G , L E H I G H VA L L E Y H E A LT H N E T W O R K , A L L E N T O W N , P E N N S Y LVA N I A ; A S S O C I AT E P R O F E S S O R O F M E D I C I N E ,

M O R S A N I C O L L E G E O F M E D I C I N E , U N I V E R S I T Y O F S O U T H F L O R I D A , TA M PA , F L O R I D A

F O R M E R LY, A S S I S TA N T P R O F E S S O R O F C A R D I O VA S C U L A R D I S E A S E S

M AY O C L I N I C C O L L E G E O F M E D I C I N E

MAYO CLINIC SCIENTIFIC PRESS OXFORD UNIVERSITY PRESS

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.

3
Oxford University Press is a department of the University of Oxford.
It furthers the University’s objective of excellence in research, scholarship,
and education by publishing worldwide.

Oxford New York

Auckland Cape Town Dar es Salaam Hong Kong Karachi
Kuala Lumpur Madrid Melbourne Mexico City Nairobi
New Delhi Shanghai Taipei Toronto

With offices in
Argentina Austria Brazil Chile Czech Republic France Greece
Guatemala Hungary Italy Japan Poland Portugal Singapore
South Korea Switzerland Thailand Turkey Ukraine Vietnam

Oxford is a registered trademark of Oxford University Press in the UK and certain other
countries.

Published in the United States of America by

Oxford University Press
198 Madison Avenue, New York, NY 10016

© 2008, 2015 by Mayo Foundation for Medical Education and Research.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted,
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior
permission of Mayo Foundation for Medical Education and Research. Inquiries should be addressed to
Scientific Publications, Plummer 10, Mayo Clinic, 200 First St SW, Rochester, MN 55905.

You must not circulate this work in any other form

and you must impose this same condition on any acquirer.

Library of Congress Cataloging-in-Publication Data

Mayo Clinic guide to cardiac magnetic resonance imaging / [edited by] Kiaran P. McGee, Eric E. Williamson, Matthew W. Martinez.—Second edition.
p. ; cm.
Guide to cardiac magnetic resonance imaging
Includes bibliographical references and index.
ISBN 978–0–19–994118–6 (alk. paper)
I. McGee, Kiaran P., editor. II. Williamson, Eric E., editor. III. Martinez, Matthew W., editor. IV. Mayo Clinic, issuing body.
V. Title: Guide to cardiac magnetic resonance imaging.
[DNLM: 1. Heart Diseases—diagnosis. 2. Magnetic Resonance Imaging—methods. WG 141.5.M2]
RC683.5.E5
616.1′207547—dc23
2014030936

Mayo Foundation does not endorse any particular products or services, and the reference to any products or
services in this book is for informational purposes only and should not be taken as an endorsement by the
authors or Mayo Foundation. 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 contents of 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 selection and dosage set forth
in this text are in accordance with current recommendations and practice 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 wordings and precautions. This is particularly important
when the recommended agent is a new or infrequently employed drug.

Some drugs and medical devices presented in this publication have US Food and Drug Administration (FDA)
clearance for limited use in restricted research settings. It is the responsibility of the health care providers
to ascertain the FDA status of each drug or device planned for use in their clinical practice.

9 8 7 6 5 4 3 2 1
Printed in the United States of America
on acid-free paper
 Kiaran P. McGee, PhD
To Cora, whose faith, courage, perseverance, and strength of character inspire me, motivate me, and fill me with
admiration every day. Keep the faith, fight the good fight, and never give up.—Dad

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

Matthew W. Martinez, MD
To my wife, Anna, whose strength and continued support in all aspects of our life together are unmatched. Nothing
matters until I share it with you.
 FOR EWOR D
This second edition of the Mayo Clinic Guide to Cardiac
Magnetic Resonance Imaging is written as a practical guide,
designed to provide truly useful information to radiologists,
along with other physicians, fellows, residents, technologists,
and medical physicists. The book will be at home beside the
magnetic resonance imaging (MRI) scanner console, in the
reading room, and on the desk of anyone training in the art
of cardiac MRI.
Since the publication of the first edition, this book has
undergone major revision and updating, including an expan-
sion from 4 to 14 chapters. New chapters covering anatomy,
imaging protocols, and MRI safety have been included.
Another new feature of the second edition is the inclusion of
120 board-style multiple-choice questions and answers. More
than 60 clinical case studies are included and illustrated with
hundreds of clinical images. Topics of the case studies include
myocardial ischemia and infarction, nonischemic myocar-
dial disease, pericardial disease, cardiac masses, and valvular
disease.
The second edition clearly reflects the growth of this
remarkable modality. Within Mayo Clinic, clinical cardiac
MRI patient volumes have grown in excess of 10% each year
during the past decade. Growth has been driven by new
capabilities stemming from engineering advances such as
vii
high-speed gradients, multiple-channel receive coil technol-
ogy, adaptation of gadolinium-based contrast agents, paral-
lel imaging techniques, and advanced 2-dimensional and
3-dimensional imaging sequences that provide anatomic and
functional information unique to MRI.
At Mayo Clinic, the steady growth of this modality is also
a testament to visionary radiologists such as Dr. Paul Julsrud
and Dr. Jerome Breen, who saw the potential of this nascent
technology long before it attained its present capabilities.
Finally, this book reflects the remarkable and synergis-
tic power resulting from the collaboration between clinical
imaging physicians, medical physicists, and engineers. It can
truly be said that cardiac MRI, unlike other medical imaging
modalities, is an imaging technology that was invented by its
users. The steady pace of invention is well illustrated in this
second edition. I highly recommend this book to all.
Richard L. Ehman, MD
Consultant, Department of Radiology,
Mayo Clinic;
Professor of Radiology
Mayo Clinic College of Medicine
 PR EFACE
The Mayo Clinic Guide to Cardiac Magnetic Resonance Imag­
ing, Second Edition, represents a major expansion of the
first edition of this text. Not only has the format of the text
changed, but new sections and chapters have been added to
keep this work current and topical. In keeping with the highly
clinical focus of this text, additional case studies and examples
have been provided to expand the clinical section of the text.
This section includes a medical history for each case, the indi-
cation for performing the cardiac magnetic resonance imaging
(MRI) examination, and a discussion of the imaging findings
from each study. In addition, 120 questions, answers, and cor-
responding explanations are provided in the final section of
the text. The objective of this section is to assist in learning of
the sometimes complex and challenging field of cardiac MRI.
The overall focus of the text remains unchanged, which is to
provide a practical handbook for cardiac MRI that will be
useful for physicians at all phases of their professional careers,
technologists both new and experienced, and medical physi-
cists involved in clinical cardiac MRI.
We would be remiss if we did not recognize our colleagues
who contributed both directly and indirectly to the content
of this text. We would like to identify, among the professional
staff of Mayo Clinic, Ron Kuzo, MD, Nandan Anavekar,
MD, Thomas Foley, MD, Philip Araoz, MD, Terri Vrtiska,
MD, James Glockner, MD, PhD, Phillip Young, MD, Robert
Watson, MD, PhD, Nila Akhtar, MD, and Ethany Cullen,
MD, for all of their input and assistance. We would also like
to recognize our gifted and talented team of MRI technolo-
gists who help to “keep us honest” on a daily basis. Finally,
we thank the members of our 3-dimensional imaging labo-
ratory and our colleague and friend David Larson for all of
their hard work in ensuring that we provide the best imaging
services to our patients and colleagues.
As cardiac MRI continues to grow, we hope that this text
will contribute to the dissemination of knowledge necessary to
perform complex, and at times challenging, MRI examinations
of the heart, increase the knowledge base of all practitioners,
and facilitate the growth and dissemination of cardiac MRI
beyond the boundaries of academic medicine into the broader
community.
Finally, we would like to recognize the landmark contri-
butions to the development of cardiovascular MRI, not only
within Mayo Clinic but worldwide, made by our good friends
and colleagues Paul Julsrud, MD, and Jerome Breen, MD.
ix
Paul and Jerry, this book is testimony to your leadership and
hard work, and we thank you.
I N T RODUC T ION TO T H E S E C O N D
E DI T ION OF T H E M AYO C L I N I C
G U I DE TO C A R DI AC M AG N ET I C
R E S O N A NC E I M AGI NG
This book is designed to meet the needs of 3 distinct yet
integrated groups, namely MR technologists, clinicians,
and MRI scientists and physicists. To achieve this goal, this
book is divided into 4 separate sections. Section I provides
information for MRI technologists who wish to acquire
consistent high-quality cardiac MR images. This includes an
overview of electrocardiographic gating, standard anatomy
of the heart, methods for acquiring standard imaging planes
of the heart, pulse sequences used for cardiac MRI, and mod-
ular imaging protocols for the most common indications for
a cardiac MRI examination. Section II provides case stud-
ies covering 6 broad disease categories representing the most
common indications for cardiac MRI. Within each disease
category, numerous clinical cases are presented, beginning
with a description of the initial indication for cardiac MRI,
followed by the recommended imaging protocol, identifica-
tion of imaging findings, and a summary of these findings
within the context of the identified disease. The target audi-
ence of this section includes clinicians in training (residents
and fellows), as well as those involved in academic or routine
clinical practice. Section III provides technical information
relevant to MRI scientists and physicists involved in car-
diac MRI. Emphasis is placed on common imaging artifacts
and methods to either reduce or eliminate them, as well as a
description of basic MRI safety as it pertains to cardiac MRI.
Finally, Section IV provides “board-type” questions and
answers designed to test the knowledge of clinicians involved
in cardiac MRI. Examination questions cover a range of top-
ics including MRI physics, anatomy and physiology, and
identification of key imaging findings of diseases described
throughout the text.
Kiaran P. McGee, PhD
Eric E. Williamson, MD
Matthew W. Martinez, MD
 CONT ENTS

Contributors xiii 9. Cardiac Masses 163

Ethany L. Cullen, MD, and Philip A. Araoz, MD
S E C T ION I 10. Congenital Disease 183
B A S IC PR I N C I PL E S OF C A R D I AC M R I Nandan S. Anavekar, MB, BCh, and
Paul R. Julsrud, MD
1. ECG Gating and Associated Artifacts 3 11. Valvular Heart Disease 203
Kiaran P. McGee, PhD, and James F. Glockner, MD, PhD
Matthew W. Martinez, MD
2. Cardiac Anatomy 16
Matthew W. Martinez, MD S E C T ION I I I
3. Standard Imaging Planes in Cardiac MR Imaging 27 T ROU B L E S H O O T I N G —M R I A RT I FAC T S A N D
Matthew W. Martinez, MD, Eric E. Williamson, MD, SA FET Y
and Kiaran P. McGee, PhD
4. Pulse Sequence Basics 45
12. Common MR Imaging Artifacts 231
Kiaran P. McGee, PhD, and
Kiaran P. McGee, PhD, and
Matthew A. Bernstein, PhD
Matthew A. Bernstein, PhD
5. Modular Cardiac MR Imaging Protocols 74
13. Cardiac MRI Safety 246
Phillip M. Young, MD, Eric E. Williamson, MD,
Kiaran P. McGee, PhD, Robert E. Watson Jr, MD, PhD,
and James F. Glockner, MD
and Eric E. Williamson, MD

S E C T ION I I
C L I N IC A L A PPL IC AT IO N S A N D S E C T ION I V
CA SE ST U DI E S R E V I E W QU E S T IO N S

6. Myocardial Ischemia and Infarction 83 14. Board-Type Questions and Answers 259
Thomas A. Foley, MD Kiaran P. McGee, PhD, Matthew W. Martinez, MD,
7. Nonischemic Myocardial Disease 105 and Eric E. Williamson, MD
Nila J. Akhtar, MD, Matthew W. Martinez, MD,
and Eric E. Williamson, MD Index  313
8. Pericardial Disease 143
Phillip M. Young, MD

xi
 CONT R I BUTOR S

Nila J. Akhtar, MD Paul R. Julsrud, MD

Senior Associate Consultant, Department of Radiology, Supplemental Consultant, Department of Radiology, Mayo
Mayo Clinic, Rochester, Minnesota; Assistant Professor, Clinic, Rochester, Minnesota; Professor of Radiology,
Mayo Clinic College of Medicine Mayo Clinic College of Medicine

Nandan S. Anavekar, MB, BCh Matthew W. Martinez, MD

Senior Associate Consultant, Division of Cardiovascular
Diseases, Mayo Clinic, Rochester, Minnesota; Assistant
Professor of Medicine, Mayo Clinic College of Medicine
Philip A. Araoz, MD
Consultant, Department of Radiology, Mayo Clinic, Rochester,
Minnesota; Professor of Radiology, Mayo Clinic College of
Medicine
Matthew A. Bernstein, PhD
Consultant, Department of Radiology, Mayo Clinic, Rochester,
Minnesota; Professor of Medical Physics, Mayo Clinic
College of Medicine
Director, Sports Cardiology & Hypertrophic Cardiomyopathy
Programs and Cardiovascular Imaging, Lehigh Valley Health
Network, Allentown, Pennsylvania; Associate Professor of
Medicine, Morsani College of Medicine, University of South
Florida, Tampa, Florida
Formerly, Assistant Professor of Cardiovascular Diseases,
Mayo Clinic College of Medicine
Kiaran P. McGee, PhD
Consultant, Department of Radiology, Mayo Clinic, Rochester,
Minnesota; Associate Professor of Medical Physics and
Assistant Professor of Biomedical Engineering, Mayo Clinic
College of Medicine

Ethany L. Cullen, MD Robert E. Watson Jr, MD, PhD

Physician, Mayo Clinic Health System—Austin, Austin,
Minnesota
Thomas A. Foley, MD
Consultant, Division of Diagnostic Radiology, Mayo Clinic,
Rochester, Minnesota; Assistant Professor of Radiology,
Mayo Clinic College of Medicine
James F. Glockner, MD, PhD
Consultant, Division of Diagnostic Radiology, Mayo Clinic,
Rochester, Minnesota; Assistant Professor of Radiology,
Mayo Clinic College of Medicine
Chair, Division of Neuroradiology, Mayo Clinic, Rochester,
Minnesota; Assistant Professor of Radiology, Mayo Clinic
College of Medicine
Eric E. Williamson, MD
Chair, Division of Cardiovascular Radiology, Mayo Clinic,
Rochester, Minnesota; Associate Professor of Radiology,
Mayo Clinic College of Medicine
Phillip M. Young, MD
Chair, Division of Body Magnetic Resonance Imaging, Mayo
Clinic, Rochester, Minnesota; Associate Professor of
Radiology, Mayo Clinic College of Medicine

xiii
Cardiac MR Acronyms a

M ANUFACTUR ER

PHILIPS MEDICAL
IM AGING COMPONENT & TER M SIEMENS MEDICAL SOLUTIONS GE HEALTHCAR E SYSTEMS

Magnetization Preparation

Phase contrast PC PC PC
Chemical fat saturation Fat Sat Fat Sat, Chem Sat SPIR, SPAIR
Tagging Tagging Tagging Tagging
Flow compensation Flow comp, GMR Flow comp Flow comp
Inversion recovery IR, TIR IR, MPIR, FastIR IR-TSE
Phase-sensitive inversion recovery PSIR PSIR PSIR
T2 signal preparation T2-Prep
T1 signal preparation MOLLI, T1-Scout CineIR

Echo Formation

Gradient echo
Spoiled
Gradient-recalled echo GRE GRE FFE
Spoiled GRE FLASH SPGR T1-FFE
Fast gradient echo TurboFLASH FGRE, FSPGR TFE
3D Fast gradient echo MPRAGE, 3D FLASH 3D FGRE, 3D FSPGR 3D TFE
Volume-interpreted GRE VIBE FAME, LAVA THRIVE
Steady state
Balanced SSFP True FISP FIESTA BFFE
SSFP–FID FISP GRASS FE
SSFP–echo PSIF SSFP T2-FFE
Spin echo SE SE SE
Gradient and spin echo TurboGSE, TGSE GRASE GRASE

Data Acquisition

Single-shot spin echo HASTE SSFSE SS TSE

Multishot (echo train) spin echo TSE, RARE FSE TSE
Number of echoes in spin-echo echo Turbo factor ETL Turbo factor
train
Iterative Dixon fat-water separation DIXON IDEAL mDIXON
Echo planar imaging EPI EPI EPI
Time-resolved MR angiography TWIST TRICKS TRACS
Balanced SSFP–based noncontrast NATIVE-trueFISP Inhance Inflow IR B-TRANCE
MR angiography

Rapid Imaging

Image based mSENSE ASSET SENSE

k-Space based GRAPPA ARC

Imaging Mode

Two dimensions 2D 2D 2D
Three dimensions 3D 3D 3D
Single image Static Static Static
Multiframe image Cine Cine Cine

Abbreviations: ARC, autocalibrating reconstruction for Cartesian imaging; ASSET, array spatial sensitivity encoding technique; B-TRANCE, balanced-SSFP–triggered
angiography, non–contrast enhanced; ETL, echo train length; FAME, fast acquisition with multiple excitation; FE, field echo; FFE, fast-field echo; FID, free induc-
tion 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; IDEAL, iterative decomposition of water and fat with echo asymmetry and least-squares
estimation; IR, inversion recovery; LAVA, liver acquisition with volume acceleration; MOLLI, modified Look-Locker imaging; MPIR, multiplanar inversion recovery;
MPRAGE, magnetization prepared rapid acquired gradient echoes; MR, magnetic resonance; mSENSE, modified sensitivity encoding; NATIVE, noncontrast MR
angiography of arteries and veins; PSIF, reversed fast imaging with SSFP; 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; SSFP, steady-state free precession;
TFE, turbo field echo; TGSE, turbo gradient spin echo; THRIVE, T1 high-resolution isotropic volume estimation; TIR, turbo inversion recovery; TRACS, time-resolved
angiography using CENTRA (contrast-enhanced timing robust angiography) and SENSE; TRICKS, time-resolved imaging of contrast kinetics; TSE, turbo spin echo;
TWIST, time-resolved angiography with interleaved stochastic trajectories; VIBE, volumetric interpolated breath-hold examination.
a
Imaging terms and corresponding acronyms used by different MR scanner manufacturers.
 SEC T ION I
BA SIC PR I NCI PL E S OF C A R DI AC M R I
 1.
ECG GATING A ND ASSOCI ATED ARTIFACTS
Kiaran P. McGee, PhD, and Matthew W. Martinez, MD
I
n routine clinical cardiac magnetic resonance (MR) imag-
ing, most morphologic (ie, static) and functional (ie, cine)
imaging involves the use of segmented data acquisition
methods that are synchronized with the patient’s electrocar-
diographic (ECG) waveform. The process of synchronizing
data acquisition with the ECG waveform of the patient is
known as ECG gating. The purpose of this chapter is to pro-
vide an overview of the importance of ECG gating, describe
the relationship between a normal ECG waveform and the
appearance of the heart on MR imaging (MRI) throughout
the cardiac cycle, and provide an overview of methods for
ensuring robust ECG gating in the MR environment. Finally,
different types of artifacts introduced into the ECG wave-
form by the MR environment and methods to reduce them
will be discussed.
S E G M E N T E D DATA AC QU I S I T ION
A N D E C G G AT I NG
In most cases, cardiac MR data are not acquired in a continu-
ous fashion. Rather, only a fraction or segment of the total
image data is acquired at one time (ie, at a given phase of the
cardiac cycle). The R wave of the ECG waveform is usually
detected first (the trigger point), because it is typically the
most prominent and reproducible feature of the ECG trac-
ing, followed by the acquisition of a given segment of data
after a predetermined delay. To complete the imaging process,
data are acquired over multiple cardiac cycles (ie, R-R inter-
vals); this is most commonly referred to as segmented data
acquisition.
Segmented data can be acquired both prospectively and
retrospectively. If data acquisition is prospective, the MR
scanner will begin collecting image data after a predetermined
delay, known as the trigger delay. If retrospective data collec-
tion is performed, data are acquired continuously throughout
the cardiac cycle, and the trigger point is used to determine
in which portion of the cardiac cycle the data were acquired.
After enough data are collected to reconstruct 1 or more
images, as in the case of a cine series, data are retrospectively
sorted according to their temporal location within the cardiac
cycle, as determined from the time between the ECG trigger
and data acquisition. If the heart rate is regular, all the data
3
collected will reflect a given phase of the cardiac cycle, with
data acquired shortly after the R wave, reflecting systole, and
data acquired toward the end of the R-R interval, reflecting
diastole.
Irregular heart rates caused by atrial fibrillation or fre-
quent premature ventricular contractions will result in data
inconsistencies, with some data collected and arranged into
the wrong phase of the cardiac cycle. Collection of data in
this manner often results in degradation of image quality and
production of artifacts, which in turn can decrease the repro-
ducibility of measurements derived from these images. The
most common reason for failure of a cardiac MR examination
is the inability to synchronize data acquisition with the cor-
rect phase of the cardiac cycle. Because the ECG waveform
is the method of synchronization, ensuring that a robust and
reliable waveform is achieved for each patient is essential to
success (Box 1.1).
E V E N T S OF T H E C A R DI AC C YC L E
(L E F T H E A RT )
The heart consists of 2 separate but interrelated systems that
control the distribution throughout and return of blood from
the body. The left side of the heart (“left heart”) is the func-
tional unit that regulates the systemic circulation of blood
throughout the body, while venous return of blood is governed
by the pulmonary circulation and therefore controlled by the
right side of the heart (“right heart”). Accurate and reproduc-
ible assessment of cardiac function is important; therefore,
a thorough understanding of the interrelationship between
Box 1.1 TAKE-HOME POINTS—WHY USE ECG
GATING IN MR STUDIES?
• To enable accurate 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
• To allow correct sorting of static and dynamic data obtained
over multiple R-R intervals using segmented acquisition schemes
 4 • S ection I : B asic P rinciples of C ardiac M R I

the various cardiac events is also important. Figure 1.1 shows
the physiologic events of the left heart throughout the car-
diac cycle. The relationships of pressure, volume, and flow to
the electrical potential of the heart as a whole (as measured
by ECG) are shown. Note that the percentage values shown
for the time intervals of systole (40%) and diastole (60%) are
valid only for the given heart rate of 70 beats per minute. As
heart rate 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 1.1 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 indicates end-diastolic
volume; ESV, end-systolic volume; HR, heart rate. (Modified from Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. Philadelphia: Lippincott
Williams & Wilkins; c2006. Used with permission of Mayo Foundation for Medical Education and Research.)
 1. E C G G ating and A ssociated A rtifacts  • 5

M R I C H A R AC T E R I S T IC S OF T H E the ventricle is most relaxed, with maximal chamber volume

C A R DI AC C YC L E and minimal myocardial wall thickness.

Figure 1.2 shows the relationship between the electrical

activity of the heart as a whole and the corresponding MR
images acquired as part of a cine imaging series in both the
4-chamber long-axis and 2-chamber short-axis views of the
left ventricle. Typical cine sequences acquire 20 images corre-
sponding to fixed time points or phases of the cardiac cycle. In
this figure, only 10 images for both views are reproduced, rep-
resenting every even or odd phase of the cardiac cycle. Viewed
as a dynamic display, these cine loops simulate real-time imag-
ing and are used to interpret the contractility of the heart.
The figure also shows enlarged 4- and 2-chamber views of the
heart at end systole (red outline) and end diastole (blue out-
line). At end systole, the cavity of the left ventricle is smallest,
with maximal thickness of the myocardium; at end diastole,
M E A S U R I N G T H E H E A RT ’ S
E L E C T R IC A L AC T I V I T Y: T H E
E I N T HOV E N L E A D
A R R A NGEM EN T
The heart’s electrical activity was first assessed in 1889 by
Augustus Desiré Waller, who measured the electrical potential
difference (voltage) across electrode pairs placed at 5 separate
anatomical locations (2 on the arms, 2 on the legs, and 1 at the
mouth). Waller’s method of measuring the time-varying volt-
age signals across various electrode pairs (lead combinations) is
commonly referred to as the electrocardiogram, or ECG. The
original configuration suggested by Waller was modified by

Figure 1.2 Four-chamber long-axis (top row) and 2-chamber 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).
 6 • S ection I : B asic P rinciples of C ardiac M R I

Willem Einthoven in 1908. The so-called Einthoven configura-
tion or Einthoven’s triangle required placement of electrodes at
3 locations; the left and right arms and the left leg (Figure 1.3).
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).
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 1.4). This complex
waveform can be decomposed into separate waveforms that
describe the various phases of the cardiac cycle. Key com-
ponents of the ECG waveform include the P wave, which
signifies the onset of atrial depolarization, the QRS complex,
which represents ventricular depolarization, and finally the
T wave, which indicates ventricular repolarization.
PAT I E N T PR E PA R AT ION F OR
G AT I N G I N M R I
ECG gating in MRI involves identification of the appro-
priate anatomical locations for placement of the ECG elec-
trodes, followed by adequate preparation of the patient’s
skin surface. Identification of the appropriate lead locations
is described in more detail in the next section, but 3 rules
should be observed:
1) Lead locations should be placed as far as possible from
the sternum, particularly if the patient has had prior
cardiothoracic surgery and sternal wires are present.

Figure 1.3 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; c1995. Used with permission.)
 1. E C G G ating and A ssociated A rtifacts  •
Figure 1.4 ECG and components of the cardiac cycle. (From Bernstein MA, et al. Handbook of MRI pulse sequences. Amsterdam: Elsevier
Academic Press; c2004. Used with permission.)
2) For women with large, pendulous breasts, an alternative
location along the chest wall and 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 men, this
typically requires shaving the chest around the region of the
electrodes. Caution should be exhibited if this procedure is
performed in the MR scan room because most disposable
razors use steel blades that can represent a projectile haz-
ard if brought too close to the MR scanner. Commercial
abrasive gels are available to remove keratinized skin from
the epidermis; this reduces the electrical impedance of the
skin and thereby creates 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 to remove oil
and dirt.
When the appropriate electrode locations are identi-
fied 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 appropri-
ate type of electrode either directly or through a third-party
supplier.
7
E C G L E A D PL AC E M E N T
A major contributor to a prolonged cardiac examination is
the amount of time spent attempting to optimize lead place-
ment either immediately before or during the cardiac MR
examination. The Division of Cardiac Radiology at Mayo
Clinic has developed several lead-placement configurations
(“the Mayo configuration”) that hold the most promise
for gating success. A second lead-placement set is also rec-
ommended when the MR scanner is equipped with VCG
gating.
M AYO C ON F IGU R AT ION
Figure 1.5 describes the 4 lead placement configurations rec-
ommended by Mayo Clinic. The Mayo lead placements are
not optimized on the basis of electrophysiologic models of the
ideal patient; rather, they represent the most successful con-
figurations derived from extensive experience with various
placement iterations.
M R-I N DUC E D E C G A RT I FAC T S
Figure 1.6 shows an ECG waveform from lead II for a healthy
volunteer. Unfortunately, the MR environment is particu-
larly hostile for ECG measurement. Table 1.1 lists some of
the more common sources of interference that exist in a typi-
cal MR environment, along with their amplitude and fre-
quency ranges.
 8 • S ection I : B asic P rinciples of C ardiac M R I

Figure 1.5 The Mayo Configuration. The 4 recommended configurations for 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.

M AG N E TOH Y DRODY N A M IC E F F E C T
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 comprises
salts (sodium, potassium, calcium, magnesium, chloride,
and bicarbonate), plasma proteins (albumin, fibrinogen, and
globulins), and other substances (nutrients, waste products,
respiratory gases, and hormones). When dissolved, the salts
in the plasma disassociate into ions and, left alone, do not
contribute to the ECG signal. However, when in motion
and in the presence of a magnetic field, they will experience
an external Lorentz force. Charge separation occurs, induc-
ing a time-varying electrical dipole signal that is a function
of the velocity and direction of flow within the field of the
MR scanner. This dipole is detected as a time-varying elec-
trical 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
 1. E C G G ating and A ssociated A rtifacts  • 9

Figure 1.6 ECG waveform from lead II from a normal (healthy) volunteer.

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 unreli-
able triggering and poor image quality. Figure 1.7 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 com-
plex, also known as T-wave swelling.
Effect on MR Data Acquisition
If ECG triggering is based on the peak voltage of the wave-
form, the scanner could trigger off the T wave or switch
between the R-wave and T-wave peaks. Detection-peak

Table 1.1 SOURCES OF ECG NOISE IN MR IMAGING

INDUCED ELECTR ICAL VOLTAGE FR EQUENCY SPECTRUM

SOURCE (TYPICAL R ANGE) (TYPICAL R ANGE)

ECG reference signal 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 Several mV Several Hz

motion due to respiration or other
motion

RF body coil switching 40–700 mV depending on RF pulse type and location 2–70 kHz
within magnet bore (isocenter smallest)

Gradient switching 100–600 mV depending on location within MR scanner 32–125 kHz

(ie, gradient amplitude)
RF field from body coil Induced electric fields are multiple orders of magnitude Resonant frequency of scanner
greater than the frequency spectrum of the ECG wave- (64 MHz at 1.5T)
form and do not contribute substantially to the noise
spectrum

Abbreviations: ECG, electrocardiographic; MR magnetic resonance; RF, radiofrequency.

 10 • S ection I : B asic Principles of C ardiac M R I
Figure 1.7 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.
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 acquisi-
tion time. Increases in scan time are unacceptable, particu-
larly 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. Miscalculation of the R-R interval resulting from false
ECG triggers degrades the image quality because data are col-
lected at a different phase of the cardiac cycle than expected.
This is particularly true for segmented cine data acquisition
schemes.
VCG Configuration
To overcome magnetohydrodynamic effects, VCG-based
triggering systems are used at most institutions. VCG gat-
ing involves measurement of the ECG dipole projected
onto 2 orthogonal axes. When the ECG waveform is mea-
sured in this way, T-wave swelling that occurs as a result of
the magnetohydrodynamic effect can be isolated from the
QRS complex waveform. VCG gating allows electrical activ-
ity to be depicted temporally and spatially from all 3 leads,
which is more accurate for detecting cardiac activity. Because
the T-wave swelling can be so large that the amplitude of the
T wave is greater than that of the R wave, the MR sequence
may be triggered incorrectly. Inconsistent synchronization
with the cardiac cycle is the most common reason for a failed
cardiac MRI study. Most MR scanners offer a modified form
of the original VCG concept. Lead placement for VCG gat-
ing is similar to 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. The general lead placement for VCG gat-
ing is shown in Figure 1.8.
T R I B OE L E C T R IC E F F E C T
The triboelectric effect is the build-up of static charge due to
the rubbing of 2 different materials against each other (for
example, an ungrounded conductor and the insulation of the
ECG cable).
Effect on ECG Waveform
Introduces a slowly varying change in the baseline voltage
(baseline drift) of the ECG signal (Figure 1.9).
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 nega-
tive. 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.
 1. E C G G ating and A ssociated A rtifacts  • 11

Figure 1.8 Vector ECG lead placement. The 2 configurations of lead placement are based on measurement of the ECG dipole projected onto 2
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 (see Figure 1.5).

R A DIOF R E QU E NC Y B ODY
C OI L S W I TCH I NG
The radiofrequency (RF) body coil functions in 1 of 2 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 opposite-polarity (±) volt-
ages on the order of several hundred volts to pin diodes within
the body coil circuit.

Figure 1.9 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.
 12 • S ection I : B asic P rinciples of C ardiac M R I
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 system 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 elec-
tric 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 1.10).
G R A DI E N T S W I TCH I NG
Image formation in MR is achieved, in part, by applying gradient
magnetic fields with amplitudes that vary linearly with spatial
Figure 1.10 Noise spikes in the ECG waveform caused by on/off switching of the body coil.
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.
In accordance with Faraday’s law of induction, expo-
sure of the ECG circuit (patient, electrodes, and cable) to a
time-varying magnetic field induces a time-varying electri-
cal voltage in the ECG circuit. This induced voltage is great-
est 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 be many
times larger than the ECG voltage (Figure 1.11).
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.
S T E R N A L W I R E S OR C L I P S
Sternal wires used to close the chest cavity after thoracic sur-
gery create conducting loops that can induce additional elec-
tric fields that are superimposed onto the ECG signal during
imaging.
 1. E C G G ating and A ssociated A rtifacts  • 13

Figure 1.11 Examples of gradient switching interference in ECG waveforms from 2 separate pulse sequences. In each set, 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.
 14 • S ection I : B asic Principles of C ardiac M R I
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 ster-
num. This is most commonly achieved by placing the elec-
trodes along the lateral chest wall of the patient.
S PE C I A L C I RC U M S TA NC E : G AT I N G
DU R I NG C H E M IC A L S T R E S S
Monitoring the ECG when using dobutamine or vasodila-
tor stress testing can be difficult. Gating during a chemically
induced stress MRI examination can be particularly prob-
lematic because of rapidly changing heart rates and increased
artifacts from physiologic effects (tachypnea) and other
adverse effects. ECG in the setting of ischemia is not reliable
because of possible artifact-related ECG changes described
previously in this chapter. In the ischemic cascade, ECG
changes occur after perfusion, and wall-motion abnormali-
ties are detectable. A substantial body of literature now exists
documenting the safety of both dobutamine and vasodilator
cardiac MRI stress testing. Nevertheless, constant monitor-
ing of both the patient for symptoms and the ECG tracing
for tachyarrhythmias such as ventricular tachycardia or heart
block that may occur during chemical stress testing is impera-
tive for patient safety.
ECG monitoring in the magnetic field also has techni-
cal limitations. In general, adequate patient preparation and
monitoring of the ECG signal throughout the cardiac exami-
nation is 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 described in
Figure 1.12 Schematic representation of a pulse profile from a peripheral photo-pulse sensor on the finger.
the next section. Therefore, it is a good idea to place the pulse
unit on the patient’s finger before beginning the examination.
Because the electrical activity of the heart precedes the flow of
blood into the system, the peripheral photo-pulse gating trig-
ger 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.
PE R I PH E R A L PHO TO -PU L S E
S E N S OR
Under certain circumstances, it may not be technically fea-
sible 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
poor-quality waveform for a gated MR angiography sequence
is sufficient. Under these conditions, a peripheral photo-pulse
waveform can be used as an ECG substitute.
Blood flowing in the capillaries of peripheral tissues (eg,
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 transmit-
ting 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 the left ventricle, the waveform has an
inherent delay from the peak of the R wave of the QRS com-
plex 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 very reliable and,
as such, is a standard feature on all high-performance car-
diac MR scanners. Often, a second peak can be seen on the
photo-pulse waveform, which corresponds to the left atrial
contraction following left ventricular contraction. Figure 1.12
shows a typical photo-pulse waveform.
 1. E C G G ating and A ssociated A rtifacts  • 15

S UG G E S T E D R E A DI N G Vector ECG Gating

ECG Physiology
Hobbie RK, Roth BJ. Intermediate physics for medicine and biology.
New York (NY): Springer; c2007.
Malmivuo J, Plonsey R. Bioelectromagnetism: principles and applica-
tions of bioelectric and biomagnetic fields. New York (NY): Oxford
University Press; c1995.
Chia JM, Fischer SE, Wickline SA, Lorenz CH. Performance of QRS
detection for cardiac magnetic resonance imaging with a novel vec-
torcardiographic triggering method. J Magn Reson Imaging. 2000
Nov;12(5):678–88.
Fischer SE, Wickline SA, Lorenz CH. Novel real-time R-wave detection
algorithm based on the vectorcardiogram for accurate gated magnetic
resonance acquisitions. Magn Reson Med. 1999 Aug;42(2):361–70.
 2.
CAR DI AC A NATOMY
Matthew W. Martinez, MD

T
he purpose of this chapter is to provide an overview
of cardiac anatomy. Distinguishing cardiac anatomic
features can be difficult, especially in persons with
congenital heart disease. Imaging the heart by magnetic reso-
nance (MR) provides several advantages over other imaging
methods. In addition to providing a multiplanar approach
to the assessment of cardiac and cardiovascular structures,
cardiac MR imaging (MRI) provides high spatial- and
contrast-resolution images in every imaginable plane without
restricted image orientation or the need to administer con-
trast agents. Cardiac MRI also offers imaging planes in tra-
ditional radiographic imaging planes such as axial, coronal,
and sagittal, as well as atypical imaging planes such as sagit-
tal oblique for “candy cane” views. In addition, traditional
17-segment model imaging planes are easily attained and are
consistent with other imaging modalities traditionally used
in cardiology such as echocardiography. The wide field of
view offered by MRI also allows us to view cardiovascular
structures as they relate to the surrounding nonvascular
structures. With this in mind, a thorough knowledge of both
cardiac anatomy and the structures surrounding the heart is
critical for interpreting cardiac MR images with expertise.
This chapter provides a brief overview of common anatomy
and provides real-life examples of views typically encoun-
tered when interpreting cardiac MR images. Continuous
review of normal cardiac anatomy is an ongoing process for
the cardiac imager.
G L OB A L C A R DI AC A N ATOM Y
The heart is located centrally in the thorax and is bordered
by the lungs on either side, the sternum anteriorly, and the
diaphragm inferiorly. Posterior to the heart lies the esopha-
gus and spine. Anatomically, the heart consists of 2 atria
and 2 ventricles (Figure 2.1). The atria collect blood, which

Figure 2.1 Schematic representation of the heart in cross-section showing the 4 chambers and the conduction system that regulates the function of
the heart throughout the cardiac cycle. AV indicates aortic valve; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; LVOT, left ventricular
outflow tract; RA, right atrium; RV, right ventricle; SVC, superior vena cava.

16
 2 . C ardiac A natomy  • 17

is then pumped into their connected ventricles. The ven-
tricles supply both the arterial and venous systems with
blood. The right side of the heart (atrium and ventricle)
represents the low-pressure, venous return portion of the
cardiovascular system and is characterized by relatively thin
myocardium. In contrast, the left side of the heart (atrium
and ventricle) creates the pressure necessary to supply the
arterial system with blood and is characterized by thicker
myocardium than on the right side. The right ventricle
(RV) is the most anterior cardiac structure. Twisting of the
ventricular outflow tracts causes the aorta to emerge from
the left ventricle (LV) in a right-sided position relative to
the pulmonic valve when viewed from the anterior vantage
point.
In 2002, the American Heart Association Writing Group
on Myocardial Segmentation and Registration for Cardiac
Imaging recommended a 17-segment model for description
of the LV (Figure 2.2). This model describes segments of the
LV using a recognized nomenclature that provides consis-
tency across cardiac imaging modalities and allows for easier

Figure 2.2 American Heart Association–recommended 17-segment model for standardized segmentation and description of the left ventricle.
(Adapted from Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WK, 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 Jan 29;105[4]‌:539–42. Used with permission.)
 18 • S e ction I : B asic P rincipl e s o f C ardiac M R I

correlation across modalities when localizing and comparing

structures. Myocardial segments are named and localized
with reference to both the long axes of the ventricle and the
360° circumferential locations on the short-axis views. The
terms basal, midcavity, and apical define the location along
the long axis of the ventricle from the base to apex. These
divisions are based on autopsy data that the heart can be
divided evenly by myocardial size and mass when divided
roughly into thirds. The 17-segment model provides a mass
distribution of 35%, 35%, and 30% for the basal, midcav-
ity, and apical portions of the heart, which is close to the
observed autopsy data.

AT R I A

The right atrium (RA) is at the upper right in the normal

heart. Blood flows into the RA from the superior and inferior
vena cava and the coronary sinus (Figure 2.3). The eustachian
valve (valve of the inferior vena cava) often is not seen but can
be visualized as a normal structure within the RA and may be
mistaken for an RA mass. The RA has a septum secundum,
which forms part of the interatrial septum. The crista termi-
nalis is one of the defining features of the RA. In the RA, the
pectinate muscles arise from the peak of the crista terminalis at
right angles and run directly into the RA appendage. The RA
appendage typically has a triangular appearance with a broad
opening.
The left atrium (LA) forms the posterior cardiac silhou-
ette and has an appendage that extends anteromedially. The
normal LA wall is smooth, making it easily distinguishable
from the RA. Within the LA, the pectinate muscles are con-
fined to the LA appendage, and the LA does not contain a
crista terminalis. The LA appendage can be seen anterior to
the left upper pulmonary vein and has a narrow-mouthed
opening compared with the RA appendage. The LA receives
blood from 4 or more of the pulmonary veins. Normal pulmo-
nary venous anatomy includes 2 right and 2 left pulmonary
veins each draining the upper and lower lungs, respectively.
Pulmonary venous anatomy can vary considerably, however;
multiple pulmonary veins entering the LA from each lung is
not unusual. Investigation of the pulmonary veins is typically Figure 2.3 Images of the thoracic cavity in a sagittal plane showing
performed before pulmonary vein isolation and for symptom selected anatomical landmarks. Top, Balanced steady-state free precession
evaluation post procedure, as needed. A fibrous projection image. Bottom, Volume-rendered cross-sectional view identifying normal
within the LA forms the posterior wall of the LA appendage anatomy. IVC indicates inferior vena cava; SVC, superior vena cava.
and the anterior wall of the left upper pulmonary vein. This
may sometimes be mistaken for a thrombus or atrial mass, but Box 2 .1 IDENTIFYING AND DISTINGUISHING
it is a normal LA structure, often referred to as the “coumadin THE ATRIA BY MRI
ridge” or the “Q-tip” because of its appearance. The LA con-
tains the septum primum, which forms part of the interatrial • The RA has a crista terminalis
septum (Box 2.1). • In the RA, the pectinate muscles arise from the peak of the
crista terminalis and run directly into the RA appendage
• The RA appendage typically has a triangular appearance
R IG H T V E N T R IC L E with a broad opening
• The LA has a narrow opening to the LA appendage
The RV (Figures 2.1 and 2.4) is crescent shaped in its • The LA wall is smooth, making the LA easily distinguish-
normal state and lies on the diaphragmatic surface supe- able from the RA
rior to the liver, forming the inferior and anterior cardiac
 2 . C ardiac A natomy  • 19

Figure 2.4 Images of the heart in a 4-chamber, wide field of view with selected landmarks identified. Top, Balanced steady-state free precession
image. Bottom, Volume-rendered cross-sectional view identifying normal anatomy.
 20 • S e ction I : B asic Principl e s o f C ardiac M R I

Figure 2.5 (Continues, legend on page 22)

 2 . C ardiac A natomy  •
Figure 2.5 (Continues, legend on page 22)
silhouette. The RV receives blood directly from the RA
through the tricuspid valve. The RV is identified through
its extensive trabeculae carnae, which are irregular
21
projections that arise from the outer surface and body of
the RV. Along with the moderator band, these features dis-
tinguish the RV from the LV in the setting of congenital
heart disease.
The RV outflow tract is a muscular and tubular-shaped
ring that supports the 3 semilunar leaflets of the pulmonic
valve, which serves as the border of the RV outflow tract. The
supraventricular crest is a muscular ridge that separates the
pulmonary and tricuspid orifice from the infundibulum of
the outflow portion of the RV.
Papillary muscles in the RV are attached to the chordae
tendineae, which ultimately attach to the tricuspid valve
in a parachutelike fashion. The papillary muscles may arise
from the floor of the RV apex or from the septal-parietal
band. The moderator band contains the right bundle
conduction system and attaches to the RV free wall.
Identification of the tricuspid valve as it inserts in the crux
of the heart, more apically than the mitral valve, is a way to
distinguish the RV.
Volumetric assessment and functional assessment of the
RV have been described in both the axial plane and short-axis
plane. Because of the unusual shape of the RV, it is difficult
to image adequately and reproducibly. Cardiac MRI, which
is able to measure the RV in multiple planes, is often referred
to as the reference standard for RV functional and volumetric
assessment.
L EF T V E N T R IC L E
The LV has the shape of an extended ellipse and has thicker
walls than the RV does (Figure 2.5). The wall thickness
throughout the LV is not uniform and tapers, with gradual
thinning toward the apex, which can often be extremely
thin (Figure 2.5A and B). The walls have a fine trabecular
pattern and no moderator band, which is distinctively dif-
ferent from the RV morphology. The LV contains a tubular
fibrous outflow tract that is in direct continuity with the
aortic valve (Figure 2.5A). The mitral valve (Figure 2.5A
and C) is behind and to the left of the aortic valve, attach-
ing to the septum toward the base of the heart. The mitral
valve annulus is continuous with the outflow tract. This
so-called aortic-mitral fibrous continuity is referred to as
the intervalvular fibrosa. This easily identifiable structure
helps distinguish the LV outflow tract from the muscular
RV outflow tract. In its usual state, the LV has 2 large papil-
lary muscles (anterior and posterior) that typically attach
to the lateral wall (Figure 2.5D). Although often singular,
papillary muscles may be bifid or trifid. In rare instances,
there may be just 1 papillary muscle supplying both mitral
valve leaflets, which is referred to as a parachute mitral
valve.
As with the RV, LV assessment can be performed in mul-
tiple planes with cardiac MRI (Box 2.2).
 22 • S e ction I : B asic Principl e s o f C ardiac M R I

Figure 2.5 Images of the heart with selected anatomical landmarks identified. Top, Balanced steady-state free precession image.
Bottom, Volume-rendered cross-sectional view identifying normal anatomy. A, Three-chamber view. LVOT indicates left ventricular outflow tract;
MV, mitral valve. B, Two-chamber view. C, Basal short-axis view. D, Two-chamber view.
 2 . C ardiac A natomy  •
Figure 2.6 (Continues, legend on page 24)
Box 2 .2 IDENTIFYING AND DISTINGUISHING
THE VENTRICLES BY MRI
• The atrioventricular valves are linked to the ventricles: the tricus-
pid valve connects to the RV and the mitral valve to the LV
• The RV has a muscular outflow tract
• The LV has a fibrous outflow tract that is continuous with
the mitral valve
• The RV has a moderator band
• The RV contains extensive trabeculae carnae that arise from
the outer surface and body of the RV
23
VA LV E S
In its normal state, the heart has 2 cardiac valves on the right
side and 2 valves on the left side. The aortic valve and pulmonic
valve are similar in that they are both trileaflet valves. The 3
cusps of the aortic valve are the noncoronary cusp and the left
and right coronary cusps (Figure 2.6A). The left cusp is iden-
tified by the origin of the left main coronary artery, and the
right cusp is identified via the right coronary artery ostium.
The right coronary artery typically arises from its respective
sinus higher than does the left coronary artery from the left
main ostium. During systole, the normal aortic valve can be
visualized as a triangular opening. Absence of the normal
appearance helps to identify abnormal valve morphology such
as a bicuspid or quadricuspid aortic valve. The pulmonary
artery arises from the infundibulum of the RV. The 3 cusps
 24 • S e ction I : B asic Principl e s o f C ardiac M R I

Figure 2.6 Images visualizing different cardiac valves. Top, Balanced steady-state free precession image. Bottom, Volume-rendered cross-sectional
view identifying normal anatomy. A, Short-axis view of the aortic valve showing the 3 coronary cusps. The blue arrows identify the noncoronary cusp;
red arrows, right coronary cusp; green arrows, left coronary cusp. B, Oblique view of the mitral valve showing the mitral valve leaflets along with their
corresponding scallops. A indicates anterior; P, posterior. Numbering identifies the cusp position (1, most lateral; 2, middle; 3, most medial) for each
valve leaflet, respectively. C, Short-axis view (top) at the base of the left ventricle bisecting the mitral valve. The dashed line represents an imaging plane
that results in a 4-chamber view (bottom). The blue arrows identify the anterior leaflet of the mitral valve; red arrows, posterior leaflet. D, Short-axis
view of the tricuspid valve showing the 3 leaflets. The blue arrows identify the anterior leaflet; red arrows, septal leaflet; green arrows, posterior leaflet.
E, Short-axis view (top) identifying the tricuspid valve. The dashed line represents an imaging plane that results in a 4-chamber view (bottom). The blue
arrows identify the anterior leaflet; red arrows, septal leaflet; green arrow, posterior leaflet.

of the pulmonic valve are the posterior cusp and the left and
right coronary cusp. The right and left cusps are identified by
their respective anatomic positions because there are no coro-
nary artery attachments from the pulmonic valve as the aortic
valve has.
Embryologically, the valvular structures are connected to
the ventricular muscle; identification of the respective valves
allows for identification of the morphologic ventricles in per-
sons with congenital heart disease. That is, the mitral valve is
connected to the morphologic LV, and the tricuspid valve is
connected to the morphologic RV.
The mitral valve is the only cardiac valve with 2 leaflets,
anterior and posterior (Figure 2.6B and C). A characteristic
feature of the mitral valve is that it has no chordal attach-
ments to the ventricular septum. The mitral valve is behind
and to the left of the aortic valve and attaches to the septum
at the crux of the heart above the insertion of the tricuspid
valve. As described earlier, this forms the aortic-mitral fibrous
 2 . C ardiac A natomy  •
Figure 2.6 (Continued, legend on page 24)
continuity known as the intervalvular fibrosa. The mitral
valve is supported by a pair of LV papillary muscles, which
are embedded in the anterolateral and posteromedial walls.
With cardiac MRI, off-axis views are performed to visualize
the various scallops of the anterior and mitral valve leaflets
(Figure 2.6B).
The tricuspid valve has 3 leaflets: septal, anterior, and
posterior (Figure 2.6D and E). The muscular support for the
tricuspid valve consists of the anterior muscle, which is the
largest and arises from the septal trabeculations. The tricus-
pid valve has chordae tendineae that attach to the septal leaf-
let on the ventricular septum. This is helpful in identifying
the RV because the septal surface of the LV never contains
chordal attachments.
25
PE R IC A R DI U M
The pericardium typically encircles the entire heart, the
superior portions of the aortic arch vessels, and the ostia of
the pulmonary veins as they enter the LA. The pericardium
is usually described as being divided into the visceral and
parietal pericardium. The visceral pericardium is virtually
indistinguishable from the epicardial surface of the myocar-
dium. The typical thickness of the pericardium should be
less than 3 mm and contains 10 to 15 mL of pericardial fluid
between the myocardium and pericardial surface. In addi-
tion, variable amounts of pericardial fat may be present in
the normal state.
Cardiac MRI visualizes the normal pericardial sac as a
thin curvilinear structure with low signal intensity. It is best
visualized over the right side of the heart and cardiac apex. It
is often continuous with the myocardium over the LV and is
indistinguishable from the myocardium.
T H E G R E AT V E S S E L S
The aorta arises from the LV to the right of the pulmonic
valve. It courses superiorly and then slightly anteriorly to
the right, forming the proximal portion of the descending
aorta. The sinus of Valsalva begins at the aortic annulus and
is separated from the ascending aorta by the sinotubular
junction.
The main pulmonary artery originates from the distal
portion of the infundibulum off the RV. The pulmonary
artery arises posteriorly to the aorta in normal hearts and
travels superiorly and posteriorly before dividing into the
right and left pulmonary artery branches. The left pulmo-
nary artery is seen as a continuation from the main trunk
and travels posteriorly and superior to the left main bron-
chus (Figure 2.7). The right pulmonary artery arises from
the main pulmonary artery at a greater angle and travels
behind the aortic arch and anterior to the right main bron-
chus. The ligamentum arteriosum is a remnant of the ductus
arteriosus and extends from the pulmonary trunk into the
descending aorta.
These anatomic features are important and are easily iden-
tified by the multiplanar imaging that typically is incorpo-
rated into cardiac MRI.
The aortic arch typically has 3 branches. The first is the
right brachiocephalic artery, which then bifurcates into
the right common carotid artery and right subclavian artery.
The second branch arising from the aortic arch is the left
common carotid artery. In up to 3% of the population, the
so-called bovine arch is present. This is defined as a common
origin of the right brachiocephalic and left common carotid
arteries. This is easily recognized when only 2 great vessels are
identified from the aortic arch. The third branch is the left
subclavian artery.
The superior vena cava is a large-diameter vein that car-
ries deoxygenated blood from the upper half of the body to
 26 • S e ction I : B asic Principl e s o f C ardiac M R I

Figure 2.7 Images in a true axial plane with selected landmarks identified. Top, Balanced steady-state free precession image. Bottom,
Volume-rendered cross-sectional view identifying normal anatomy. SVC indicates superior vena cava.

the RA. It is located in the anterior right superior mediasti- S UG G E S T E D R E A DI N G

num. The left and right brachiocephalic veins join together to
form the superior vena cava. The azygos vein joins the superior
vena cava just before it enters the RA.
The inferior vena cava is a large vein that carries deoxy-
genated blood from the lower half of the body into the RA.
It is a retroperitoneal structure located posterior to the
abdominal cavity and running along the right side of the
vertebral column. The left and right common iliac veins join
to form the inferior vena cava along with the azygos venous
plexus vein systems adjacent to the right side of the verte-
bral column.
Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey
WK, et al; American Heart Association Writing Group on
Myocardial Segmentation and Registration for Cardiac Imaging.
Standardized myocardial segmentation and nomenclature for tomo-
graphic 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. Int J Cardiovasc
Imaging. 2002 Feb;18(1):539–42.
Marieb EN, Hoehn K. Fundamentals of anatomy and physiology, 7th ed.
San Francisco (CA): Pearson/Benjamin Cummings; c2007.
Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. Philadelphia
(PA): Lippincott Williams & Wilkins; c2006.
 3.
STA NDAR D IM AGING PLA NES IN CAR DI AC MR IM AGING
Matthew W. Martinez, MD, Eric E. Williamson, MD, and Kiaran P. McGee, PhD
T
he purpose of this chapter is to provide step-by-step
protocols for acquiring common cardiac magnetic res-
onance (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 con-
sistent cardiac examinations. However, they do promote both
consistent visualization of the most clinically relevant cardiac
anatomy and completion of the cardiac examination in a prac-
tical time frame for the patient and imaging department alike.
I M AG I NG T H E L E F T V E N T R IC L E
MR imaging of the heart most commonly includes visualiza-
tion of the left ventricle (LV). Views of the LV in MR imag-
ing include 2-chamber, 4-chamber, long-axis, and 3-chamber
views, in addition to short-axis imaging planes. These are
analogous to the views seen with other cardiovascular imaging
techniques such as transthoracic echocardiography and single-
photon emission computed tomography. These imaging planes
are designed to view the LV wall in 2 orthogonal planes.
Figure 3.1 shows the order in which these planes are typi-
cally acquired, as well as their temporal and spatial relationships.
Each study begins by acquiring a lower-resolution set of localizer
images comprising 3 orthogonal planes (axial, coronal, and sag-
ittal) that cover most of the thoracic cavity. This acquisition is
commonly referred to as a 3-plane localizer. A 2-chamber image
is obtained by prescribing the imaging plane from the local-
izer data, using the axial slice as the main image for prescrip-
tion. Similarly, short-axis views are prescribed off a 4-chamber
image. Imaging planes identified by solid arrows are considered
standard planes for visualizing the left side of the heart (“left
heart”); additional, optional planes are identified by dashed
arrows. The 2 optional planes are repeat acquisitions and should
be acquired if the original prescriptions do not represent true 2-
and 4-chamber long-axis views of the left heart, such as when the
prescription image is not a double-oblique (ie, short-axis) image.
M U LT I PL A N E L O C A L I Z E R I M AG E S
The first step in prescribing the various imaging planes
acquired during a cardiac MR examination is to obtain a
series of localizer images that include the entire volume of
27
the heart (Figure 3.2). This is an essential first step because all
subsequent planes are prescribed from these data. When pre-
scribing these localizer or scout images, choose enough slices
to cover the entire heart. These data are typically acquired as
nongated breath-hold acquisitions with a wide field of view in
3 orthogonal radiographic planes: axial, coronal, and sagittal.
The use of a wide field of view often allows for visualization
of the noncardiac structures within the thoracic cavity and
upper abdomen. Key anatomical structures to be identified
from the localizer views include the 4 chambers and great
vessels of the heart. Review of these images shows the oblique
orientation of the heart within the thoracic cavity. The apex
of the heart lies on top of the diaphragm at the level of the
fifth intercostal space, and the base of the heart is posterior
to the apex at the level of the third rib. The left and right sides
of the heart can be seen by scrolling from left to right through
the sagittal images.
L E F T V E N T R IC U L A R 2- CH A M BE R
(V E RT IC A L L ONG -A X I S) V I E W
A vertical long-axis view, as shown in Figure 3.3, bisects the
LV, illustrating its anterior and inferior walls, parallel to
the interventricular septum. This orientation is commonly
known as a 2-chamber view because 2 chambers (the left
atrium [LA] and LV) are visualized. This view is analogous to
the vertical long-axis view obtained by nuclear imaging and
the 2-chamber view by echocardiography.
To obtain a 2-chamber image from the localizer images,
perform the following steps:
• Scroll through the localizer images and find an axial image
in which the apex of the LV can be clearly identified.
• 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 in the axial plane.
• Scroll through the complete set of localizer images to
ensure that the imaging plane bisects both the apex and
mitral valve planes.
• Make sure the center of the imaging plane is at the center
of the LV.
 28 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

Figure 3.1 Imaging planes used to characterize the LV of the heart. The figure demonstrates the order in which these planes are acquired. Arrows indicate
the relationship between prescription and resultant image. Solid arrows indicate typical imaging planes; dashed arrows indicate optional planes.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 29

Figure 3.2 Anatomical reference showing the location of axial, coronal, and sagittal localizer planes acquired as a 3-plane localizer set with respect
to the heart and chest wall. The corresponding MR sagittal, coronal, and axial imaging planes are shown. Renderings of representative slices for each
plane identify relevant anatomical landmarks.

The proper 2-chamber image will demonstrate the LV,

LA, LA appendage, and mitral valve. Figure 3.3 shows the
placement of the 2-chamber imaging plane with landmarks
annotated.
Figure 3.3 also shows the placement of the imaging plane
on the axial localizer image and the resultant image. Angula­
tion of the imaging plane in this manner allows the imaging
slice to approximately bisect both chambers of the heart.
L E F T V E N T R IC U L A R 4 - CH A M BE R
(HOR I Z ON TA L L ONG -A X I S) V I E W
A 4-chamber long-axis view of the left and right ventricles
can be obtained by prescribing an imaging plane through the
2-chamber view that is perpendicular to the interventricular
septum and centered on the LV. A true 4-chamber view of the
heart will illustrate both the right and left ventricles separated
 30 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

Figure 3.3 MR prescription planes (red lines) at 2 separate anatomical locations (top), resultant MR image, and rendered anatomical reference of the
LV in a 2-chamber long-axis view. The rendered image identifies relevant anatomical landmarks and associated cardiac anatomy.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 31

by the inferior septum as it bisects the left and right chambers

of the heart along the long axis. Care should be taken such
that the aortic valve is not visible in this view. Figure 3.4 illus-
trates a true 4-chamber view with landmarks annotated. This
view is analogous to the horizontal long-axis view obtained by
nuclear imaging.
To prescribe a true 4-chamber long-axis view, perform the
following steps:

• Prescribe an imaging plane that bisects the LV from the

base of the heart to the cardiac apex in the 2-chamber
view. The plane should be placed in the lower third of
the ventricle to avoid the outflow tract. Reviewing the
prescription plane on the coronal localizer is useful for
avoiding the 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.
• Make sure the center of the imaging plane is at the center
of the LV.

Figure 3.4 shows the placement of the 4-chamber imaging

plane. The angle between the plane and the interventricular
septum is approximately 90°. 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 pro-
duces the resultant image.

L E F T V E N T R IC U L A R S HORT-A X I S
V IEWS
Short-axis images of the heart show a view “down the bar-
rel” of the LV, perpendicular to the long axis or septum of the
heart. Figure 3.5 shows the placement of a short-axis imag-
ing plane in relation to the heart and the resultant anatomi-
cal 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). The base image is
closest to the great vessels and includes the left and right ven-
tricles, whereas the apex image typically includes only the LV.
Acquisition of the 4-chamber view, as already described,
provides the anatomical landmarks necessary for prescrib-
ing the various LV short-axis views. Depending on the type
of study, 3 or more slices will be acquired. If only 3 slices are
needed, these should be through the apex, mid ventricle,
and base of the LV. Figure 3.5 illustrates the mid and basal
short-axis slices with landmarks annotated.
To prescribe short-axis views of the LV, perform the
following steps:

• From the 4-chamber long-axis data set acquired previously,

identify the image that is approximately at end diastole. Figure 3.4 MR prescription plane (red line), resultant MR image, and
This will be the image in which the heart is relaxed and the rendered anatomical reference of the LV in a 4-chamber long-axis
view. The rendered image identifies relevant anatomical landmarks and
chamber is maximally dilated. associated cardiac anatomy.
 32 • S ecti o n I : B asic Principles o f C ar d iac M R I

Figure 3.5 MR prescription planes (red lines), resultant MR images, and rendered anatomical references of the LV in a short-axis view. Solid red
lines equate to the resultant images in the red-outlined boxes; dashed lines are planes typically prescribed but not shown in this example. The MR
imaging planes should be parallel to the septum of the heart and centered within the middle of the LV. The resultant images show representative
slices through the heart at the base, middle (mid), and apex of the LV. The rendered images identify relevant anatomical landmarks and associated
cardiac anatomy.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 33

• 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 be
roughly parallel to one another and perpendicular to the
septum. A series of images slicing through the base, mid
ventricle, and apex of the heart will result. Be certain to
start high enough to include the basal outflow tract, which
is needed to plot the 3-chamber view.

Figure 3.5 shows the placement of several imaging planes

perpendicular to the septum on the 4-chamber long-axis
view and perpendicular to the long axis of the ventricle in
the 2-chamber view. The orientation of these planes in rela-
tion to the anatomical orientation of the heart is also shown.
Placement of several imaging planes parallel to one another
produces the resultant images.

L E F T V E N T R IC U L A R
3 - CH A M BE R V I E W
A 3-chamber long-axis view bisects the LV through the aortic
root and lateral LV 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. Figure 3.6 illustrates the 3-chamber view with
landmarks annotated.
To prescribe a 3-chamber long-axis view of the LV, per-
form 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 that is oblique to the
interventricular septum and bisects the aortic root, as
shown in Figure 3.6. The angle of rotation is measured
away from the septum toward the right ventricle (RV),
resulting in a plane that bisects both the RV and LV.
• Make sure the center of the imaging plane is at the center
of the LV.

This imaging plane can also be obtained by copying the

prescription from the 2-chamber acquisition and rotating
the imaging plane a further 45° toward the interventricular
septum.
Figure 3.6 shows the placement of the 3-chamber imag-
ing plane. The angle between the plane and the interven-
tricular septum is approximately 45°. In this instance the
imaging plane is measured from the septum toward the Figure 3.6 MR prescription plane (red line), resultant MR image, and
RV. The orientation of this plane in relation to the ana- rendered anatomical reference of the LV in a 3-chamber long-axis view.
The short perpendicular line on the prescription image represents
tomical orientation of the heart is also shown. Placement the center of the field of view and the length of the line, the width of
of the imaging plane at mid ventricle produces the resul- the imaging slice. The rendered image identifies relevant anatomical
tant image. landmarks and associated cardiac anatomy.
 34 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

L E F T V E N T R IC U L A R 2- CH A M BE R
(V E RT IC A L L ONG -A X I S) V I E W
(OP T ION A L)
In certain circumstances, 2-chamber views prescribed from
the 3-plane localizer images cannot be prescribed such that
the imaging plane bisects the LV through its anterior and
inferior walls, parallel to the interventricular septum. The
result of this is suboptimal visualization of the LA and LV. In
this situation, an additional 2-chamber view can be acquired
in which previously acquired short-axis views are used as the
prescription image.
To prescribe this 2-chamber long-axis view of the LV, per-
form 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.
• Make sure the center of the imaging plane is at the center
of the LV.

Figure 3.7 shows the placement of the 2-chamber imaging

plane. The orientation of this plane in relation to the anatom-
ical orientation of the heart is also shown. Placement of the
imaging plane at mid ventricle produces the resultant image.

L E F T V E N T R IC U L A R 4 - CH A M BE R
(HOR I Z ON TA L L ONG -A X I S) V I E W
(OP T ION A L)
If, as in the case of the 2-chamber acquisition, the initial
4-chamber view does not bisect the heart perpendicular to
the interventricular septum allowing visualization of both
the LV and RV, a more accurate 4-chamber view can be pre-
scribed off the previously acquired short-axis data sets. This is
a true 4-chamber view of the heart because it is perpendicular
to the septum, is centered on the LV, and bisects the left and
right chambers of the heart along the long axis.
To prescribe a true 4-chamber long-axis view, 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 perpendicular to the
interventricular septum.
• Make sure the center of the imaging plane is at the center
of the LV.
Figure 3.7 MR prescription plane (red line), resultant MR image, and
rendered anatomical reference of the LV in a 2-chamber long-axis view.
The short perpendicular line on the prescription image represents
the center of the field of view and the length of the line, the width of
the imaging slice. The rendered image identifies relevant anatomical
landmarks and associated cardiac anatomy.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 35

This imaging plane can also be obtained by copying the

prescription from either the 2- or 3-chamber acquisition and
rotating the imaging plane so that it is perpendicular to the
interventricular septum.
Figure 3.8 shows the placement of the 4-chamber imaging
plane. The orientation of this plane in relation to the anatomi-
cal orientation of the heart is also shown. Placement of the
imaging plane at mid ventricle produces the resultant image.

I M AG I NG T H E R IG H T
V E N T R IC L E

Visualization and interpretation of the structure and function

of the RV is an important part of many cardiac MR examina-
tions. Under most circumstances, adequate visualization can
be achieved from the short-axis planes used for imaging the
LV. Under certain circumstances, however, additional imag-
ing planes are required, such as axial imaging planes. In other
specific instances, more complex RV views are required, such
as in the diagnosis of arrhythmogenic RV dysplasia or Ebstein
anomaly. Figure 3.9 provides an overview of the typical work-
flow for imaging the right side of the heart when these addi-
tional views are required.

C ON V E N T ION A L A X I A L R IG H T
V E N T R IC U L A R C I N E V I E W
The sagittal localizer image set provides the anatomical land-
marks necessary for prescribing the axial RV cine data. Axial
cine images provide the best visualization of the RV and are not
the same as the axial images acquired from the 3-plane localizer
view. In comparison, axial localizer images provide dynamic
information (ie, cine) and are of higher resolution. Using the
axial plane can facilitate tracing the RV for calculating RV vol-
umes and ejection fraction. In general, high-resolution straight
axial cine data sets provide a more complete and easy method
to identify the 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 3.10 shows the placement of the axial image planes

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.
R IG H T V E N T R IC U L A R I N F L OW T R AC T
L ONG -A X I S V I E W
Acquisition of the 4-chamber view provides the anatomical
landmarks necessary for prescribing additional RV views.
Therefore, it is assumed that the 4-chamber view used for the
Figure 3.8 MR prescription plane (red line), resultant MR image, and
rendered anatomical reference of the LV in a 4-chamber long-axis view.
The short perpendicular line on the prescription image represents
the center of the field of view and the length of the line, the width of
the imaging slice. The rendered image identifies relevant anatomical
landmarks and associated cardiac anatomy. It is useful to scroll through
several short-axis views to ensure that the imaging plane includes both
the left and right sides of the heart.
 36 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

Figure 3.9 Imaging planes used to characterize the RV of the heart. The figure demonstrates the order in which these planes are acquired. Arrows
indicate the relationship between prescription and resultant image. The blue arrows describe protocols specific to imaging the right side of the heart,
and the red arrows describe those planes acquired when imaging the left heart.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 37

Figure 3.10 MR prescription planes, resultant MR images, and rendered anatomical references of the conventional axial view of the RV. The sagittal
localizer image shows the location of the prescription planes (red lines), which are orthogonal to the sagittal imaging planes acquired initially. The
short perpendicular line on the prescription image represents the center of the field of view and the length of the line, the width of the imaging slice.
 38 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

prescription image is acquired using the protocol described

for the left heart (see sections on “Left Ventricular 2-Chamber
[Vertical Long-Axis] View” and “Left Ventricular 4-Chamber
[Horizontal Long-Axis] View”). The RV inflow tract long-axis
view should be oriented parallel to the interventricular sep-
tum and centered at the mid ventricular point of the RV.
To prescribe RV inflow long-axis views, perform the
following steps:

• From the 4-chamber data set acquired as described

previously, 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 3.11 shows the placement of a single imaging plane

parallel to the septum on the 4-chamber view and centered
at the middle of the RV 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 pro-
duces the resultant image.

R IG H T V E N T R IC U L A R OU T F L OW
T R AC T V I E W
Axial images provide the relevant anatomical landmarks nec-
essary 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:

• On the axial data, prescribe a sagittal imaging plane that is

centered on the pulmonic 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 3.12 shows the placement of a single imaging

plane on an axial image showing the main pulmonary artery.
Placement of the imaging plane at mid ventricle produces the
resultant image.

AORT IC I M AG I NG

AORT IC C ORON A L V I E W
Coronal views of the aorta are often helpful for measurement
of the sinus of Valsalva and the proximal ascending aorta.
To prescribe a coronal view of the aorta, perform the
following:
Figure 3.11 MR prescription plane (red line), resultant MR image, and
• On the axial data, prescribe a center line perpendicular to the rendered anatomical reference of the RV inflow tract in the long-axis
aorta. The resultant image will show the LV, aortic valve, and view. The short perpendicular line on the prescription image represents
the center of the field of view and the length of the line, the width of the
outflow tract. In addition, oblique views of the pulmonary imaging slice. The imaging plane on the prescription image bisects the
artery, right atrium, and RV will be seen (Figure 3.13). RV and right atrium.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 39

Figure 3.13 MR prescription image (red lines), resultant MR image,

Figure 3.12 MR prescription plane (red line), resultant MR image,
and rendered anatomical reference of the outflow tract of the RV in
the sagittal view. The short perpendicular line on the prescription
image represents the center of the field of view and the length of the
line, the width of the imaging slice. To ensure correct placement of
the prescription imaging plane, it is recommended to verify its correct
location on several localizer images (not shown).
and rendered anatomical reference of the aorta in the coronal view.
Solid red line equates to the resultant image in the red-outlined box;
dashed lines are planes typically prescribed but not shown in this
example. The short perpendicular line on the prescription image
represents the center of the field of view and the length of the line, the
width of the imaging slice.
 40 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

S AG I T TA L OBL IQU E
(“C A N DY C A N E ”) V I E W
Figure 3.14 illustrates how to prescribe candy cane views of the
ascending and descending aorta. This view allows for evaluation
of the ascending aorta, aortic arch branching, and descending
thoracic aorta without requiring contrast media. This view is
often used for evaluation of coarctation of the aorta and aortic
aneurysms or dissections. The name candy cane derives from
the appearance of the ascending and descending aorta and its
similarity to that of a candy cane.

Figure 3.14 MR prescription image (red lines), resultant MR image, and rendered anatomical reference in a sagittal oblique view. Solid red line
equates to the resultant image in the red-outlined box; dashed lines are planes typically prescribed but not shown in this example. The short
perpendicular line on the prescription image represents the center of the field of view and the length of the line, the width of the imaging slice. This
view is typically referred to as a candy cane view of the aorta.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 41

Figure 3.15 Imaging of the pulmonic (or pulmonary) valve. The red lines show the location of the respective prescription planes. Using the axial
image, a view of the RV outflow tract is obtained. A second imaging plane bisecting the outflow tract provides a double oblique view of the
pulmonic outflow tract with a view of the pulmonic valve. This image is then used to prescribe a final imaging plane that bisects the valve plane,
providing the view of the valve in cross-section.
 42 • S ecti o n I : B asic P rinciples o f C ar d iac M R I

Figure 3.16 Visual representation of method for prescribing the aortic valve in cross-section. The red lines show the location of the respective
prescription planes. Short-axis and 3-chamber views are used to localize the LV outflow tract. The aortic valve plane can be visualized by
precribing an imaging plane (dashed line on 3-chamber view) orthogonal to the outflow tract. Or, a double oblique LV outflow tract view can be
used to prescribe a slice orthogonal to the outflow tract, which provides an imaging slice that bisects the valve plane and allows visualization of the
aortic valve.
 3 . S tan dar d I maging Planes in C ar d iac M R I maging  • 43

To prescribe the candy cane view, perform the following

steps:

• On the cine axial data, identify the ascending and

descending thoracic aorta.
• Place 1 or more imaging planes parallel to the ascending
and descending thoracic aorta. The resultant image will
illustrate the ascending aorta, aortic arch, and descending
thoracic aorta in the sagittal oblique plane. The right
pulmonary artery may also be visualized in the short axis.

V I S UA L I Z AT IO N OF C A R DI AC
VA LV E PL A N E S

Assessment of valvular heart disease is an important part of

imaging in many cardiac disease states. This assessment typi-
cally includes prescribing imaging planes that visualize the
pulmonic, aortic, and mitral valves. For improved conspicuity
of valvular anatomy such as valve leaflet cusps, a gradient echo
sequence that produces high blood-pool/myocardium con-
trast, such as a balanced steady-state free precession sequence,
should be used. To improve visualization of the valve leaflets,
a large flip angle (≈60°) should be used. This diminishes over-
all contrast but improves the conspicuity of the leaflets, which
often can be difficult to see with smaller flip angles.

PU L MON IC VA LV E PL A N E
To prescribe the pulmonic (or pulmonary) valve view, per-
form the following steps:

• If not already acquired, obtain an axial view of the heart.

• From the axial data, obtain an imaging plane that bisects
the RV outflow tract.
• On the RV outflow tract image, prescribe an imaging
plane that is centered perpendicular to the pulmonic
valve. This will view the pulmonary artery and pulmonic
valve. In addition, this image will provide limited views
of the LV and LA, as demonstrated in Figure 3.15,
labeled as the double-oblique view of the pulmonic
outflow tract.
• On the double-oblique view, place the prescription plane
parallel to the pulmonic valve plane.

The resultant image plane will demonstrate the pulmonic

Figure 3.17 Two-, 3-, and 4-chamber views acquired using prescription
valve in the short axis.
methods described already can be used to localize the mitral and
tricuspid valves and associated valve planes. All 3 imaging planes AORT IC VA LV E PL A N E
can be used to localize the mitral valve. The solid red line represents
the imaging plane that can be prescribed on each of these images to To prescribe the aortic valve plane in cross-section
visualize the valve in cross-section. The 4-chamber view provides (Figure 3.16), perform the following steps:
visualization of both the mitral and tricuspid valve planes. The solid line
identifies the plane that can be prescribed to visualize the mitral valve
plane in cross-section, and the dashed line identifies the imaging plane • Obtain short-axis and 3-chamber views of the left heart as
that will visualize the tricuspid valve plane in cross-section. previously described.
 44 • S ecti o n I : B asic P rinciples o f C ar d iac M R I
• To visualize the aortic valve directly, place an imaging
slice perpendicular to the outflow tract at the level of
the aortic annulus, as shown by the dashed line on the
3-chamber view.
• Alternatively, prescribe a double-oblique LV outflow tract
view by placing an imaging plane parallel to the LV outflow
tract, as shown by the solid line on the 3-chamber view.
• On the double-oblique LV outflow tract view, prescribe
a plane parallel to the aortic valve at the level of the
aortic annulus. This will illustrate the aortic valve in the
short axis.
M I T R A L A N D T R IC US PI D VA LV E
PL A N E S
Several standard imaging planes already described provide
excellent visualization of both the mitral and tricuspid valves.
For example, at the level of the valve plane, a 2-chamber
short-axis view will bisect both the mitral and tricuspid valves.
In addition, the 4-chamber view will illustrate the mitral and
tricuspid valves. RV inflow tract views illustrate long-axis
views of the tricuspid valve. Imaging planes bisecting each
valve plane can be obtained by prescribing imaging slices per-
pendicular to the valve orifice, as shown in Figure 3.17.
 4.
PULSE SEQUENCE BASICS
Kiaran P. McGee, PhD, and Matthew A. Bernstein, PhD

T
he purpose of this chapter is to describe pulse
sequences that are most commonly applied in routine
clinical cardiac magnetic resonance (MR) imaging.
A conceptual overview of a pulse sequence is first provided by
considering each sequence as consisting of 5 separate modules
or categories. These categories include magnetization prepara-
tion, echo formation, data acquisition, rapid imaging, and the
imaging mode used to acquire the data. The resultant image
is then described by the signal of both the myocardium and
blood pool. The effects of the choice of imaging parameters
on overall image quality are illustrated with several exam-
ples. Using this framework, individual pulse sequences and
sequence-specific variables, their recommended values, and
example images are provided. Pulse sequences are also distin-
guished according to their application—imaging of cardiac
morphology or function.
New to this edition is the inclusion of examples dem-
onstrating the effect on image quality when typical pulse
sequence imaging parameters are modified. In addition, we
describe several emerging techniques and pulse sequences that
have recently become available for routine clinical practice.
A N ATOM Y OF A C A R DI AC M R
I M AG I NG PU L S E S E QU E NC E
Conceptually, a cardiac MR pulse sequence can be broken
down into 5 constituent categories (boxes 1–5 in Figure 4.1).
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 mor-
phology). Figure 4.1 shows these 5 categories and the resul-
tant image (box 6 in Figure 4.1), as defined by the blood pool
signal. This section describes each category and provides a list
of components that make up each category.
M AG N E T I Z AT ION PR E PA R AT ION
Magnetization preparation is the application of radiofre-
quency (RF) and gradient pulses to prepare the MR signal
and, hence, image contrast before data acquisition. Five differ-
ent components of magnetization preparation are described
below.
Saturation Recovery—Application of a series of 90° RF
pulses to convert longitudinal into transverse magnetiza-
tion. Recovery of the longitudinal magnetization will occur
as a result of T1 relaxation effects. By choosing the appropri-
ate delay between the RF pulses (ie, the pulse repetition time
[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
the selection of a delay between the 180° pulse and the com-
mencement 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 that is spec-
trally tuned to the resonant frequency of lipids, followed by
gradient-induced spoiling. This RF pulse–gradient combi-
nation dephases only 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.
Tagging—Application of an RF pulse to create transverse
magnetization, followed by gradient-induced spatial modula-
tion 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 gradi-
ent waveforms before data acquisition to encode the velocity
(ie, speed and direction) of moving tissues into the phase of

Figure 4.1 Cardiac MR imaging pulse sequences.

45
 46 • S ection I : B asic Principles of C ardiac M R I

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 mini-
mum 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.
E CHO FOR M AT ION
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 produces the final MR image. The various compo-
nents of echo formation are described below and illustrated
in Figure 4.2.
Spin Echo—Formation of the k-space signal by applica-
tion of 2 RF pulses (90° and 180°). The formation of the sig-
nal (RF spin echo) occurs at a time after the 90° pulse equal
to twice the interval between the 2 pulses. For a standard
spin echo, each TR interval consists of a single 90°–180° RF
pulse pair. Multiecho spin echoes can be formed by repeat-
ing the 180° pulse. These additional echoes are typically phase

Figure 4.2 Pulse sequence diagrams for the 4 basic pulse sequence types used in cardiac MR imaging: spin echo, multiecho spin echo (or multiple-
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 the sequence generates the k-space data necessary for image reconstruction. Multiple gradient waveforms are
shown on the phase-encoding axis. Arrows on the phase-encoding gradient waveforms indicate the temporal sequence of the gradient waveforms: a
downward arrow indicates that the maximum positive to maximum negative gradient waveforms are applied in sequential order; an upward arrow
indicates the reverse, with the first gradient being the maximum negative, increasing sequentially until the maximum positive gradient is reached.
α indicates the flip angle of the RF pulse—the angle by which the longitudinal magnetization is rotated into the transverse plane. Notations of 90o
and 180o for RF pulses on the spin echo and multiple-spin echo sequences refer to the value of the associated flip angle.
 4 . P ulse S equence B asics  •
encoded, which allows for multiple lines of k-space data to be
acquired within a single TR—as in fast spin echo or turbo
spin echo methods—thus decreasing overall imaging time.
The amplitude of the series of spin echoes (also known as echo
trains) formed by the application of multiple 180° refocusing
pulses is attenuated by T2 signal relaxation effects. For long
echo trains, this can produce image blurring for tissues with a
short T2 relaxation time.
Gradient Echo—Formation of an echo signal and subse-
quent image by application of an RF pulse with a flip angle
typically much less than 90° (eg, <45°). Immediately after
the RF pulse, the transverse magnetization is dephased by
application of a negative-polarity gradient pulse along the
readout direction, followed by a contiguous positive-polarity
gradient pulse that reverses the effect of the negative gradi-
ent and results in the formation of the image echo. Additional
gradient fields are added for slice selection and phase encod-
ing, necessary to complete the image acquisition sequence.
Short image echo times, on the order of 1 millisecond, can be
achieved with the high-performance gradient systems avail-
able on most modern imaging systems. Gradient echo imag-
ing 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 equilib-
rium as a result of the trade-off between magnetization loss
from the application of RF pulses and gain from T1 recovery.
The 2 most commonly used types of gradient echoes in car-
diac imaging are spoiled and balanced, the latter of which
will be the focus in this chapter. Other types of gradient echo
imaging include coherent gradient-recalled echo and reversed
steady-state free precession (SSFP).
Spoiled gradient echo—Residual transverse magnetization
is eliminated (spoiled) by varying the phase of the RF pulses
and/or by applying additional gradient lobes. A spoiled gradi-
ent echo image is typically T1 weighted but can display bright
blood signal as a result of inflow.
Balanced gradient echo—Residual transverse magnetiza-
tion is maintained and strongly contributes to the net signal.
As shown in Figure 4.2, the net gradient area on each axis is
nulled (balanced) in each TR interval. Maintaining zero net
phase accumulation along all 3 spatial encoding axes pro-
vides 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 AC QU I S I T ION
Data acquisition refers to the method by which echoes, either
spin or gradient, are collected as part of the process of acquir-
ing the k-space data necessary for image reconstruction.
Components of data acquisition are described below.
47
Single Echo—Acquisition of a single line of data per rep-
etition (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 1 image echo or
line of data per TR by applying additional RF (eg, fast or
turbo spin echo sequences) or gradients (for multiecho gradi-
ent 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 for an image are acquired
within a single TR or “shot.” This allows for very rapid image
acquisition.
Multishot—An echo train that requires more than 1 rep-
etition (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.
If there is a remainder, the quotient is rounded up to the next
highest integer.
Segmented Data Acquisition—The acquisition of a lim-
ited number of lines (views) of image data at a given phase
(segment) of the cardiac cycle. Acquisition of the complete set
of lines required for a single image occurs over multiple car-
diac 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 acqui-
sition 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 seg-
ment is known as the views per segment (VPS). The VPS is
adjusted on the basis of heart rate (HR) in order to maintain
sufficient temporal resolution of each image in the cine series,
with a smaller value of VPS improving temporal resolution
but increasing the overall acquisition time.
View Sharing—Lines of k-space are shared between
images representing adjacent phases of the cardiac cycle,
thereby increasing the number of reconstructed cardiac
phases.
R A PI D I M AG I NG
Rapid imaging comprises a group of imaging techniques
designed to reduce the total acquisition time by undersam-
pling of the k-space data, followed by image reconstruction.
Rapid imaging components are described below.
Image-Based Parallel Imaging (SENSE)—Decreasing
the number of phase encodings acquired in a standard
acquisition intentionally induces aliasing (wrap) in the
phase-encoded direction, followed by unwrapping (unalias-
ing) to produce an effectively larger field of view (FOV) image.
(In a 3-dimensional [3D] acquisition, decreasing the number
of phase encodings along 2 of the directions sometimes is pos-
sible for further acceleration.) Differences in spatial sensitivity
 48 • S ection I : B asic Principles of C ardiac M R I
of the elements of a phased-array coil are used to mathemati-
cally 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 sepa-
rate 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 phase-encoding process.
Hybrid (Spatial-Temporal)—Techniques to improve the
temporal resolution or total acquisition of a time series (eg,
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 (k-Space)—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 synthe-
sized by applying a homodyne reconstruction technique or
simply setting those data to zero (zero filling).
Rectangular (Fractional)-Phase FOV—The spacing
between k-space lines is inversely proportional to the FOV.
Reducing 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. To avoid image wrap (ie, aliasing),
rectangular-phase FOV must be carefully matched to the
shape of the anatomy of interest.
I M AG I NG MODE
Imaging mode defines the type of data set acquired. The 4
imaging mode components are described below. It is impor-
tant to appreciate that the final image can be a combination of
2 or more of these modes, for example, a 2-dimensional (2D)
cine acquisition is a common imaging mode in cardiac MR
imaging.
Single Frame (Static)—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 ana-
tomical location (prescription) but over a given time interval.
For the large majority of cardiac acquisitions, the time inter-
val over which a cine series is acquired is the electrocardio-
graphic (ECG) R-R interval, or multiples thereof.
2D—A plane of data whose orientation can be defined by
any 3 points in physical space. A matrix of data points (pix-
els) fills the plane. The dimensions of the 2D image are given
by the matrix size, which can be thought of as the number
of rows and columns, respectively, in the reconstructed image
matrix (or columns and rows, depending on the orientation
of the image). The matrix size can be greater than the num-
bers of acquired points N X and N Y in the frequency- and
phase-encoded directions, respectively, if interpolation such
as zero filling is used. Multiple 2D planes can be acquired
with or without gaps to cover an imaging volume. For 2D
acquisitions, each imaging plane (also called a section or
slice), is reconstructed individually with its own 2D Fourier
transform.
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 2 perpendicular 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. For 3D acquisitions, the entire
set of imaging planes is reconstructed as a group with a 3D
Fourier transform.
BL O OD P O OL
Blood pool refers to the intensity of the blood pool signal in
the final MR image. The blood pool signal is most commonly
described by 1 of the 3 terms below.
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 com-
monly 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 approx-
imately equal to the background signal (zero). Blood pool
signal suppression is typically achieved by application of 1 or
more inversion pulse(s), followed by a spin echo or a gradient
echo imaging sequence.
I M AG I NG PA R A M E T E R S
The alteration of MR imaging parameters is a common prac-
tice in routine clinical cardiac MR imaging and is necessitated
by the variation in body habitus, patient age, and anatomic
differences between males and females. It is important to
appreciate that, as with MR in general, a compromise typically
results from modifying any imaging parameter. For example,
an increase in the imaging FOV, when all other parameters
are held constant, will increase the image signal-to-noise ratio
(SNR) as a result of the increased pixel dimensions. However,
image resolution will be decreased, which may affect the abil-
ity to distinguish small but important anatomical structures.
It is thus important to understand how the modification
of commonly used imaging variables affects overall image
quality.
One measure of image quality, the SNR, for a 2D MR
image is given by the general equation:
N avg × N X × N Y × ∆X × ∆Y × ∆Z
SNR 2D = const × (1)
BW
 4 . P ulse S equence B asics  • 49

where Navg is the number of signal averages; N X is the num-

ber of data points along the frequency-encoding axis; N Y
is the number of phase-encoding steps; ΔX, ΔY, and ΔZ
are the pixel resolutions along the frequency-, phase-, and
slice-encoding directions, respectively; and BW is the
receiver bandwidth of the imaging sequence. Bandwidth
values typically are stated as either total bandwidth of the
receiver signal (in units of kHz) or bandwidth per pixel (in
units of Hz/pixel). The bandwidth per pixel is obtained by
dividing the total bandwidth (ie, twice the ± value often pro-
vided on image annotation) by the number of pixels in the
frequency-encoding direction. In general, the FOV—in this
case along the frequency-encoding direction—is given by the
product of N X and ΔX. The constant of proportionality in
Equation 1 depends on various factors, including the main
magnetic field strength and the RF coil design.
During image prescription, it is common to modify 1
or more of these parameters. For example, the FOV may be
increased to survey a larger anatomical region or to decrease
image aliasing. It is important to appreciate the effect of modi- Figure 4.3 Short-axis balanced SSFP image obtained from a healthy
fying these parameters in terms of spatial resolution and SNR volunteer. Basic image with a relative SNR of 100%.
(or both). This section provides an explanation of each param-
eter, examples of the effects of their modification, and reasons
for their alteration. MR scanner field strength = 1.5T. This image is assigned
an arbitrary SNR value of 100%.

BA S E AC QU I S I T ION E X A M PL E S IG N A L AV E R AG E S OR E XC I TAT IONS

Figures 4.3 through 4.8 show examples of how vary-
ing different imaging parameters affects SNR, using
short-axis balanced SSFP images obtained from a healthy
volunteer. Figure 4.3 shows a typical short-axis bal-
anced SSFP image at mid diastole. The imaging param-
eters are: FOV = 44 cm, slice thickness = 8 mm, N X ,
N Y = 192/192, TR/TE = 3.1/1.3 ms, BW = 976 Hz/pixel
or ±125 kHz (bandwidth per pixel is calculated by divid-
ing the receiver bandwidth of 250 kHz by the number of
pixels along the frequency-encoded direction in the recon-
structed image, namely 256), Navg = 1, flip angle = 50°, phase
FOV = 1.0 (ie, no rectangular-phase FOV), VPS = 16, and
Increasing the number of signal averages (or excitations)
improves image SNR but does so at the expense of increased
imaging time. Because SNR is proportional to the square root
of the number of signal averages, doubling this value will only
increase the SNR by 41%, since the square root of 2 is ≈1.41. For
imaging of moving organs such as the heart, increasing the num-
ber of signal averages increases the likelihood of image artifacts
due to acquisition of data from different phases of the cardiac
cycle for segmented acquisitions or due to increased likelihood of
breath-hold loss by the patient because of increased imaging time.
The acquisition for Figure 4.4 is identical to that in Figure 4.3,
but with number of excitations varying from 0.75 to 1.0 to 2.0.

     

Figure 4.4 Similar short-axis balanced SSFP images as in Figure 4.3, but with varying signal averages (or excitations). The number of excitations in
the images varies from 0.75 to 2.0. Relative SNR values of the 3 images are 87%, 100%, and 141%, respectively.
 50 • S ection I : B asic P rinciples of C ardiac M R I

  

  

Figure 4.5 Similar short-axis balanced SSFP images as in Figure 4.3, but with varying bandwidth. The bandwidth in the images varies from
±62.5 kHz (488 Hz/pixel) to ±125 kHz (976 Hz/pixel). Corresponding relative SNR values for the 4 images are 141%, 112%, 106%, and 100%,
respectively.

     

Figure 4.6 Similar short-axis balanced SSFP images as in Figure 4.3, but with varying FOV. The FOV in the images varies from 34 cm to 44 cm.
Relative SNR values for the 3 images are 60%, 79%, and 100%, respectively.
 4 . P ulse S equence B asics  • 51

     

Figure 4.7 Similar short-axis balanced SSFP images as in Figure 4.3, but with varying matrix size. The FOV in the images is fixed, with matrix size
varying from 1922 to 384 2. The relative SNR values for the 3 images are 100%, 133%, and 50%, respectively. The 384 2 matrix acquisition (right) has
been cropped to a dimension of 2562.

     

Figure 4.8 Similar short-axis balanced SSFP images as in Figure 4.3, but with varying slice thickness. The slice thickness in the images varies from
8 mm to 16 mm. Relative SNR values in the 3 images are 100%, 150%, and 200%, respectively.

BA N DW I DT H
The imaging bandwidth, or the inverse of the time spent
acquiring each data point along the frequency-encoding
axis, is one of the most commonly varied parameters by
pulse sequence programmers and imaging technologists.
A large bandwidth decreases the minimum TE and TR, as
in the case of balanced SSFP imaging, or can decrease the
spacing between echoes in a multiecho acquisition such as
multiecho or single-shot spin echo techniques commonly
used in black blood imaging. Although increasing the
bandwidth decreases the fat-water chemical shift and arti-
facts from metal, it also decreases image SNR according to
Equation 1. Figure 4.5 demonstrates a balanced SSFP image
with bandwidths ranging from ±62.5 kHz (488 Hz/pixel)
to ±125 kHz (976 Hz/pixel).
F I E L D OF V I E W
For a given data matrix, increasing the FOV will increase
the pixel size and, hence, increase SNR. This is an effective
method for increasing the SNR of the image without an asso-
ciated penalty in imaging time. Increasing the FOV can also
be advantageous for eliminating artifacts due to aliasing (ie,
wrap). However, assuming that the number of image pixels
remains the same, increasing the FOV will decrease spatial
resolution, as shown in Figure 4.6.
M AT R I X (PI X E L S I Z E)
The SNR of the image is proportional to the square root of
the number of data points (N X × N Y). Increasing this param-
eter for a fixed FOV will decrease the image SNR, however,
because of the decrease in the dimensions of the pixel (ie, ΔX
= FOV/NX) along this axis. Figure 4.7 shows the effect of
increasing the number of data points while maintaining a fixed
 52 • S ection I : B asic P rinciples of C ardiac M R I
pixel size. Because standard image reconstruction matrix sizes
are 2562 and 5122, acquisition matrix sizes of 2562 or less will
be reconstructed to this dimension, whereas an acquisition
matrix size of 3842 will be reconstructed to a 5122 dimension
using zero-filling methods. In this example, the 3842 matrix
acquisition was reconstructed into a 5122 image, halving the
pixel dimension ΔX, or doubling the effective resolution.
PI X E L DI M E NS IONS
Image SNR is linearly proportional to the volume of the
acquired image voxel. (Image interpolation, however, such
as by zero filling the reconstruction, does not affect SNR.)
A larger voxel volume will increase the SNR by integrating
signal from a larger volume of tissue. However, the result is
decreased spatial resolution and increased partial volume
effects. For the through-plane direction, increasing the slice
thickness can degrade image quality of irregularly shaped or
curved objects such as the papillary muscles, thus increasing
the potential for image blurring. Figure 4.8 shows the effect of
increasing the through-plane pixel dimension.
Figure 4.9 Imaging components: balanced gradient echo cine.
PU L S E S E QU E N C E S F OR I M AG I NG
C A R DI AC MOR PHOL O G Y
BA L A NC E D G R A DI E N T E CHO
(BA L A NC E D S S F P) C I N E
This method (Figure 4.9) is the most common sequence used
for assessment of cardiac morphology and function. The image
signal is roughly proportional to the ratio of the 2 relaxation
parameters (T2/T1); therefore, fluid is bright despite the short
TE and TR values used. This sequence provides high blood
pool–to-myocardial contrast (Figure 4.10).
Sequence-Specific Variables
Views Per Segment
VPS is 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 HR
(in beats per minute [bpm]) (Table 4.1). A decrease in the VPS
will increase imaging time. Thus, a compromise is often struck
 4 . P ulse S equence B asics  • 53

between s­ ufficient temporal resolution and breath-hold dura-

tion. To keep imaging times within normal breath-hold dura-
tions (<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.

Table 4.1 TYPICAL VPS VERSUS HEART R ATE

HEART R ATE, bpm VPS

≤60 10–12

61–95 8–10

96–125 6–8

126–155 4–6
≥156 ≤4
Figure 4.10 Balanced gradient echo image, short-axis view.

Cardiac Phases
This is the number of images reconstructed across the
cardiac cycle. Each image represents a specific time point or
phase of the cardiac cycle. The greater the number of cardiac
phases, the higher the temporal resolution of the cine series.
Most commonly, 20 cardiac phases are reconstructed for cine
sequences.
S P OI L E D G R A DI E N T E CHO C I N E
This method (Figure 4.11) 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 (Figure 4.12).

Figure 4.11 Imaging components: spoiled gradient echo cine.

 54 • S ection I : B asic Principles of C ardiac M R I

Sequence-Specific Variables
Views Per Segment
VPS is 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
HR (Table 4.1). 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 imag-
ing times within normal breath-hold duration (<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.

Table 4.1 TYPICAL VPS VERSUS HEART R ATE

HEART R ATE, bpm VPS

Figure 4.12 Spoiled gradient echo image, short-axis view.
≤60 10–12
61–95 8–10

96–125 6–8 L AT E G A D OL I N I U M E N H A NC E M E N T
126–155 4–6 This method (Figure 4.13) comprises inversion recovery, single-
≥156 ≤4 shot, or multishot spoiled gradient echo. Myocardial inversion
time (TImyo) is chosen so that signal from normal myocardium
is suppressed and signal from gadolinium contrast-enhanced
Cardiac Phases infarcted myocardium is maximized (Figure 4.14).
This is the number of images reconstructed across the car-
diac cycle. Each image is at a specific time point or phase of Sequence-Specific Variables
the cardiac cycle. The greater the number of cardiac phases,
the higher the temporal resolution of the cine series. Most Myocardial Inversion Time
commonly, 20 cardiac phases are reconstructed for cine This is the delay time from the application of the RF
sequences. inversion pulse to data acquisition. TI myo is chosen so that
the longitudinal magnetization of normal myocardium
is zero at the time of data collection. The choice of TI myo
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 mul-
tishot sequences that acquire multiple lines of data for a
single inversion pulse, TI myo 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

 4 . P ulse S equence B asics  • 55

Figure 4.13 Imaging components: late gadolinium enhancement.

Figure 4.14 Late gadolinium enhancement 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 (arrow) are
bright due to delayed uptake of the contrast agent.
 56 • S ection I : B asic P rinciples of C ardiac M R I

Figure 4.15 Imaging components: double inversion recovery.

D OU BL E I N V E R S ION R E C OV E RY
This is an inversion recovery pulse sequence (Figure 4.15)
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 inver-
sion time (TIblood) and is chosen so that the blood signal is
nulled at the time of the imaging sequence (Figure 4.16). This
is not a fat-suppressed imaging sequence.

Sequence-Specific Variables
Blood Inversion Time
This is 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.
Figure 4.16 Double inversion recovery image, short-axis view.
Typical TIblood = 650 milliseconds at 1.5T field strength and HR
of 60 bpm
(For more information, see Simonetti et al and Greenman
et al in Suggested Reading.)
 4 . P ulse S equence B asics  • 57

T R I PL E I N V E R S ION R E C OV E RY Inclusion of both inversion pulses allows complete sup-

pression of signal from blood and lipids (fat) (Figure 4.18).
This is an inversion recovery with 3 inversion pulses, followed
Note that both TIblood and TI lipid values vary with HR and
by an echo train spin echo imaging sequence (Figure 4.17).
field strength. When imaging at higher field strengths (3.0T),
This sequence is similar to the double inversion recovery
it is advisable to check TIblood and TIlipid.
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 third RF pulse and the imag- Typical TIblood
ing sequence is known as the fat inversion time (TI lipid). = 625 milliseconds at 1.5T field strength and HR
of 60 bpm (assuming T1 blood = 1,200 ms)
Sequence-Specific Variables = 700 milliseconds at 3.0T field strength and HR
of 60 bpm (assuming T1 blood = 1,550 ms)
Blood Inversion Time
TIblood is the time delay between the RF inversion pulse and Typical TIlipid
data acquisition. A non–slice-selective (hard) RF pulse is applied  173 milliseconds at 1.5T field strength and HR
=
in order to invert the MR signal from all of the blood within the of 60 bpm (assuming T1 lipid = 250 ms)
imaging volume. This value is field strength and HR dependent.
= 248 milliseconds at 3.0T field strength and HR
Fat Inversion Time of 60 bpm (assuming T1 lipid = 360 ms)
TIlipid is the time delay between the application of a spa-
tially selective RF pulse and data acquisition. This inversion
time is shorter than TIblood and is placed after the RF pulse
and before data acquisition.

Figure 4.17 Imaging components: triple inversion recovery.

 58 • S ection I : B asic P rinciples of C ardiac M R I

S PI N E CHO T 1 W E IG H T E D
This method (Figure 4.19) involves a conventional or fast spin
echo, with TE chosen to allow blood within the imaging volume
to flow out of the slice before data collection begins. This effec-
tively eliminates any signal from the blood pool (Figure 4.20).

Sequence-Specific Variables
TE/2
This is the time between the 90° and the first of the 180°
RF pulses. This value must be large enough to allow for blood
to flow out of the imaging slice (or volume), thereby not con-
tributing to the signal within the image.
TR
This is the time between successive repetitions of the 90°
RF pulse or lines of data.
The TE should be as short as possible and is recommended
not to exceed 50 milliseconds. This is particularly important for
multiple (ie, fast) spin echo imaging in which the effective TE is
Figure 4.18 Triple inversion recovery image, short-axis view. proportional to the number of echoes in the echo train.
A typical TR is equal to 1 R-R interval and should
TI times are calculated from the equation: not exceed 800 milliseconds for primarily T1 (rather than
proton-density) weighting.
Note that slow-flowing blood can be mistaken for patho-
 − TR  logic processes within the cardiac chambers because the blood
 1 + e T1

TI null = −T1 × ln   (2) does not wash out of the imaging slice during the time TE/2
 2  and therefore contributes to signal within the chambers in the
 
slice of interest.

where TInull is the desired inversion time, TR the pulse repetition

time (TR ≈ 2 R-R intervals), and T1 the spin-lattice relaxation
time of the tissue to be nulled. That is, T1 blood and T1 lipid are the T1
relaxation times for blood and lipid, respectively, at a given field
strength.
Note that estimates of T1 relaxation time for lipids vary by
several tens of milliseconds in the MR literature. The relax-
ation times given above are therefore approximate values. (For
more information see Simonetti et al and Greenman et al in
the Suggested Reading.)
 4 . P ulse S equence B asics  • 59

Figure 4.19 Imaging components: spin echo T1 weighted.

Figure 4.20 Fat-suppressed, T1-weighted axial image.

 60 • S ection I : B asic Principles of C ardiac M R I

PU L S E S E QU E NC E S F OR I M AG I N G Sequence-Specific Variables
C A R DI AC F U NC T IO N
Centric View Order Encoding
G R A DI E N T E CHO (BA L A NC E D A N D
k-Space views are acquired based on their radial distance
S P OI L E D) C I N E
from the center of k-space, typically starting from the center
of k-space. Data acquisition is typically initiated upon arrival
See previous section (Pulse Sequences for Imaging Cardiac of the bolus peak within the imaging volume.
Morphology, pages 52–54) for a complete description.
Sequential View Order Encoding
3D M R A NG IO G R A PH Y k-Space views are acquired in a rectilinear, sequential
This method (Figure 4.21) uses a 3D spoiled gradient echo order.
sequence with 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 back-
ground tissue (Figure 4.22).

Figure 4.21 Imaging components: 3D MR angiography.

 4 . P ulse S equence B asics  • 61

Figure 4.22 Maximum-intensity projection images from 4 different perspectives (rotation angles) of the imaging volume.
 62 • S ection I : B asic P rinciples of C ardiac M R I

C I N E PH A S E C ON T R A S T Table 4.2 VELOCITY ENCODING PAR AMETERS

This method (Figure 4.23) involves gradient-recalled echo MEASUR EMENT TYPICAL VENC VALUES, cm/s
(coherent or spoiled) with motion-sensitizing gradients
added between RF excitation and acquisition of the image Vessel
data. The velocity of flowing blood is encoded into the phase Internal and common <120
of the MR signal. The velocity encoding (VENC) parame- carotid artery
ter is the maximal velocity that is represented in the image Thorax
without flow-related aliasing (Table 4.2). Given the cross-sec-
Ascending aorta <175 (range, 100–250)
tional area of a vessel, flow rate (typically expressed in units
of mL/min) can be calculated by multiplying through-plane Descending aorta <175 (range, 100–250)
velocity and cross-sectional area. Vena cava <40
Sequence-Specific Variables Abdomen

Velocity Encoding Aorta <100

This is the maximum velocity that is mapped to the high- Pathologies
est phase value in the image (180° or π ≈ 3.14159 radians). Aortic valve stenosis
Valvular insufficiency
Carotids
Prestenotic
Intrastenotic
<800 (range, 200–800)
<400 (range, 200–400)
<50 (range, 5–50)
<500 (range, 100–500)

Figure 4.23 Imaging components: cine phase contrast.

 4 . P ulse S equence B asics  • 63

Flow-Encoding Direction
This is the direction that is sensitized to flow; often
described as along the 3 imaging axes (frequency, phase,
and slice). To obtain the 3 components of the flow vector,
the imaging sequence must be repeated 3 separate times,
along with 1 reference acquisition. It is most common to
choose the flow direction solely along the slice-encoding
direction, which only requires 2 acquisitions. Encoding
along all directions requires 4 separate acquisitions and
thereby causes a reduction in temporal resolution for inter-
leaved acquisitions.

Reconstruction Type
This is the phase difference or complex difference—the
method by which the velocity (phase) data are reconstructed.
Phase difference calculates the difference in the phase of the 2
data sets acquired in the cine phase-contrast sequence and is used
for quantitative analysis. Other reconstruction methods, such as
complex difference, can be used to visualize anatomical details
of vessels but only provides qualitative velocity information.

Views Per Segment

VPS is 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 HR
(Table 4.1). A decrease in the VPS will increase imaging time.
Thus, a compromise is often struck between sufficient tem-
poral resolution and breath-hold duration. To keep imaging
times within normal breath-hold durations (<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.
Figure 4.24 Phase (top) and magnitude (bottom) images of the
Table 4.1 TYPICAL VPS VERSUS HEART R ATE ascending and descending aorta. The 2 directions of flow in the phase
image are represented by the bright and dark signal within the vessel
HEART R ATE, bpm VPS
lumen.
≤60 10–12

61–95 8–10

96–125 6–8

126–155 4–6
≥156 ≤4

Cardiac Phases
This is the number of images reconstructed across the cardiac
cycle. Each image (Figure 4.24) is at a specific time point or phase
of the cardiac cycle. The greater the number of cardiac phases,
the higher the temporal resolution of the cine series. Most com-
monly, 20 cardiac phases are reconstructed for cine sequences.
 64 • S ection I : B asic Principles of C ardiac M R I
Figure 4.25 Imaging components: perfusion.
PE R F US ION
This method (Figure 4.25) uses a saturation recovery preparation
pulse, followed by a spoiled or balanced gradient echo readout.
Sequence-Specific Variables
Phases Per Slice
This is the number of samples (images) over which the per-
fusion bolus wash-in and wash-out are measured. Each image
represents a separate time point (Figure 4.26). Total imag-
ing time is proportional to this value, which can be between
20 and 40 seconds. For larger phases (≈40), total imaging
time can be longer than 1 minute.
TAG G I NG
This method (Figure 4.27) involves a tagging preparation
before initiation of a spoiled gradient echo imaging sequence.
Sequence-Specific Variables
Tag Spacing
This is 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).
Views Per Segment
VPS is 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 HR (Table 4.1). 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 durations
(<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.
Table 4.1 TYPICAL VPS VERSUS HEART R ATE
HEART R ATE, bpm VPS
≤60 10–12
61–95 8–10
96–125 6–8
126–155 4–6
≥156 ≤4
Cardiac Phases
This is the number of images reconstructed across the cardiac
cycle. Each image is at a specific time point or phase of the cardiac
cycle (Figure 4.28). The greater the number of cardiac phases,
the higher the temporal resolution of the cine series. Most com-
monly, 20 cardiac phases are reconstructed for cine sequences.
 4 . P ulse S equence B asics  • 65

Figure 4.26 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 filling of the left ventricle. Overall
contrast diminishes over time as the contrast is diluted into the blood pool.
 66 • S ection I : B asic Principles of C ardiac M R I

Figure 4.27 Imaging components: tagging.

Figure 4.28 Tagged short-axis images at systole (left), mid diastole (middle), and late diastole (right) showing tag fading over time.
 4 . P ulse S equence B asics  •
Figure 4.29 Imaging components: quantification of T1 relaxation time.
PA R A M E T R IC A S S E S S M E N T
QUA N T I F IC AT ION OF
T 1 R E L A X AT ION T I M E
This method (Figure 4.29) uses an emergent imaging sequence
involving an inversion recovery, balanced SSFP acquisition.
Images are acquired at varying inversion times (TI values) at
a given cardiac phase. The most commonly applied sequence
is known as a modified Look-Locker imaging (MOLLI)
sequence, which refers to the method of rapidly acquiring
multiple ECG-gated images with differing inversion times
(Figure 4.30). Postprocessing of image data is required to spa-
tially resolve myocardial T1.
Sequence-Specific Variables
R-R Intervals
Between 2 and 4 intervals are used, depending on the
pulse sequence implementation.
Number of TI Values
Depending on the MOLLI implementation, up to 8
images, each with differing TI values, are acquired, ranging
from several hundred to several thousand milliseconds.
67
Typical Values for T1 Tissue Characterization
T1 mapping using MOLLI or other inversion recovery
approaches can be performed before and after administration
of gadolinium contrast agents. Changes in T1 are suggestive of
myocardial fibrosis. Caution should be taken when interpret-
ing T1 maps because values for both normal and scarred regions
vary with and without contrast administration and vary with
the type of T1 mapping sequence. In different studies, precon-
trast T1 values for normal myocardium have been reported as
980 ± 43 ms and 1,030 ± 34 ms at 1.5T, and 1,471 ± 31 ms at
3.0T. Postcontrast T1 relaxation time depends on the amount of
contrast, the patient’s HR, and the delay from administration to
imaging.
T1 is estimated by fitting an equation of the form:
− TTi∗
Si = A − Be 1 (3)
where Si is the signal for a time Ti, A and B are general fitting
variables, and T1* is the apparent T1 value. T1 is then calculated
by solving for T1 where T1 = T1* ([B/A] – 1). The use of variables
A and B allows flexibility in the fitting algorithm because they
are applicable to both saturation recovery and inversion recovery
sequences.
 68 • S ection I : B asic Principles of C ardiac M R I

Figure 4.30 Short-axis views of an infarction within the lateral wall of the left ventricle. Images include balanced SSFP, late gadolinium
enhancement, saturation recovery balanced SSFP MOLLIs with varying TIs, and a T1 parametric map. T1 MOLLI data were acquired 3 minutes
post contrast administration before gadolinium chelate contrast was able to fully perfuse the infarcted region. As a result, the T1 of the infarcted
region is longer because of fibrotic tissue. At longer delay times, the presence of contrast agent within the infarction will decrease the T1 of this
tissue compared with normally perfused myocardium.

QUA N T I F IC AT ION OF
T 2 R E L A X AT ION T I M E
Two different methods—black blood (multiecho spin echo)
or magnetization prepared bright blood (balanced SSFP)
(Figure 4.31)—can be applied to measure the T2 of the
myocardium. Both sequences acquire a single static image
at each slice location but with increasing echo times, typi-
cally at mid to late systole, when the myocardium is thickest
(Figure 4.32). Postprocessing of the image data is required to
generate T 2 maps.
 4 . P ulse S equence B asics  • 69

Figure 4.31 Imaging components: quantification of T2 relaxation time. A, Inversion recovery (black blood), multiecho spin echo. B, Balanced SSFP
imaging sequence.
 70 • S ection I : B asic P rinciples of C ardiac M R I

Figure 4.32 Short-axis views of an infarction in the lateral wall of the left ventricle. Images include balanced SSFP, late gadolinium enhancement,
single echo T2-weighted spin echo, and a T2 parametric map. The color scale indicates that the infarction (red arrows) has a smaller T2 value than
other segments of the myocardium, which indicates that there is little fluid content and therefore that this is a nonacute infarction.

Sequence-Specific Variables For multiecho black blood sequences, T2 is estimated by

fitting an equation of the form:
R-R Intervals
Two or 3 are used, depending on the type of imaging
− TE i

sequence and the patient’s HR.   Si = Ae T 2

+ B (4)

Number of Echoes
For black blood spin echo, 3 to 4 images are acquired, each
with separate TEs, each within a single R-R interval. For bal-
anced SSFP, 3 separate images with separate T2 preparation
times are acquired.
Views Per Segment
For black blood spin echo, between 4 and 8 views (echoes)
are acquired per TE, depending on HR. For balanced SSFP,
data are acquired in a single shot within each selected R-R
interval.
Typical Values for T2 Tissue Characterization
The T2 relaxation time of normal myocardium has been
reported to range from ≈40 to 73 ms at 1.5T. As a function of
field strength, T2 increases: 40 ± 6 ms for 1.5T vs 47 ± 11 ms
for 3.0T. Edematous myocardium will have T2 values greater
than normal ranges.
where Si is the signal intensity at TE i and A and B are gen-
eral fitting parameters. A represents the signal at TE = 0
and B the estimate of the noise within each pixel in the
image.
For balanced SSFP T2 mapping methods, TEi is replaced
with TET2Pi in the above equation and is equal to the amount
of T2 preparation time for the echo i.
The T2 distribution is typically displayed as a color-
wash image. T2 quantification is performed in combination
with late gadolinium enhancement imaging to distinguish
between edema and infarction, particularly for acute myocar-
dial infarctions.
QUA N T I F IC AT ION OF T 2 *
R E L A X AT ION T I M E
This method (Figure 4.33) is an ECG-gated multiecho spoiled
gradient echo sequence acquired at a single cardiac phase, most
commonly at mid to late systole to ensure that the optimal
 4 . P ulse S equence B asics  • 71

Figure 4.33 Imaging components: quantification of T2* relaxation time.

thickness of the myocardium is imaged (Figure 4.34). As a Number of TEs

result of the ferromagnetic properties of iron, its presence results
in a decrease in T2*. This parameter can therefore be used to
estimate iron concentration in the heart and, more specifically,
iron overload, such as in patients with thalassemia major.
Sequence-Specific Variables
Views Per Segment
Typically between 8 and 12 are used. Fewer echoes are gener-
ally needed for patients with severe iron overload because the sig-
nal at longer TEs can approach the noise level of the image. Most
commonly, 20 cardiac phases are reconstructed for cine sequences.
T2* is estimated by fitting the general equation for signal
strength as a function of echo time, TEi:
− TE i

VPS depends on the patient’s HR (Table 4.1): between 4 Si ( TE i ) = Ae T2∗

+B (5)
and 16, but typically 8.
Table 4.1 TYPICAL VPS VERSUS HEART R ATE where A is the signal at zero TE, TEi is the TE of the ith echo,
and B is an estimate of the noise level in the image.
HEART R ATE, bpm VPS Myocardial iron load [Fe] (Table 4.3) in units of mg Fe per
gram of tissue can then be estimated by substitution of T2*
≤60 10–12
into the equation:
61–95 8–10
( )
−1.22

96–125 6–8
[Fe ] = 45 T2∗ (6)

126–155 4–6 Table 4.3 R EFER ENCE VALUES OF T 2 * AND [Fe] FOR
≥156 ≤4 NOR MAL MYOCAR DIUM AND MODER ATE AND
SEVER E MYOCAR DIAL IRON OVER LOAD

CAR DI AC TISSUE T 2*, ms [Fe], mg/g TISSUE

R-R Intervals
Typically 1 or 2 are used, depending on the patient’s HR Normal >20 <1.16
(<80 bpm, 1 R-R interval; ≥80 bpm, 2 R-R intervals).
Mild to moderate 10–20 1.16–2.71
hemochromatosis
Severe hemochromatosis <10 >2.71
 72 • S ection I : B asic P rinciples of C ardiac M R I

Note that cardiac T2* < 10 ms represents severe cardiac iron

loading, with the risk of heart failure increasing sharply as
T2* decreases. Patients with a T2* < 6 ms have a 50% risk of
heart failure developing within 1 year. All values are at a field
strength of 1.5T.

DI XON FAT A N D WAT E R S E PA R AT ION

This is a multiecho gradient or spin echo sequence that uses
the chemical shift effect of the second kind. First described
by Thomas Dixon, this method acquires 2 separate image
echoes in which the fat and water signals are in and out of
phase from one another. Addition and subtraction of the
2 image sets generates images containing either water-only
or fat-only signals. Iterative methods that acquire 3 or more
echoes address off-resonance effects due to B0 inhomoge-
neities, which increases the accuracy of water- and fat-only
image reconstruction. For late gadolinium enhancement
imaging, Dixon-based approaches are useful for distinguish-
ing between fat and infarcted regions, in comparison to non–
fat-suppressed late gadolinium enhancement images, which
are heavily T1 weighted and therefore have a high fat signal.

Sequence-Specific Variables
Various applications of iterative Dixon-based methods exist
(eg, ECG gated, non–ECG gated, cine, static, spin echo, and
gradient echo); therefore, sequence-specific variables are not
applicable in this instance.
When using Dixon-based reconstruction methods, at least
2 separate data sets are acquired. In the simplest case, 2 images
are acquired (Figure 4.35). The first image is typically acquired
at a TE in which the fat and water signals are out of phase (Δθ
= 180o) and therefore subtract. The second, or in-phase, image
is acquired with a choice of TE such that fat and water signals
within each voxel are aligned or in phase (Δθ = 0o) and there-
fore add constructively. Processing of the in- and out-of-phase
Figure 4.34 Examples from patients with (left) and without (right)
data produce images with either fat-only or water-only content.
hemochromatosis, with associated T2* maps in units of milliseconds.
The 4 gradient echoes (TE1,2,3,4) are acquired at increasing echo
times: 1.35, 4.57, 7.78, and 11 ms (left) and 1.63, 5.90, 10.2, and 14.5
ms (right). The positive case shows a lower T2* in the left ventricle, S UG G E S T E D R E A DI N G
indicating an increased concentration of iron compared with the
normal example.
Cardiac MR
Bogaert J, Dymarkowski S, Taylor AM. Clinical cardiac MRI: with
interactive CD-ROM. Berlin: Springer; c2005.
Lee VS. Cardiovascular MRI: physical principles to practical protocols.
Philadelphia (PA): Lippincott Williams & Wilkins; c2006.

Dixon Methods
Dixon WT. Simple proton spectroscopic imaging. Radiology. 1984
Oct;153(1):189–94.
 4 . P ulse S equence B asics  •
Figure 4.35 Late gadolinium-enhancement images with the Dixon-based data reconstruction method for separation of water and fat signals. At
TE1, the water and fat signals are out of phase (Δθ = 180o), whereas at TE2, water and fat signals are aligned or in phase (Δθ= 0o).
Glover GH. Multipoint Dixon technique for water and fat pro-
ton and susceptibility imaging. J Magn Reson Imaging. 1991
Sep-Oct;1(5):521–30.
Reeder SB, McKenzie CA, Pineda AR, Yu H, Shimakawa A, Brau AC,
et al. Water-fat separation with IDEAL gradient-echo imaging.
J Magn Reson Imaging. 2007 Mar;25(3):644–52.
Flow and Velocity Measures
Jager KA, Ricketts HJ, Strandness DE Jr. Duplex scanning for the
evaluation of lower limb arterial disease. In: Bernstein EF, editor.
Noninvasive diagnostic techniques in vascular disease. 3rd ed. St.
Louis (MO): Mosby; c1985. p. 619–31.
MR Acronyms
Boyle GE, Ahern M, Cooke J, Sheehy NP, Meaney JF. An interac-
tive taxonomy of MR imaging sequences. Radiographics. 2006
Nov-Dec;26(6):e24.
Brown MA, Semelka RC. MR imaging abbreviations, definitions, and
descriptions: a review. Radiology. 1999 Dec;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 Feb;15
Suppl 2:B10–6.
MR Physics and Pulse Sequences
Bernstein MA, King KF, Zhou XJ. Handbook of MRI pulse sequences.
Amsterdam: Elsevier Academic Press; c2004.
Greenman RL, Shirosky JE, Mulkern RV, Rofsky NM. Double inversion
black-blood fast spin-echo imaging of the human heart: a comparison
between 1.5T and 3.0T. J Magn Reson Imaging. 2003 Jun;17(6):648–55.
Simonetti OP, Finn JP, White RD, Laub G, Henry DA. “Black blood”
T2-weighted inversion-recovery MR imaging of the heart. Radiology.
1996 Apr;199(1):49–57.
73
T1 Look-Locker Sequences
Look DC, Locker DR. Time saving in measurement of NMR and EPR
relaxation times. Rev Sci Instrum. 1970 Feb;41(2):250–1.
Messroghli DR, Plein S, Higgins DM, Walters K, Jones TR, Ridgway
JP, et al. Human myocardium: single-breath-hold MR T1 mapping
with high spatial resolution: reproducibility study. Radiology. 2006
Mar;238(3):1004–12. Epub 2006 Jan 19.
Messroghli DR, Radjenovic A, Kozerke S, Higgins DM, Sivananthan
MU, Ridgway JP. Modified Look-Locker inversion recovery
(MOLLI) for high-resolution T1 mapping of the heart. Magn Reson
Med. 2004 Jul;52(1):141–6.
Song T, Stainsby JA, Ho VB, Hood MN, Slavin GS. Flexible cardiac T1
mapping using a modified Look-Locker acquisition with saturation
recovery. Magn Reson Med. 2012 Mar;67(3):622–7. Epub 2012 Jan 3.
T2
Giri S, Chung YC, Merchant A, Mihai G, Rajagopalan S, Raman SV,
et al. T2 quantification for improved detection of myocardial edema.
J Cardiovasc Magn Reson. 2009 Dec 30;11:56.
Kellman P, Aletras AH, Mancini C, McVeigh ER, Arai AE. T2-prepared
SSFP improves diagnostic confidence in edema imaging in acute
myocardial infarction compared to turbo spin echo. Magn Reson
Med. 2007 May;57(5):891–7.
T 2*
Carpenter JP, He T, Kirk P, Roughton M, Anderson LJ, de Noronha SV,
et al. On T2* magnetic resonance and cardiac iron. Circulation. 2011
Apr 12;123(14):1519–28. Epub 2011 Mar 28.
T1 , T2 versus Field Strength
Stanisz GJ, Odrobina EE, Pun J, Escaravage M, Graham SJ, Bronskill
MJ, et al. T1, T2 relaxation and magnetization transfer in tissue at
3T. Magn Reson Med. 2005 Sep;54(3):507–12.
 5.
MODULAR CAR DI AC MR IM AGING PROTOCOLS
Phillip M. Young, MD, Eric E. Williamson, MD, and James F. Glockner, MD
T
he process of “protocoling” a cardiac magnetic
resonance (MR) imaging examination—determin-
ing which imaging protocol, or variant thereof, a
patient requires—can be confusing to the novice. The pulse
sequences used are somewhat different from MR examina-
tions of other parts of the body, as are the imaging planes.
However, both the sequences used and the planes in which
they are prescribed have specific utility for investigation of
cardiovascular disease. As an aid to demystifying the pro-
cess of protocoling a cardiac MR examination, it is helpful
to view protocols as composed of a series of distinct modules
that are designed to answer specific questions according to
the clinical information required.
The purpose of this chapter is to describe 6 specific cardiac
imaging modules, to describe the pulse sequences that make
up each module, and to demonstrate how these modules can
be combined to generate imaging protocols for specific car-
diac imaging indications. The 6 modules discussed in this
chapter are given descriptive names that indicate the specific
application: localizer, late gadolinium enhancement/viability,
perfusion, tissue characterization, vascular flow, and structure
and function modules. The protocols provided in this chapter
are by no means comprehensive but instead cover the more
common indications for cardiac MR imaging. These modules
and protocols can be adapted to the specific needs of each
reader’s practice.
Pulse sequences within certain modules include a descrip-
tion of standard imaging planes such as short-axis and 2-, 3-,
and 4-chamber views of the heart, as described, for example,
in the Structure and Function module. The methods to
prescribe these planes are outlined in Chapter 3, Standard
Imaging Planes in Cardiac MR Imaging. Thus, Chapter 3
should be considered a companion to this chapter, and the
reader is recommended to cross-reference the methods out-
lined in Chapter 3, as needed. In addition, specific informa-
tion on the pulse sequences used in each module can be found
in Chapter 4, Pulse Sequence Basics.
Finally, in many of the imaging sequences that make
up the individual modules, some type of parallel imaging
is used. It is important to recognize that parallel imag-
ing approaches and methods vary across scanner manufac-
turers and software platforms and that persons building
74
cardiac MR protocols should be aware of the performance
and limitations of each method. Some form of parallel
imaging can be used for most of the sequences below; judi-
cious use of acceleration factors and appropriate field-of-
view selection will greatly affect the quality of images
obtained.
L O C A L I Z E R MODU L E
All cardiac MR examinations should begin with local-
izer images, which serve to orient the technologist to the
patient’s anatomy and to identify landmarks that will
be used to prescribe the various required standard car-
diac imaging planes. The purpose of the localizer module
(Table 5.1) is to describe imaging planes and pulse sequences
that enable a rapid survey of the thoracic cavity and key ana-
tomical landmarks of the heart. Images obtained from this
module are used to prescribe standard views of the heart
and represent the starting point of the cardiac examination.
In our practice, the localizer or first imaging series consists
of a 3-plane image set acquired with a balanced steady-state
free precession (SSFP) imaging sequence. The 3-plane local-
izer acquires orthogonal imaging planes in the axial, cor-
onal, and sagittal planes. A large field of view with thick
slices (≈10 mm) and spacing describe each slice and enable
coverage of most of the chest cavity. Single-shot, multiecho,
spin echo sequences work equally well and are preferred in
some practices.
In addition to the 3-plane localizer set, it is often a good
idea to obtain a fast set of ungated axial balanced SSFP images
covering the whole chest. These have the advantage of quickly
surveying the entire chest for abnormalities that otherwise
might not be easily apparent, such as a left-sided superior vena
cava or anomalous pulmonary venous return.
Images from either the axial data or the 3-plane local-
izer set can be used to set up a 2-chamber localizer, from
the mitral valve plane to the apex of the left ventricle. This,
in turn, is used to generate the 4-chamber localizer image,
again prescribed from the mitral valve plane to the apex.
In general, these should be acquired in diastole to improve
reproducibility.
 5 . M odular C ardiac M R I mag i n g Pro t ocol s • 75

Table 5.1 LOCALIZER MODULE SEQUENCES Table 5.2 STRUCTUR E AND FUNCTION MODULE
SEQUENCES
DESCR IPTION IM AGING PLANE a SEQUENCE b
DESCR IPTION IM AGING PLANE a PULSE SEQUENCE b
3-Plane localizer Axial, coronal, and sagittal Balanced SSFPc
planes orthogonal to one Short axis Double oblique, mitral valve Balanced SSFP
another plane to apex, on 2- and
4-chamber localizer
2-Chamber Mitral valve plane to apex Balanced SSFP images
localizer on axial image
2-Chamber Mitral valve plane to apex, Balanced SSFP
4-Chamber Mitral valve plane to apex Balanced SSFP
(VLA) parallel to ventricular
localizer on 2-chamber long-axis
septum and perpendicular
image
to anterior and inferior
walls on short-axis image
Abbreviation: SSFP, steady-state free precession.
4-Chamber Mitral valve plane to apex, Balanced SSFP
a
See Chapter 3 for imaging plane prescription details.
(HLA) perpendicular to septum
b
Pulse sequence details described in Chapter 4. and lateral walls, on
c
Single-shot multiecho spin echo images in the axial plane can also be acquired short-axis image
to complement the 3-plane acquisition.
3-Chamber Mitral valve plane to apex, Balanced SSFP
(LVOT) with third point set at mid
aortic valve
This module should also include any required calibra-
tion scans for parallel imaging or surface coil intensity Axial RV Straight (true) axial Balanced SSFP
correction.
LVOT stack Identical to 3-chamber but Balanced SSFP
performed in a stack of
several images
ST RUC T U R E A N D
F U NC T IO N MODU L E Abbreviations: HLA, horizontal long axis; LVOT, left ventricular outflow tract;
RV, right ventricle; SSFP, steady-state free precession; VLA, vertical long axis.
One of the advantages of MR for cardiac imaging is the abil- a
See Chapter 3 for imaging plane prescription details.
ity to obtain dynamic cine images, which depict regional wall b
Balanced SSFP imaging sequences are preferred for these imaging planes.
motion and valvular motion and allow accurate quantifica- However, this sequence can be substituted with spoiled gradient-recalled echo
imaging sequences as needed.
tion of ventricular volumes and other parameters such as ejec-
tion fraction.
The purpose of the structure and function module is to
the heart. Using spoiled gradient-recalled echo instead of
provide a list of imaging planes and sequences that will enable
balanced SSFP sequences can be a useful alternative. These
the assessment of volumes, function, and regional wall-motion
sequences also generally demonstrate more dephasing than
abnormalities (Table 5.2). Most of the sequences described
balanced SSFP and can occasionally be useful to demon-
in this module will be electrocardiography (ECG)-gated,
strate valvular pathology or a small shunt because of T2*
balanced SSFP images because of their speed, high spatial
dephasing.
resolution, and excellent blood/myocardial contrast. These
sequences also allow a reasonable assessment of valvular mor-
phology and often visualize valvular stenosis or insufficiency
because of intravoxel dephasing. The structure and function T I SS U E C H A R AC T E R I Z AT IO N
module typically follows the localizer module. Images from MODU L E
the localizer module are used as prescription series for several
of the structure and function imaging series, the first of which The purpose of this module is to describe pulse sequences
is a stack of short-axis images prescribed in double-oblique that can be used to quantify the intrinsic magnetic proper-
fashion. This sequence is commonly followed by long-axis 2-, ties of the heart and surrounding tissues (ie, T1, T2, and T2*
3-, and 4-chamber imaging series that are obtained for supple- relaxation time), which are used to characterize myocardial
mental assessment. The 2- and 4-chamber long-axis views are pathologic processes. The most common approaches involve
acquired if the localizer views do not accurately visualize the multiecho spin echo–based techniques, but gradient echo–
heart in these planes. They are therefore considered optional based sequences have also been recently developed (Table 5.3).
sequences in this module. For multiecho spin echo sequences, the pulse repetition time
In small (pediatric) patients, significant off-resonant (TR) is governed by the patient’s heart rate and is set to every
artifacts in balanced SSFP imaging sequences can occur at R-R interval (shorter TR, more T1 weighting) or every other
the spatial resolution necessary for accurate depiction of R-R interval (longer TR, more T2 weighting). It is important
 76 •  Sec t io n I : B a s ic Pri n ciple s of C ardiac M R I

Table 5.3 TISSUE CHAR ACTER IZATION MODULE Table 5.4 PER FUSION MODULE

IM AGING DESCR IPTION IM AGING PLANE PULSE SEQUENCE a

DESCR IPTION PLANE PULSE SEQUENCE a
Ultrashort TE and Most commonly Spoiled gradient echo
T1-weighted (1 R-R ­interval) Variable Double inversion TR T1-weighted prescribed as Balanced SSFP-based
and T2-weighted (2 R-R recovery multiecho gradient echo short-axis viewsb sequences can also
intervals) without fat spin echo imaging acquired be applied
suppression as short-axis views
T1-weighted (1 R-R ­interval) Variable Triple inversion
and T2-weighted (2 R-R recovery multiecho Abbreviations: SSFP, steady-state free precession; TE, echo time; TR, pulse
intervals) with fat spin echo repetition time.
suppression a
Pulse sequence details described in Chapter 4.
b
Long-axis views can also be prescribed, particularly if imaging a mass to obtain
T1 parametric mapping Variable Look-Locker inver- perfusion information. Some pulse sequences provide the flexibility to acquire
(quantification) sion recovery T1 multiple oblique imaging planes within the same imaging sequence (eg, short-
mapping sequence and long-axis views), thereby allowing visualization of the heart and question-
able anatomical features in multiple imaging planes.
T2 parametric mapping Variable Multiple TE spin echo
(quantification) or T2-weighted bal-
anced SSFP
triple inversion recovery, multiecho, spin echo sequences with
T2* parametric mapping Variable Multiple TE spoiled
(quantification) gradient- the same prescription.
recalled echo

PE R F US ION MODU L E
Abbreviations: SSFP, steady-state free precession; TE, echo time.
a
Pulse sequence details described in Chapter 4.
The purpose of the perfusion module (Table 5.4) is to describe
sequences and imaging planes that can be used to dynami-
cally assess first-pass myocardial perfusion after injection of a
to note that, with this approach, the amount of T1 and T2 bolus of gadolinium contrast. Myocardial perfusion imaging
weighting is variable, dependent on the patient’s heart rate, can be performed using either spoiled or balanced gradient
and generally less “pure” than what is achieved in images of echo imaging sequences. Spoiled gradient echo approaches
other parts of the body. Although conventional ECG-gated
spin echo imaging sequences are infrequently applied in most Table 5.5 LATE GADOLINIUM ENHANCEMENT/
cardiac imaging protocols because of their long acquisition VIABILITY MODULE
time, they can occasionally be useful in patients who cannot
hold their breath at all, because respiratory compensation IM AGING
DESCR IPTION PLANE PULSE SEQUENCE a
techniques can be used. More commonly used today are dou-
ble inversion recovery multiecho spin echo sequences. These T1 localizer/scout Short axis Inversion recovery fast
employ long echo trains to shorten acquisition time to within for inversion time T1 mapping (inversion
a single breath hold. The use of 2 inversion pulses (ie, double selection and recovery or saturation
inversion) increases the “black blood” effect of flow voids, optimization recovery)
and a “triple inversion” recovery adds a nonselective inversion Late gadolinium Short axis Inversion recovery gradi-
pulse to null the fat signal. Both double and triple inversion enhancementb ent echo (spoiled or
techniques can be used with either T1 or T2 weighting. balanced SSFP)
T1-weighted imaging can be useful to identify normal Late gadolinium Long axis Inversion recovery gradi-
anatomic structures, including the pericardium and lymph enhancementb ent echo (spoiled or
nodes, as well as pathologic features, such as an aortic intra- balanced SSFP)
mural hematoma or fat in the right ventricular myocardium.
Late gadolinium Variable Inversion recovery gradi-
T2-weighted imaging is generally used to look for evidence of enhancementb ent echo (spoiled or
myocardial edema in the acute setting, such as suspected api- balanced SSFP)
cal ballooning cardiomyopathy, acute myocarditis, or acute
myocardial infarction. Abbreviation: SSFP, steady-state free precession.
In the setting of arrhythmogenic right ventricular dyspla- a
Pulse sequence details described in Chapter 4.
sia/cardiomyopathy, the diagnostic criteria no longer include b
Inversion time is chosen to suppress the signal from normal myocardium. The
the presence of right ventricular fat. However, it is common T1 localizer is used to assist in the selection and optimization of this inversion
to screen for it using axial or short-axis, T1-weighted, double time. Because of contrast kinetics within normal and infarcted myocardium,
this sequence can be repeated to track the evolution of the inversion time if sig-
inversion recovery, multiecho, spin echo sequences. If fat is nificant delays are encountered between execution of the various late gadolinium
suspected, this can be confirmed by performing T1-weighted, enhancement series.
 5 . M odular C ardiac M R I mag i n g Pro t ocol s • 77

Box 5.1 LATE GADOLINIUM-ENHANCEMENT IMAGING KEY POINTS

1. It is not possible to reproducibly quantify nonischemic late gadolinium enhancement using standard, clinically available techniques.
The technique is based on the idea of nulling the “normal” myocardium and highlighting pathologic scar tissue against that back-
ground. In the setting of diffuse or nonischemic fibrosis, it is not clear which myocardium is “normal,” or even if there is normal
myocardium.
2. The inversion time, which is the parameter used to suppress the signal from normal myocardium, must be correctly chosen.
3. Some viability sequences use a balanced SSFP readout instead of a spoiled gradient-recalled echo readout. This approach has the
advantage of speed and generally works well for assessing myocardium. However, this approach has a T2 component to the signal.
A pericardial effusion may appear bright with this approach and may be mistaken for pericardial enhancement. This, in theory,
could also happen with myocardial edema.
4. In the setting of nonischemic heart disease, the percentage thickness of late gadolinium enhancement is key to predicting viability.
These images should be obtained at end systole and the trigger delay set appropriately to obtain systolic images.
5. Fat-suppressed late gadolinium-enhancement imaging sequences can be useful for distinguishing between enhancing myocardium
and fatty infiltration.

Abbreviation: SSFP, steady-state free precession.

are preferred because they are more purely T1 weighted and Look-Locker sequence is not available, some trial and error is
the contrast opacification of myocardium is more conspicu- involved in the process of selecting an inversion time for sup-
ous. There is a tradeoff among the number of slices obtained, pression of the signal from normal myocardium (Box 5.1).
spatial resolution, and temporal resolution. In general, an R-R
interval of 2, 7 slices in the short axis covering myocardium, an
acceleration factor of 1.75 to 2, and a field of view outside the VA S C U L A R A N D F L OW MODU L E
patient’s skin are the imaging parameters of choice for most
patients. Visualization of the vascular structures and quantitative
assessment of blood flow within vessels can be accomplished
using the pulse sequences described in the Vascular and Flow
L AT E G A D OL I N I U M Module listed below (Table 5.6).
E N H A NC E M E NT/ V I A B I L I T Y
MODU L E
Table 5.6 VASCULAR AND FLOW MODULE
The late gadolinium enhancement/viability module (Table 5.5) IM AGING
describes the combination of pulse sequences and imaging DESCR IPTION PLANE PULSE SEQUENCE a
planes used for identification and classification of myocardial
scar tissue or fibrosis. The assessment of myocardial fibrosis Magnetic resonance Variable 3D spoiled or balanced
angiographyb gradient echo
or scar is based on its uptake of gadolinium relative to normal
myocardium at specific time points. The increased extracel- Flow quantificationc Variable Phase-contrast gradient
lular space of the fibrotic scar tissue will gradually accumulate echo pulse sequence
gadolinium after intravenous injection, while normal myo-
cardium will rapidly perfuse but rapidly wash out. This differ- Abbreviation: 3D, 3-dimensional.
ence is exploited by using an inversion pulse to selectively null a Pulse sequence details described in Chapter 4.
the “normal” myocardial signal. The scar, with higher gado- b Various sequences can be applied to perform 3D angiography of the vascular
linium concentration, will recover signal and appear “bright” system. The most common involves the use of gadolinium-based contrast
agents using spoiled gradient echo imaging sequences (see Chapter 13, Cardiac
next to the dark myocardium. Imaging occurs after a delay of MRI Safety, for important considerations with the use of gadolinium-based
10 minutes or longer after contrast is administered, as part contrast agents). Non–contrast-enhanced techniques are becoming commer-
of a dynamic contrast enhancement (ie, perfusion) sequence. cially available for patients in whom contrast is contraindicated and can use
balanced steady-state free precession or multiecho spin echo imaging sequences.
Because of the delay, this type of myocardial fibrosis imaging is Alternatively, conventional time-of-flight techniques can be used for imaging
referred to as late gadolinium enhancement imaging. blood flow and the vascular system but have the disadvantage of long acquisi-
Some MR scanner manufacturers have provided Look- tion times.
c
Locker sequences similar to quantitative T1-mapping meth- typically It is most common to encode flow in a single direction only. The direction
chosen is orthogonal to the imaging slice or through plane. Full 3D
ods described in the Tissue Characterization Module, which flow encoding allows for quantification of the true flow vector (direction and
obtains images at multiple inversion times to allow the user to amplitude) but requires long acquisition times. Four-dimensional flow (3 spatial
select the optimal null point for myocardium before proceed- dimensions and 1 time dimension) sequences are being translated into clinical
practice but are not routinely used. These sequences involve long acquisition
ing with the late gadolinium-enhancement images. If a robust times and sophisticated postprocessing tools for flow visualization.
Protocol 5.1 MYOCAR DIAL ISCHEMIA & INFARCTION

MODULE COMMENTS

Localizer
Structure and function
Tissue characterization Short-axis, T2-weighted, triple inversion recovery, multiecho spin
echo sequence can be used if there is suspicion of an acute
myocardial infarction, to look for edema
Perfusion
Late gadolinium enhancement/viability

Protocol 5.2 NONISCHEMIC MYOCAR DIAL DISEASE

MODULE COMMENTS

Localizer
Structure and function
Perfusion
Late gadolinium enhancement/viability
Additional/optional sequences
Tissue characterization module:
Short-axis, T2-weighted, triple IR If suspected myocardial edema, particularly in the setting of
­possible myocarditis or apical ballooning syndrome
T2* -weighted images Used for assessment of iron overload
Long- or short-axis double and triple IR Useful for assessment of myocardial fat in suspected ARVC
Structure and function module:
Any balanced SSFP cine Optional for hypertrophic cardiomyopathy
prescribed as an LVOT stack
Any balanced SSFP cine prescribed as a Used to quantify right ventricular function, such as in ­suspected ARVC
straight axial image

Abbreviations: ARVC, arrhythmogenic right ventricular dysplasia; IR, inversion recovery; LVOT, left ventricular outflow tract; SSFP,
steady-state free precession.

Protocol 5.3 PER ICAR DITIS

MODULE COMMENTS

Localizer
Structure and function
Tissue characterization Axial, T1-weighted, double inversion recovery (fat-suppressed),
multiecho spin echo sequence to look for pericardial thickening
or mediastinal fat stranding
Short-axis, T2-weighted, triple inversion recovery (fat-suppressed),
multiecho spin echo sequence to look for edema
Perfusion
Late gadolinium enhancement/viability Axial late gadolinium enhancement (optional for pericarditis)
Additional/optional sequences
Structure and function module:
Any balanced SSFP cine To evaluate respirophasic change in position of the interventricu-
lar septum. Modified to allow imaging during free-breathing,
low-resolution, nongated, nonsegmented, multiphase, continu-
ous acquisition
Myocardial tagginga To evaluate adhesions (see Chapter 4 for pulse sequence details)

Abbreviation: SSFP, steady-state free precession.

a
This pulse sequence is not described in any of the modules because of its infrequent use.
Protocol 5.4 VALVULAR HEART DISEASE

MODULE COMMENTS

Localizer
Structure and function Including RV long axis
Vascular and flow module:
Cine phase contrast Above or below valves of interest: above to quantify forward flow or
peak velocity, below to quantify regurgitation (see Chapter 4 for
pulse sequence details)
MR angiography Pulmonary artery or aorta to look for aneurysm or stenosis.
Obtaining phase-contrast postgadolinium images will also
increase signal-to-noise ratio in the phase-contrast data (see
Chapter 4 for pulse sequence details)

Abbreviations: MR, magnetic resonance; RV, right ventricular.

Protocol 5.5 PULMONARY VEIN

MODULE COMMENTS

Localizer
Structure and function Can be considered an optional module if localizer image sufficiently
visualizes pulmonary veins
Additional/optional sequences
Vascular and flow module:
MR angiography Timing of the bolus arrival should be based on the timing of flow
into the pulmonary veins (see Chapter 4 for pulse sequence details)

Abbreviation: MR, magnetic resonance.

Protocol 5.6 CAR DIAC MASS

MODULE COMMENTS

Localizer
Structure and function Straight axial data can be prescribed from any of the balanced SSFP
sequences in this module to determine the location of the mass
Tissue characterization T1-weighted double inversion recovery (non–fat-suppressed),
T2-weighted triple inversion recovery (fat-suppressed), multiecho
spin echo images prescribed through mass
Perfusion Imaging planes prescribed through mass to assess perfusion,
vascularity
Late gadolinium enhancement/viability Imaging planes prescribed to cover the mass, as well as screen
­myocardium, pericardium, and possibly other tissues as needed
Additional/optional sequences
Structure and function module:
Any balanced SSFP cine or spoiled Images prescribed as straight axials. These images can be used to
gradient echo images survey the remainder of the chest to check for metastases

Abbreviation: SSFP, steady-state free precession.

 80 •  Sec t io n I : B a s ic Pri n ciple s of C ardiac M R I

Protocol 5.7 CONGENITAL HEART DISEASE

MODULE COMMENTS

Localizer
Structure and function Including long-axis RV when appropriate
Additional/optional sequences
Structure and function module:
Any balanced SSFP cine sequence Useful for quantifying ventricular function, imaging baffles, or
conduits
Any balanced SSFP cine or spoiled Prescribed as long-axis images through valves, baffles, and conduits.
­gradient echo images Useful for visualizing specific anatomical features
Vascular and flow module:
MR angiography Useful for delineation of stenosis or aneurysms
Cine phase contrast Quantification of flow direction, volume, or velocity
Late gadolinium enhancement/viability
module:
Postcontrast late gadolinium Useful for assessment of scar tissue
enhancement

Abbreviations: MR, magnetic resonance; RV, right ventricle; SSFP, steady-state free precession.

S UGG E ST E D R E A DI NG Foundation Task Force on Expert Consensus Documents. J Am Coll

American College of Cardiology Foundation Task Force on Expert
Consensus Documents; Hundley WG, Bluemke DA, Finn JP,
Flamm SD, Fogel MA, Friedrich MG, et al. ACCF/ACR/AHA/
NASCI/SCMR 2010 expert consensus document on cardiovascular
magnetic resonance: a report of the American College of Cardiology
Cardiol. 2010 Jun 8;55(23):2614–62.
Kramer CM, Barkhausen J, Flamm SD, Kim RJ, Nagel E; Society for
Cardiovascular Magnetic Resonance Board of Trustees Task Force
on Standardized Protocols. Standardized cardiovascular magnetic
resonance imaging (CMR) protocols, Society for Cardiovascular
Magnetic Resonance: Board of Trustees Task Force on Standardized
Protocols. J Cardiovasc Magn Reson. 2008 Jul 7;10:35.
 SEC T ION I I
CL I N IC A L A PPL IC AT IONS
A N D C A SE S T U DI E S
 6.
MYOCAR DI A L ISCHEMI A A ND INFARCTION
Thomas A. Foley, MD

C
ardiac magnetic resonance (MR) imaging is an essen-
tial method for visualization of myocardial ischemia
and infarction. The modality provides information
on the extent and stage of infarction, regional and global
myocardial function, and physiologic status by showing myo-
cardial perfusion and tissue characterization. Complications
from myocardial infarction, such as aneurysm formation,
thrombus formation, wall rupture, and ischemic mitral valve
regurgitation can be detected using MR. MR imaging (MRI)
can also be used to detect inducible ischemia. Either pharma-
cologic agents (eg, adenosine or dobutamine) or exercise can
be used as stress agents to perform an MRI “stress test.”
Figure 6.1 shows the anatomical location of the 3 main
coronary arteries and the myocardial territories that they sup-
ply, using the 17-segment model described by the American
Heart Association. It is recommended that the anatomic
locations of findings associated with ischemic heart disease,
particularly in terms of involved myocardial segments, are
described with reference to this model. The purpose of this
chapter is to present case studies of different clinical scenarios
of myocardial ischemia and infarction, suggest recommended
imaging protocols, and provide examples of their appearance
on cardiac MR images.

Figure 6.1 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 3 main coronary arteries,
as well as the 3 parallel planes that correspond to the short-axis slices shown at bottom. (Adapted from Imaging guidelines for nuclear cardiology
procedures, part 2. American Society of Nuclear Cardiology. J Nucl Cardiol. 1999 Mar–Apr;6[2]‌:G47–84. Used with permission.)

83
 84 • S ection I I : C linical A pplications and C ase S tudies

CASE 6A

Figure 6.2 Short-axis late gadolinium-enhancement images at the base (A), mid ventricle (B), and apex (C) show transmural enhancement (high
signal intensity) in the anterior wall, septum, and apex (arrows)—a distribution typical of an LAD territory myocardial infarction. Low signal
intensity in the subepicardial myocardium signifies regions of microvascular obstruction. D, Short-axis dynamic perfusion image shows decreased
signal in the anterior wall and septum (arrowhead) consistent with decreased or absent perfusion in this region.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
I N FA RC T ION I N VA RY I NG
C A R DI AC T E RR I TO R I E S
I N FA RC T CH A R AC T E R I S T IC S : L E F T
A N T E R IOR DE S C E N DI NG A RT E RY
T E R R I TORY, T R A NS M U R A L
E X T E N T W I T H M IC ROVA S C U L A R
OB S T RUC T ION
Clinical History and Presentation
A 57-year-old man sought care at his local emergency depart-
ment after having chest pain of several hours’ duration while
working on his farm. Electrocardiography upon arrival
showed ST-segment elevation, and he was transferred for
cardiac catheterization. A proximal left anterior descending
coronary artery (LAD) occlusion was identified and treated.
Clinical Question
Cardiac MRI (Figure 6.2) was performed the next day to
assess for viability and evaluate the extent of infarction for
prognosis.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
Imaging Findings
The images obtained demonstrated late gadolinium
enhancement in the anterior wall, septum, and apex of the
left ventricle (LV) on postcontrast images—a distribution
typical of an LAD territory myocardial infarction. Within
the late gadolinium enhancement, an area of low signal
intensity was present in the myocardium due to microvascu-
lar obstruction (MVO). A perfusion defect was also noted in
the anterior wall and septum on dynamic perfusion images.
Akinesis was present in the anterior wall, septum, and apex
on cine balanced steady-state free precession (SSFP) images
(not shown).
85
Summary
After confirmation of the extent of the ST-segment eleva-
tion myocardial infarction on MRI, the patient underwent
pharmacologic management of his hyperlipidemia and
hypertension. Follow-up imaging studies demonstrated no
improvement in the function of the myocardium where the
MVO was present.
Outcomes after a myocardial infarction depend on sev-
eral factors, including age and time to reperfusion, which is
related to infarction size and ejection fraction. Assessment
of the infarction size and ejection fraction can be completed
in a single study with cardiac MRI. During the administra-
tion of gadolinium contrast, a dynamic first-pass sequence can
demonstrate myocardial perfusion defects in regions of myo-
cardium with decreased or absent blood flow. The amount
of viable myocardium and infarction size has important
prognostic information for recovery of function and risk of
arrhythmia post infarction.
Late gadolinium-enhancement images have a key role
in the evaluation of patients with ischemic heart disease.
Infarcted myocardium, in both the acute and chronic stages,
has been shown to take up gadolinium-based contrast
agents to a greater degree than normal myocardium on late
gadolinium-enhancement images. This allows the extent of
infarcted myocardium (eg, nontransmural vs transmural) to
be determined. Contrast uptake by noninfarcted but isch-
emic myocardium is normal on late gadolinium-enhancement
images. Infarcted regions can also be seen on triple inversion
images as bright areas, indicating edema.
MVO is due to lack of blood flow through microvessels
in the heart and can occur even when epicardial coronary
artery patency has been reestablished. The cause of obstruc-
tion may be local tissue injury, inflammation and edema,
microvascular embolism, or any combination of these. With
late gadolinium-enhancement images, MVO appears as
an area with absent gadolinium uptake (black), often sur-
rounded by infarcted, avidly enhancing tissue. The presence
of MVO has been shown to be a predictor of poor func-
tional recovery in the affected area and poor outcomes after
infarction.
 86 • S ection I I : C linical A pplications and C ase S tudies

CASE 6B

Figure 6.3 Short-axis late gadolinium-enhancement images at the base (A), mid ventricle (B), and apex (C) show subepicardial enhancement (high
signal intensity) in the lateral wall at the base and mid ventricle (arrows) with sparing of the apex—a distribution typical of a circumflex territory
myocardial infarction. D, Short-axis, T2-weighted, fat-suppressed, black blood image from the mid ventricle shows increased signal in the LV lateral
wall consistent with edema (arrowhead).
 6 . M yoca r dial I sc h emia and I n fa r ction  •
I N FA RC T
CH A R AC T E R I S T IC S : S U BE PIC A R DI A L
A N D C I RC U M F L E X A RT E RY
T E R R I TOR I E S
Clinical History and Presentation
A 44-year-old man sought care at the emergency depart-
ment for intermittent chest pain of 2 days’ duration.
Electrocardiography showed ST-segment depression. The
patient had recurrent symptoms despite optimal medical
management. Cardiac catheterization was performed, and a
stent was placed to open an occluded left circumflex coronary
artery.
Clinical Question
Cardiac MRI (Figure 6.3) was performed 2 days after the
catheterization to evaluate the extent of infarction.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
Imaging Findings
Subendocardial myocardial enhancement was present
in the lateral wall at the base and mid ventricle on late
gadolinium-enhancement images—a distribution typical of
a nontransmural circumflex territory myocardial infarction.
Increased myocardial signal was also present in the lateral
wall on T2-weighted fat-suppressed (triple inversion recov-
ery) images, which was consistent with edema.
87
Summary
After confirmation of the size and extent of the myocardial
infarction by MRI, the patient subsequently underwent cardiac
rehabilitation and pharmacologic therapy for dyslipidemia.
Myocardial infarction spreads transmurally from the
endocardium to the epicardium, and the extent of wall thick-
ness involved depends on the severity of the ischemic insult.
In myocardial infarction, the myocardial enhancement on
late gadolinium-enhancement images always involves the
subendocardial layer. If myocardial enhancement does not
involve the subendocardial layer, a nonischemic myocardial
disease, such as myocarditis, must be considered as the cause
of the enhancement.
For patients with chronic ischemic heart disease who are
being considered for revascularization, cardiac MRI is an
accurate way to determine myocardial viability. Segments
with decreased function with no myocardial enhancement, or
with enhancement involving less than 25% of the wall thick-
ness, on myocardial late gadolinium-enhancement images
have a high probability of improved function after revascular-
ization. Conversely, the probability of functional recovery of
a segment decreases with increasing extent of mural enhance-
ment on late gadolinium-enhancement images.
In acute ischemic insults, similar data can be inferred by
the total amount of scar tissue present, which has been shown
to be a predictor of recovery of ejection fraction after an acute
myocardial infarction. In addition, the volume of late gado-
linium enhancement provides prognostic information about
the amount of recovery of ejection fraction after infarction.
Myocardial salvage is defined as the difference between the
actual and potential infarction size, the latter defined as the
initial area at risk during acute coronary occlusion. This is
calculated by determining the volume difference between the
edematous region and scar tissue.
 88 • S ection I I : C linical A pplications and C ase S tudies

CASE 6C

Figure 6.4 Short-axis late gadolinium-enhancement images at the base (A), mid ventricle (B), and apex (C) demonstrate transmural enhancement
(high signal intensity; arrows) in the inferior septum and inferior wall at the base and mid ventricle with sparing of the apex—a distribution
typical of a right coronary artery territory myocardial infarction. Late gadolinium enhancement is also present in the right ventricular free wall. D,
Midventricular, short-axis, T2-weighted, fat-suppressed, black blood image showing increased signal (arrowhead) in the same territory, consistent
with edema. High signal in the pericardial space is due to a pericardial effusion.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
I N FA RC T CH A R AC T E R I S T IC S : R IG H T
C ORON A RY A RT E RY T E R R I TORY,
T R A N S M U R A L I N FA RC T ION
W I T H M VO, E DE M A , A N D R IG H T
V E N T R IC U L A R I N FA RC T ION
Clinical History and Presentation
A 72-year-old woman sought care from her primary
care provider for a 3-day history of shortness of breath.
Electrocardiography showed ST-segment elevation. She
was referred for cardiac catheterization, which identified an
occluded mid right coronary artery that was opened with
angioplasty.
Clinical Question
Cardiac MRI (Figure 6.4) was performed the next day to
assess for viability and evaluate the extent of infarction for
prognosis.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
Imaging Findings
On late gadolinium-enhancement images, transmural myo-
cardial enhancement was present in the inferior wall and
inferior septum at the base and mid ventricle of the LV and
in the inferior wall of the right ventricle—a distribution typi-
cal of a transmural right coronary artery territory myocar-
dial infarction. A small region of subendocardial MVO was
noted in the inferior wall at the base. Increased myocardial
89
signal was present in the inferior wall and inferior septum on
T2-weighted, fat-suppressed (triple inversion recovery), black
blood images, which was consistent with edema. Akinesis was
present in the same territory on cine images. A small pericar-
dial effusion was also present.
Summary
As a result of the MRI findings indicating the extent of the
myocardial infarction, a course of outpatient cardiac rehabili-
tation and counseling regarding lifestyle changes, including
smoking cessation, was initiated.
T2-weighted (“edema-weighted”) imaging identifies
regions of myocardium with increased water content (edema).
In ischemic heart disease, myocardial T2 signal intensity can
increase within 30 minutes of onset of ischemia. In acute coro-
nary syndromes, myocardium with increased T2 signal, in the
absence of late gadolinium enhancement, indicates the area of
salvaged myocardium—that is, the area that would have been
infarcted if the artery was not opened quickly. This indicates
the area at risk for infarction that benefitted the most from
intervention.
In acute myocardial infarction, cine images (eg, cine
balanced SSFP images) provide detailed images of cardiac
motion with relatively high temporal resolution. These
sequences are important in the MRI evaluation of patients
with acute ischemic heart disease, since assessment of
cardiac function is a core measure required post myocar-
dial infarction. Wall-motion abnormalities may indicate
infarcted, stunned, or hibernating myocardium; these can
be distinguished using cardiac MRI. In addition, ventric-
ular volumes and ejection fraction can also be measured
from cine images and used for prognosis and therapeutic
decision making.
 90 • S ection I I : C linical A pplications and C ase S tudies

CASE 6D

Figure 6.5 End-systolic (A) and end-diastolic (B) balanced SSFP long-axis images show paradoxical outpouching of the apical anterior wall during
systole with a wide neck, consistent with a true aneurysm. C, A thin enhancing wall is present on the late gadolinium-enhancement image. All 3
myocardial layers were believed to be intact. Low signal intensity along the endocardial surface of the aneurysm on the balanced SSFP images and
the late gadolinium-enhancement image is consistent with mural thrombus.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
A N E U RY S M W I T H T HROM BUS
T RU E A N EU RY S M
Clinical History and Presentation
A 48-year-old woman with a history of coronary artery dis-
ease sought care from her cardiologist for episodic chest pain
and heart failure symptoms. Prior treatments included angio-
plasty and stenting of the LAD.
Clinical Question
Cardiac MRI (Figure 6.5) was performed to evaluate cardiac
function.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
Imaging Findings
The apical anterior wall was noted to be thinned on all
sequences, with paradoxical outpouching of this wall dur-
ing systole seen on the balanced SSFP cine images. Abnormal
91
enhancement on late gadolinium-enhancement images was
also seen. These findings are consistent with a myocardial
infarction with true aneurysm formation. A small area of low
signal intensity in the ventricular cavity was seen on balanced
SSFP images and late gadolinium-enhancement images,
which is consistent with mural thrombus.
Summary
After confirmation of the extent of myocardial infarction by
MRI, the patient continued to have shortness of breath and
chest discomfort. The patient underwent coronary artery
bypass grafting surgery of 3 coronary arteries and resection of
the LV apical aneurysm.
An LV true aneurysm results from ventricular remodel-
ing after an infarction that leads to an abnormal contour with
either dyskinetic or paradoxical wall motion (ie, bulges out-
ward during systole). True aneurysms typically have a wide
neck and encompass all 3 myocardial layers. They typically
grow slowly and have a low probability of rupture compared
with pseudoaneurysms. A pseudoaneurysm, in contrast, is
narrow necked (acting more like a contained myocardial rup-
ture), is thought to have a high risk of rupture, and typically
is treated surgically. All aneurysms are associated with an
increased incidence of thrombus formation.
 92 • S ection I I : C linical A pplications and C ase S tudies

CASE 6E

Figure 6.6 Long-axis balanced SSFP (A) and late gadolinium-enhancement (B) images show transmural infarction at the apex with focal disruption
of the myocardium at the apex consistent with a false aneurysm (pseudoaneurysm). Laminated thrombus (low signal intensity) is present at the apex
and extends through the defect into the false aneurysm. Note the narrow neck of the false aneurysm.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
FA L S E A N EU RY S M
Clinical History and Presentation
An 81-year-old man with a several-week history of dyspnea
on exertion and decreasing exercise tolerance was referred for
cardiac MRI. The patient had severe LAD stenosis on a recent
cardiac catheterization.
Clinical Question
Cardiac MRI (Figure 6.6) was ordered to evaluate myocardial
function (ie, ejection fraction).
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
Imaging Findings
Myocardial enhancement consistent with a transmural
infarction was present at the apex on all myocardial late
gadolinium-enhancement images. A small focal area of
myocardial disruption with a narrow neck consistent with
93
a false aneurysm (pseudoaneurysm) was present in the
infarcted region. A laminated thrombus extended from
the apex through the myocardial defect into the contained
rupture. Quantitative analysis of short-axis cine balanced
SSFP images identified decreased systolic function, with an
LV ejection fraction of 30%. The right ventricle was deter-
mined to be of normal size and function, with an ejection
fraction of 47%.
Summary
After identification and measurement of the myocardial
infarction and identification of the pseudoaneurysm from the
MRI examination, the patient underwent surgical repair of
the aneurysm and coronary artery bypass grafting.
A false aneurysm (pseudoaneurysm) is a contained myo-
cardial rupture. This occurs in the acute or subacute setting
after an infarction when weakened myocardium ruptures
but is contained by overlying adherent pericardium. Over
time this may grow and eventually rupture. As opposed to
true aneurysms, false aneurysms are often treated surgically
because of the higher risk of rupture. False aneurysms typi-
cally have a narrow neck, compared with the wide neck typi-
cally seen with true aneurysms.
 94 • S ection I I : C linical A pplications and C ase S tudies

CASE 6F

Figure 6.7 Short-axis balanced SSFP images at the base in end diastole (A) and end systole (B) show a markedly dilated LV (end-diastolic volume,
405 mL) and poor systolic function (ejection fraction, 14%). The best-preserved systolic function was in the lateral wall. The myocardium was
thinned, most prominently in the anterior wall. Short-axis late gadolinium-enhancement images at the base (C) and mid ventricle (D) show areas of
transmural and nontransmural enhancement involving large areas of the myocardium, consistent with infarction.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
I S C H E M IC C A R DIOM YOPAT HY
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 44-year-old man with a history of congestive heart fail-
ure was admitted to the hospital with worsening dyspnea.
Cardiac catheterization was performed, which showed severe
obstructive coronary artery disease predominantly involving
the LAD and right coronary arteries and branches.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 6.7) was performed to evaluate cardiac
function and myocardial viability.
C A R DI AC M R I PROTO C OL
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
I M AG I NG F I N DI NG S
Balanced SSFP cine images showed a severely dilated LV
(end-diastolic volume, 405 mL) with severely decreased LV
ejection fraction (14%), akinesis, and myocardial thinning
of the anterior wall. Late gadolinium-enhancement images
showed areas of transmural and nontransmural myocardial
enhancement in an ischemic pattern, predominantly involv-
ing the anterior, septal, inferior, and apical walls, with relative
sparing of the lateral wall.
95
S U M M A RY
After confirmation and quantification of the extent of myo-
cardial infarction and bilateral heart failure by MRI, medical
management was instituted. Subsequent evaluations by echo-
cardiography indicated a slow recovery of heart function over
time.
After a myocardial infarction, some degree of LV dys-
function is expected, and the degree of dysfunction usually
correlates with the extent and location of myocardial injury.
With multiple or large myocardial infarctions, global LV
function can become markedly decreased, and LV remodel-
ing can occur with resultant dilatation of the LV cavity. This
condition of a dilated LV with decreased function is termed
ischemic cardiomyopathy. The use of gadolinium in these
patients is important in the search for evidence of an ischemic
enhancement pattern to distinguish ischemic from nonisch-
emic dilated cardiomyopathy, which can be difficult.
In chronic ischemic heart disease, cardiac MRI can accu-
rately determine myocardial viability without the need for
radiation exposure. Segments with decreased function with-
out late gadolinium enhancement, or with enhancement
involving less than 25% of the wall thickness, have a high
probability (>80%) of improved function after revasculariza-
tion. Conversely, the probability of functional recovery for a
segment decreases with increasing mural extent of enhance-
ment on late gadolinium-enhancement images. That is, dys-
functional myocardial segments without late gadolinium
enhancement indicate viable myocardium and those with
dysfunction and transmural late gadolinium enhancement
indicate nonviable myocardium.
 96 • S ection I I : C linical A pplications and C ase S tudies

CASE 6G

Figure 6.8 LV outflow tract balanced SSFP images at end systole (A) and diastole (B) identify severe akinesis of the LV anterior wall in an LAD
distribution pattern (arrows). C, Late gadolinium enhancement in a 4-chamber view shows no significant areas of infarction (arrowhead), which
indicates viable myocardium. D, Fat-suppressed, T2-weighted, black blood image shows hyperintense signal in the LV anterior wall, identifying
edema in an LAD distribution. This represents an example of completely salvaged myocardium—a large area of edema without infarction in the
LAD territory.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
I S C H E M IC C A R DIOM YOPAT HY
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 51-year-old woman sought care at the emergency depart-
ment for acute-onset dyspnea of 20 minutes’ duration. She
had a history of hypertension and was an active smoker.
Electrocardiography revealed ST-segment elevation. Cardiac
catheterization identified a proximal LAD occlusion.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 6.8) was ordered to evaluate the extent
of infarction and assess viability for prognosis.
C A R DI AC M R I PROTO C OL
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78).
I M AG I NG F I N DI NG S
Thinning of the LV free wall was seen during end systole and
end diastole. No subendocardial late gadolinium enhance-
ment was seen, but an area of edema was noted. This distribu-
tion is typical of LAD territory stenosis without evidence of
97
myocardial infarction. Increased myocardial signal was seen
in the anterior wall on T2-weighted fat-suppressed images,
consistent with edema.
S U M M A RY
After MRI, the patient was informed regarding the success
of the cardiac catheterization procedure and the absence of
permanent myocardial injury (ie, infarction). The overall
prognosis for this patient is excellent. Postimaging treatment
included initiation of conventional pharmacologic therapy.
For patients with chronic ischemic heart disease, and in
the acute phase after an infarction, cardiac MRI is an accu-
rate way to determine myocardial viability and prognostic
information, on the basis of the amount of scar tissue present.
The amount of infarction present is also a predictor of myo-
cardial functional recovery. In addition, MRI can be used to
determine myocardial salvage—the area that would have been
infarcted if not for the intervention (potential vs actual infarc-
tion), or the amount of muscle saved by rapid intervention on
the occluded vessel. Myocardial salvage is calculated as the
difference between the volume of edema and the volume of
scar tissue; currently many research studies are using this as a
marker to determine successful interventions. In this case, the
entire amount was salvaged myocardium, which shows the
importance of rapid intervention. Follow-up imaging indi-
cated complete resolution of the wall-motion abnormality.
 98 • S ection I I : C linical A pplications and C ase S tudies

CASE 6H

Figure 6.9 Midventricular stress (A) and resting (B) perfusion short-axis images show normal perfusion, which indicates no inducible ischemia. C,
Corresponding late gadolinium-enhancement image shows no areas of enhancement to indicate prior myocardial infarction.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
PH A R M AC OL O G IC S T R E S S
T E S T I NG
NOR M A L R E S U LT S
Clinical History and Presentation
A 76-year-old man with a recent diagnosis of pelvic chondro-
sarcoma and a history of diabetes mellitus, hyperlipidemia,
and intermittent chest pain was referred initially for stress
echocardiography for preoperative evaluation. Diagnostic
echocardiographic images, however, could not be obtained.
Clinical Question
Adenosine stress MRI (Figure 6.9) was ordered for preopera-
tive evaluation because of unsuccessful completion of exercise
stress echocardiography.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78). The perfusion sequence is performed during admin-
istration of adenosine and at rest.
Imaging Findings
No perfusion abnormalities were present on either stress
or resting dynamic perfusion sequences. No regional
wall-motion abnormalities on balanced SSFP cine images
99
at rest (not shown) or myocardial enhancement on late
gadolinium-enhancement images were present. The study was
considered normal with no evidence of inducible ischemia or
infarction.
Summary
Because cardiac function and MRI findings were normal,
including no evidence of ischemia, no further therapies were
initiated.
Cardiac stress testing can be performed with cardiac
MRI using either exercise or vasodilator (eg, adenosine,
regadenoson) or inotropic (eg, dobutamine) pharmacologic
stress agents. Exercise usually consists of the patient riding a
special MRI-compatible recumbent bicycle during scanning.
Exercise cardiac MRI using a treadmill has been described
but is not used in most institutions. Stress testing with cardiac
MRI has similar sensitivity and specificity as other noninva-
sive stress tests such as stress echocardiography and nuclear
stress testing.
With stress testing using dobutamine or exercise, cine
bright blood images (eg, balanced SSFP images) are acquired
at rest and during dobutamine infusion or exercise. Infarcted
myocardial segments will have wall-motion abnormali-
ties at rest and with stress. Ischemic myocardial segments
have normal wall motion at rest but develop wall-motion
abnormalities with dobutamine infusion or exercise. Late
gadolinium-enhancement images are also performed to evalu-
ate for areas of infarction and peri-infarct ischemia.
 100 • S ection I I : C linical A pplications and C ase S tudies

CASE 6I

Figure 6.10 Dynamic perfusion short-axis images from the mid ventricle show a subepicardial perfusion defect in the anteroseptum and anterior
wall (arrows) on both stress (A) and resting (B) images, consistent with myocardial infarction in these segments. C and D, Corresponding late
gadolinium-enhancement images show subepicardial enhancement in the same distribution (arrowheads), confirming prior myocardial infarction.
 6 . M yoca r dial I sc h emia and I n fa r ction  •
F I N DI NG S OF I N FA RC T ION
Clinical History and Presentation
A 65-year-old man with known coronary artery disease and
prior stenting of the proximal LAD after a myocardial infarc-
tion sought care for recurrent chest pain with exertion.
Clinical Question
Adenosine stress MRI (Figure 6.10) was ordered to evaluate
for inducible ischemia.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78). The perfusion sequence is performed during admin-
istration of adenosine and at rest.
Imaging Findings
An anteroseptal and anterior wall perfusion defect was pres-
ent on the dynamic perfusion images obtained both dur-
ing adenosine infusion (stress images) and at rest. There was
101
associated nontransmural myocardial enhancement on late
gadolinium-enhancement images in the anteroseptal and
anterior walls, along with hypokinesis of these segments on
balanced SSFP cine images. The study was considered positive
for nontransmural myocardial infarction in the anteroseptal
and anterior walls but negative for inducible ischemia.
Summary
The results of stress MRI confirmed the presence of a prior
myocardial infarction without evidence of peri-infarct isch-
emia. The patient’s condition was managed medically.
With vasodilator stress testing, dynamic myocardial per-
fusion imaging is performed using intravenous gadolinium
both during administration of the stress agent (eg, adenosine)
and at rest. Infarcted myocardial segments have decreased
perfusion at rest and with stress. The perfusion defect may be
less visible on the resting images compared with stress images
because of late enhancement in the infarcted myocardium
from the prior stress injection. An infarction will be present
on late gadolinium-enhancement images. Resting perfusion
defects extending beyond the infarcted areas represent peri-
infarct ischemia.
 102 • S ection I I : C linical A pplications and C ase S tudies

CASE 6J

Figure 6.11 Midventricular dynamic perfusion short-axis images showing a subepicardial perfusion defect in the anterior wall (arrow) with stress
(A) and normal perfusion at rest (B), indicating inducible ischemia in this segment. C, Corresponding late gadolinium-enhancement image without
evidence of enhancement to indicate prior myocardial infarction.
 6 . M yoca r dial I sc h emia and I n fa r ction  • 103

F I N DI NG S OF I S CH E M I A enhancement on late gadolinium-enhancement images were

Clinical History and Presentation
A 79-year-old man with known coronary artery disease discov-
ered on prior cardiac catheterization sought care from his pri-
mary care provider for a several-month history of chest pain.
Clinical Question
Adenosine stress MRI (Figure 6.11) was ordered to evaluate
for inducible ischemia and viability.
Cardiac MRI Protocol
Use Myocardial Ischemia & Infarction Protocol 5.1 (see
page 78). The perfusion sequence is performed during admin-
istration of adenosine and at rest.
Imaging Findings
An anterior wall perfusion defect was present on the
dynamic perfusion images obtained during adenosine infu-
sion (stress images). No perfusion defect was present on the
resting dynamic perfusion image. No regional wall-motion
abnormalities on balanced SSFP cine images or myocardial
noted. The study was considered positive for inducible ante-
rior wall ischemia with no evidence of myocardial infarction.
Summary
Adenosine stress MRI revealed myocardial ischemia with
severe coronary stenosis at cardiac catheterization. With vaso-
dilator stress testing, dynamic myocardial perfusion imag-
ing is performed using intravenous gadolinium both during
administration of the stress agent (eg, adenosine) and at rest.
Two injections of gadolinium contrast must be administered
for this type of study. Typically, the stress images are acquired
before the resting images so that stress-induced defects will not
be obscured by a prior administration of gadolinium. Ischemic
myocardial segments have normal perfusion at rest and
decreased perfusion with stress. Late gadolinium-enhancement
images, acquired after the perfusion images, will show no
infarction. Functional (cine) imaging can also be performed to
evaluate for wall-motion abnormalities.
A schematic representation of a protocol for chemical
stress testing using the vasodilator adenosine is shown in
Figure 6.12 and describes the timeline of events that can be
performed in a “typical” stress MRI examination.

Figure 6.12 Protocol for performing chemical stress testing for the diagnosis of coronary artery disease by means of cardiac MRI. Imaging
modules and sequences are described in Chapter 5. Times listed represent approximate values. The 3 rows identify the sequence of events typically
performed during a pharmacologic stress MRI test. (Adapted from Kim HW, Klem I, Kim RJ. Detection of myocardial ischemia by stress perfusion
cardiovascular magnetic resonance. Magn Reson Imaging Clin N Am. 2007 Nov;15[4]‌:527–40. Used with permission.)
 104 • S ection I I : C linical A pplications and C ase S tudies
S UG G E S T E D R E A DI N G
Aneurysm With Thrombus
Kumbasar B, Wu KC, Kamel IR, Lima JA, Bluemke DA. Left ventricular
true aneurysm: diagnosis of myocardial viability shown on MR imag-
ing. AJR Am J Roentgenol. 2002 Aug;179(2):472–4.
Infarct Characteristics: Left Anterior Descending Artery
Territory, Transmural Extent With Microvascular Obstruction
Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, et al.
Relationship of MRI delayed contrast enhancement to irreversible
injury, infarct age, and contractile function. Circulation. 1999 Nov
9;100(19):1992–2002.
Wu KC, Zerhouni EA, Judd RM, Lugo-Olivieri CH, Barouch LA,
Schulman SP, et al. Prognostic significance of microvascular obstruc-
tion by magnetic resonance imaging in patients with acute myocar-
dial infarction. Circulation. 1998 Mar 3;97(8):765–72.
Infarct Characteristics: Right Coronary Artery Territory,
Transmural Infarction With MVO, Edema, and Right
Ventricular Infarction
Raman SV, Simonetti OP, Winner MW 3rd, Dickerson JA, He X,
Mazzaferri EL Jr, et al. Cardiac magnetic resonance with edema
imaging identifies myocardium at risk and predicts worse outcome in
patients with non-ST-segment elevation acute coronary syndrome. J
Am Coll Cardiol. 2010 Jun 1;55(22):2480–8.
Infarct Characteristics: Subepicardial and
Circumflex Artery Territories
Selvanayagam JB, Kardos A, Francis JM, Wiesmann F, Petersen SE,
Taggart DP, et al. Value of delayed-enhancement cardiovascular mag-
netic resonance imaging in predicting myocardial viability after sur-
gical revascularization. Circulation. 2004 Sep 21;110(12):1535–41.
Epub 2004 Sep 7.
Ischemic Cardiomyopathy
Nagel E, Lehmkuhl HB, Bocksch W, Klein C, Vogel U, Frantz E, et al.
Noninvasive diagnosis of ischemia-induced wall motion abnormali-
ties with the use of high-dose dobutamine stress MRI: comparison
with dobutamine stress echocardiography. Circulation. 1999 Feb
16;99(6):763–70.
Sakuma H, Suzawa N, Ichikawa Y, Makino K, Hirano T, Kitagawa K, et al.
Diagnostic accuracy of stress first-pass contrast-enhanced myocardial
perfusion MRI compared with stress myocardial perfusion scintigra-
phy. AJR Am J Roentgenol. 2005 Jul;185(1):95–102.
 7.
NONISCHEMIC MYOCAR DI A L DISEASE
Nila J. Akhtar, MD, Matthew W. Martinez, MD, and Eric E. Williamson, MD
C
ardiomyopathies are a heterogeneous group of car-
diac diseases that are either ischemic (see Chapter
6) or nonischemic. Nonischemic myocardial disease
includes but is not limited to dilated cardiomyopathy (DCM),
hypertrophic cardiomyopathy (HCM), infiltrative cardiomy-
opathy, and arrhythmogenic right ventricular (RV) cardiomy-
opathy/dysplasia, to name a few (Figure 7.1). Some etiologies
are chronic, whereas others may be transient, such as viral-
induced DCMs or the so-called ballooning syndromes (eg,
apical ballooning cardiomyopathy).
As with other cardiac diseases, cardiac magnetic reso-
nance imaging (MRI) provides information on regional
and global myocardial dysfunction, edema, and fibrosis
in the left and right ventricles. It also can visualize ana-
tomic features including abnormal trabecular patterns,
wall thinning, and hypertrophy. In this chapter, we
introduce and describe the most commonly encountered
nonischemic cardiomyopathies and their associated MRI
characteristics.
H Y PE RT ROPH IC
C A R DIOM YOPAT H Y
HCM is defined as myocardial hypertrophy in the absence of
an identifiable cause to account for the degree of myocardial
hypertrophy. Excluding other causes of hypertrophy—such as
long-standing severe hypertension, Fabry disease, and amy-
loid heart disease—is critical before confirming the clinical
diagnosis of HCM. HCM primarily affects the left ventricle
(LV) but can also involve the RV. HCM is the most common
genetic nonischemic cardiomyopathy and the most common
genetic cardiovascular disorder. Numerous genes are known
to cause HCM, with hundreds of associated mutations.
Inheritance is autosomal dominant with variable penetrance
and phenotypic expression.
The clinical presentation of HCM ranges from asymp-
tomatic to symptomatic; symptoms may include exertional
dyspnea, fatigue, palpitations, presyncope, syncope, or sudden
cardiac death. Symptoms can vary widely and are not depen-
dent on the degree of hypertrophy present. Pathophysiologic
mechanisms for symptoms include diastolic dysfunction and
105
left ventricular outflow tract (LVOT) obstruction with asso-
ciated mitral valve regurgitation, which is present in up to
60% of patients with HCM.
Cardiac MRI is used to assess the maximum myocar-
dial thickness in patients with HCM, along with the mor-
phology and distribution of hypertrophy, before surgical
or interventional treatment. It can detect the presence of
both LVOT obstruction and mitral valve regurgitation,
which are identified by turbulence-related signal flow
void. However, the severity of mitral regurgitation cannot
be judged by the subjective degree of the signal flow void
because it is highly dependent on sequence parameters
and the imaging plane. Cardiac MRI is rarely used to mea-
sure the LVOT pressure gradient because of the difficulty
in both obtaining an imaging plane perpendicular to the
outflow tract flow for phase-contrast imaging and assess-
ing gradients during provocative maneuvers. The nonin-
vasive reference standard for determining the presence
and severity of LVOT obstruction is echocardiography.
There are 4 morphologic HCM subtypes: sigmoid,
reverse curve, apical, and neutral (Figure 7.2). Distinction
of the 4 subtypes is important clinically because the type
of HCM is closely related to the presence or absence of
HCM-related genetic mutations. MRI is an important
complementary imaging modality to echocardiography for
assessment of HCM because it better depicts HCM mor-
phology owing to its larger field of view, higher spatial reso-
lution, and excellent tissue contrast. Echocardiography may
underestimate the degree of hypertrophy when compared
with MRI, which may affect disease management. In addi-
tion, a finding of myocardial fibrosis on MRI is an emerging
risk factor that may help predict which patients are at risk
for sudden cardiac arrest.
Septal hypertrophy is the most common distribution of
hypertrophy in HCM. This can be either the sigmoid mor-
phologic subtype or the reverse curve morphologic subtype.
The sigmoid subtype has a characteristic asymmetric basal
septal myocardial hypertrophy, which results in a promi-
nent basal septal convexity. The remainder of the septum is
predominantly concave to the LV cavity. The reverse curve
morphologic subtype has a crescent-shaped septum, which
is predominantly convex to the LV cavity. This is the classic
 106 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

Figure 7.1 Classification and subtypes of nonischemic myocardial disease in relation to all myocardial diseases. (Data from Maron BJ, Towbin JA,
Thiene G, Antzelevitch C, Corrado D, Arnett D, et al; American Heart Association; Council on Clinical Cardiology, Heart Failure and
Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary
Working Groups; Council on Epidemiology and Prevention. Contemporary definitions and classification of the cardiomyopathies: an American
Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care
and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology
and Prevention. Circulation. 2006 Apr 11;113[14]:1807–16. Epub 2006 Mar 27.)

morphology most often associated with HCM. The reverse
curve subtype is most commonly associated with genetic
mutations known to cause HCM.
The apical morphologic subtype has characteristic apical
myocardial hypertrophy. There may be an associated “apical
pouch,” which occurs when the very tip of the apex develops
a thinned portion and may contain an apical LV thrombus.
This finding is often associated with myocardial fibrosis and
has been shown to be associated with adverse cardiovascular
events.
The neutral morphologic subtype has a uniform or
nearly uniform hypertrophy involving all the myocardial
walls. This subtype is often difficult to distinguish from
hypertension-induced hypertrophy or changes related to elite
athletic performance. The following cases highlight these dif-
ferent types of HCM.
 7.  No n ischemic M yocardia l D isease  • 107

Figure 7.2 Four-chamber, balanced (SSFP) images in end diastole show the 4 morphologic subtypes of HCM: sigmoid (A), reverse curve (B), apical
(C), and neutral (D), along with corresponding stylized examples. Each subtype has been described as being more likely to be associated with genetic
mutations. “Gene +” indicates the percentage of patients with each subtype who have a myofilament mutation, one type of mutation associated with
HCM. (Adapted from Binder J, Ommen SR, Gersh BJ, Van Driest SL, Tajik AJ, Nishimura RA, et al. Echocardiography-guided genetic testing in
hypertrophic cardiomyopathy: septal morphological features predict the presence of myofilament mutations. Mayo Clin Proc. 2006 Apr;81[4]‌:459–
67. Used with permission of Mayo Foundation for Medical Education and Research.)
 108 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

C A S E 7A

Figure 7.3 Reverse curve HCM. A, Three-chamber balanced SSFP image showing reverse curve septal hypertrophy (arrowhead) characteristic of
HCM, and LVOT obstruction with resultant mitral valve regurgitation identified by the presence of a posteriorly directed regurgitant jet (arrow)
into the left atrium. B, Late gadolinium-enhancement 3-chamber view showing abnormal enhancement patterns throughout the LV (arrow). C
and D, Midventricular, short-axis, balanced SSFP images at end systole (C) and end diastole (D). E, Short-axis perfusion image showing diffuse
subepicardial and midmyocardial enhancement of the myocardium along the anteroseptal and inferoseptal segments of the LV (arrow). F, Late
gadolinium-enhancement image showing patchy subepicardial and midmyocardial enhancement in the corresponding segments.
 7.  No n ischemic M yocardia l D isease  •
R E V E R S E C U RV E HC M
Clinical History and Presentation
A 40-year-old man who had received a diagnosis of HCM
6 years earlier sought care for worsening symptoms,
including chest pains, dyspnea, palpitations, and fatigue.
Echocardiography revealed increased LV wall thickening and
resting LVOT obstruction despite maximal medical therapy.
Clinical Question
MRI (Figure 7.3) was ordered to assess the extent of hypertro-
phy preoperatively and to look for the presence of myocardial
fibrosis.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced steady-state free precession (SSFP) LVOT stack.
Imaging Findings
The key MR images indicated a diagnosis of HCM with
LVOT obstruction and myocardial fibrosis. Balanced SSFP
images identified reverse-curve septal hypertrophy charac-
teristic of HCM and increased thickening of the LV with
109
a maximum diastolic septal thickness of 37 mm. Cine bal-
anced SSFP images demonstrated systolic anterior motion
(SAM) of the mitral valve apparatus with LVOT obstruc-
tion and posteriorly directed mitral regurgitation. LVOT
obstruction and mitral valve regurgitation were indicated
by the presence of a regurgitant jet in the left atrium and
flow turbulence with SAM in the LVOT. Late gadolinium-
enhancement images demonstrated abnormal enhancement
patterns throughout the LV septum in a nonischemic pat-
tern. Quantitative assessment of the short-axis cine images
showed a normal LV ejection fraction of 75%. Short-axis,
first-pass, perfusion images showed early enhancement of
the myocardium along the septum of the LV.
Summary
The patient had continued symptoms despite optimal medical
therapy. MRI findings confirmed severe LVOT obstruction
with massive LV hypertrophy and myocardial fibrosis. The
patient was recommended for surgical myectomy and place-
ment of an implantable cardioverter-defibrillator (ICD).
The reverse curve morphologic subtype has a
crescent-shaped septum, which is predominantly convex to
the LV cavity. This is the classic morphology that is most often
associated with HCM. Patients with the reverse curve mor-
phologic subtype most commonly have a genetic mutation
known to cause HCM.
 110 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7B

Figure 7.5 Another example of sigmoid HCM in a different patient.

Figure 7.4 Sigmoid HCM with SAM of the mitral valve. A and
B, Three-chamber (A) and short-axis (B) balanced SSFP images
in end diastole demonstrating asymmetric LV basal anteroseptal
hypertrophy. C, Three-chamber balanced SSFP image in systole shows
hypointense signal flow void in the LVOT (arrow). SAM of the mitral
valve apparatus is seen, along with posteriorly directed mitral valve
regurgitation (arrowhead).
Balanced SSFP 3-chamber images of the LVOT before (A) and after (B)
myectomy in a patient with an initial diagnosis of neutral morphology
HCM. Before surgery, dynamic LVOT obstruction is seen, marked
by the regurgitant jet (arrow), which is no longer present after surgery.
(Adapted from Binder J, Ommen SR, Gersh BJ, Van Driest SL, Tajik
AJ, Nishimura RA, et al. Echocardiography-guided genetic testing
in hypertrophic cardiomyopathy: septal morphological features
predict the presence of myofilament mutations. Mayo Clin Proc. 2006
Apr;81[4]‌:459–67. Used with permission.)
 7.  No n ischemic M yocardia l D isease  •
S IG MOI D OB S T RUC T I V E HC M
W ITH SA M
Clinical History and Presentation
A 45-year-old man with known HCM who was maintained
on optimal medical therapy was evaluated for increasing
exertional dyspnea and light-headedness. The patient had no
obstructive coronary artery disease. Echocardiography dem-
onstrated an LVOT gradient of 31 mm Hg at rest and 92 mm
Hg with provocation. The patient was referred for surgical
septal myectomy.
Clinical Question
MRI (Figure 7.4) was ordered to assess LV morphology and
the distribution of hypertrophy before surgery.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
The MR images obtained were used to determine the diagno-
sis of a sigmoid morphologic subtype obstructive HCM with
SAM of the mitral valve. Balanced SSFP gradient echo images
in end diastole demonstrated asymmetric LV basal anterosep-
tal hypertrophy with a maximum myocardial thickness of 19
111
mm. A similar image in systole demonstrated turbulent flow
in the LVOT. SAM of the mitral valve apparatus was easily
identified, along with posteriorly directed mitral valve regur-
gitation. The presence of SAM, the contact site of the mitral
valve leaflets on the septum, and the morphology of the papil-
lary muscles are important features to describe before surgical
myectomy.
Summary
On the basis of the MRI findings, the patient underwent sur-
gical intervention for HCM. This involved an extended septal
myectomy with the goal of decreasing the severity of LVOT
obstruction. Successful myectomy widens the outflow tract,
removing the outflow obstruction.
The definitive treatment for medically refractory obstruc-
tion in HCM is septal myectomy. Surgical myectomy via aor-
totomy debulks the myocardial hypertrophy to relieve the
obstruction (Figure 7.5). In some cases, an extended myectomy
may be needed with wider excision and extension to the level
of the papillary muscles, along with reduction of the subval-
vular mitral valve apparatus. The procedure-related mortality
risk is less than 0.5%, and the combined risk of mortality and
severe complication is 1% to 2% when performed in experi-
enced centers. More than 90% of patients have considerable
symptomatic improvement with durable results.
Alcohol septal ablation is an alternative treatment to sur-
gical myectomy and is a less-invasive procedure but is usually
reserved for patients whose HCM is refractory to medical
therapy and who are not otherwise good surgical candidates.
 112 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

C A S E 7C

Figure 7.6 Sigmoid morphologic subtype obstructive HCM. A-C, Short-axis images showing abnormalities in basal anteroseptal (arrows) and
inferoseptal segments (arrowheads). Perfusion defects in these locations (A) can be seen, along with corresponding transmural enhancement, with
central nonenhancing foci in early (B) and late (C) gadolinium-enhancement images. These findings are consistent with transmural myocardial
infarction with central microvascular obstruction. D, Three-chamber balanced SSFP image in systole shows persistent hypointense signal flow in
the left atrium indicating persistent mitral regurgitation from LVOT obstruction with SAM of the mitral valve (arrow).
 7.  No n ischemic M yocardia l D isease  •
S IG MOI D OB S T RUC T I V E HC M
Clinical History and Presentation
A 73-year-old man with known HCM who was maintained
on medical therapy underwent a cardiology evaluation for
fatigue and exertional dyspnea. Echocardiography findings
included a resting LVOT gradient of 61 mm Hg. Septal reduc-
tion therapy was recommended, but surgical myectomy was
thought to be a high-risk procedure. No obstructive coronary
artery disease was identified by coronary angiography. A large
septal perforator artery that was amenable to alcohol septal
ablation was also identified.
Clinical Question
MRI (Figure 7.6) was ordered 1 week after septal myocardial
alcohol ablation to assess myocardial fibrosis and to assess for
complications of the procedure.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
MR images obtained after endovascular septal myocardial
alcohol ablation helped determine the diagnosis of sigmoid
morphologic subtype obstructive HCM. A first-pass perfu-
sion, short-axis view of the heart identified a basal anterosep-
tal and inferoseptal segmental perfusion defect. Early and
113
late gadolinium-enhancement images showed correspond-
ing transmural enhancement with central nonenhancing
foci, consistent with transmural myocardial infarction with
central microvascular obstruction. Cine balanced SSFP
images demonstrated corresponding segmental akinesis.
Balanced SSFP images of the heart in systole also showed
persistent hypointense signal flow void in the LVOT indica-
tive of turbulence and consistent with dynamic LVOT
obstruction and persistent mitral regurgitant hypointense
signal void.
Summary
Because the patient was believed to be at too high risk for surgi-
cal myectomy, alcohol ablation was offered for relief of medi-
cally refractory symptoms. No postablation complications were
identified, and the patient experienced symptomatic relief.
Alcohol septal ablation is considered as a treatment option
for relieving obstruction in selected patients with HCM with
medically refractory LVOT obstruction. The septal perforator
artery supplying the basal septal wall is injected with alcohol,
which causes a local myocardial infarction and relief of the
obstruction. Obstruction is decreased acutely by akinesis of
the infarcted basal septum, and further relief occurs over time
as postinfarction negative myocardial remodeling occurs.
MRI evaluation can assess the infarction size and distribu-
tion on myocardial late gadolinium-enhancement images.
Alcohol septal ablation results in a variable pattern of myocar-
dial infarction often involving the inferior aspect of the basal
septum with extension to the RV side. Cardiac MRI can also
assess for small ventricular septal defects or acute pericarditis
post ablation.
 114 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7D

Figure 7.7 Sigmoid nonobstructive HCM. Short-axis late gadolinium-enhancement images at the basal (A), mid (B), and apical (C) levels of the LV
showing the sigmoid morphologic subtype of HCM with focal areas of subepicardial and midmyocardial enhancement (arrows) in the anteroseptal
and inferoseptal segments consistent with myocardial fibrosis.
 7.  No n ischemic M yocardia l D isease  •
S IG MOI D NONOB S T RUC T I V E HC M
Clinical History and Presentation
A 53-year-old man with known HCM undergoing medical
therapy was referred for evaluation of increasing palpitations.
Clinical Question
MRI (Figure 7.7) was ordered to evaluate for possible myo-
cardial fibrosis for risk stratification of sudden cardiac arrest.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
The MR images obtained were used to diagnose a sigmoid
morphologic subtype nonobstructive HCM with myocardial
fibrosis. Late gadolinium-enhancement images showed focal
areas of subepicardial and midmyocardial enhancement in
the anteroseptal and inferoseptal segments consistent with
myocardial fibrosis.
115
Summary
The presence of myocardial fibrosis may be a risk factor for
sudden cardiac death; as such, it is used in conjunction with
other patient factors in the decision-making process for rec-
ommending an ICD. The patient had no other major risk
factors for sudden cardiac death and was otherwise asymp-
tomatic. His care involved continuation of medical therapy
and regular cardiovascular follow-up.
The detection of myocardial late gadolinium enhance-
ment on MRI is an emerging factor used in risk stratification
to identify those who may benefit from an ICD. However,
there is insufficient evidence to place an ICD on the basis of
myocardial late gadolinium enhancement alone, despite publi-
cations showing the correlation between myocardial late gado-
linium enhancement and detection of ventricular arrhythmias.
Between 40% and 70% of patients with HCM have myocar-
dial late gadolinium enhancement, with a wide variability of
distribution. Late gadolinium enhancement can be patchy and
multifocal, involving the RV insertion points, but is most often
found in the areas of greatest hypertrophy. The precise cause of
late gadolinium enhancement in this setting is not well under-
stood. A proposed mechanism is increased myocardial collagen
from microvascular ischemia leading to fibrosis from intramu-
ral coronary arteriole dysplasia. An alternative theory is sarco-
meric gene mutations resulting in the phenotypic expression of
increased myocardial connective tissue deposition.
 116 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7E

Figure 7.8 Apical obstructive HCM. A and B, Four-chamber balanced SSFP images in end diastole (A) and end systole (B) showing asymmetric
biventricular apical myocardial hypertrophy (arrowhead). Also noted is a small LV akinetic apical pouch in the absence of an apical thrombus.
A subtle linear hypointense signal void in the LV mid cavity is also seen (B), indicating the presence of turbulent flow (arrow). C, Four-chamber
late gadolinium-enhancement image shows moderate, patchy, biventricular, apical subepicardial and midmyocardial enhancement indicative of
myocardial fibrosis.
 7.  No n ischemic M yocardia l D isease  •
A PIC A L HC M
Clinical History and Presentation
During a routine cardiology examination, a 30-year-old man
who was asymptomatic was noted on echocardiography to
have apical variant HCM.
Clinical Question
MRI (Figure 7.8) was ordered to assess for the presence of an
apical pouch and myocardial fibrosis.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
The MR images obtained led to a diagnosis of apical morpho-
logic subtype obstructive HCM with biventricular involvement,
akinetic LV apical pouch, and myocardial fibrosis. Balanced
SSFP images of the heart in end diastole and end systole iden-
tified asymmetric biventricular apical myocardial hypertrophy
with the greatest end-diastolic myocardial thickness of 21 mm
117
noted in the LV apex. Also noted was a small LV akinetic api-
cal pouch in the absence of an apical thrombus. A subtle lin-
ear hypointense signal void in the LV mid cavity was also seen,
indicating turbulent flow. As is typical for isolated apical HCM,
there was no SAM of the mitral valve or mitral regurgitation.
Late gadolinium-enhancement images demonstrated moderate,
patchy, biventricular subendocardial, midmyocardial, and sub-
epicardial apical enhancement indicative of myocardial fibrosis.
Summary
MRI confirmed the presence of an apical pouch and myocar-
dial fibrosis. Although the patient was asymptomatic, young,
and leading a relatively active lifestyle, he was considered to be
at sufficient risk for sudden cardiac death, which warranted
consideration of ICD placement.
Cardiac MRI is an excellent approach for visualizing the
apex of the heart. The apical pouch has important prognos-
tic implications for this subtype of HCM. It is suspected
that those with an apical pouch may be at increased risk for
complications including arrhythmias and stroke. An apical
pouch may be the result of a severe increase in wall stress in
the apical region causing diffuse subendocardial ischemia.
The ensuing apical fibrosis and wall-motion abnormalities
may predispose these patients to arrhythmia and thrombus
formation.
 118 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7F

Figure 7.9 Arrhythmogenic RV cardiomyopathy/dysplasia. Axial balanced SSFP images in end diastole (A) and end systole (B) showing multiple
microaneurysms of the RV basal inferolateral wall (arrows) with characteristic dyskinesis, as well as myocardial thinning and probable fatty
infiltration.
 7.  No n ischemic M yocardia l D isease  •
A R R H Y T H MO G E N IC
R IG H T V E N T R IC UL A R
C A R DIOM YOPAT H Y/ DY S PL A S I A
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
After reporting episodic palpitations for more than a year, a
46-year-old woman underwent clinical work-up to determine
the cause of the palpitations. Exercise stress testing revealed
frequent episodes of nonsustained ventricular tachycardia.
An electrophysiology study revealed ventricular tachycardia
originating from the RV outflow tract.
C L I N IC A L QU E S T ION
MRI (Figure 7.9) was ordered to assess for arrhythmogenic
right ventricular cardiomyopathy/dysplasia (ARVC/D).
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a long- or
short-axis double and triple inversion recovery sequence,
and cine balanced SSFP prescribed as a straight axial.
I M AG I NG F I N DI NG S
The MR images contributed to a multidisciplinary diag-
nosis of moderate RV enlargement with segmental RV
dysfunction and RV free wall microaneurysms consistent
with ARVC/D. Balanced SSFP views at end diastole and
end systole demonstrated multiple microaneurysms of the
119
RV basal inferolateral wall. Review of axial images in cine
mode revealed associated dyskinesia. Both images dem-
onstrated marked thinning and possible fatty infiltration
of the basal inferolateral wall. There was moderate RV
enlargement with an end-diastolic volume of 200 mL/m 2
and a severely decreased ejection fraction of 26%. Late gad-
olinium-enhancement images did not demonstrate abnor-
mal enhancement.
S U M M A RY
MRI identified one of the major criteria for the multidisciplinary
diagnosis of ARVC/D. The patient underwent placement of
an automatic ICD system. ARVC/D is an uncommon genetic
nonischemic cardiomyopathy with an estimated prevalence of
0.02%. Although the etiology of ARVC/D is unknown, it is
found in 30% to 50% of family members studied noninvasively.
The histopathologic finding in ARVC/D is fatty or fibrofatty
tissue replacement of the RV myocardium (much less commonly
of the LV).
The diagnosis of ARVC/D is not based on MRI alone,
is often challenging, and requires a multidisciplinary
approach guided by the proposed major and minor diagnos-
tic criteria. The criteria include structural and functional
abnormalities identified by cardiac imaging—cross-sec-
tional techniques such as MRI are favored. Current diag-
nostic imaging criteria for ARVC/D focus on regional and
global morphologic and functional abnormalities, includ-
ing akinesia, dyskinesia, or dyssynchrony of the RV. These
are often referred to as RV free wall microaneurysms or
dyskinesis. Additional imaging-based criteria include the
amount of RV dilation and the presence of decreased RV
systolic function.
 120 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

C A S E 7G

Figure 7.10 Isolated LV noncompaction. A and B, Short-axis (A) and 4-chamber (B) balanced SSFP images in end diastole demonstrating
hypertrabeculation of the LV apical inferolateral segment and apex (arrows). The LV is moderately dilated. C, Four-chamber late gadolinium-
enhancement view demonstrates no ventricular thrombus or abnormal enhancement.
 7.  No n ischemic M yocardia l D isease  •
L E F T V E N T R IC UL A R
NO NC OM PAC T IO N
I S OL AT E D LV NONC OM PAC T ION
Clinical History and Presentation
A 34-year-old woman with nonsustained polymorphic ven-
tricular tachycardia and a family history of sudden cardiac
death in a first-degree relative was referred to a cardiologist for
further evaluation. A comprehensive work-up did not identify
a cause of the tachycardia. Echocardiography revealed mild
LV enlargement and a severe global decrease in LV systolic
function.
Clinical Question
The overall quality of the echocardiogram was poor. Therefore,
MRI (Figure 7.10) was ordered to assess biventricular func-
tion and to determine possible causes of presumed nonisch-
emic cardiomyopathy.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
On the basis of the MR images obtained, left ventricular
noncompaction (LVNC) was diagnosed. Balanced SSFP
images demonstrated hypertrabeculation of the LV apical
121
inferolateral segment and apex. The ratio of noncompacted
to compacted myocardium was 3 to 1. The LV was moder-
ately dilated. Review of images in cine mode also revealed
moderate global LV hypokinesis with an ejection fraction of
33%. On late gadolinium-enhancement views, no ventricular
thrombus or abnormal enhancement could be seen.
Summary
After the confirmation of LVNC and because the patient had
several episodes of rapid polymorphic ventricular tachycardia,
placement of an ICD was recommended.
LVNC is characterized by increased ventricular trabecu-
lations and deep intertrabecular recesses. Most consider the
morphologic appearance of LVNC to be the result of an
abnormal embryologic arrest of normal myocardial devel-
opment during weeks 5 through 8 of gestation. Myocardial
compaction normally occurs from the epicardium to the
endocardium, from the base to apex, and from the septum to
free wall. Thus, the timing of the embryologic arrest deter-
mines the severity of LVNC. The mid inferolateral LV wall
and apex are the most common locations for LVNC, and
the apex is always involved. Associated hypokinesis is almost
always present.
LVNC can be diagnosed by either echocardiography or
MRI according to the ratio of noncompacted to compacted
myocardial thickness. For echocardiography, an end-systolic
thickness ratio of more than 2 is considered diagnostic for
noncompaction. For MRI, an end-diastolic thickness ratio of
more than 2.3 is considered diagnostic. Advantages of MRI
include the acquisition of true LV short-axis images used for
measurement and superior visualization of the apex.
 122 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7H

Figure 7.11 LV noncompaction. A and B, Short-axis (A) and 4-chamber (B) balanced SSFP images in end diastole demonstrating diffuse LV
hypertrabeculation (arrows) and LV chamber enlargement. Hypertrabeculation of the RV is also seen to a lesser extent, with normal RV chamber
size. C, Four-chamber late gadolinium-enhancement image demonstrates the absence of ventricular thrombus or abnormal enhancement.
 7.  No n ischemic M yocardia l D isease  •
LV NONC OM PAC T ION W I T H
DE C R E A S E D S Y S TOL IC F U NC T ION
Clinical History and Presentation
As part of routine management, a 33-year-old asymptomatic
woman with known ventricular noncompaction underwent
echocardiography, which revealed decreased LV systolic func-
tion compared with prior evaluations.
Clinical Question
MRI (Figure 7.11) was ordered to assess the degree and distri-
bution of LVNC and to quantify LV function and the pres-
ence and extent of myocardial fibrosis.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
MR imaging findings showed extensive biventricular non-
compaction with decreased LV systolic function, without
myocardial fibrosis or thrombus. Balanced SSFP images in
123
end diastole showed diffuse LV hypertrabeculation. The basal-
to-apical wall measurement with the greatest ratio of noncom-
pacted to compacted myocardium was 4 to 1. In both short- and
long-axis balanced SSFP images, no discrete papillary muscles
could be identified. Images also identified hypertrabeculation
of the RV to a lesser extent, with mild dilation and normal sys-
tolic function. Late gadolinium-enhancement images showed
no ventricular thrombus or abnormal enhancement.
Summary
After confirmation of ventricular noncompaction by MRI,
the patient underwent longitudinal assessment of her ven-
tricular function. Since the understanding of ventricular
noncompaction syndrome is evolving, current management
includes expectant observation for the development of symp-
toms and reimaging at that time.
Patients with LVNC may be asymptomatic or may have
LV systolic dysfunction and heart failure, thromboembolism,
and arrhythmias. The extent and distribution of noncompac-
tion and the presence of late gadolinium enhancement may
relate to clinical disease severity. The continued improvement
and utilization of cardiac imaging has resulted in identifica-
tion of patients with increased trabeculations within the LV.
This may represent a normal variant, especially in those with
preserved LV systolic function.
 124 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7I

Figure 7.12 DCM without fibrosis. A and B, Four-chamber (A) and short-axis (B) balanced SSFP images in end diastole demonstrating biatrial and
biventricular chamber enlargement with mild diffuse myocardial thinning. C, Short-axis late gadolinium-enhancement image shows no abnormal
enhancement, suggesting the absence of myocardial fibrosis.
 7.  No n ischemic M yocardia l D isease  •
DI L AT E D C A R DIOM YOPAT H Y
D C M W I T HOU T F I BRO S I S
Clinical History and Presentation
A 28-year-old man with dyspnea attributed to asthma was
found to have an enlarged heart on chest radiography. The
patient reported a flulike illness within the past year. As part
of a routine cardiology work-up, echocardiography identified
severe biventricular enlargement and severe biventricular sys-
tolic dysfunction. In addition, no obstructive coronary artery
disease was identified by coronary angiography. As a result of
these findings, a preliminary diagnosis of nonischemic cardio-
myopathy was made.
Indication for MRI
MRI (Figure 7.12) was ordered to determine the causes of the
patient’s cardiomyopathy.
Clinical Question
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T2-weighted, fat-suppressed, black blood (triple
inversion recovery) and long- or short-axis, non–fat-sup-
pressed (double inversion recovery) and fat-suppressed
(triple inversion recovery) images.
Imaging Findings
The MR images identified extensive biventricular enlargement
and dysfunction without myocardial fibrosis or thrombus.
125
Balanced SSFP images in end diastole demonstrated biatrial
and biventricular enlargement with mild diffuse myocardial
thinning. Quantitative analysis of the cine data determined
that the LV and RV ejection fractions were 10% and 12%,
respectively. Late gadolinium-enhancement images showed
no abnormal enhancement, which suggested the absence of
myocardial fibrosis.
Summary
The MRI findings confirmed DCM without prior myocar-
dial infarction, fibrosis, or inflammation. This is consistent
with a diagnosis of idiopathic DCM. After receiving this
diagnosis the patient underwent medical therapy, lifestyle
changes, and routine follow-up. Subsequent echocardiogra-
phy studies demonstrated a marked increase in cardiac func-
tion with an increase in his LV ejection fraction from 10%
as determined by MRI to 38% approximately 12 months
later.
DCM is characterized by ventricular chamber dilation
with decreased systolic function in the absence of signifi-
cant ischemic heart disease. The histopathology of DCM is
ventricular myocyte degeneration and interstitial fibrosis.
Assessment of a patient with newly diagnosed DCM requires
evaluation of potentially reversible forms of all types of car-
diomyopathies. MRI provides the single best noninvasive
assessment of cardiomyopathies. Identification of unrecog-
nized myocardial infarctions has been shown in as much as
15% of cases thought to be nonischemic cardiomyopathies.
In nonischemic cardiomyopathies, several studies have shown
that identification of an alternative diagnosis such as hemo-
chromatosis can lead to marked changes in management and
patient outcomes.
 126 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies
CASE 7J
Figure 7.13 DCM with fibrosis. A, Four-chamber balanced SSFP
image demonstrating biatrial and biventricular enlargement (asterisks)
with mild diffuse myocardial thinning (arrow). B, Short-axis late
gadolinium-enhancement image demonstrates linear anteroseptal and
inferoseptal midmyocardial enhancement (ie, a midmyocardial “stripe”)
(arrowhead) indicative of myocardial fibrosis.
D C M W I T H F I BRO S I S
Clinical History and Presentation
A 67-year-old man with a history of hypertension and DCM
diagnosed 1 year earlier was admitted to our institution after
a new diagnosis of congestive heart failure by his primary
care physician. As part of his clinical work-up, echocardiog-
raphy revealed severe biventricular enlargement and a severe
decrease in biventricular systolic function. No obstructive
coronary artery disease was detected by coronary angiography.
Clinical Question
MRI (Figure 7.13) was ordered to assess biventricular func-
tion and to identify possible causes of a presumed nonisch-
emic cardiomyopathy.
Cardiac MRI Protocol
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include a cine bal-
anced SSFP LVOT stack.
Imaging Findings
The MR images obtained led to a diagnosis of extensive
biventricular dysfunction with myocardial fibrosis, without
thrombus, in the LV. Late gadolinium-enhancement images
demonstrated a linear anteroseptal and inferoseptal mid-
myocardial enhancement or “stripe” indicative of myocardial
fibrosis. A 4-chamber view identified biatrial and biventric-
ular enlargement with mild diffuse myocardial thinning.
Quantitative analysis of the cine balanced SSFP images indi-
cated an LV ejection fraction of 18% and an RV ejection frac-
tion of 36%. These findings were consistent with DCM.
Summary
Most patients with DCM have no abnormal late gadolin-
ium enhancement on postcontrast enhanced MR images.
However, up to 30% of patients with DCM have a character-
istic, distinct, nearly pathognomonic area of fibrosis. This is
identified in the midmyocardial septum as a thin stripe pat-
tern of myocardial late gadolinium enhancement that spares
the endocardium (Figure 7.14). Sparing of the endocardium
allows for distinction from a myocardial infarction and corre-
lates with focal fibrosis on autopsy. This is an important find-
ing and is reported to be an independent predictor of all-cause
mortality, sudden cardiac death, and cardiovascular hospi-
talization. It should also be noted that the differential diag-
nosis for this midmyocardial late gadolinium enhancement
includes myocarditis, which can be complicated by a DCM.
Healed nonrecovered myocarditis has been proposed as a
potential cause of idiopathic DCM. Absence of myocardial
edema on T2-weighted images (fat-suppressed, triple inversion
recovery images) helps to distinguish acute from chronic myo-
carditis when the midmyocardial stripe is identified.
 7.  No n ischemic M yocardia l D isease  • 127

One caveat when reviewing MR images of a DCM is
that it is difficult to distinguish DCM without fibrosis
from severe 3-vessel ischemic heart disease with hibernating
myocardium. In some cases, 3-vessel ischemic heart disease
will have no late gadolinium enhancement in any distri-
bution and can mimic a DCM. Hibernating myocardium
results in chronic underperfusion of the myocardium as
the culprit for the LV dysfunction. It is important to note
this possibility, although it is an uncommon occurrence.
Review of coronary angiography studies showing absence
of 3-vessel obstructive coronary artery disease is instructive
in this regard.

Figure 7.14 Example of fibrosis along the midmyocardial septum. A, Two-chamber late gadolinium-enhancement image showing an LV septal
midmyocardial stripe (arrow) characteristic of DCM. B-E, Short-axis late gadolinium-enhancement images from the base (B) through the mid
ventricle (E), including and extending beyond the septal wall of the LV, demonstrating a midmyocardial stripe (arrows).
 128 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7K

Figure 7.15 Acute myocarditis. A and B, Four-chamber balanced SSFP images during systole (A) and diastole (B) demonstrating normal
biventricular systolic function. C and D, Four-chamber (C) and 3-chamber (D) late gadolinium-enhancement images demonstrating abnormal
subepicardial enhancement of the LV mid and apical inferolateral segments and overlying pericardium (arrow).
 7.  No n ischemic M yocardia l D isease  •
M YO C A R DI T I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 29-year-old man with no significant past medical history
was evaluated in the emergency department for sudden onset
of chest pressure radiating to the left arm. Cardiac biomarkers
were increased, and electrocardiography studies showed non-
specific T-wave abnormalities. Echocardiography showed no
abnormalities, and coronary angiography did not reveal sig-
nificant coronary artery disease.
C L I N IC A L QU E S T ION
MRI (Figure 7.15) was ordered to assess for the cause of increased
troponin levels and to investigate the occurrence of a non–
ST-segment elevation myocardial infarction or myocarditis.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T2-weighted, fat-suppressed, black blood (triple
inversion recovery) and long- or short-axis, non–fat-sup-
pressed (double inversion recovery) and fat-suppressed
(triple inversion recovery) images.
I M AG I NG F I N DI NG S
The MR images obtained provided a diagnosis of myocar-
dial necrosis or fibrosis in a nonischemic pattern suggestive
of acute myocarditis. Balanced SSFP images in systole and
129
diastole illustrated normal systolic function. Late gadolinium-
enhancement images showed epicardial distribution of myo-
cardial fibrosis. There was no evidence of a pericardial effusion
or abnormal T2 signal indicating edema in the lateral wall.
S U M M A RY
The patient was given a diagnosis of acute myocardi-
tis and treated medically. A 6-month follow-up imaging
study revealed complete resolution of the myocarditis and
normal ventricular function. No long-term sequelae have
occurred.
Myocarditis is myocardial inflammation secondary to
infectious or noninfectious causes. Infectious causes include
viral and bacterial etiologies. Coxsackie viruses A and B,
human herpesvirus 6, parvovirus B19, adenovirus, echo-
virus, and poliovirus are the common viruses involved.
Noninfectious causes include autoimmune diseases, pharma-
cologic agents, and traumatic injury.
Patients with myocarditis often have acute chest pain,
abnormal electrocardiography findings, and increased car-
diac biomarkers, mimicking acute coronary syndrome.
MRI is the primary noninvasive imaging modality for the
diagnosis of clinically suspected myocarditis. MRI allows
the clinician to distinguish patients with acute myocar-
ditis from those with an acute coronary syndrome such as
a non–ST-segment elevation myocardial infarction. MR
signal abnormalities related to myocarditis include charac-
teristic subepicardial and midmyocardial late gadolinium
enhancement. This can present as patchy diffuse involve-
ment throughout the myocardium or in any regional dis-
tribution of the myocardium. A classic location is the basal
lateral wall of the LV.
 130 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7L

Figure 7.16 Nonischemic pattern of myocardial fibrosis suggestive of myocarditis. A, Fat-suppressed, black blood (triple inversion recovery), short-
axis image demonstrating subepicardial and midmyocardial hyperintensity in the LV basal posterolateral segment (arrow) indicative of edema.
B, The corresponding gadolinium enhancement image demonstrating early enhancement 2 minutes after contrast administration is indicative of
hyperemia. C, Late gadolinium-enhancement image shows enhancement indicative of necrosis or fibrosis (arrowhead).
 7.  No n ischemic M yocardia l D isease  •
AC U T E M YO C A R DI T I S W I T H
F I B RO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
An 18-year-old woman with no significant past medical his-
tory sought care at the emergency department for acute chest
pain and palpitations. Clinical evaluation revealed increased
cardiac biomarker levels, an electrocardiogram with nonspe-
cific T-wave changes, and a normal echocardiogram.
C L I N IC A L QU E S T ION
MRI (Figure 7.16) was ordered to assess for causes of the
increased troponin level and to rule out a non–ST-segment
elevation myocardial infarction or myocarditis.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T2-weighted, fat-suppressed, black blood (triple
inversion recovery) and long- or short-axis, non–fat-sup-
pressed (double inversion recovery) and fat-suppressed
(triple inversion recovery) images.
I M AG I NG F I N DI NG S
The MR images indicated a diagnosis of myocardial edema,
hyperemia, and necrosis or fibrosis in a nonischemic pattern
suggestive of acute myocarditis. A black blood, fat-suppressed
(triple inversion recovery) image demonstrated subepicardial
and midmyocardial hyperintensity in the LV basal posterolat-
eral segment indicative of edema. Corresponding abnormal
early gadolinium enhancement indicative of hyperemia was seen
2 minutes post gadolinium contrast administration. A corre-
sponding late gadolinium-enhancement short-axis view showed
abnormal enhancement indicative of necrosis or fibrosis. Review
131
of balanced SSFP cine images demonstrated normal LV size and
systolic function with no regional wall-motion abnormalities,
with the presence of a very small pericardial effusion.
S U M M A RY
Although the MRI examination confirmed the presence of
myocardial necrosis or fibrosis, the normal ventricular size
and function required only periodic follow-up with the refer-
ring cardiology service.
MRI assessment of myocarditis involves the acquisition
of an additional 3 imaging sequences after acquisition of
the standard imaging planes for assessment of myocardial
function with balanced SSFP imaging techniques. First, a
fat-suppressed, T2-weighted, black blood sequence (triple
inversion recovery) is acquired. These images are used for
the detection of myocardial edema, which correlates with
serum biomarkers of acute myocardial injury and can help
identify acute versus chronic changes on later imaging.
Second, early postcontrast (approximately 2-4 minutes post
contrast injection) inversion recovery gradient echo images
are acquired. Myocardial early gadolinium enhancement is
indicative of hyperemia up to approximately 4 weeks after
the onset of acute myocarditis. Third, late gadolinium-
enhancement images (approximately 10-15 minutes post
contrast injection) are acquired to detect significant myo-
cardial late gadolinium enhancement relative to precontrast
images. Myocardial late gadolinium enhancement is indica-
tive of necrosis or fibrosis.
Commonly, qualitative assessment of an MRI signal
abnormality is used to diagnose myocarditis. It is often dif-
ficult to quantify abnormal myocardial signal intensity as
being due to myocardial inflammation in accordance with the
guidelines provided by the International Consensus Group on
Cardiac Magnetic Resonance Diagnosis of Myocarditis, also
known as the Lake Louise Criteria, because of artifacts aris-
ing from respiratory motion, arrhythmia, or artifact(s) inher-
ent to the MR acquisition, particularly with edema-sensitive
sequences. In addition, the abnormal signal of edematous or
enhancing myocardium is subtle and patchy.
 132 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7M

Figure 7.17 Apical ballooning cardiomyopathy. A and B, Two-chamber balanced SSFP images at end diastole (A) and end systole (B) show LV basal
and mid hyperkinesis and apical akinesis and dilation. C, Two-chamber late gadolinium-enhancement image shows no detectable enhancement to
suggest myocardial fibrosis.
 7.  No n ischemic M yocardia l D isease  •
A PIC A L B A LL O O N I NG
C A R DIOM YOPAT H Y
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 71-year-old woman without known coronary artery disease
was emergently transferred to our institution for cardiac cath-
eterization after sudden onset of chest pain, increased cardiac
biomarkers, and ST-segment elevation in the anterior precor-
dial leads. Mild nonobstructive coronary artery disease was
identified by coronary angiography. Left ventriculography
revealed bulging out of the LV apex with a hypercontractile
base. Her personal history was remarkable for the recent sud-
den death of her husband.
C L I N IC A L QU E S T ION
MRI (Figure 7.17) was ordered to assess for causes of the
increased troponin levels and to rule out a non–ST-segment
elevation myocardial infarction or regional myocarditis.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T 2-weighted, fat-suppressed, black blood (triple
inversion recovery) images and a cine balanced SSFP
LVOT stack.
I M AG I NG F I N DI NG S
On the basis of the clinical MR images, a diagnosis of apical
ballooning cardiomyopathy, or takotsubo cardiomyopathy,
was made. Balanced SSFP images at end diastole and systole
demonstrated hyperdynamic basal segments with akinesis
and dilation of the apical segments of the LV. Late gadolin-
ium-enhancement images showed no myocardial fibrosis or
infarction. Markedly increased edema in the apical myocar-
dium without thrombus formation was also noted. Based on
quantitative analysis of short-axis balanced SSFP images, the
LV ejection fraction was 37%.
133
S U M M A RY
The MRI study confirmed the clinical suspicion of apical
ballooning cardiomyopathy. She was treated medically with
symptom relief. Repeat imaging with echocardiography dur-
ing the index hospitalization demonstrated near-resolution of
the regional wall-motion abnormalities.
Apical ballooning cardiomyopathy is a temporary, severe,
LV systolic dysfunction usually involving the apex, most com-
mon in postmenopausal women with nonobstructive coronary
artery disease. This is classically identified after significant emo-
tional stress. In our patient, the recent, unexpected death of her
husband most likely represented the major emotional stressor.
Proposed pathophysiologic mechanisms are cardiotoxicity from
catecholamine release and vasospasm.
Patients with apical ballooning cardiomyopathy have signs
and symptoms that mimic acute coronary syndrome and
include chest pain, acute heart failure, electrocardiographic
changes that may include ST-segment elevation, and increased
levels of cardiac biomarkers.
The diagnosis of apical ballooning cardiomyopathy is usually
first suspected during coronary catheter angiography prompted
by the acute coronary syndrome–like clinical presentation.
Coronary angiography shows normal coronary arteries or non-
obstructive coronary artery disease. However, left ventriculogra-
phy reveals the characteristic LV wall-motion abnormalities of
apical ballooning. In some cases, the severe apical wall-motion
abnormalities can be a nidus for LV apical thrombus formation.
MRI is often performed to exclude acute myocardial
infarction and acute severe myocarditis, which have similar
clinical presentations, and to confirm the diagnosis of apical
ballooning syndrome. MRI findings include LV apical severe
hypokinesis or akinesis and basal hyperdynamic systolic func-
tion on gradient echo cine images. The shape of the LV dur-
ing systole on left ventriculography and MRI is analogous to
a Japanese octopus trap or takotsubo. There is increased sig-
nal intensity on fat-suppressed, black blood (triple inversion
recovery) images within the LV apex, indicative of myocardial
edema. However, there is no corresponding myocardial late
gadolinium enhancement that would normally be seen with
myocarditis or an acute myocardial infarction.
Apical ballooning cardiomyopathy generally has a good
prognosis. Recovery can occur within days to weeks.
 134 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7N

Figure 7.18 Cardiac amyloidosis. A-D, End-diastolic balanced SSFP images. Basal (A), mid (B), and apical (C) short-axis and 4-chamber (D) views
demonstrating diffuse concentric myocardial thickening, small ventricular cavities, and biatrial chamber enlargement (D). Panel B shows a small
pericardial effusion (arrow). Panel D shows thickening of the interatrial septum and mild thickening of the mitral and tricuspid valves. E, Coronal
balanced SSFP scout image demonstrates small bilateral pleural effusions (arrowheads). F and G, Midventricular, late gadolinium-enhancement,
short-axis (F) and 4-chamber (G) images showing diffuse patchy enhancement of the myocardium characteristic of amyloid plaque deposition
(arrows) with poor overall myocardial signal suppression compared with normal muscle (arrowhead).
 7.  No n ischemic M yocardia l D isease  •
C A R DI AC A M Y L OI D O S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 67-year-old man with a history of hypertension and a new
diagnosis of primary (AL) systemic amyloidosis was evaluated
by his primary care physician for increasing exertional dys-
pnea and syncope. Preliminary clinical work-up revealed that
all coronary arteries were normal by coronary angiography,
and echocardiography revealed preserved LV systolic func-
tion, LV hypertrophy, and increased LV filling pressures.
C L I N IC A L QU E S T ION
MRI (Figure 7.18) was ordered to assess for the presence of
cardiac amyloidosis.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2
(see page 78). Additional/optional sequences include T2*-
weighted images.
I M AG I NG F I N DI NG S
The clinical MR images identified morphologic findings most
consistent with amyloidosis. Balanced SSFP images demon-
strated diffuse concentric myocardial thickening and small
ventricular cavities, thickening of the interatrial septum, mild
thickening of the mitral and tricuspid valves, and a small pericar-
dial effusion. Severe biatrial enlargement was also noted, along
with small bilateral pleural effusions. Late gadolinium-enhance-
ment images demonstrated diffuse enhancement throughout
the myocardium characteristic of amyloid plaque deposition.
Quantitative analysis of short-axis balanced SSFP images indi-
cated that biventricular systolic function was preserved.
135
S U M M A RY
After MRI confirmation of myocardial amyloidosis, the
patient underwent subcutaneous proteasome inhibitor ther-
apy (bortezomib) as a systemic treatment.
Amyloidosis is characterized by insoluble proteinaceous
deposits, or amyloid, as a result of misfolding of a precursor
protein. The histopathologic finding of cardiac amyloidosis is
the deposition of amyloid within the myocardial interstitium.
Deposition is usually widespread, including in ventricles, atria,
valves, and coronary arteries.
The most common types of amyloidosis affecting
the heart are immunoglobulin light chain–derived (AL
type), which includes primary systemic amyloidosis and
commonly affects the heart; transthyretin gene–related
(ATTR type), which primarily affects the heart and ner-
vous system; and senile amyloidosis (SSA type), which is
seen in the elderly, is often asymptomatic, and is isolated
to the heart. The recognition of cardiac amyloidosis is
important because it carries a poor prognosis for patients
with AL amyloidosis. Patients with cardiac amyloidosis
may have classic symptoms reflecting severe restrictive
physiology or arrhythmias that result from amyloid pro-
tein deposition.
Characteristic morphologic findings of cardiac amyloi-
dosis include diffuse biventricular myocardial thickening
resulting in small ventricular cavities, atrial wall thicken-
ing, especially of the interatrial septum, atrial enlargement
due to ventricular diastolic dysfunction, and multivalvu-
lar leaflet thickening. Pericardial and pleural effusions are
also commonly seen. Postcontrast images reveal a diffuse
patchy distribution of late gadolinium enhancement with
either difficulty nulling the myocardium at all or diffuse
subendocardial late gadolinium enhancement. The area of
enhancement corresponds to the histologic findings found
at autopsy and may represent the distribution of amyloid
protein.
 136 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

C A S E 7O

Figure 7.19 Cardiac siderosis. A and B, Sagittal spoiled gradient echo scout images show hepatosplenomegaly and diffuse signal nulling in the liver
and spleen consistent with siderosis. C, Four-chamber balanced SSFP image at end diastole also shows diffuse signal nulling in the myocardium and
normal biatrial and biventricular size. Biventricular systolic function was normal. The liver, spleen, and myocardium illustrate the characteristic
dark black appearance on pregadolinium balanced SSFP images.
 7.  No n ischemic M yocardia l D isease  •
C A R DI AC S I DE RO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 25-year-old woman with hepatitis C–induced liver cirrhosis
and a history of beta thalassemia major requiring blood cell
transfusions each month was undergoing clinical work-up for
consideration of a liver transplant.
C L I N IC A L QU E S T ION
MRI (Figure 7.19) was ordered to assess for the presence of
cardiac iron deposition.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2
(see page 78). Additional/optional sequences include T2*-
weighted images.
I M AG I NG F I N DI NG S
From the MR images obtained, a diagnosis of LV dysfunc-
tion with abnormal myocardial T 2* relaxation values con-
sistent with myocardial iron overload was made. Spoiled
gradient echo scout images demonstrated hepatospleno-
megaly and diffuse signal nulling in the liver, spleen, and
myocardium, consistent with siderosis. A balanced SSFP
image at end diastole also demonstrated normal biatrial and
biventricular size. Quantitative assessment of short-axis
balanced SSFP cine images revealed normal biventricular
systolic function.
137
S U M M A RY
The patient continued to be evaluated by the gastrointestinal
and hepatobiliary services. The iron deposition in the myocar-
dium was used to help with further risk stratification.
Siderosis is deposition of iron in skin and internal organs
secondary to iron-overload disease states. Iron-overload disease
states are divided into primary hemochromatosis, an autoso-
mal recessive disorder of accelerated intestinal iron absorption,
and secondary hemochromatosis, which results from multiple
blood transfusions in persons with hereditary anemias, includ-
ing beta thalassemia anemia and sickle cell anemia.
Iron deposition in siderosis occurs first in the liver, followed
by the spleen, pancreas, and heart, and causes related organ tox-
icity. Patients with cardiac siderosis are initially asymptomatic,
but arrhythmias, systolic and diastolic dysfunction, and sudden
death occur when iron levels are high. Heart failure secondary
to siderosis is the leading cause of death in these patients. This
is a reversible form of a cardiomyopathy when identified early
and treated with iron-chelating agents. Cardiac MRI is ideal
for identification of iron deposition in the heart. Paramagnetic
iron particles in tissues create localized regions of magnetic field
inhomogeneity, resulting in signal dephasing (ie, loss), quanti-
tatively described by a decrease in the T2* relaxation constant.
Qualitative assessment identifies the characteristic signal drop-
out from iron deposition in the myocardium, liver, and spleen.
Assessment of hepatic and cardiac T2* and cardiac function
can be performed concurrently in a single MRI examination.
Myocardial iron deposition can be reproducibly quantified
using myocardial T2*—the most important variable for pre-
dicting when to use iron-chelation therapy for iron overload.
A T2* value less than 20 milliseconds (see also Chapter 12 for
more information on T2* quantification) is indicative of cardiac
iron overload and predictive of myocardial dysfunction.
 138 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

CASE 7P

Figure 7.20 Endomyocardial fibrosis. A and B, Four-chamber (A) and apical short-axis (B) balanced SSFP images in diastole demonstrating
severe diffuse LV myocardial thickening, which is greatest in the apex (white arrow). A small pericardial effusion (red arrow) and bilateral pleural
effusions (arrowheads) are also present. C and D, Two-chamber (C) and apical short-axis (D) late gadolinium-enhancement images showing diffuse
subendocardial enhancement (arrow). Small nonenhancing hypointense masses (C) that abut the enhancing apical endocardium (arrowheads) are
thrombi.
 7.  No n ischemic M yocardia l D isease  •
E N D OM YO C A R DI A L F I B RO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 57-year-old woman with a history of ulcerative colitis and a
previous liver transplant was hospitalized for new-onset con-
gestive heart failure. As part of her clinical work-up, resting
echocardiography suggested apical HCM, and blood testing
revealed peripheral eosinophilia.
C L I N IC A L QU E S T ION
MRI (Figure 7.20) was ordered to determine the degree of api-
cal hypertrophy.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T2-weighted, fat-suppressed, black blood (triple
inversion recovery) and long- or short-axis, non–fat-sup-
pressed (double inversion recovery) and fat-suppressed
(triple inversion recovery) images.
I M AG I NG F I N DI NG S
The clinical MR images provided a diagnosis of endomyocar-
dial fibrosis, possibly secondary to a drug allergy. This find-
ing was verified by RV endomyocardial biopsy, which showed
fibrosis and eosinophils. Balanced SSFP images in diastole
demonstrated severe diffuse LV myocardial thickening, which
was greatest at the apex. A small pericardial effusion and bilat-
eral pleural effusions were also seen. Late gadolinium-enhance-
ment views identified diffuse subendocardial enhancement
and small nonenhancing hypointense masses abutting the
enhancing apical endocardium, which were thrombi.
S U M M A RY
Therapy with corticosteroids produced a favorable response,
and the patient was able to resume normal day-to-day activities.
139
Endomyocardial fibrosis is characterized by fibrosis of the
apical endocardium of the LV, RV, or both. It encompasses 2
entities with different clinical features and geographic dis-
tributions but similar pathologic and imaging features. The
first is Loeffler endomyocarditis, which is idiopathic, is most
common in nontropical countries, and is associated with
eosinophilia. The second is endomyocardial fibrosis, which
is secondary to parasitic infection, drug toxicity, or allergy, is
most common in tropical countries, and is not usually associ-
ated with eosinophilia.
Traditionally, left ventriculography was used for diag-
nosis, along with endomyocardial biopsy. MRI is now the
preferred noninvasive imaging modality and can aid in
determining the stage of endomyocardial fibrosis. The
initial phases of the disease are characterized by diffuse
or focal endomyocardial inflammation with eosinophilic
infiltration of the LV and/or the RV, primarily involving
the ventricular apex and inflow tract. The outflow tracts
are usually spared. On MRI, the early endomyocardial
infiltrative stage manifests as thickening and hyperinten-
sity of the endomyocardium on T 2-weighted sequences,
with corresponding regional wall-motion abnormali-
ties. The ventricular cavity is small, and there is atrioven-
tricular regurgitation with associated enlargement of the
atrium, reflecting the restrictive filling of the ventricles.
Subsequent endomyocardial damage has 3 sequential
stages: acute subendocardial necrosis and microabscess for-
mation, subendocardial denudation and thrombus forma-
tion in the ventricular cavity, and endomyocardial fibrosis.
As the disease progresses, the later stages have a characteris-
tic 3-layered appearance on MRI. The layers from ventricu-
lar cavity outward are nonenhancing thrombus/fibrous
tissue, enhancing thickened endomyocardium, and diffuse
myocardial thickening.
Overall, the prognosis for both Loeffler endomyocardi-
tis and endomyocardial fibrosis is poor. Early detection is of
great importance; early initiation of therapy can help prevent
progression to the fibrotic phase. Corticosteroid therapy is
used for Loeffler endomyocarditis. Identification and treat-
ment of the underlying cause is necessary in endomyocardial
fibrosis.
 140 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies

C A S E 7Q

Figure 7.21 Cardiac sarcoidosis. A, Short-axis, black blood, fat-suppressed (triple inversion recovery) image showing mild myocardial edema in the
LV mid anteroseptal segment (white arrow). B and C, Short-axis (B) and 4-chamber (C) late gadolinium-enhancement images identifying patchy
enhancement in the LV basal anterior, basal and mid anteroseptal, and inferoseptal (red arrow) segments, and the RV free wall (arrowhead). D,
Single-shot, spin echo, axial scout image demonstrates subcarinal and bilateral hilar lymphadenopathy and small bilateral pleural effusions.
 7.  No n ischemic M yocardia l D isease  •
C A R DI AC S A RC OI D O S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 45-year-old man was hospitalized for atrial fibrillation
with rapid ventricular response. Clinical work-up including
echocardiography showed systolic dysfunction. The patient
also reported a history of chronic cough. Additional clini-
cal assessment identified mediastinal and hilar lymphade-
nopathy, along with hepatosplenomegaly with abnormal liver
enzymes and hypercalcemia.
C L I N IC A L QU E S T ION
MRI (Figure 7.21) was ordered to assess for cardiac sarcoidosis.
C A R DI AC M R I PROTO C OL
Use Nonischemic Myocardial Disease Protocol 5.2 (see
page 78). Additional/optional sequences include short-
axis, T2-weighted, fat-suppressed, black blood (triple
inversion recovery) and long- or short-axis, non–fat-sup-
pressed (double inversion recovery) and fat-suppressed
(triple inversion recovery) images.
I M AG I NG F I N DI NG S
The MR images obtained provided the diagnosis of restric-
tive cardiomyopathy with patchy fibrosis within the myo-
cardium. A black blood, fat-suppressed view demonstrated
mild myocardial edema in the LV anteroseptal wall. Late
141
gadolinium-enhancement images showed patchy enhance-
ment in the LV anteroseptal wall and RV free wall. A single-
shot spin-echo scout image demonstrated subcarinal and
bilateral hilar lymphadenopathy and small bilateral pleural
effusions.
S U M M A RY
As a result of the MRI findings of restrictive cardiomyopathy
with areas of abnormal myocardial late gadolinium enhance-
ment, the patient was started on corticosteroid therapy for
presumed cardiac sarcoidosis.
Sarcoidosis is a multisystem granulomatous disease
of unknown etiology. The histopathologic diagnosis is
made by the identification of noncaseating granulomas.
Pulmonary involvement is most common, with up to 20%
of patients having cardiac involvement; clinically signifi-
cant cardiac sarcoidosis is much less common. Cardiac
involvement may precede, follow, or concurrently exist
with other organ involvement and typically affects the LV
more than the RV. Patients with cardiac sarcoidosis have
a poor prognosis and may have conduction abnormalities,
arrhythmias, and heart failure. Increasingly, MRI has been
shown to be useful in detecting cardiac sarcoidosis, which is
often subclinical and not easy to identify by echocardiogra-
phy or endomyocardial biopsy. Myocardial thickening and
increased signal abnormality on T 2-weighted sequences
are indicative of edema associated with granulomatous
infiltration. Myocardial late gadolinium enhancement is
generally patchy, subepicardial, and midmyocardial; it can
occur anywhere in the ventricle but is classically seen at the
basal septum.
 142 • S ectio n I I : C l i n ica l A ppl icatio n s a n d C ase S t u dies
S UG G E S T E D R E A DI NG
Apical Ballooning Cardiomyopathy
Eitel I, Behrendt F, Schindler K, Kivelitz D, Gutberlet M, Schuler G,
et al. Differential diagnosis of suspected apical ballooning syndrome
using contrast-enhanced magnetic resonance imaging. Eur Heart J.
2008 Nov;29(21):2651–9. Epub 2008 Sep 27.
O’Donnell DH, Abbara S, Chaithiraphan V, Yared K, Killeen RP,
Martos R, et al. Cardiac MR imaging of nonischemic cardiomyopa-
thies: imaging protocols and spectra of appearances. Radiology. 2012
Feb;262(2):403–22.
Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia
Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke DA,
et al. Diagnosis of arrhythmogenic right ventricular cardiomy-
opathy/dysplasia: proposed modification of the task force criteria.
Circulation. 2010 Apr 6;121(13):1533–41. Epub 2010 Feb 19.
Cardiac Amyloidosis
Maceira AM, Joshi J, Prasad SK, Moon JC, Perugini E, Harding I,
et al. Cardiovascular magnetic resonance in cardiac amyloidosis.
Circulation. 2005 Jan 18;111(2):186–93. Epub 2005 Jan 3.
Cardiac Sarcoidosis
Gupta A, Singh Gulati G, Seth S, Sharma S. Cardiac MRI in restrictive
cardiomyopathy. Clin Radiol. 2012 Feb;67(2):95–105. Epub 2011
Oct 4.
Patel MR, Cawley PJ, Heitner JF, Klem I, Parker MA, Jaroudi WA,
et al. Detection of myocardial damage in patients with sarcoidosis.
Circulation. 2009 Nov 17;120(20):1969–77. Epub 2009 Nov 2.
Dilated Cardiomyopathy
Rihal CS, Nishimura RA, Hatle LK, Bailey KR, Tajik AJ. Systolic and
diastolic dysfunction in patients with clinical diagnosis of dilated
cardiomyopathy: relation to symptoms and prognosis. Circulation.
1994 Dec;90(6):2772–9.
Endomyocardial Fibrosis
Syed IS, Martinez MW, Feng DL, Glockner JF. Cardiac magnetic reso-
nance imaging of eosinophilic endomyocardial disease. Int J Cardiol.
2008 Jun 6;126(3):e50–2. Epub 2007 Mar 30.
Hypertrophic Cardiomyopathy
Kwon DH, Setser RM, Popovic ZB, Thamilarasan M, Sola S,
Schoenhagen P, et al. Association of myocardial fibrosis, electrocar-
diography and ventricular tachyarrhythmia in hypertrophic cardio-
myopathy: a delayed contrast enhanced MRI study. Int J Cardiovasc
Imaging. 2008 Aug;24(6):617–25. Epub 2008 Jan 19.
Rubinshtein R, Glockner JF, Ommen SR, Araoz PA, Ackerman MJ,
Sorajja P, et al. Characteristics and clinical significance of late gad-
olinium enhancement by contrast-enhanced magnetic resonance
imaging in patients with hypertrophic cardiomyopathy. Circ Heart
Fail. 2010 Jan;3(1):51–8. Epub 2009 Oct 22.
Syed IS, Ommen SR, Breen JF, Tajik AJ. Hypertrophic cardiomyopa-
thy: identification of morphological subtypes by echocardiography
and cardiac magnetic resonance imaging. JACC Cardiovasc Imaging.
2008 May;1(3):377–9.
Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Breen
JF, et al. Comparison of surgical septal myectomy and alcohol septal
ablation with cardiac magnetic resonance imaging in patients with
hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 2007
Jan 23;49(3):350–7. Epub 2007 Jan 4.
Left Ventricular Noncompaction
Dodd JD, Holmvang G, Hoffmann U, Ferencik M, Abbara S, Brady TJ,
et al. Quantification of left ventricular noncompaction and trabecu-
lar delayed hyperenhancement with cardiac MRI: correlation with
clinical severity. AJR Am J Roentgenol. 2007 Oct;189(4):974–80.
Harris SR, Glockner J, Misselt AJ, Syed IS, Araoz PA. Cardiac MR imag-
ing of nonischemic cardiomyopathies. Magn Reson Imaging Clin N
Am. 2008 May;16(2):165–83.
Myocarditis
Abdel-Aty H, Simonetti O, Friedrich MG. T2-weighted cardiovas-
cular magnetic resonance imaging. J Magn Reson Imaging. 2007
Sep;26(3):452–9.
Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P,
Cooper LT, et al; International Consensus Group on Cardiovascular
Magnetic Resonance in Myocarditis. Cardiovascular magnetic reso-
nance in myocarditis: a JACC White Paper. J Am Coll Cardiol. 2009
Apr 28;53(17):1475–87.
Zagrosek A, Abdel-Aty H, Boye P, Wassmuth R, Messroghli D, Utz W,
et al. Cardiac magnetic resonance monitors reversible and irreversible
myocardial injury in myocarditis. JACC Cardiovasc Imaging. 2009
Feb;2(2):131–8.
 8.
PER ICAR DI A L DISEASE
Phillip M. Young, MD

T
he pericardium is a flask-shaped sac composed of
2 virtually inelastic layers, with a small amount of
fluid between them, surrounding the heart. Its func-
tions are to anchor the heart in the mediastinum, prevent the
heart from extreme dilatation in acute settings, and poten-
tially act as a barrier to the spread of disease from contiguous
organs. Pathologic changes in its stiffness or in the amount
of fluid it contains can alter normal heart function. The
purpose of this chapter is to provide examples of pericardial
pathology-induced changes and to identify their appearance
on magnetic resonance imaging (MRI).

143
 144 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8 A

Figure 8.1 Pericardial effusion. A, Short-axis balanced SSFP view showing extensive pericardial fluid (white arrow) completely enveloping the heart.
The arrowhead identifies an infarction, with thinning of the inferior wall of the left ventricle. B, T2-weighted, non–fat-suppressed, black blood
image demonstrates simple pericardial fluid (white arrow) without marked thickening of the pericardium (yellow arrow). C, Late gadolinium-
enhancement image demonstrates the effusion (white arrow), enhancement of the infarction (arrowhead), and lack of thickening of the right
ventricular pericardium (yellow arrow).
 8 .  Pe r i c a r d i a l D i s e a s e
S I M PLE PERICARDIAL E F F US ION
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 71-year-old man sought care for evaluation of shortness of
breath and lower extremity edema. The patient had a history
of coronary artery disease and prior myocardial infarction.
Echocardiographic images were limited but suggested a peri-
cardial effusion.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.1) was ordered to assess left ventricular
(LV) function and to investigate possible pericardial disease.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views.
I M AG I NG F I N DI NG S
The key clinical images obtained showed a large simple
pericardial effusion without hemodynamic compromise.
A balanced steady-state free precession (SSFP) view iden-
tified extensive pericardial fluid around the entire heart.
• 145
Non–fat-suppressed black blood imaging demonstrated peri-
cardial fluid without marked thickening of the pericardium.
A late gadolinium-enhancement image showed an effusion.
A myocardial scar was present in the inferior wall without
enhancement of the pericardium to suggest active pericarditis.
S U M M A RY
Normally, only 15 to 50 mL of fluid is present in the pericar-
dium, and visually increased amounts of fluid are termed peri-
cardial effusion. Simple pericardial effusions are usually not
imaged with MRI; echocardiography is the standard imaging
technique to determine the presence or absence of tamponade
in the urgent setting. Imaging of pericardial effusions is occa-
sionally performed to assess for an underlying mass or inflam-
mation as the cause or when echocardiographic images are
insufficient. On the basis of the imaging findings of this study,
the diagnosis of a pericardial effusion without evidence of
active pericarditis was made. Echocardiography-guided peri-
cardiocentesis was performed for both therapeutic and diag-
nostic purposes. On analysis, the fluid was without suspicious
features, and the patient had symptomatic improvement.
Effusions can be secondary to an inflammatory process,
such as pericarditis, or can be noninflammatory, due to hypo-
thyroidism or cirrhosis, for example. Rapid or significant
accumulation of pericardial fluid can lead to tamponade, a
life-threatening state of impaired ventricular diastolic filling.
This is generally not encountered in the MRI setting.
 146 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8B

Figure 8.2 Constrictive pericarditis. Real-time, free-breathing, short-axis, balanced SSFP images of the heart during inspiration (A) and expiration
(B). Respirophasic flattening of the interventricular septum (arrow) is seen with inspiration (A) but not with expiration (B).
 8 .  Pe r i c a r d i a l D i s e a s e
CON S TRICTI V E PH Y S IOLO G Y ON
F REE-B REAT H IN G I M AG IN G
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 57-year-old man sought care from his family physician for
chronic shortness of breath and fluid retention.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.2) was ordered to determine the pres-
ence or absence of pericarditis and constrictive physiology.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views, and short-
axis, free-breathing, balanced SSFP imaging to assess res-
pirophasic changes in the interventricular septum.
I M AG I NG F I N DI NG S
Short-axis balanced SSFP images were obtained during
free-breathing. Although these images are of inferior quality
compared with breath-held images, they demonstrated tran-
sient flattening of the interventricular septum during inspira-
tion, which was not evident during expiration. This reflects
the constraint imposed on the total heart volume by non-
compliant pericardium. During inspiration, negative intra-
thoracic pressures cause increased systemic venous pressures
• 147
in the chest and decreased pulmonary venous pressures. The
increase in right ventricular (RV) filling during inspiration
comes at the expense of LV filling because of the constraint
in volume.
S U M M A RY
On the basis of the MRI findings, the patient was given a
diagnosis of constrictive pericarditis with pericardial thicken-
ing and enhancement. Because of multiple comorbid condi-
tions, including severe heart failure with ascites and edema,
the patient elected medical management rather than the sur-
gical option of pericardiectomy.
MRI is often used to assess for pericardial inflammation
(manifested by edema on T2-weighted imaging or postcon-
trast late gadolinium enhancement), as well as to confirm
clinical suspicion of constriction. Static images suggestive of
constriction include pericardial thickening, effusion, inflam-
mation/enhancement, calcification (best seen on computed
tomography [CT]), and findings secondary to the abnor-
mal filling pressures, such as septal bounce, a D-shaped LV,
increased atrial size, and large coronary sinus and/or inferior
vena cava. Free-breathing short- or long-axis images will typi-
cally show increased filling of the RV with inspiration at the
expense of LV filling, manifested as a leftward shift of the ven-
tricular septum.
Constrictive pericarditis is a condition (typically chronic)
in which pericardial fibrosis or calcification limits diastolic
filling and preload of the ventricles. The clinical manifestation
of these abnormal hemodynamics is congestive symptoms,
including weight gain, abdominal bloating and discomfort,
shortness of breath, fatigue, and edema.
 148 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8 C

Figure 8.3 Myopericarditis. A, Short-axis, T2-weighted, fat-suppressed, black blood image showing pericardial edema (arrowheads). Myocardial
edema is identifiable by the hyperintensity within the myocardium (arrow). B, Short-axis, T1-weighted, late gadolinium-enhancement image
showing a focal region of enhancement within the inferior wall indicating the presence of myocardial infarction (arrow). The arrowheads identify
pericardial enhancement.
 8 .  Pe r i c a r d i a l D i s e a s e
ACUTE M YOPERICARDITI S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 42-year-old woman with a history of systemic lupus ery-
thematosus sought care for atypical chest pain. Evaluation
showed increased troponin levels, and coronary arteriography
showed normal results. As a result of this finding, either myo-
carditis or pericarditis was suspected.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.3) was ordered to determine the pres-
ence or absence of myocarditis and pericarditis.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78).
I M AG I NG F I N DI NG S
T2-weighted, fat-suppressed, black blood images and
T1-weighted late gadolinium-enhancement images dem-
onstrated circumferential pericardial edema and enhance-
ment, as well as a focal region of subepicardial myocardial
• 149
edema and enhancement in the inferior wall. The use of fat
suppression on T2-weighted imaging allows hyperintense
signal to be more clearly distinguished from signal arising
from lipid, providing a more definitive diagnosis of fluid or
edema. Hyperintense signal within the myocardium on late
gadolinium-enhancement images indicated the presence of
myocardial scar. Hyperintense signal in both T2-weighted
and late gadolinium-enhancement images indicated both
active inflammatory processes and fibrosis, suggesting recent
myocardial injury.
S U M M A RY
As a result of the MRI findings, myopericarditis was diag-
nosed concurrent with systemic lupus erythematosus. The
symptomatic presentation was thought to be due to an
inflammatory flare and was monitored with subsequent MRI
examinations. Follow-up examinations demonstrated resolu-
tion of the myocardial edema but persistence of enhancement,
suggesting myocardial necrosis and fibrosis.
Myopericarditis is an infrequent finding on imaging.
Electrocardiographic changes are often present in acute peri-
carditis, however, which suggests that myocardial involvement
may be more common than is realized. Myocardial involve-
ment may result in tissue necrosis, although this is certainly
not necessarily the case.
 150 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8D

Figure 8.4 Acute flare of chronic pericarditis. A, Axial, T1-weighted, non–fat-suppressed, black blood image demonstrates extensive pericardial
thickening (arrows) and adjacent fat stranding. B, Axial, postcontrast, fat-suppressed, T1-weighted, spoiled gradient echo image showing
enhancement within the pericardium (arrowhead) with a small amount of loculated fluid. C and D, A short-axis, late gadolinium-enhancement
image from the current examination (C) shows significant pericardial thickening and enhancement with some loculated foci of pericardial fluid,
which were not present on a similar image from a previous study (D).
 8 .  Pe r i c a r d i a l D i s e a s e
ACUTE F LARE OF C H RONIC
RECURRENT PERICARDITI S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 40-year-old man with a history of chronic recurrent peri-
carditis sought care from his family physician for return of his
typical symptoms suggesting a flare of disease activity.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.4) was ordered to document the pres-
ence and severity of pericardial inflammation.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views.
I M AG I NG F I N DI NG S
Axial, T1-weighted, non–fat-suppressed, black blood imag-
ing demonstrated extensive pericardial thickening and
adjacent fat stranding. Postcontrast, T1-weighted, spoiled
• 151
gradient echo imaging with fat suppression demonstrated
significant pericardial enhancement with the presence
of some loculated fluid. Comparison of postcontrast late
gadolinium-enhancement images from the current examina-
tion and a previous study confirmed that the current study’s
findings were a new development.
S U M M A RY
On the basis of both the findings of the MRI examination and
comparison with previous cardiac MRI studies performed at
an outside institution, an acute flare of chronic recurrent peri-
carditis was diagnosed. The cause of the patient’s pericarditis
was thought to be an autoimmune phenomenon secondary to
a subclinical viral infection or other environmental exposure.
The patient subsequently underwent curative pericardiec-
tomy because of his long history of recurrent symptoms and
intolerance of colchicine therapy.
Acute pericarditis results from active inflammation of the
pericardium. Potential causes include viral, postoperative, or
autoimmune phenomena, but it often is idiopathic. Patients
classically have sharp retrosternal pain, which is often pleu-
ritic and worse in the recumbent position and sometimes radi-
ates to the shoulder, arm, or epigastrium. Recurrent episodes
may occur, often after withdrawal of corticosteroids given for
a previous episode.
 152 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8E

Figure 8.5 Constrictive pericarditis. Axial, T1-weighted, non–fat-suppressed, black blood image demonstrates pericardial thickening (yellow arrow),
a dilated suprahepatic inferior vena cava (arrowhead), and a right pleural effusion (white arrow).
 8 .  P e r i c a r d i a l D i s e a s e
CON S TRICTI V E PERICARDITI S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 55-year-old man saw his cardiologist after a 1-year history
of progressive lower extremity swelling, shortness of breath,
and dyspnea on exertion. Previous CT pulmonary angiogra-
phy noted right pleural effusion and pericardial calcifications.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.5) was ordered to assess for evidence
of pericarditis and constriction.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views.
I M AG I NG F I N DI NG S
Axial, T1-weighted, non–fat-suppressed, black blood imaging
demonstrated pericardial thickening, a dilated suprahepatic
• 153
inferior vena cava, and right pleural effusion. Although vari-
ous imaging data were acquired in this study, the single black
blood image described the constellation of findings that are
suggestive of constrictive pericarditis. Functional analysis of
short-axis balanced SSFP images demonstrated normal LV
systolic function, with an ejection fraction of 62%; the RV
systolic function was slightly decreased, with an ejection frac-
tion of 42%.
S U M M A RY
After confirmation of constrictive pericarditis by MRI, the
patient underwent surgical pericardiectomy. Because this
procedure is considered curative, no further treatment was
initiated except periodic outpatient cardiology follow-up
examinations.
Because of the restricted diastolic filling of both ventricles,
secondary anatomic signs can be very helpful in diagnosing
constriction. Among the suggestive findings are enlargement
of the cardiac atria, pleural effusion, distortion of ventricular
contours (“acorn heart”), thickened pericardium, and dilated
inferior vena cava.
 154 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8F

Figure 8.6 Subtotal pericardiectomy. A, Axial, T1-weighted, non–fat-suppressed, black blood image demonstrates anterior pericardial scarring
(arrow). B, Axial, fat-suppressed, late gadolinium-enhancement image demonstrates significant effusion and enhancement in the remaining
pericardium (arrowhead).
 8 .  P e r i c a r d i a l D i s e a s e
RECURRENT CON S TRICTION
A F TER S U B TOTAL
PERICARDIECTOM Y
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 37-year-old man had a history of recurrent effusive-
constrictive pericarditis. A “pericardiectomy” had been pre-
viously performed at an outside institution because of the
inability to wean the patient from corticosteroid therapy and
the need for recurrent pericardiocentesis. After the procedure,
the patient remained symptomatic.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.6) was ordered to assess for the pres-
ence of any constrictive physiology.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views, and short-
axis, free-breathing, balanced SSFP imaging to assess res-
pirophasic changes in the interventricular septum.
• 155
I M AG I NG F I N DI NG S
Axial, T1-weighted, non–fat-suppressed, black blood imag-
ing demonstrated some anterior scarring at the site of a
partial pericardial resection and a large circumferential peri-
cardial effusion in the remaining pericardial space. An axial,
postcontrast, fat-suppressed, late gadolinium-enhancement
image demonstrated significant enhancement and scarring.
Short-axis balanced SSFP images revealed a small LV cavity
with normal LV systolic function (ejection fraction, 71%)
and slightly decreased RV systolic function (ejection frac-
tion, 44%).
S U M M A RY
On the basis of the MRI findings, including the presence of
active inflammation in the pericardium, it was determined
that the previous pericardiectomy had been subtotal. As a
result, the patient subsequently underwent completion peri-
cardiectomy, which was curative.
Pericardiectomy is infrequently performed but can be
curative for either constrictive pericarditis or chronic recur-
rent pericarditis that is refractory to medical therapy. The best
results are obtained with aggressive removal of pericardial tis-
sue, usually only leaving a small amount of tissue posteriorly
to spare the phrenic nerves.
 156 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8 G

Figure 8.7 Pericardial cyst. A and B, Axial, T1-weighted, non–fat-suppressed (A) and T2-weighted, fat-suppressed (B) black blood images
demonstrating a simple, well-circumscribed cystic structure on the surface of the pericardium (arrows). C, Axial, first-pass, myocardial perfusion
image during arrival of the contrast bolus in the LV. In combination, these images indicate the presence of a nonperfused mass containing fluid,
indicating a cyst.
 8 .  P e r i c a r d i a l D i s e a s e
PERICARDIAL C Y S T
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 45-year-old woman was incidentally found to have a peri-
cardial cyst after undergoing abdominal CT.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.7) was ordered to evaluate and char-
acterize the lesion, which was only partially visualized by
abdominal CT.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78).
I M AG I NG F I N DI NG S
Axial, T1-weighted, non–fat-suppressed, and T2-weighted,
fat-suppressed, black blood images demonstrated a simple,
well-circumscribed, cystic structure along the left lateral
• 157
surface of the pericardium. The cyst was relatively isointense
on the non–fat-suppressed image, suggesting a relatively
long T1, and bright on the fat-suppressed image, indicating
a long T 2, both of which are indicative of fluid. Dynamic
perfusion images demonstrated no enhancement of the wall
of the cyst. The findings were compatible with a simple peri-
cardial cyst.
S U M M A RY
On the basis of the MRI examination findings, the mass was
definitively diagnosed as a simple pericardial cyst. Although
the size of the cyst was considerable, the patient remained
asymptomatic. As a result, no further work-up was required.
Pericardial cysts are infrequently seen but are character-
ized by smooth walls with barely perceptible enhancement
and characteristics of simple or mildly proteinaceous fluid.
The use of both non–fat-suppressed and fat-suppressed black
blood imaging allows for distinction of masses by determin-
ing the degree, if any, of fatty infiltration, as well as the overall
consistency of the mass (solid vs liquid). Advanced Dixon-
based imaging methods provide fat-water separation within a
single imaging series.
 158 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8H

Figure 8.8 Pericardial constriction. An axial, T1-weighted, non–fat-suppressed, black blood image demonstrates thickened pericardium distorting
the RV (yellow arrow), biatrial enlargement, and right pleural effusion (white arrow), which are definitive for constriction. A parallel imaging
artifact across the center of the image (arrowhead) is due to the choice of an acceleration factor at the upper limit for the number of radiofrequency
channels in the receiver coil.
 8 .  P e r i c a r d i a l D i s e a s e
PERICARDIAL CON S TRICTION
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 70-year-old man saw his primary care physician with a 1-year
history of progressive shortness of breath and intermittent
edema, weight gain, and increased abdominal girth. The patient
was given a preliminary diagnosis of pericardial constriction
on hemodynamic investigation with echocardiography.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.8) was ordered to confirm the pres-
ence of pericardial constriction.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78). Additional/
optional sequences include late gadolinium-enhancement
imaging in both short- and long-axis views, and short-
axis, free-breathing, balanced SSFP imaging to assess res-
pirophasic changes in the interventricular septum.
• 159
I M AG I NG F I N DI NG S
Axial, T1-weighted, non–fat-suppressed, black blood imag-
ing demonstrated focally thickened pericardium distorting
the contour of the RV, which suggested the likelihood of
pericardial constriction. This portion of the pericardium was
noted to be calcified on CT. Also evident was biatrial enlarge-
ment and a right pleural effusion, which was also compatible
with constrictive physiology. Septal flattening of the RV
with worsening upon inspiration suggested right-sided heart
strain and ventricular interdependence. Dilation of the pul-
monary arteries was also noted, which suggested pulmonary
hypertension.
S U M M A RY
As a result of the MRI findings, pericarditis and constrictive
physiology were diagnosed. The patient underwent curative
pericardiectomy. The postoperative course was complicated
by a localized mediastinal infection and nonunion of the ster-
notomy, but at 1-year follow-up the patient was happy with
his progress.
 160 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 8I

Figure 8.9 Pericardial abscess. A, Axial, T1-weighted, non–fat-suppressed, black blood image demonstrating a slightly T1-hyperintense, loculated
pericardial effusion (arrowhead) with thick walls and some adjacent fat stranding, along with fluid in the lungs (arrow). B, Axial, T2-weighted,
fat-suppressed, black blood image clearly showing fluid in the mass (arrowhead) and lungs (arrow). Increased image noise is a result of the use of
the radiofrequency body coil for signal reception to eliminate spatial variation in the received signal commonly found on phased-array receive-only
surface coils. C, Axial late gadolinium-enhancement image approximately 14 minutes post contrast administration. The inversion time of 250
milliseconds was selected to provide optimal enhancement of the mass with the consequential incomplete suppression of the signal from normal
myocardium. The peripherally enhancing fluid collection, along with the presence of a fever, indicates a high probability that the mass is an abscess.
 8 .  P e r i c a r d i a l D i s e a s e • 161

PERICARDIAL A B S CE S S imaging demonstrated a slightly T1-hyperintense, loculated

C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 72-year-old man underwent a left atrial ablation procedure,
after which an esophageal rupture developed into the pericar-
dium, with subsequent development of persistent fevers and
an increased leukocyte count.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 8.9) was ordered to investigate for the
presence of a pericardial abscess.
C A R DI AC M R I PROTO C OL
Use Pericarditis Protocol 5.3 (see page 78).
I M AG I NG F I N DI NG S
The images obtained were used to confirm a pericardial
abscess. Axial, T1-weighted, non–fat-suppressed, black blood
pericardial effusion with thick walls and some adjacent fat
stranding. T2-weighted, fat-suppressed, black blood imaging
demonstrated that the lesion was hyperintense, suggesting the
presence of fluid. Axial late gadolinium-enhancement imag-
ing showed intense enhancement of the lesion walls, indicat-
ing that the lesion capsule was fibrotic.
S U M M A RY
As a result of the MRI examination and the concurrence of
fever, the mass was diagnosed as a pericardial abscess result-
ing from esophageal perforation to the pericardium and
mediastinum. The patient underwent surgical repair of an
esophageal-pericardial fistula and recovered after a long
course of antibiotics.
Pericardial abscesses are quite rare and are most likely to
occur after surgery. They may occur as a complication of endo-
carditis. Treatment is decided on an individualized basis and
may include surgery, antibiotic therapy, percutaneous drain-
age, or a combination of these.
 162 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s
S UG G E S TED READIN G
Anavekar NS, Wong BF, Foley TA, Bishu K, Kolipaka A, Koo CW, et al.
Index of biventricular interdependence calculated using cardiac MRI: a
proof of concept study in patients with and without constrictive pericar-
ditis. Int J Cardiovasc Imaging. 2013 Feb;29(2):363–9. Epub 2012 Jul 21.
Croisille P, Revel D. MR imaging of the heart: functional imaging. Eur
Radiol. 2000;10(1):7–11.
Giorgi B, Mollet NR, Dymarkowski S, Rademakers FE, Bogaert J.
Clinically suspected constrictive pericarditis: MR imaging assessment
of ventricular septal motion and configuration in patients and healthy
subjects. Radiology. 2003 Aug;228(2):417–24. Epub 2003 Jun 11.
Hurrell DG, Nishimura RA, Higano ST, Appleton CP, Danielson GK,
Holmes DR Jr, et al. Value of dynamic respiratory changes in left and
right ventricular pressures for the diagnosis of constrictive pericardi-
tis. Circulation. 1996 Jun 1;93(11):2007–13.
Karia DH, Xing YQ, Kuvin JT, Nesser HJ, Pandian NG. Recent role
of imaging in the diagnosis of pericardial disease. Curr Cardiol Rep.
2002 Jan;4(1):33–40.
Kojima S, Yamada N, Goto Y. Diagnosis of constrictive pericarditis by
tagged cine magnetic resonance imaging. N Engl J Med. 1999 Jul
29;341(5):373–4.
Masui T, Finck S, Higgins CB. Constrictive pericarditis and restric-
tive cardiomyopathy: evaluation with MR imaging. Radiology. 1992
Feb;182(2):369–73.
Matsouka H, Hamada M, Honda T, Kawakami H, Abe M,
Shigematsu Y, et al. Evaluation of acute myocarditis and pericarditis
by Gd-DTPA enhanced magnetic resonance imaging. Eur Heart J.
1994 Feb;15(2):283–4.
Rajiah P. Cardiac MRI: part 2, pericardial diseases. AJR Am
J Roentgenol. 2011 Oct;197(4):W621–34.
Rienmuller R, Groll R, Lipton MJ. CT and MR imaging of pericardial
disease. Radiol Clin North Am. 2004 May;42(3):587–601.
Taylor AM, Dymarkowski S, Verbeken EK, Bogaert J. Detection of peri-
cardial inflammation with late-enhancement cardiac magnetic reso-
nance imaging: initial results. Eur Radiol. 2006 Mar;16(3):569–74.
Epub 2005 Oct 25.
Yared K, Baggish AL, Picard MH, Hoffmann U, Hung J. Multimodality
imaging of pericardial diseases. JACC Cardiovasc Imaging. 2010
Jun;3(6):650–60.
Young PM, Glockner JF, Williamson EE, Morris MF, Araoz PA,
Julsrud PR, et al. MR imaging findings in 76 consecutive surgically
proven cases of pericardial disease with CT and pathologic corre-
lation. Int J Cardiovasc Imaging. 2012 Jun;28(5):1099–109. Epub
2011 Jul 7.
Zurick AO, Bolen MA, Kwon DH, Tan CD, Popovic ZB, Rajeswaran
J, et al. Pericardial delayed hyperenhancement with CMR imaging
in patients with constrictive pericarditis undergoing surgical peri-
cardiectomy: a case series with histopathological correlation. JACC
Cardiovasc Imaging. 2011 Nov;4(11):1180–91.
 9.
CAR DI AC M ASSES
Ethany L. Cullen, MD, and Philip A. Araoz, MD

C
ardiac masses are uncommon findings on cardiac
magnetic resonance imaging (MRI). Therefore, for
those not familiar with their presentation, their cor-
rect diagnosis can be challenging. The algorithm shown can
assist in identifying the pathologic characteristics and cause
of a cardiac mass according to findings on MRI (Figure 9.1).
Masses are classified either as arising from within the heart
or as invading masses. Masses that arise from the heart
can then be further classified as a normal variant, throm-
bus, or neoplasm. Masses that invade the heart are typically
malignant, and the differential diagnosis can be narrowed
by determining the origin of the mass. In this chapter, sev-
eral case examples of cardiac masses from each category are
presented.

Figure 9.1 Decision tree for determining cardiac mass type on the basis of MRI. Correct classification of the cause and pathologic features of a
cardiac mass begins with identification of the origin of the mass. Further stratification is achieved by identification of specific imaging findings
associated with a given tumor type. IVC indicates inferior vena cava; RA, right atrium.

163
 164 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9A

Figure 9.2 Axial images demonstrating thickening of the interatrial septum, sparing the fossa ovalis. A, Four-chamber balanced SSFP image
shows high signal thickening of the interatrial septum with a characteristic India ink artifact at the interface of the fat and blood pool. B, Late
gadolinium-enhancement image shows no enhancement of the interatrial septum (arrow). C, Four-chamber, non–fat-suppressed, black blood image
demonstrates high signal consistent with fat. D, Non–fat-suppressed black blood image demonstrates narrowing of the superior vena cava (arrow) as
a result of the lipomatous hypertrophy.
 9.  C a r d i ac M a ss e s  •
NOR M AL VARIANT S
L I P OM ATOUS H Y PE RT ROPH Y OF T H E
I N T E R AT R I A L S E P T U M
Clinical History and Presentation
A 57-year-old woman was referred for contrast-enhanced com-
puted tomography (CT) of the chest to assess for the presence
of pulmonary emboli. Although no emboli were detected, a
mass was identified within the interatrial septum.
Clinical Question
Cardiac MRI (Figure 9.2) was ordered to evaluate the mass.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79). Additional/
optional sequences include cine balanced steady-state free
precession (SSFP) prescribed as a straight axial.
Imaging Findings
The 4-chamber balanced SSFP image showed thickening of
the interatrial septum with sparing of the fossa ovalis. The
165
thickened interatrial septum had signal characteristics consis-
tent with fat on all imaging sequences. There was no late gado-
linium enhancement of the interatrial septum. Narrowing of
the superior vena cava as a result of lipomatous hypertrophy
could be seen on the non–fat-suppressed black blood image;
the narrowing was not thought to be hemodynamically
significant.
Summary
A diagnosis of benign lipomatous hypertrophy of the interatrial
septum was made. Compression of the superior vena cava is
occasionally seen in patients with this entity, as in this case, but
only rarely has it been reported to cause physiologic obstruc-
tion. In this case, as in most cases, no intervention was required.
Lipomatous hypertrophy of the interatrial septum is,
despite its name, a benign hyperplasia of normal fat cells
within the interatrial septum. It is typically asymptom-
atic but can be associated with atrial tachyarrhythmias.
Lipomatous hypertrophy of the interatrial septum is typi-
cally a dumbbell-shaped mass that spares the fossa ovalis and
has the signal characteristics of fat on all imaging sequences.
The thickness of the interatrial septum should exceed 2 cm
for diagnosis. Lipomatous hypertrophy can contain brown
fat and demonstrate increased uptake on positron emission
tomography/CT.
 166 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9B

Figure 9.3 Axial balanced SSFP image demonstrating a small, low-signal, rounded mass originating from the posterior right atrium (arrow).
 9.  C a r d i ac M a ss e s  •
PROM I N E N T C R I S TA T E R M I N A L I S
Clinical History and Presentation
A 54-year-old man with atypical chest pain and dyspnea was
referred for cardiac MRI to further evaluate an incidentally
detected right atrial mass seen on echocardiography.
Clinical Question
Cardiac MRI (Figure 9.3) was performed for further evalua-
tion of the incidental right atrial mass.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
The key diagnostic image acquired was used to identify a
low-signal, rounded mass originating from the posterior wall
167
of the right atrium. Note that a conventional 4-chamber view
was not used to visualize the right side of the heart, which is
more clearly depicted on axial images. This is the characteristic
appearance of a prominent crista terminalis, which is a benign
normal variant.
Summary
A benign normal variant such as a prominent crista terminalis
may be seen on MRI performed for an unrelated indication
or may be imaged for further evaluation after a mass has been
identified on echocardiography. The crista terminalis is the
fibromuscular ridge that separates the embryonic sinus veno-
sus from the primitive right atrium. It can be confused with a
mass arising from the posterior right atrial wall.
 168 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9 C

Figure 9.4 Balanced SSFP images demonstrating the prominent eustachian valve (arrows). A, Short-axis view. B, Right ventricular inflow view
bisecting the right atrium, inferior vena cava, and superior vena cava.
 9.  C a r d i ac M a ss e s  •
PROM I N E N T EUS TACH I A N VA LV E
Clinical History and Presentation
A 24-year-old man with sinus bradycardia was referred for
cardiac MRI to further evaluate a right atrial mass detected
incidentally on echocardiography.
Clinical Question
Cardiac MRI (Figure 9.4) was obtained for further evaluation
of the right atrial mass.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
169
Imaging Findings
The key diagnostic images were used to highlight the promi-
nence of the eustachian valve, which can also be mistaken for
a right atrial mass. The balanced SSFP short-axis view clearly
depicts the prominent eustachian valve, and the right ventric-
ular inflow balanced SSFP image allows visualization of the
right atrium, inferior vena cava, and superior vena cava.
Summary
The eustachian valve is the valve of the inferior vena cava and
is located at the junction of the inferior vena cava and right
atrium. When prominent, the valve can be mistaken for a mass
or thrombus. It is important to be familiar with these normal
variants and be able to distinguish them from a cardiac mass
that would require further evaluation and treatment.
 170 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9D

Figure 9.5 Series of 4-chamber images demonstrating a mass in the right atrium (arrows). The mass is isointense to myocardium on the balanced
SSFP image (A) and on the black blood non–fat-suppressed image (B). C, Late gadolinium-enhancement sequence shows no enhancement within
the right atrial mass. These findings are consistent with a thrombus.
 9.  C a r d i ac M a ss e s  •
INTRACARDIAC T H ROM BUS
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 42-year-old woman with severe rheumatoid arthritis was
referred for evaluation of a right atrial mass incidentally
detected during echocardiographic assessment of left ventric-
ular function. The mass was thought to be a thrombus and the
patient was started on anticoagulation therapy. The mass did
not change on serial echocardiography after 4 months.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 9.5) was performed to determine if the
right atrial mass was a solid mass or a thrombus.
C A R DI AC M R I PROTO C OL
Use Cardiac Mass Protocol 5.6 (see page 79).
I M AG I NG F I N DI NG S
A small mobile mass (4 cm total length) was detected within
the right atrium. The mass was isointense to myocardium
on the balanced SSFP and non–fat-suppressed black blood
171
sequences. On balanced SSFP cine images, the mass was seen
to arise from the right atrial free wall with several small cur-
vilinear foci projecting into the atrial cavity. No late gadolin-
ium enhancement was seen within the mass. These findings
were consistent with thrombus.
S U M M A RY
After characterization of the mass on MRI as a thrombus,
anticoagulation therapy was initiated in lieu of surgical throm-
bectomy. Follow-up MRI studies demonstrated a decrease in
mass size, confirming that the mass was a thrombus.
Thrombus is the most frequent intracardiac mass and
the most common tumor mimic. The most common sites for
thrombi to form are the left ventricular apex adjacent to an
apical myocardial infarction or in the left atrial appendage
in the setting of atrial fibrillation, but they can form in any
cardiac chamber. The T1 and T2 characteristics of thrombi
vary depending on the age of the thrombus. Thrombus is
typically dark on balanced SSFP images and can be diffi-
cult to distinguish from the myocardium if the thrombus
is small and laminated. The key finding for identifying a
thrombus is the lack of enhancement after administration of
gadolinium. On late gadolinium-enhancement sequences, a
thrombus will be hypointense compared with the myocar-
dium and the blood pool.
 172 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9E

Figure 9.6 Four-chamber long-axis views demonstrating a round left atrial mass attached to the interatrial septum (arrows). The myxoma is slightly
hyperintense compared with the myocardium on the balanced SSFP image (A), hyperintense on the fat-suppressed black blood T2-weighted image
(B), and isointense to the myocardium on the non–fat-suppressed black blood T1-weighted image (C). The mass shows no significant enhancement
on first-pass perfusion (D) and has no late gadolinium enhancement (E).
 9.  C a r d i ac M a ss e s  •
NEOPLA S M S
M Y XOM A
Clinical History and Presentation
A 77-year-old woman was referred for further evaluation
of a left atrial mass that was incidentally seen on CT of the
abdomen performed to evaluate abdominal pain. Subsequent
echocardiography confirmed a left atrial mass with features
consistent with an atrial myxoma.
Clinical Question
Cardiac MRI (Figure 9.6) was performed to further evaluate
the left atrial mass.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
MRI identified a 1.5-cm, round, left atrial mass. The mass
was attached to the interatrial septum by a very short stalk
and was slightly mobile on cine balanced SSFP. The mass was
isointense or slightly hyperintense to myocardium on the bal-
anced SSFP sequences, hyperintense on the fat-suppressed
T2-weighted black blood image, and isointense on the
T1-weighted non–fat-suppressed black blood sequence. There
was no first-pass perfusion or late gadolinium enhancement
173
of the mass. There were no findings to suggest the mass had
invaded the myocardium. The findings were consistent with a
benign atrial myxoma.
Summary
After the mass was identified on MRI, the left atrial myxoma
was successfully resected. Myxomas account for approximately
50% of primary cardiac masses. They typically occur in adults
aged 30 to 60 years and are more common in women. Most
myxomas (75%) occur in the left atrium and another 15% to
20% occur in the right atrium. Myxomas are typically spo-
radic, although they can be inherited with Carney complex. If
there are multiple myxomas or if they are in atypical locations,
consider Carney complex as the appropriate diagnosis.
Myxomas are typically rounded atrial masses that arise
from the interatrial septum, usually near the fossa ovalis. They
can be pedunculated with a stalk or can have a broad-based
attachment. Myxomas are generally isointense on T1-weighted
images but may be heterogeneous due to calcification or hem-
orrhage. On T2-weighted images, myxomas are typically
hyperintense because of their myxoid stroma. Balanced SSFP
cine images are typically hyperintense compared with myo-
cardium but hypointense compared with the blood pool. Late
gadolinium-enhancement series usually demonstrate patchy
enhancement, but enhancement can be homogeneous and
intense. Cine balanced SSFP images are helpful for determin-
ing the attachment point to the interatrial septum as well as
the mobility of the mass. Myxomas can prolapse through or
obstruct the atrioventricular valves.
 174 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9F

Figure 9.7 Four-chamber long-axis views acquired with 3 separate imaging sequences. The right ventricular mass (arrows) has high signal on the
balanced SSFP image (A), high signal on the non–fat-suppressed black blood T1-weighted image (B), and low signal on the fat-suppressed black
blood T1-weighted image (C). These findings are consistent with a lipoma.
 9.  C a r d i ac M a ss e s  •
L I P OM A
Clinical History and Presentation
A 54-year-old woman without cardiac symptoms underwent
echocardiography as part of a pre–lung transplant evaluation.
The echocardiogram identified a mass in or overlying the right
ventricle.
Clinical Question
Cardiac MRI (Figure 9.7) was performed to further evalu-
ate the location and extent of the mass and to establish a
diagnosis.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
The key images were obtained as long-axis, 4-chamber views.
The balanced SSFP image demonstrated a high-signal mass
with a dark India ink outline in the apex of the right ventricle.
This mass was bright on T1-weighted black blood images and
dark on fat-suppressed black blood T1-weighted images. These
findings were characteristic of a benign lipoma. Note that
175
triple inversion recovery sequences are generally considered T2
weighted. However, T1 weighting can be achieved by setting
the pulse repetition time equal to 1 R-R interval, as opposed
to 2 or more used to provide T2 weighting.
Summary
As a result of the MRI findings, the mass was diagnosed as a
benign lipoma that did not affect either ventricular function
or function of the tricuspid valve. Therefore, neither surgical
nor medical intervention was required. The mass was observed
on routine echocardiography.
Lipomas are typically solitary masses that arise from epi-
cardium and grow into the pericardial space, but they can be
intramyocardial or endocardial and grow into any cardiac
chamber.
Lipomas are smooth, homogeneous, encapsulated, fatty
masses. They have high signal on T1-weighted images and
should demonstrate signal drop-out when fat saturation is
applied. They may contain thin, nonenhancing septa but
should not have a soft-tissue component. Lipomas will have
high signal intensity on balanced SSFP images, similar to the
adjacent epicardial fat. If the lipoma is within a cardiac cham-
ber, there will also be an India ink artifact at the junction of
the mass and the blood pool. No late gadolinium enhance-
ment should be seen in a lipoma.
 176 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9 G

Figure 9.8 Short-axis images demonstrating the presence of a large epicardial mass (arrows) extending into the pericardial space from the right
ventricular free wall. The mass is isointense to myocardium on the balanced SSFP image (A), hyperintense on the fat-suppressed, black blood,
T2-weighted image (B), and isointense on the black blood, non–fat-suppressed, T1-weighted image (C). After the administration of gadolinium
contrast, the mass demonstrates marked enhancement on the perfusion (D) and late gadolinium-enhancement image (E).
 9.  C a r d i ac M a ss e s  •
H E M A NG IOM A
Clinical History and Presentation
An 80-year-old woman with a history of breast cancer under-
went echocardiography to evaluate the onset of a cardiac mur-
mur. The echocardiogram demonstrated thickening of the
right ventricular free wall consistent with a mass.
Clinical Question
Cardiac MRI (Figure 9.8) was ordered to evaluate the extent
of the mass and to determine if the mass was a metastasis.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
The key images acquired as short-axis views showed a 5-cm
epicardial mass arising from the right ventricular free wall.
The borders were well defined with no evidence of local inva-
sion. The mass was isointense to myocardium on the bal-
anced SSFP and non–fat-suppressed black blood T1-weighted
images and hyperintense on the fat-suppressed black blood
T2-weighted sequence. The perfusion images showed con-
trast enhancement and intense late gadolinium enhancement,
177
indicating that the mass was highly vascular. These findings
were consistent with a benign hemangioma. Quantitative
analysis of short-axis, balanced SSFP, cine images indicated
normal left ventricular size and function without regional
wall-motion abnormalities.
Summary
On the basis of the MRI examination, the mass was identified
as a benign hemangioma. Because the tumor was identified
as being highly vascularized, biopsy was not recommended.
Instead, the mass was observed by additional follow-up echo-
cardiographic imaging.
Hemangiomas are benign vascular tumors that can
occur in any cardiac chamber and can be endocardial, epi-
cardial, or intramural. They are classified by the size of their
vascular channels as capillary, cavernous, or arteriovenous
hemangiomas.
Hemangiomas are typically hypointense on balanced SSFP
sequences, heterogeneously isointense on non–fat-suppressed
black blood T1 sequences, and hyperintense on fat-suppressed
(triple inversion recovery) black blood T2 sequences. They
may contain areas of fat that present as high signal on
non–fat-suppressed (double inversion recovery) black blood
T1-weighted images. Gadolinium contrast enhancement
is intense and prolonged but may be heterogeneous due to
fibrous septa and interspersed calcification.
 178 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9H

Figure 9.9 Long-axis 4-chamber views of the heart demonstrating the presence of a bulky right atrial mass (arrows) and a small pericardial effusion
(arrowheads). The mass is isointense to the myocardium on the fat-suppressed balanced SSFP image (A) and the non–fat-suppressed, black blood,
T1-weighted image (B) and hyperintense on the fat-suppressed, black blood, T2-weighted image (C). D, Late gadolinium-enhancement image
demonstrating absence of late enhancement within the mass.
 9.  C a r d i ac M a ss e s  •
A NG IO S A RC OM A
Clinical History and Presentation
A 71-year-old woman sought care from her primary care phy-
sician for shortness of breath and hemoptysis. She was found
to have multiple pulmonary metastases. Biopsy demonstrated
poorly differentiated angiosarcoma.
Clinical Question
Cardiac MRI (Figure 9.9) was performed to identify the loca-
tion of the primary tumor.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
The acquired images demonstrated a large, invasive, lobu-
lated, right atrial mass. The interatrial portion of the mass was
mobile and prolapsed through the tricuspid valve, causing
both stenosis and regurgitation. The mass was isointense to
myocardium on balanced SSFP and non–fat-suppressed (dou-
ble inversion recovery) black blood T1-weighted sequences
and heterogeneously hyperintense on the fat-suppressed
(triple inversion recovery) black blood T2 sequence.
179
Heterogeneous enhancement was present on perfusion and
late gadolinium-enhancement sequences. There was also a
small pericardial effusion. Numerous pulmonary metastases
were also visualized but are not shown in the images.
Summary
On the basis of the imaging findings, the mass was identi-
fied as an angiosarcoma of the myocardium with metastatic
bilateral lung nodules. Pathologic confirmation identified the
primary as a grade IV angiosarcoma. Surgical resection was
not considered as a viable treatment option; therefore, the
patient underwent chemotherapy for debulking of the pri-
mary tumor.
Angiosarcoma is the most common primary cardiac
malignancy. It most often occurs in the right atrioventricular
groove. The mass is typically bulky and infiltrative, with areas
of hemorrhage and necrosis. Angiosarcomas can also present
as an infiltrative pericardial mass.
Angiosarcomas typically have heterogeneous T1 signal
with areas of hyperintensity due to hemorrhage and hypoin-
tense areas of calcification. The T2 signal is also heterogeneous
but predominantly hyperintense. Enhancement is heteroge-
neous, reflecting areas of hypervascularity and necrosis. In
cases of infiltrative pericardial angiosarcoma, a pattern of
linear contrast enhancement with a hypointense necrotic core
has been described as a sunray appearance.
 180 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 9I

Figure 9.10 Octreotide study demonstrating an area of increased activity in the region of the left ventricular apex (arrow). Additional uptake in the
mediastinum and supraclavicular region is abnormal and represents additional metastases.

Figure 9.11 Long-axis 4-chamber and short-axis views demonstrating a mass in the lateral wall of the left ventricle (arrows). The mass is isointense
on both non–fat-suppressed, black blood, T1-weighted (A) and balanced SSFP sequences (B). Short-axis late gadolinium-enhancement (C) and
fat-suppressed, black blood, T2-weighted (D) images demonstrate a T2-hyperintense mass with late gadolinium enhancement.
 9.  C a r d i ac M a ss e s  •
M E TA S TA S E S
Clinical History and Presentation
A 58-year-old woman sought care from her primary care
provider for symptoms of palpitations, hot flashes, flushing,
and abdominal fullness. CT demonstrated a large mesenteric
mass, liver metastases, and enlarged retroperitoneal lymph
nodes. Pathologic findings were consistent with a neuroen-
docrine tumor. An octreotide study (Figure 9.10) was then
performed, which demonstrated an area of myocardial or
pericardial uptake concerning for a cardiac metastasis.
Clinical Question
After the octreotide study, cardiac MRI (Figure 9.11) was
performed to evaluate possible myocardial or pericardial car-
cinoid metastases.
Cardiac MRI Protocol
Use Cardiac Mass Protocol 5.6 (see page 79).
Imaging Findings
The cardiac MRI findings demonstrated a large mass
centered in the lateral wall of the left ventricle, which
181
correlated with the area of octreotide uptake. The mass
was isointense to myocardium on the balanced SSFP and
non–fat-suppressed, black blood, T1-weighted images
and hyperintense on the fat-suppressed, black blood, T 2
sequence. There was also heterogeneous late gadolinium
enhancement.
Summary
On the basis of the MRI characteristics, the mass was iden-
tified as a metastasis arising from a primary neuroendocrine
tumor. Because surgical excision of the mass was considered
too high risk, the patient underwent systemic management of
her disease by medical oncology.
Metastases are the most common cardiac masses and are
20 to 40 times more frequent than primary cardiac malig-
nancies. The most common sources of cardiac metastases
are lung and breast carcinoma, melanoma, and lymphoma.
Imaging findings are highly variable, with pericardial effu-
sion being the most common finding. Any cardiac mass in a
patient with a known malignancy is suggestive of a metastasis.
Most malignant masses will be hypointense or isointense on
T1 imaging, except for melanoma, which will be hyperintense.
Malignancies are typically T2 hyperintense and have some
degree of late gadolinium enhancement.
 182 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s
S UG G E S TED READIN G
Angiosarcoma
Yahata S, Endo T, Honma H, Ino T, Hayakawa H, Ogawa M, et al.
Sunray appearance on enhanced magnetic resonance image of car-
diac angiosarcoma with pericardial obliteration. Am Heart J. 1994
Feb;127(2):468–71.
Benign Neoplasm
Araoz PA, Mulvagh SL, Tazelaar HD, Julsrud PR, Breen JF. CT and
MR imaging of benign primary cardiac neoplasms with echo-
cardiographic correlation. Radiographics. 2000 Sep-Oct;20(5):
1303–19.
General Overview
Syed IS, Feng D, Harris SR, Martinez MW, Misselt AJ, Breen JF, et al.
MR imaging of cardiac masses. Magn Reson Imaging Clin N Am.
2008 May;16(2):137–64.
Lipomatous Hypertrophy
O’Connor S, Recavarren R, Nichols LC, Parwani AV. Lipomatous
hypertrophy of the interatrial septum: an overview. Arch Pathol Lab
Med. 2006 Mar;130(3):397–9.
Metastases
Lam KY, Dickens P, Chan AC. Tumors of the heart: a 20-year experience
with a review of 12,485 consecutive autopsies. Arch Pathol Lab Med.
1993 Oct;117(10):1027–31.
McAllister HA Jr, Hall RJ, Cooley DA. Tumors of the heart and pericar-
dium. Curr Probl Cardiol. 1999 Feb;24(2):57–116.
Myxomas
Reynen K. Cardiac myxomas. N Engl J Med. 1995 Dec 14;333(24):1610–7.
Primary Cardiac Malignancies
Araoz PA, Eklund HE, Welch TJ, Breen JF. CT and MR imaging of primary
cardiac malignancies. Radiographics. 1999 Nov-Dec;19(6):1421–34.
 10.
CONGENITA L DISEASE
Nandan S. Anavekar, MB, BCh, and Paul R. Julsrud, MD
M
agnetic resonance imaging (MRI) has unique
capabilities compared with other noninvasive
imaging modalities which are beneficial in the
evaluation of patients with congenital heart disease. This
is especially true for older patients who have undergone
attempts at surgical repair. With echocardiography, it may
be difficult to gain optimal acoustic windows to evaluate
these patients. With cardiac MRI, however, it is possible
to select the ideal imaging planes to display the relevant
individual anatomical and physiologic abnormalities in
these often complex situations. In addition, compared with
most other imaging modalities, MRI can achieve superior
183
flow quantification and tissue characterization to exam-
ine patients with congenital heart disease. The evaluation
of patients with congenital heart disease, more so than for
other disease entities, requires a working knowledge of vari-
ous congenital heart defects, surgical procedures performed
for these defects, and potential complications that may arise.
Additionally, assessment of many, often complex, congeni-
tal heart defects is not easily accomplished with standard-
ized imaging protocols and requires more of a “hands on”
approach at the scanner. This chapter provides a rationale
for the use of MRI for congenital heart disease and describes
its application in various conditions.
 184 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 A

Figure 10.1 Balanced steady-state free precession (SSFP) axial multislice images of tetralogy of Fallot demonstrating right ventricular enlargement
and hypertrophy. All images were acquired in the axial plane to facilitate volumetric assessment of the right ventricle (arrows).
 10 .  C o n g e n i ta l D i s e a s e
TET R ALOG Y OF FALLOT
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 31-year-old woman had cyanosis immediately after her birth
and received a diagnosis of tetralogy of Fallot. She underwent
placement of a central shunt from the ascending aorta to the
right pulmonary artery. Subsequently, she underwent com-
plete repair of the tetralogy with closure of the ventricular
septal defect, pulmonary valvotomy, patch angioplasty of the
right pulmonary artery, and right ventricular (RV) outflow
tract enlargement using a pericardial patch.
C L I N IC A L QU E S T ION
The patient was referred for MRI (Figure 10.1) to assess the
degree of pulmonic valve regurgitation and for RV volumetric
analysis in the setting of worsening fatigue. She also was hav-
ing symptoms related to atrial arrhythmias.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
Note that intravenous gadolinium contrast was not adminis-
tered in this study.
I M AG I NG F I N DI NG S
The key imaging findings of this study included an enlarged
RV and wide-open pulmonic valve regurgitation. The RV end-
diastolic volume was 306 mL, which was 188 mL/m2 indexed
to body surface area.
• 185
S U M M A RY
The literature suggests the cutoff for consideration of surgi-
cal intervention to be an indexed end-diastolic volume of 150
to 160 mL/m2. As a result of the MRI findings, the patient
underwent pulmonic valve replacement.
Tetralogy of Fallot is the most common congenital
heart disease in children older than 4 years with cyanosis.
Tetralogy of Fallot is a heart defect that comprises 4 com-
ponents: obstruction of the RV outflow tract, ventricular
septal defect, deviation of the origin of the aorta to the
right, and concentric hypertrophy of the RV. The 4 salient
anatomic components of the tetralogy result from a specific
morphogenetic abnormality, which is a malalignment of the
interventricular septum wherein the infundibular septum
moves anteriorly and cephalad and is therefore not aligned
with the trabecular septum, which creates a ventricular
septal defect. A right aortic arch can be seen in up to 25%
of patients with this defect. Anomalous origin and distri-
bution of the coronary arteries are also common, includ-
ing aberrant origin of a conus branch or origin of the left
anterior descending artery from the right coronary artery
or from the right aortic sinus. A single coronary artery may
also be seen. In tetralogy of Fallot, the most common rea-
son for reoperation is progressive pulmonary valve regurgi-
tation with resultant RV dilatation and dysfunction. This is
usually manifested as RV enlargement on imaging, as well
as contractile dysfunction. The RV is especially difficult to
characterize on conventional imaging using echocardiogra-
phy, and in this regard cardiac MRI is especially well suited
to characterize morphology and function but also to quan-
tify RV volumes and therefore change in volumes over serial
assessment.
 186 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 B

   

Figure 10.2 Balanced SSFP images of a transposition of the great arteries after a Mustard procedure. A, Multislice axial imaging planes facilitate
derivation of biventricular volumetric data and also are useful in delineating the baffle connections. The asterisk identifies a dilated pulmonary
artery that arises from a morphologic left ventricle (indicated by the yellow arrow). The red arrow indicates the morphologic RV. The arrowheads
indicate the pulmonary venous baffle directing oxygenated blood to the morphologic right (systemic) ventricle. B, Single-slice oblique image
demonstrates the inferior limb of the systemic venous baffle (arrow) draining into the morphologic left atrium. Also note the markedly dilated main
pulmonary artery (asterisk); this patient also had concomitant pulmonary valvular stenosis. C, Single-slice image demonstrates the systemic venous
drainage (arrows). The inferior limb of the systemic venous baffle drains into the morphologic left atrium. The superior limb of the systemic venous
baffle is also demonstrated right below the dilated main pulmonary artery (asterisk).
 10 .  C o n g e n i ta l D i s e a s e
T R AN S PO S ITION OF T H E G R EAT
A RTE R IE S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 41-year-old woman had been born with D-transposition of
the great vessels—atrioventricular concordance and ventricu-
loarterial discordance. Previous Blalock-Taussig shunts had
been performed, with subsequent takedown of both shunts
followed by a Mustard procedure.
C L I N IC A L QU E S T ION
The patient was referred for MRI (Figure 10.2) examination
to assess systemic (morphologic right) ventricular function
and the status of the interatrial baffle.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
Note that intravenous gadolinium contrast was not adminis-
tered in this study.
I M AG I NG F I N DI NG S
The key images from this study demonstrated the systemic
ventricle to be mildly dilated and moderately hypertrophied,
with a moderate decrease in global function. The systemic
ventricle can be identified as a morphologic RV by the pres-
ence of multiple septoparietal muscle bands, including a
moderator band. The calculated systemic ventricular ejection
fraction was 41%. In addition, the pulmonary venous drain-
age has been surgically changed such that it is now received
• 187
by the morphologic right atrium, which then drains into the
morphologic RV (the systemic ventricle).
Oblique imaging planes demonstrated the inferior limb
of the systemic venous baffle, which directs venous blood
received from the inferior vena cava into the morphologic
left atrium and then into the morphologic left ventricle (LV),
which is the subpulmonic ventricle.
In combination, the MRI data demonstrated the vascular
connections and patency of the interatrial baffle system.
S U M M A RY
The patient was treated conservatively. Traditional cardio-
vascular risk factors were identified and modified. Lifestyle
modifications including dietary changes and increased exer-
cise were instituted.
The term transposition signifies that the aorta arises from
the morphologic RV and the pulmonary trunk arises from the
morphologic LV. This represents a ventriculoarterial discor-
dance. The designation of complete transposition indicates
that ventriculoarterial discordance is associated with atrio-
ventricular concordance. This alignment results in a unique
circulation in which 2 independent circulations—a pulmo-
nary and a systemic circuit—function in parallel rather than
in series, as in normal cardiovascular anatomy. As in tetralogy
of Fallot, a right-sided aortic arch can commonly be seen in
persons with transposition of the great arteries.
The Mustard procedure is an interatrial baffling proce-
dure that directs systemic venous blood into the subpulmonic
morphologic LV and pulmonary venous blood to the sub-
aortic morphologic RV. Postoperative surveillance includes
assessment of clinical signs and symptoms of systemic ven-
tricular dysfunction and imaging to assess for baffle leaks or
obstruction.
 188 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 C

Figure 10.3 Balanced SSFP images of a congenitally corrected transposition of the great arteries. A, Axial multislice acquisition showing the morphologic
RV (arrow) to the left of the terventricular septum identified by the dominant trabeculations, including a moderator band. Note the increased wall
thickness of the morphologic RV that is needed to generate systemic pressures. The morphologic LV (arrowhead) has a thinner wall. Axial data sets are
used to derive volumetric data. B, Multiple oblique, balanced SSFP, single-slice acquisition with the imaging plane through the morphologic RV (arrow),
which directs blood through the aorta (asterisk)—a demonstration of ventriculoarterial discordance. Note that the pulmonary artery (arrowhead) and
aorta arise in parallel to each other, which is a result of the anatomic defect. The morphologic RV receives pulmonary venous blood from the morphologic
left atrium (not shown). This double discordance arrangement physiologically “corrects” the circulation and can therefore be compatible with life.
 10 .  C o n g e n i ta l D i s e a s e
Figure 10.3 (Continued)
CONGENITALLY COR R ECTED
T R AN S PO S ITION OF T H E G R EAT
A RTE R IE S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 19-year-old man had been born with congenitally corrected
transposition of the great arteries. He had mild subpulmonary
obstruction due to an aneurysmal membranous septum. Over
the past few years his systemic ventricular function had grad-
ually decreased, and his systemic atrioventricular valve regur-
gitation increased slightly, but he remained asymptomatic.
C L I N IC A L QU E S T ION
The patient was referred for MRI (Figure 10.3) examination
for assessment of biventricular morphology and function.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
Note that intravenous gadolinium contrast was not adminis-
tered in this study.
I M AG I NG F I N DI NG S
Axial magnetic resonance (MR) images acquired in this study
clearly demonstrated the morphologic LV to the right of the
• 189
interventricular septum. The morphologic LV receives sys-
temic venous blood from a morphologic right atrium and
delivers this blood to the pulmonary artery. The morphologic
RV receives pulmonary venous blood from a morphologic left
atrium and delivers this to the aorta. Therefore, despite the
incorrect anatomic connection, this arrangement allows for
a physiologically correct pathway for blood flow through the
body. Due to this anatomic arrangement, the great arteries do
not cross as they arise from the base of the heart but arise in
parallel.
MRI findings showed mild systemic (morphologic right)
ventricular dilatation. The end-diastolic volume was 186 mL,
which was 106 mL/m2 indexed to body surface area. The sys-
temic ventricular contractile function was mildly decreased,
with a calculated ejection fraction of 49%.
S U M M A RY
The patient is symptomatically stable. He continues to par-
ticipate in sports at a moderate level and is not limited by
symptoms.
Congenitally corrected transposition of the great arteries
is typified by atrioventricular discordance and ventriculoar-
terial discordance. This results in pulmonary venous blood
being routed to a morphologic RV (atrioventricular discor-
dance) and subsequently to the systemic arterial circulation
via the aorta (ventriculoarterial discordance). Surveillance
includes assessment of clinical signs and symptoms of sys-
temic ventricular dysfunction.
 190 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 D

Figure 10.4 Partial anomalous pulmonary venous return. A, Balanced SSFP single-slice acquisition with the imaging plane selected to demonstrate
the superior vena cava in its long axis (arrow). It therefore demonstrates the drainage of a right upper pulmonary vein (asterisk). B, Coronal view
MR angiography demonstrates the drainage of the right upper pulmonary vein (arrowhead) into the superior vena cava (arrow).
 10 .  C o n g e n i ta l D i s e a s e
PA RTIAL ANOM ALOUS
PUL MONA RY V ENOUS R ETU R N
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 17-year-old boy sought care from his primary physician for
chest pain and dizziness. He also had a pectus excavatum.
He reported no other symptoms and participated in numer-
ous athletic activities without limitation. His chest pain was
believed to be musculoskeletal in origin. Echocardiography
revealed mild RV enlargement but otherwise normal cardiac
anatomy and function.
C L I N IC A L QU E S T ION
He was referred for cardiac MRI (Figure 10.4) to evaluate RV
size and function and to assess pulmonary venous anatomy.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
I M AG I NG F I N DI NG S
The images acquired demonstrated anomalous pulmonary
venous connection of all the right upper lobe pulmonary veins
into the superior vena cava near the entry of the azygos vein.
The right middle lobe, right lower lobe, and left-sided pulmo-
nary veins all connected normally with the left atrium. The
shunt can be quantified using phase-contrast techniques; in
this case, the calculated pulmonary flow:systemic flow ratio
was 1.3:1.
A balanced steady-state free precession (SSFP) sequence
demonstrated the anomalous pulmonary venous drain-
age. In order to achieve this, it is important to identify all
• 191
pulmonary venous connections and prescribe the correct
imaging plane that is aligned with the site of confluence of
each of the pulmonary veins to their receiving atrial cham-
ber. The resulting image may be confusing; therefore, each
step of image prescription must be appropriately labeled. MR
angiography performed in a coronal plane also demonstrated
the drainage of the right upper pulmonary vein into the supe-
rior vena cava.
S U M M A RY
Given the finding of right-sided chamber enlargement, the
patient underwent the Warden procedure, which includes
repair of partial anomalous pulmonary venous return with a
baffle of veins through a surgically created atrial septal defect
and a 16-mm interposition Gore-Tex graft connecting the
superior vena cava to the right atrial appendage.
Partial anomalous pulmonary venous connections exist
when 1 or more, but not all, pulmonary veins connect anoma-
lously to the right atrium. The finding of an anomalous pul-
monary venous connection should elicit the search for other
congenital cardiac defects, especially atrial septal defects. In
particular, both sinus venosus and ostium secundum atrial
septal defects are associated with the presence of anomalous
pulmonary venous drainage. Anomalous pulmonary venous
connections represent a site of left-to-right shunting of blood
flow. Therefore, not only is their anatomic identification
important, but also an impression of the downstream effects
of this shunt on RV geometry and function is essential to the
complete evaluation of the patient.
Cardiac MRI can be especially useful in the assessment
of the RV. Echocardiography is limited by acoustic windows
and by the RV sometimes being hidden, given its retrosternal
position. Using MRI, the venous and arterial connections are
well delineated, which makes it particularly useful for assess-
ing anomalous pulmonary venous connection.
 192 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 E

Figure 10.5 (Continues)

 10 .  C o n g e n i ta l D i s e a s e • 193

Figure 10.5 Ebstein anomaly of the tricuspid valve. A, In these axial balanced SSFP images taken before surgical repair, note the dilated right-sided
chambers (asterisk). For comparison, note the small size of the LV (arrowhead). Also note that a substantial portion of the RV is “atrialized”—thin
walled with morphologic characteristics of an atrial chamber rather than a ventricular chamber. B, Axial, balanced SSFP, multislice acquisition after
surgical repair showing the significantly improved RV size (asterisk) and the improved ratio of RV to LV (arrowhead) chamber size. C, Balanced
SSFP single-slice acquisition before surgical repair, with the imaging plane prescribed through the RV to create a 2-chamber RV view. This view can
be useful to demonstrate the inflow portion, trabecular portion, and outflow portion of the RV.

E B S TEIN ANOM ALY
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 10-year-old girl was found to have an incidental murmur during
an outpatient evaluation for dyspnea, dizziness, and perioral “blue-
ness” after swimming. Her cardiac evaluation included echocar-
diography, which demonstrated Ebstein anomaly of the tricuspid
valve. She was referred for consideration of surgical intervention.
C L I N IC A L QU E S T ION
MRI (Figure 10.5) was ordered to assess RV function and vol-
umes preoperatively, with the anticipation of surveillance of
response to surgical therapy postoperatively.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
I M AG I NG F I N DI NG S
MRI demonstrated an enlarged RV, with a significantly
enlarged atrialized portion.
S U M M A RY
The patient underwent tricuspid valve repair with plication
of the atrialized RV, right reduction atrioplasty, and suture
closure of a patent foramen ovale. The patient had an excellent
response to surgery. After repair, an additional MRI examina-
tion revealed a marked decrease in size of the right-sided cham-
ber. More than 2 years after surgery she is asymptomatic and
participates in school and extracurricular activities without
limitation.
Ebstein anomaly of the tricuspid valve is characterized by
abnormal attachments of the septal and posterior leaflets to
the tricuspid annulus. The valve orifice is displaced downward
into the RV cavity at the junction of the inlet and trabecular
components of the RV. The greater the apical displacement of
the posterior and septal leaflets, the larger the atrialized por-
tion of the RV, which results in a smaller functional portion
of the RV. The anterior leaflet of the tricuspid valve is almost
always normally attached to the atrioventricular junction. This
arrangement leads to a dysfunctional valve with a predomi-
nantly regurgitant lesion and its subsequent effects of initiating
a cycle of right-sided chamber volume overload, dilation, and
dysfunction.
The RV is notoriously difficult to image with echocardiog-
raphy given the limited acoustic windows and the unusual
geometric features of the RV, which are accentuated in the
setting of Ebstein anomaly of the tricuspid valve. Functional
assessment of the RV by MRI can be afforded by using sev-
eral imaging planes that are dedicated to the RV. Additionally,
accurate volumetric assessment is crucial in predicting and fol-
lowing outcome after surgery.
 194 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 F

Figure 10.6 Coarctation of the aorta. A, Multiple oblique, balanced SSFP, multislice acquisition with the imaging plane prescribed transverse to the
aortic root. The image on the left is in diastole (valve leaflets closed; arrow) and the image on the right is in systole (valve leaflets open; arrowhead).
Note the bicuspid aortic valve with fusion of the right and left cusps. B, MR angiography imaged before surgical intervention (left; arrow indicating
severe coarctation) and after surgical intervention (right), which involved placement of an interposition graft.
 10 .  C o n g e n i ta l D i s e a s e
COA RCTATION OF T H E AORTA
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 49-year-old woman was found to have a murmur and dis-
crepant upper extremity blood pressure on routine physi-
cal examination. Therefore, coarctation of the aorta was
suspected.
C L I N IC A L QU E S T ION
She was referred for MRI (Figure 10.6) to delineate the tho-
racic aorta and evaluate the severity of coarctation from both
anatomic and hemodynamic standpoints.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
I M AG I NG F I N DI NG S
The acquired images demonstrated the presence of a severe
discrete juxtaductal coarctation with significant collateral
flow through the superior intercostal arteries and the internal
mammary arteries, which indicated hemodynamically signifi-
cant stenosis. Balanced SSFP sequences in a plane perpendicu-
lar to blood flow at the level of the aortic root represented the
aortic valve in diastole and in systole and clearly demonstrated
bicuspid aortic valve with fusion of the right and left cusps.
• 195
S U M M A RY
The patient underwent repair of coarctation of the aorta with
the placement of an 18-mm Hemashield interposition graft.
MR angiography images demonstrated the severe coarctation
and the postsurgical result.
Coarctation of the aorta is typically located near the aor-
tic attachment of the ligamentum arteriosum or patent duc-
tus arteriosus. The ridge that forms the coarctation consists
of smooth muscle, fibrous tissue, and elastic tissue similar
in composition to a muscular arterial ductus. Intimal pro-
liferation distal to the ridge culminates in narrowing of the
lumen. The common form of coarctation of the aorta is rep-
resented by a localized constriction containing the ridge or
shelf of tissue. Less commonly, a relatively long segment of
constriction extends beyond the left subclavian artery. The
coarctation ridge is located either immediately proximal
to the aortic insertion of the ductus or opposite the aortic
insertion (juxtaductal), or immediately distal to the aortic
insertion.
MRI can be useful in delineating the severity of a coarc-
tation from anatomic and hemodynamic standpoints.
Coarctation-induced hemodynamic changes can be evalu-
ated by assessment for the presence of LV hypertrophy and
collateral vessels. Phase-contrast imaging can also be used to
assess direction of flow, when needed. When cine phase con-
trast is used to assess the significance of an obstruction, it is
important to prescribe a level above the point of obstruction.
The aim is to demonstrate retrograde flow in the intercostal
arteries to the descending thoracic aorta beyond the area of
obstruction.
 196 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 G

Figure 10.7 Balanced SSFP multislice images through a bicuspid aortic valve. The imaging plane is prescribed transverse to the aortic root in diastole
(A, valve leaflets closed) and systole (B, valve leaflets open). Note the bicuspid aortic valve with fusion of the right and left cusps (arrowhead). The
arrow indicates the noncoronary cusp.
 10 .  C o n g e n i ta l D i s e a s e
B ICUS PID AORTIC VALV E
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
The patient with coarctation of the aorta just described had
ancillary imaging during her MRI examination (Figure 10.7)
that is important to note.
C L I N IC A L QU E S T ION
The patient was referred for assessment of coarctation of the
aorta. During the examination, the aortic valve anatomy was
also assessed because coarctation of the aorta can be associ-
ated with bicuspid aortic valve.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
I M AG I NG F I N DI NG S
The acquired balanced SSFP images indicated a bicuspid aor-
tic valve. In systole, the valve leaflets were open, clearly dem-
onstrating 2 functioning leaflets. The right and left cusps were
• 197
fused, resulting in the bicuspid aortic valve. There was no sig-
nificant stenosis or regurgitation on MRI.
S U M M A RY
Because coarctation of the aorta is associated with bicus-
pid aortic valve, complete assessment of aortic coarctation
involves imaging of the aortic root to identify the presence
or absence of a bicuspid aortic valve, which tends to become
stenotic or regurgitant. Identification of such lesions has
implications with regard to surgical planning. In this patient,
imaging findings did indicate a bicuspid aortic valve, which
was neither stenotic nor significantly regurgitant. The patient
underwent surgical intervention for the coarctation of the
aorta without intervention of the aortic valve or ascending
aorta.
The images demonstrate the acquisition of an imag-
ing plane transverse to the aortic valve. This imaging plane
ensures that the subsequent image, which is perpendicular
to the plane just described, will be axial to the structure of
interest. Subsequent images made in this fashion are axial to
the aorta, which can give information regarding valvular mor-
phology and function. Phase-contrast imaging can be used to
demonstrate the presence of stenotic or regurgitant lesions
and also to quantify them.
 198 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 H

Figure 10.8 Multiple oblique balanced SSFP image of a bicuspid aortic valve. The imaging plane is prescribed longitudinal to the aortic root (the
arrowhead is at the level of the sinus of Valsalva and the arrow is at the mid ascending level). This image demonstrates a normal caliber of the
ascending aorta. The presence of a bicuspid aortic valve is associated with an ascending aortopathy; the region of the aorta most commonly dilated is
the tubular ascending aorta.
 10 .  C o n g e n i ta l D i s e a s e
B ICUS PID AORTIC VALV E
W IT HOUT A S CENDING
AORTIC DILATION
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 28-year-old man who had no significant past medical his-
tory and had been physically active with no perceived limi-
tations had a preemployment physical with his primary care
physician. During that examination, he was noted to have a
diastolic murmur. Echocardiography demonstrated a bicus-
pid aortic valve with mild to moderate regurgitation.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 10.8) for
assessment of the thoracic aorta because its echocardiographic
assessment was suboptimal.
C A R DI AC M R I PROTO C OL
Use Congenital Heart Disease Protocol 5.7 (see page 80).
I M AG I NG F I N DI NG S
The acquired images demonstrated bicuspid aortic valve with
fusion of the left and right coronary cusps. There was mild dila-
tion of the ascending aorta, which tapered to a normal caliber
• 199
at the distal ascending level. The aortic arch and descending
thoracic aorta were of normal caliber without coarctation.
S U M M A RY
As a result of the MRI findings, conservative management
was recommended. The patient undergoes surveillance in the
setting of bicuspid aortic valve as indicated by the American
Heart Association/American College of Cardiology guide-
lines and continues to do well.
Cardiac MRI is useful because the entire thoracic aorta
can be interrogated. Bicuspid aortic valve is often associated
with ascending aortopathy and coarctation, both of which
can be evaluated during the examination. With regard to
evaluating the aorta in a patient with bicuspid aortic valve,
the emphasis is on the diagnosis of ascending aortic dilation
or frank aneurysmal disease. Thereafter, periodic surveillance
is needed to time surgical repair of aneurysmal disease before
the onset of catastrophic aortic complications such as dissec-
tion or aortic rupture. Echocardiography is useful as a screen-
ing tool but is limited by the available acoustic windows,
which vary depending on several factors, including patient
factors. Both computed tomography angiography and MRI
are suited to completely assessing the aorta and its branch ves-
sels. In patients with aortic disease, surveillance imaging is
indicated lifelong. One of the great advantages of MRI is the
absence of radiation exposure to the patient and, therefore, it
may be preferred as a modality for surveillance in an other-
wise stable patient.
 200 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 10 I

Figure 10.9 Gadolinium contrast-enhanced MR angiography of a bicuspid aortic valve. A, The source image is in a plane transverse to the ascending
aorta. Note the ascending aorta anteriorly, the right branch of the main pulmonary artery (arrow) behind the ascending aorta (asterisk), and the
descending thoracic aorta posteriorly (arrowhead). B, Sagittal view maximum intensity projection image demonstrates the dilated ascending aorta
(asterisk). In patients with bicuspid aortic valve, the ascending aorta is usually dilated.
 10 .  C o n g e n i ta l D i s e a s e • 201

B ICUS PID AORTIC VALV E W IT H ascending aorta (44 mm), and mild LV dilatation with
A S CENDING AORTIC DILATION preserved contractile function. In contrast to the previous
AND AORTIC R EGU RGITATION case (Bicuspid Aortic Valve Without Ascending Aortic
Dilation), this case demonstrated the typical ascending
aortic dilation and the presence of aortic regurgitation,
C L I N IC A L H I S TORY A N D
both of which can be seen in the setting of bicuspid aortic
PR E S E N TAT ION
valve.
A 43-year-old woman had a bicuspid aortic valve with mod-
erate insufficiency and ascending aortic enlargement. As part
S U M M A RY
of her ongoing care, the patient undergoes routine follow-up
with her cardiologist for assessment of aortic size and severity The patient continues to be followed up for symptoms and
of aortic valvular regurgitation. continues to undergo surveillance imaging to assess the sever-
ity of aortic valvular disease and the stability of the ascending
aortic dilation.
C L I N IC A L QU E S T ION
Patients with bicuspid aortic valve are at risk for ascend-
She was referred for cardiac MRI (Figure 10.9) to assess ing aortic aneurysmal disease and require surveillance imag-
ascending aortic dimensions. ing. With dilation of the aortic annulus, there is risk of
significant aortic valvular regurgitation and aortic valvular
stenosis because of the inherent abnormality of the aortic
C A R DI AC M R I PROTO C OL
valve. Although the hemodynamic consequences of stenotic
Use Congenital Heart Disease Protocol 5.7 (see page 80). or regurgitant valvular heart disease traditionally have been
diagnosed using echocardiography, cardiac MRI is evolv-
ing to assess these specific lesions. Nevertheless, a complete
I M AG I NG F I N DI NG S
assessment of the thoracic aorta and associated lesions such
The acquired images demonstrated a bicuspid aortic valve as coarctation of the aorta can be useful in the evaluation of
with moderate aortic regurgitation, dilatation of the such conditions.
 202 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s
S UGGE S TED R EADING
Attenhofer Jost CH, Edmister WD, Julsrud PR, Dearani JA, Savas Tepe
M, Warnes CA, et al. Prospective comparison of echocardiography
versus cardiac magnetic resonance imaging in patients with Ebstein’s
anomaly. Int J Cardiovasc Imaging. 2012 Jun;28(5):1147–59. Epub
2011 Aug 6.
Buechel ER, Dave HH, Kellenberger CJ, Dodge-Khatami A, Pretre R,
Berger F, et al. Remodelling of the right ventricle after early pul-
monary valve replacement in children with repaired tetralogy of
Fallot: assessment by cardiovascular magnetic resonance. Eur Heart
J. 2005 Dec;26(24):2721–7. Epub 2005 Oct 7.
Gaca AM, Jaggers JJ, Dudley LT, Bisset GS 3rd. Repair of congenital
heart disease: a primer: part 1. Radiology. 2008 Jun;247(3):617–31.
Epub 2008 Mar 28.
Gaca AM, Jaggers JJ, Dudley LT, Bisset GS 3rd. Repair of congenital
heart disease: a primer: part 2. Radiology. 2008 Jul;248(1):44–60.
Epub 2008 May 5.
Jimenez-Juan L, Joshi SB, Wintersperger BJ, Yan AT, Ley S, Crean
AM, et al. Assessment of right ventricular volumes and function
using cardiovascular magnetic resonance cine imaging after atrial
redirection surgery for complete transposition of the great arteries.
Int J Cardiovasc Imaging. 2012 Jul 12. [Epub ahead of print]
Julsrud PR, Breen JF, Felmlee JP, Warnes CA, Connolly HM, Schaff
HV. Coarctation of the aorta: collateral flow assessment with
phase-contrast MR angiography. AJR Am J Roentgenol. 1997
Dec;169(6):1735–42.
Julsrud PR, Ehman RL. The “broken ring” sign in magnetic resonance
imaging of partial anomalous pulmonary venous connection to the
superior vena cava. Mayo Clin Proc. 1985 Dec;60(12):874–9.
Kilner PJ. Imaging congenital heart disease in adults. Br J Radiol. 2011
Dec;84 Spec No 3:S258–68.
Malaisrie SC, Carr J, Mikati I, Rigolin V, Yip BK, Lapin B, et al. Cardiac
magnetic resonance imaging is more diagnostic than 2-dimensional
echocardiography in determining the presence of bicuspid aortic
valve. J Thorac Cardiovasc Surg. 2012 Aug;144(2):370–6. Epub 2011
Dec 10.
Perloff PK, Marelli AJ. Perloff’s clinical recognition of congenital heart
disease. 6th ed. Philadelphia (PA): Elsevier; c2012.
Vesely TM, Julsrud PR, Brown JJ, Hagler DJ. MR imaging of partial
anomalous pulmonary venous connections. J Comput Assist Tomogr.
1991 Sep-Oct;15(5):752–6.
 11.
VA LV ULAR HEART DISEASE
James F. Glockner, MD, PhD
E
valuation of valvular heart disease with magnetic reso-
nance imaging (MRI) has generated an extensive body
of literature over the past 20 years, although it remains
uncertain whether this indication will see widespread clini-
cal application. Echocardiography has several inherent advan-
tages in the assessment of cardiac valves, including higher
temporal and spatial resolution and generally more accurate
measurement of peak velocities of stenotic and regurgitant
flow jets. Echocardiography is also portable and generally less
expensive than MRI.
Nevertheless, in some occasions transthoracic echocar-
diography is limited or is unsuccessful in the evaluation of
cardiac valves, or, in other cases, successive examinations
reveal widely discrepant results. In these cases, MRI can be
a useful alternative. MRI is also attractive for its ability to
obtain a global assessment of valvular function, ventricular
size and function, and maximal diameter of the ascending
aorta (in the case of aortic valve disease) or pulmonary artery
(pulmonic valve disease).
Assessment of valves with MRI begins with localiza-
tion of the valve in question. For the aortic valve, standard
3-chamber balanced steady-state free precession (SSFP) cine
images provide a view through the left ventricular (LV) out-
flow tract and aortic valve. This can be followed by a coronal
oblique acquisition prescribed orthogonal to the 3-chamber
images. Transverse balanced SSFP images are then obtained
through the valve plane using both the 3-chamber and
coronal oblique images for prescription. Transverse images
allow assessment of valve morphology (eg, bicuspid vs tri-
cuspid valve, leaflet thickening or calcification, and leaflet
203
coaptation). Orthogonal long-axis views allow visualization
of stenotic or regurgitant flow jets, which generally appear as
flow voids on one side of the valve and result from intravoxel
dephasing generated by the rapid disordered motion of blood
within the regurgitant jet. The size and duration of the flow
jet may roughly correlate with the severity of the valve lesion;
however, visualization is also affected by the slice thickness
and orientation, the presence or absence of gadolinium con-
trast, and the particular imaging parameters chosen, so these
images should be interpreted with caution.
Quantification of the severity of valve lesions generally
involves cine phase-contrast velocity and flow measurements.
Transverse slices positioned at the valve plane, or slightly
above or below the valve, allow measurement of the amount
of blood flowing backward across the valve during dias-
tole—this is the regurgitant volume. For aortic insufficiency,
the regurgitant volume is often indexed to the LV stroke
volume to obtain the regurgitant fraction. The LV stroke
volume can be determined from short-axis balanced SSFP
cine images or by measuring the systolic forward flow in the
proximal ascending aorta with a cine phase-contrast acquisi-
tion. Quantification of stenotic valve lesions generally relies
on measuring the peak and mean systolic velocity, again with
cine phase-contrast acquisitions, or measuring the maximal
cross-sectional valve area in systole, which can be obtained
from either transverse balanced SSFP or cine phase-contrast
images. The purpose of this chapter is to describe the most
commonly encountered cardiac valvular diseases and to illus-
trate their unique characteristics on cardiac MRI through
specific case study presentations.
 204 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11 A

Figure 11.1 Aortic insufficiency with a bicuspid aortic valve. A and B, Three-chamber balanced SSFP images during early (A) and late (B) diastole
showing a regurgitant jet (arrows). The loss of signal is due to the high flow velocity–induced intravoxel phase dispersion. C, Axial balanced SSFP
image through the aortic valve in systole demonstrates a bicuspid aortic valve. D and E, Systolic (D) and diastolic (E) combined phase-contrast
magnitude and flow images showing forward flow (red-yellow) and reverse flow (blue). F, Time-vs-flow plot demonstrating quantitative assessment
of flow throughout the cardiac cycle. RV indicates regurgitant volume; SV, stroke volume.
 11. Va lv u l a r H e a r t D i s e a s e • 205

AORTIC IN S U F F ICIENC Y W IT H
B ICUS PID AORTIC VALV E
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
During a routine physical examination, a diastolic murmur
was detected in an asymptomatic 33-year-old man.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 11.1) to
assess for the presence of aortic insufficiency.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
The images obtained indicated a diagnosis of aortic insuffi-
ciency. Diastolic, 3-chamber, balanced SSFP images revealed
a dark aortic insufficiency flow jet, which was relatively
small in early diastole and more prominent in late diastole.
A systolic balanced SSFP image from a transverse acquisi-
tion through the aortic valve demonstrated a bicuspid aortic
valve. Color-flow images in systole and diastole generated
from a cine phase-contrast slice across the aortic valve dem-
onstrated normal forward flow in systole and a prominent
blue regurgitant jet in late diastole. Aortic regurgitation was
quantified with a time-versus-flow plot obtained from cine
phase-contrast data. The forward flow (area under the curve
above baseline) in systole represents the stroke volume, and
the backward flow (area under the curve below baseline) in
diastole is the regurgitant volume. The regurgitant fraction
is obtained by dividing the regurgitant volume by the stroke
volume. Analysis of short-axis balanced SSFP cine images
indicated that the patient had normal LV size and function,
no dilatation of the ascending aorta, and moderate aortic
insufficiency, with 38 mL of regurgitant volume per heartbeat
and a regurgitant fraction of 24%.
S U M M A RY
The findings of the MRI examination indicated that the
patient did not require valve replacement. Close continued
follow-up was initiated so that valve replacement surgery can
be performed at the appropriate time. Given the patient’s
young age, it is unlikely that valve degeneration alone is
responsible for his moderate aortic insufficiency—the pres-
ence of a congenitally bicuspid aortic valve was also confirmed
by MRI.
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 includ-
ing Marfan syndrome, aortic aneurysm, bicuspid aortic valve,
rheumatic heart disease, and endocarditis. Combined aortic
insufficiency and stenosis is common, since both conditions
can result from an abnormal valve configuration or degenera-
tion of valve leaflets. Patients are often asymptomatic despite
severe LV volume overload and may have irreversible LV dys-
function 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 provides accurate determination of LV size and func-
tion (the current diagnostic standard), measurement of maxi-
mal aortic diameter, assessment of valve morphology, and
evaluation of the valve lesion both qualitatively (based on size
of flow jets) and quantitatively (based on cine phase-contrast
flow measurement, or by comparing the difference in stroke
volume between the right ventricle [RV] and LV, provided
no additional valve lesions are present). Quantitative estima-
tion of the severity of aortic insufficiency by MRI (Table 11.1)
agrees fairly well with that obtained by echocardiography.

Table 11.1 QUANTIFICATION OF AORTIC INSUFFICIENCY

R EGURGITANT VOLUME, R EGURGITANT

CLASSIFICATION mL/HEART BEATa FR ACTION, %

Mild <30 15–20

Moderate 30–60 21–40

Severe >60 >40

a
The regurgitant volume can be calculated from the stroke volume in the aorta minus the stroke volume in the main
pulmonary artery, or from the stroke volume in the aorta minus the mitral valve inflow, all of which are derived from
phase-contrast measurements. Regurgitant volume can also be derived from short-axis balanced SSFP data by taking
the difference between the LV and RV stroke volumes.
 206 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11 B

Figure 11.2 Aortic insufficiency with LV enlargement. A and B, Balanced SSFP views of the aortic outflow tract during diastole in the coronal (A) and
sagittal oblique (B) planes showing a large regurgitant jet. C, Short-axis balanced SSFP image during diastole demonstrating dilation of the LV. D,
Phase-contrast composite magnitude and velocity profile showing positive flow (red) and regurgitant flow (blue) through the aortic valve during
diastole. E, Axial, fat-suppressed, balanced SSFP image demonstrating aneurysmal dilatation of the ascending aorta.
 11. Va lv u l a r H e a r t D i s e a s e
AORTIC IN S U F F ICIENC Y W IT H
LV ENLARG E M ENT
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 56-year-old woman saw her primary care physician
with a report of chest discomfort while shoveling snow.
Subsequent echocardiography revealed a dilated LV and aor-
tic insufficiency.
C L I N IC A L QU E S T ION
The patient was referred for MRI (Figure 11.2) to confirm the
suspicion of aortic regurgitation.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
On the basis of the MRI findings, the patient was given a diag-
nosis of severe aortic insufficiency and enlargement of the LV.
Cine balanced SSFP images acquired during diastole demon-
strated a large regurgitant jet extending from the aortic valve
to the inferior septal wall of the LV. An irregular, dark signal
at the valve plane represented thickened, calcified leaflets. An
• 207
end-diastolic image obtained from a short-axis cine balanced
SSFP acquisition revealed moderate dilatation of the LV.
A diastolic color-flow image through the aortic valve demon-
strated a large regurgitant jet extending from the aortic valve
into the LV. Quantitative measurement of the regurgitant
flow yielded a regurgitant volume of 105 mL, consistent with
severe aortic insufficiency. A fat-suppressed balanced SSFP
image demonstrated aneurysmal dilatation of the ascending
aorta.
S U M M A RY
The MRI examination provided the definitive diagnosis
of severe aortic insufficiency, as well as sequelae including
LV dilatation and an associated ascending aortic aneurysm.
Whether the episode of chest pain was truly related to the
patient’s valve disease is uncertain. However, even if the
patient were completely asymptomatic, valve surgery was rec-
ommended on the basis of the severely dilated LV. As a result,
the patient underwent replacement of the diseased aortic
valve with an aortic valve prosthesis.
In addition to the MRI findings described above, quanti-
tative assessment of MRI data can be used to derive a range of
useful metrics for assessment of patients with aortic insuffi-
ciency, including LV end-diastolic volume and dimension, LV
ejection fraction, regurgitant volume and fraction per heart-
beat, maximal diameter of the ascending aorta, and valve
morphology.
 208 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11C

Figure 11.3 Aortic stenosis with dilation of the ascending aorta. A and B, Coronal (A) and 3-chamber (B) balanced SSFP images of the aortic
valve and ascending aorta showing a high-velocity jet (arrowheads). C, Axial balanced SSFP image of the aortic valve (arrow) during systole. D,
Composite magnitude and velocity image through the aortic valve showing a large forward-flowing jet (red-yellow).
 11. Va lv u l a r H e a r t D i s e a s e
AORTIC S TENO S I S W IT H
DILATION OF T H E A S CENDIN G
AORTA
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 60-year-old man sought care from his primary care physi-
cian for shortness of breath on exertion.
C L I N IC A L QU E S T ION
Dilation of the aorta and possible aortic aneurysm were iden-
tified on initial echocardiography. The patient was referred for
MRI (Figure 11.3) to confirm the finding of aortic aneurysm.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
The images obtained of the aortic valve clearly depicted the pres-
ence of aortic stenosis. End-systolic images from cine balanced
SSFP acquisitions demonstrated a prominent dark flow jet
extending from the aortic valve into the ascending aorta, dilata-
tion of the ascending aorta, doming of the valve leaflets, and thick-
ening and reduced signal intensity of the visualized valve leaflets.
A transverse cine balanced SSFP image through the aortic valve
during systole demonstrated a bicuspid valve with thickened leaf-
lets and markedly decreased valve area. A composite magnitude
and velocity image acquired in a plane transverse to the aortic
valve plane showing the distribution of velocities during systole
demonstrated the narrow flow jet extending superiorly from the
aortic valve toward the medial wall of the ascending aorta.
S U M M A RY
Based on the MRI findings, a diagnosis of aortic stenosis
and moderate dilation of the ascending aorta was made. The
patient underwent surgical replacement of the aortic valve
with a biological prosthesis and replacement of the ascending
aorta and hemiarch.
As with aortic insufficiency, the most common cause of aor-
tic stenosis is idiopathic degeneration of a normal valve. The
next most common cause is degeneration of a bicuspid valve,
typically occurring with earlier onset, followed less frequently
by rheumatic heart disease. Supravalvular and subvalvular
stenosis usually are congenital lesions; however, subvalvular
functional stenosis also occurs in the setting of hypertrophic
obstructive cardiomyopathy. Classic symptoms include dys-
pnea on exertion, exertional syncope, and angina, accompa-
nied by a holosystolic murmur. Symptoms usually appear late
in the course of the disease, and patients often have rapid func-
tional decline if the valve is not replaced. Aortic stenosis causes
obstruction of LV outflow, increased LV pressures, decreased
cardiac output, and compensatory LV hypertrophy.
Visualization of aortic stenosis with MRI is usually straight-
forward—3-chamber, coronal oblique, and transverse cine bal-
anced SSFP images through the valve plane demonstrate limited
excursion of the valve leaflets, congenital abnormalities such as
• 209
a bicuspid valve, and systolic jets of high velocity flow in the
ascending aorta, seen as dark flow voids. Ventricular function,
as well as the presence or absence of LV hypertrophy, can be
assessed on short-axis, cine balanced SSFP images, and the max-
imal diameter of the ascending aorta should also be measured.
Quantitative assessment of aortic stenosis can be performed
either by direct planimetry (ie, tracing the maximal opening
area of the aortic valve on a transverse cine balanced SSFP or
phase-contrast acquisition) or by measuring the peak velocity
across the valve with a cine phase-contrast acquisition. Peak sys-
tolic velocity measurements can also be used to estimate pres-
sure gradients according to the modified Bernoulli equation:
Peak pressure gradient = 4 ( Vmax )
2
where the pressure gradient is measured in mm Hg and Vmax is the
maximal velocity of the stenotic jet in the proximal aorta in m/s.
The mean pressure gradient can be obtained from the
equation:
Mean pressure gradient = ( 4Σ [ Vmax ] ∆t1 )/ ∆t 2
2
where Δt1 is the time interval for the phase-contrast cine
image in which Vmax is measured and Δt2 is the interval over
which these velocities are summed (typically 1 R-R interval).
This measurement is the time average of Vmax over systole. For
this measurement, it is best to choose a small region of inter-
est that encompasses the highest velocity portion of the flow
jet—this is somewhat arbitrary.
The aortic valve area can be estimated by the equation:
Aortic valve area = A OT ( VOT ) / Vmax
where AOT is the outflow tract area, VOT is the outflow tract
maximum velocity, and Vmax is the maximum velocity of
the stenotic jet in the proximal aorta. Valve area can also be
directly measured if cine images of sufficient quality have been
acquired through the stenotic valve. Table 11.2 lists MRI mea-
surements associated with varying degrees of aortic stenosis.
Attention to detail is very important in obtaining accurate
cine phase-contrast velocity and flow measurements—the
velocity-encoding parameter, VENC, should be set to a value
slightly higher than the expected peak velocity, slices should be
positioned perpendicular to the direction of flow, and tempo-
ral and spatial resolution must be adequate to ensure accurate
depiction of the vessel borders as well as complete visualiza-
tion of rapid flow components (with the unfortunate caveat
that improving either temporal or spatial resolution results in
a longer acquisition time).
Table 11.2 QUANTIFICATION OF AORTIC STENOSIS
DEGR EE OF AORTIC AORTIC VALVE PEAK SYSTOLIC
STENOSIS AR EA, cm 2 VELOCITY, m/s
Normal 2.0–4.0 1–2.4
Mild 1.1–1.9 2.5–2.9
Moderate 0.75–1.0 3.0–4.0
Severe <0.75 >4.0
 210 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11D

Figure 11.4 Mitral valve insufficiency. A-C, Sequential 3-chamber balanced SSFP views during early systole identifying a high-velocity jet (dark;
ie, hypointense signal) due to mitral insufficiency (arrows). The arrowheads identify mitral annular calcification. D and E, Three- and 4-chamber
balanced SSFP images during early systole showing a high-velocity jet (arrows). The low signal intensity of the jet is a result of high-flow–induced
intravoxel phase dispersion of the blood pool signal.
 11. Va lv u l a r H e a r t D i s e a s e
M ITRAL IN S U F F ICIENC Y
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 77-year-old woman saw her primary care physician for
increasing dyspnea on exertion.
C L I N IC A L QU E S T ION
Limited echocardiographic images suggested aortic stenosis.
The patient was referred for cardiac MRI (Figure 11.4) to con-
firm the initial diagnosis of aortic valve stenosis.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
A 3-chamber cine balanced SSFP acquisition demonstrated
a prominent high-velocity jet of mitral insufficiency directed
toward the posterior wall of the left atrium. Thickening of
the anteroseptal myocardium and flow disturbance in the LV
outflow tract could also be seen. In addition, a round, low-
signal-intensity lesion adjacent to the posterior attachment
of the mitral valve represented mitral annular calcification,
• 211
which was more easily appreciated by computed tomogra-
phy. Balanced SSFP views acquired in early systole demon-
strated a large posterior lateral jet of mitral insufficiency, left
atrial enlargement, and thickening of the interventricular
septum. On the basis of these key images, mitral valve insuf-
ficiency due to hypertrophic cardiomyopathy (HCM) was
diagnosed.
S U M M A RY
Cardiac MRI confirmed the diagnosis of HCM with dynamic
outflow obstruction. The patient subsequently underwent car-
diac surgery, which included LV septal myectomy, to relieve
the obstruction. The patient experienced significant relief of
her cardiac symptoms postoperatively.
HCM is a common indication for cardiac MRI. Cardiac
MRI allows for further evaluation of myocardial hypertro-
phy and visualization of the LV outflow tract obstruction.
Although echocardiography is usually performed to evaluate
valvular disease, MRI allows accurate assessment of both the
LV outflow tract obstruction and mitral regurgitation asso-
ciated with obstructive HCM. It is worthwhile to remember
that patients with HCM may have additional reasons for their
mitral regurgitation besides systolic anterior motion of the
mitral valve; a regurgitant jet not directed toward the poste-
rior lateral wall of the left atrium should suggest that an addi-
tional etiology may be involved.
 212 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11 E

Figure 11.5 Mitral valve prolapse. A and B, Sequential, 3-chamber, balanced SSFP images acquired during systole show a central jet of mitral valve
insufficiency (arrows).
 11. Va lv u l a r H e a r t D i s e a s e • 213

M ITRAL VALV E PROLAP S E
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 43-year-old asymptomatic man with a known and
long-standing cardiac murmur had a recent diagnosis of mitral
valve prolapse and regurgitation from an outside institution.
Analysis of cardiac MRI data can generate a range of use-
ful metrics for assessment of both mitral valve stenosis and
regurgitation, as shown in Box 11.1.
Table 11.3 GRADE OF MITRAL VALVE
REGURGITATION VS REGURGITANT VOLUME
DERIVED FROM MRI

GR ADE OF MITR AL R EGURGITANT

C L I N IC A L QU E S T ION R EGURGITATION CLASSIFICATION VOLUME, mL

The patient was referred for cardiac MRI (Figure 11.5) to I/IV Mild <30
assess cardiac function.
II/IV Moderate 30–44

III/IV Moderately severe 45–59

C A R DI AC M R I PROTO C OL
IV/IV Severe ≥60
Use Valvular Heart Disease Protocol 5.4 (see page 79).

I M AG I NG F I N DI NG S
Balanced SSFP views demonstrated prolapse of both the ante-
rior and posterior leaflets of the mitral valve across the mitral
annular plane into the left atrium. Also noteworthy was sig-
nal void across the valve indicating the presence of a central jet
of mitral insufficiency.
S U M M A RY
The findings of the MRI examination confirmed the pres-
ence of prolapse of both leaflets of the mitral valve with severe
mitral valve regurgitation. On the basis of this information, the
patient underwent mitral valve repair. The patient responded
well to surgical repair, returning to normal daily activities.
Mitral regurgitation is the most common valve disorder in
the United States and can result from dysfunction involving
any component of the valve apparatus. Mitral valve prolapse
due to myxomatous degeneration is the leading cause of mitral
insufficiency and is defined as systolic bowing of a mitral
leaflet more than 2 mm beyond the annular plane into the
atrium. Abnormal fibroelastic connective tissue within the
valve leaflets, chordae, and annulus lead to elongated dysfunc-
tional leaflets, chordal elongation and thinning, and annular
thickening and dilatation. Mitral regurgitation is graded on
the basis of MRI-derived regurgitant volume (Table 11.3).
Mitral valve prolapse is diagnosed from 3-chamber bal-
anced SSFP images. In severe cases, a flail leaflet may occur
secondary to rupture of a chordae tendineae and is defined as
eversion of the leaflet tip into the left atrium during systole.
Box 11.1 MRI METRICS FOR MITRAL VALVE
EVALUATION
• Regurgitant volume per beat, which can be calculated by:
1. The difference between flow in the proximal main pulmo-
nary artery and proximal aorta
2. Measurement of LV stroke volume by tracing end-systolic
and end-diastolic short-axis images and subtracting flow
in the proximal aorta as measured by a phase-contrast
sequence
3. Direct phase-contrast flow measurement of a regurgi­
tant jet in the left atrium. For accurate quantification it is
important that the velocity-encoding parameter, VENC, is
set high enough and that the slice is oriented perpendicu-
lar to the direction of flow
4. Measurement of inflow through the mitral valve
plane minus LV stroke volume as calculated from
phase-contrast images through the proximal aorta
5. LV minus RV 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
LV diameter at end systole and end diastole at the mid
ventricular level (this is to duplicate standard echocardio-
graphic measurement)
• Reversal of flow in pulmonary veins
 214 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11F

Figure 11.6 Mitral valve stenosis. A-C, Multiple balanced SSFP views indicating stenosis of the mitral valve. A, Three-chamber view during early
diastole showing restricted opening of the mitral valve leaflets (arrow). B, Four-chamber view identifying left atrial enlargement (arrowhead). C,
Short-axis view showing restricted opening of the mitral valve (arrow).
 11. Va lv u l a r H e a r t D i s e a s e
M ITRAL S TENO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 60-year-old woman sought care from her primary care phy-
sician for progressive shortness of breath.
C L I N IC A L QU E S T ION
Cardiac MRI (Figure 11.6) was ordered to assess for mitral valve
stenosis.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
Balanced SSFP images illustrated the presence of mitral
valve stenosis. Various views revealed restricted opening of
the mitral valve leaflets, a dilated left atrium, and left atrial
enlargement with bowing of the anterior mitral valve leaflet
in a “hockey stick” configuration. A short-axis view revealed
restricted opening of the mitral valve, with a “fish mouth”
appearance.
S U M M A RY
On the basis of the imaging findings, a sclerotic mitral valve
with limited motion consistent with mitral valve stenosis
• 215
was diagnosed. Over the course of several years, the patient
continued to experience worsening of symptoms, and per-
cutaneous mitral valve balloon valvuloplasty was eventually
performed.
Rheumatic heart disease is by far the most common cause
of mitral stenosis in the developed world. Stenosis of the mitral
valve leads to increased atrial pressures, which in turn cause
atrial dilatation and pulmonary hypertension. Long-standing
mitral stenosis and pulmonary hypertension may also cause
right-sided heart failure. Atrial fibrillation is a fairly com-
mon complication of mitral stenosis, which complicates MRI
assessment of these patients.
Restricted opening of the stenotic mitral valve may result
in a fish mouth appearance on short-axis balanced SSFP
images. Bowing of a thickened anterior leaflet during diastole
may result in the characteristic diastolic doming or so-called
hockey stick appearance, which can be seen on 4-chamber or
2-chamber balanced SSFP images. Stenotic flow jets can be
seen on the ventricular side of the mitral valve on cine bal-
anced SSFP images, and peak velocity or pressure gradients
can be quantified with cine phase-contrast acquisitions.
Planimetry of the maximal opening area of the mitral valve
can also be performed. MRI allows comprehensive assessment
of the additional effects of mitral stenosis, including measure-
ment of left atrial volume and RV size and function.
 216 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11G

Figure 11.7 Parachute mitral valve with mitral stenosis. A, Three-chamber balanced SSFP image showing anterior and posterior chordae attaching
to the same papillary muscle (arrow). B, Basal, short-axis, balanced SSFP image demonstrating restricted opening of the mitral valve. The arrowhead
identifies the leaflets (dark lines) of the valve.
 11. Va lv u l a r H e a r t D i s e a s e
PARAC H UTE M ITRAL VALV E
W IT H M ITRAL S TENO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 21-year-old woman with a history of Shone syndrome had
undergone previous repair of an aortic coarctation.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 11.7) to assess
the previously performed coarctation repair and to compare
the results with a prior cardiac MRI performed 2 years earlier.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
The images obtained provided a diagnosis of mitral valve
stenosis and identified anatomical features characteristic
of a so-called parachute mitral valve. Various SSFP images
• 217
demonstrated chordae from the anterior and posterior mitral
valve leaflets attaching to the same papillary muscle and
restricted opening of the mitral valve.
S U M M A RY
The results of the cardiac MRI examination and comparison
with the prior study showed that the patient’s graft was widely
patent without evidence of aneurysmal dilation or stenosis
and was unchanged from the prior study. A parachute mitral
valve with mild stenosis was also noted, which was consistent
with Shone syndrome. Because the graft was patent and the
patient was asymptomatic, the patient was recommended for
follow-up echocardiography in 5 years.
Shone syndrome was initially described by Shone et al in
1963 and consists of 4 left-sided obstructive lesions, including
supravalvular mitral ring, parachute mitral valve, subaortic
stenosis, and coarctation.
The parachute mitral valve describes a valve with normal
leaflets but with chordae tendineae that attach to a single
large papillary muscle, which typically results in a stenotic
orifice. The valve and chordae are said to resemble a parachute
canopy and shroud.
 218 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11H

Figure 11.8 Cardiac amyloidosis with mitral and tricuspid regurgitation. A-D, Consecutive 4-chamber balanced SSFP images acquired during early
systole demonstrating regurgitant jets (white arrows) from both the mitral and tricuspid valves. The red arrows identify pleural and pericardial
effusions, and the arrowheads identify LV hypertrophy.
 11. Va lv u l a r H e a r t D i s e a s e
CARDIAC A M Y LOIDO S I S W IT H
M ITRAL AND TRICUS PID
RE GURG ITATION
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 70-year-old man sought care from his cardiologist for
increasing shortness of breath over the past 12 months.
Decreased LV function was diagnosed on the basis of echo-
cardiography findings.
C L I N IC A L QU E S T ION
The patient was referred for MRI (Figure 11.8) to assess for
cardiac amyloidosis based on pathologic results showing amy-
loid protein deposition in a subcutaneous fat biopsy specimen.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
The key diagnostic images from this study included a cine bal-
anced SSFP acquisition that demonstrated regurgitant jets
• 219
extending from the tricuspid and mitral valves into the atria.
Small pericardial and bilateral pleural effusions were also
seen, as well as diffuse LV thickening.
S U M M A RY
Based on the MRI study, the patient was given a diagnosis
of concentric RV and LV hypertrophy, decreased LV systolic
function (ejection fraction, 50%), and a small to moderate
pericardial effusion. Thickening of both the mitral and tricus-
pid valve leaflets was noted, along with mitral and tricuspid
regurgitation. Mild, diffuse, late gadolinium enhancement
with abnormal nulling was consistent with cardiac amyloido-
sis. The patient underwent chemotherapy for amyloidosis and
had a subsequent diagnosis of multiple myeloma.
Amyloidosis represents a heterogeneous group of dis-
eases all characterized by deposition of amyloid proteins
in the extracellular matrix of 1 or more organs. Amyloid
deposits, regardless of their composition, have a character-
istic appearance on light microscopy, staining pink with
Congo red dye and exhibiting apple-green birefringence
under polarized light.
 220 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11I

Figure 11.9 Tricuspid valve insufficiency. A and B, Balanced SSFP 4-chamber views demonstrate a regurgitant jet through the tricuspid valve at
different time points during systole (arrows). C and D, Composite magnitude and velocity images from a cine phase-contrast acquisition during
diastole (C) and systole (D) show forward flow (red-yellow) and regurgitant flow (blue-green) across the tricuspid valve.
 11. Va lv u l a r H e a r t D i s e a s e
TRICUS PID IN S U F F ICIENC Y
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 48-year-old man with a history of congenital pulmonic
valve stenosis, for which he underwent pulmonary valvotomy
as a child, was seen in the cardiology department for manage-
ment of subsequent right-sided heart failure.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 11.9) to
assess the status of the tricuspid valve.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
Balanced SSFP images demonstrated marked right atrial
enlargement, moderate RV enlargement, and prominent
regurgitant flow jets extending from the tricuspid valve into
the right atrium. Diastolic and systolic composite magnitude
and velocity images generated from a cine phase-contrast
acquisition across the tricuspid valve plane demonstrated nor-
mal forward flow into the RV during diastole, with marked
• 221
regurgitant flow in systole. Quantitative analysis of short-axis
cine balanced SSFP images revealed decreased LV and RV
ejection fractions of 39% and 43%, respectively.
S U M M A RY
On the basis of the MRI study, the patient was noted to have a
markedly enlarged RV and right atrium, with severe tricuspid
and pulmonic valve regurgitation. The patient subsequently
underwent surgical replacement of both pulmonic and tricus-
pid valves.
Tricuspid regurgitation is most often a result of a dilated
RV and tricuspid annulus rather than intrinsic valvular dis-
ease. Our case is an illustration of this principle: the patient’s
pulmonary valvotomy eventually led to severe pulmonic
valve regurgitation and subsequent RV volume overload and
dilatation, which in turn caused enlargement of the tricus-
pid annulus and consequent poor coaptation of the tricuspid
valve leaflets. The long-standing pulmonic and tricuspid valve
lesions led to marked RV and right atrial enlargement.
The tricuspid valve is also the most common valve affected
in intravenous drug abusers with infectious endocarditis,
since left-sided valves are protected by the filtration system of
the lungs. Likewise, the tricuspid and, to a lesser extent, pul-
monic valves are predominantly affected in carcinoid heart
disease, in which endothelial damage, fibrosis, and eventual
dysfunction of valve leaflets is caused by vasoactive substances
released into the bloodstream by hepatic metastases.
 222 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11J

Figure 11.10 Ebstein anomaly. Balanced SSFP images in a 4-chamber end-diastolic view (A) and an axial early systolic view (B) demonstrating
apical displacement of the septal leaflet of the tricuspid valve (arrowhead) and severe regurgitation (arrow).
 11. Va lv u l a r H e a r t D i s e a s e
E B S TEIN ANOM ALY
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 27-year-old woman was given a diagnosis of a congeni-
tal heart anomaly from an outside institution. The patient
self-referred to our institution for consideration of surgery for
Ebstein anomaly.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 11.10) to
confirm the presence of Ebstein anomaly diagnosed on a prior
MRI study at an outside institution.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
End-diastolic 4-chamber and early systolic balanced SSFP
axial images demonstrated apical displacement of the septal
• 223
leaflet of the tricuspid valve, atrialization of the RV, and severe
tricuspid regurgitation. The RV was enlarged, with leftward
bowing of the interventricular septum on the 4-chamber
image.
S U M M A RY
On the basis of the imaging findings, the diagnosis of Ebstein
anomaly was confirmed. In addition, the right atrium and
ventricle were severely enlarged, with displacement of the tri-
cuspid valve resulting in severe tricuspid regurgitation. The
patient underwent surgical repair of the tricuspid valve and
a right-sided maze procedure with ablation of the right atrial
isthmus.
Ebstein anomaly represents approximately 1% of adult
congenital heart disease and is characterized by apical dis-
placement of the septal leaflet of the tricuspid valve (and the
functional annulus), with adherence of the septal and pos-
terior leaflets to the underlying myocardium. The excluded
portion of the RV is said to be atrialized and does not con-
tribute to normal RV function. The displaced valve leaflets
are usually dysfunctional, and severe tricuspid regurgita-
tion is frequently observed, with consequent right atrial
enlargement.
 224 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11K

Figure 11.11 Severe pulmonic regurgitation and pulmonary artery aneurysm. A-D, Sagittal, oblique, balanced SSFP views during 2 time points in
systole (A and B) and 2 time points in diastole (C and D) showing a regurgitant jet through the pulmonic valve (arrow). E and F, Velocity-encoded
images from a phase-contrast acquisition across the pulmonic valve during systole (E) and diastole (F) confirm the presence of the large regurgitant
jet (arrowhead). G and H, Axial balanced SSFP image at the level of the main pulmonary artery in systole (G) and a maximum intensity projection
image from a 3-dimensional MR angiography acquisition (H) identify the severely dilated main pulmonary artery.
 11. Va lv u l a r H e a r t D i s e a s e
S E V ERE PUL MONIC
RE GURG ITATION AND
PUL MONARY ARTERY ANEURY S M
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 62-year-old woman had a history of an enlarged pulmonary
artery and mildly decreased exercise tolerance.
C L I N IC A L QU E S T ION
The patient was referred for cardiac MRI (Figure 11.11) to
assess the status of her pulmonary arteries and establish the
source of her exercise intolerance.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
Key diagnostic images, including balanced SSFP images of
the RV outflow tract and main pulmonary artery, demon-
strated marked aneurysmal dilatation of the main pulmo-
nary artery with poor coaptation of the valve leaflets in
• 225
diastole and a prominent regurgitant jet. Systolic and dia-
stolic velocity-encoded images from a cine phase-contrast
acquisition across the pulmonic valve confirmed promi-
nent regurgitant flow in diastole. A systolic balanced
SSFP image at the level of the main pulmonary artery
and a maximum intensity projection image from 3D
contrast-enhanced MR angiography of the pulmonary
arteries demonstrated marked dilatation of the main pul-
monary artery.
S U M M A RY
The MRI findings indicated a diagnosis of severe RV enlarge-
ment with severe pulmonic regurgitation. The main pulmo-
nary artery was noted to be severely dilated with a maximum
diameter of 6.4 cm. As a result of these findings, surgical
repair of the identified pulmonary artery aneurysm and pul-
monic valve replacement were recommended.
Pulmonic regurgitation is most frequently caused by dila-
tation of the annulus secondary to pulmonary hypertension.
Less common causes include direct damage to the valve cusps
from rheumatic heart disease, infectious endocarditis, or car-
cinoid disease. In this case, the pulmonary artery aneurysm
led to a dilated pulmonic annulus and poor coaptation of the
valve leaflets.
 226 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s

CA S E 11L

Figure 11.12 Pulmonic stenosis. A and B, Axial balanced SSFP images in systole identifying thickening of the pulmonic valve leaflets (A, white
arrow) and aneurysmal dilatation of the main pulmonary artery (B). C and D, Systolic balanced SSFP sagittal image through the RV outflow tract
(C) and coronal image of the pulmonic valve (D) demonstrating turbulence and signal voids (red arrow). E, Sagittal oblique velocity-encoded image
of the pulmonic valve acquired during systole demonstrating a narrow jet of flow across the valve (arrowhead).
 11. Va lv u l a r H e a r t D i s e a s e
PUL MONIC S TENO S I S
C L I N IC A L H I S TORY A N D
PR E S E N TAT ION
A 69-year-old woman had a known fusiform dilation of the
main pulmonary artery previously diagnosed by MRI at an
outside institution.
C L I N IC A L QU E S T ION
Follow-up MRI (Figure 11.12) at our institution was ordered
to assess the status of the pulmonary artery.
C A R DI AC M R I PROTO C OL
Use Valvular Heart Disease Protocol 5.4 (see page 79).
I M AG I NG F I N DI NG S
Balanced SSFP images revealed thickened pulmonic valve leaf-
lets with restricted opening and aneurysmal dilatation of the
main pulmonary artery. Images through the RV outflow tract
and pulmonic valve in systole demonstrated flow dephasing dis-
tal to the valve in the dilated main pulmonary artery. A systolic
velocity-encoded image from a cine phase-contrast acquisition
showed a narrow jet of flow across the pulmonic valve directed
anteriorly against the wall of the main pulmonary artery.
• 227
S U M M A RY
When compared with the MRI study from 5 years earlier,
the current MRI findings showed that the main pulmo-
nary artery had increased in diameter by 5 mm from its
prior dimension. In addition, the pulmonic valve leaf lets
were thickened, with stenosis and regurgitation through
the valve. Although the MRI examination demonstrated
continued worsening of the pulmonary artery aneurysm,
the lack of clinical data supporting the benefit of surgi-
cal repair in the patient did not support surgical inter-
vention. As a result, the patient underwent watchful
waiting and monitoring involving repeat cardiac MRI
examinations.
Pulmonic stenosis is a congenital lesion in approximately
95% of cases. It is usually an isolated lesion but can be a com-
ponent of complex congenital disease, such as tetralogy of
Fallot. Acquired pulmonic stenosis can occur in the setting of
rheumatic fever or carcinoid syndrome.
Pulmonic stenosis may produce RV pressure and volume
overload, with resultant RV hypertrophy, dilatation, and
eventual dysfunction. Poststenotic enlargement of the main
and left pulmonary arteries is a frequent association. The right
main pulmonary artery is frequently spared because the path
of the flow jet extends posteriorly through the main pulmo-
nary artery and into the origin of the left artery; the right pul-
monary artery originates at nearly a right angle to the main
pulmonary artery and is therefore spared some of the conse-
quences of the stenotic flow jet.
 228 • S e c t i o n II : C l i n i c a l A ppl i c at i o n s a n d C a s e S t u d i e s
S UG G E S TED READIN G
Bhattacharyya S, Toumpanakis C, Burke M, Taylor AM, Caplin ME,
Davar J. Features of carcinoid heart disease identified by 2- and
3-dimensional echocardiography and cardiac MRI. Circ Cardiovasc
Imaging. 2010 Jan;3(1):103–11. Epub 2009 Nov 17.
Chen JJ, Manning MA, Frazier AA, Jeudy J, White CS. CT angiogra-
phy of the cardiac valves: normal, diseased, and postoperative appear-
ances. Radiographics. 2009 Sep-Oct;29(5):1393–412.
Irwin RB, Luckie M, Khattar RS. Tricuspid regurgitation: contempo-
rary management of a neglected valvular lesion. Postgrad Med J. 2010
Nov;86(1021):648–55. Epub 2010 Oct 18.
Lee C, Kim YM, Lee CH, Kwak JG, Park CS, Song JY, et al. Outcomes of
pulmonary valve replacement in 170 patients with chronic pulmonary
regurgitation after relief of right ventricular outflow tract obstruc-
tion: implications for optimal timing of pulmonary valve replacement.
J Am Coll Cardiol. 2012 Sep 11;60(11):1005–14. Epub 2012 Aug 22.
Lotz J, Meier C, Leppert A, Galanski M. Cardiovascular flow measure-
ment with phase-contrast MR imaging: basic facts and implementa-
tion. Radiographics. 2002 May-Jun;22(3):651–71.
Mordi I, Tzemos N. Bicuspid aortic valve disease: a comprehensive
review. Cardiol Res Pract. 2012;2012:196037. Epub 2012 May 28.
Morris MF, Maleszewski JJ, Suri RM, Burkhart HM, Foley TA,
Bonnichsen CR, et al. CT and MR imaging of the mitral valve:
radiologic-pathologic correlation. Radiographics. 2010 Oct;30(6):
1603–20.
Myerson SG. Valvular and hemodynamic assessment with CMR. Heart
Fail Clin. 2009 Jul;5(3):389–400. Erratum in: Heart Fail Clin. 2011
Apr;7(2):x.
Pibarot P, Dumesnil JG. Prosthetic heart valves: selection of the opti-
mal prosthesis and long-term management. Circulation. 2009 Feb
24;119(7):1034–48.
Shone JD, Sellers RD, Anderson RC, Adams P Jr, Lillehei CW, Edwards
JE. The developmental complex of “parachute mitral valve,” supraval-
vular ring of left atrium, subaortic stenosis, and coarctation of aorta.
Am J Cardiol. 1963 Jun;11:714–25.
Vogel-Claussen J, Pannu H, Spevak PJ, Fishman EK, Bluemke DA. Cardiac
valve assessment with MR imaging and 64-section multi-detector
row CT. Radiographics. 2006 Nov-Dec;26(6):1769–84.
Yalonetsky S, Tobler D, Greutmann M, Crean AM, Wintersperger
BJ, Nguyen ET, et al. Cardiac magnetic resonance imaging and the
assessment of Ebstein anomaly in adults. Am J Cardiol. 2011 Mar
1;107(5):767–73. Epub 2011 Jan 19.
 SEC T ION I I I
T ROU BL E SHO OT I NG —M R I A RT I FAC TS
A N D S A F ET Y
 12.
COMMON MR IM AGING ARTIFACTS
Kiaran P. McGee, PhD, and Matthew A. Bernstein, PhD

C
ardiac magnetic resonance (MR) imaging involves
the use of a complex and sensitive imaging device to
obtain high temporal- and spatial-resolution images
of the heart as it changes shape, size, and position throughout
the cardiac cycle. Because of this inherent complexity, mea-
surement errors inevitably occur, which results in artifacts
within the reconstructed image. Even when the MR scanner
is functioning correctly, inappropriate choice of specific imag-
ing parameters also can result in image artifacts. Successful
cardiac imaging, therefore, requires knowledge of not only
the most commonly encountered artifacts and their sources
but also methods to reduce them. The purpose of this chapter
is to describe several commonly encountered imaging arti-
facts, their causes, and countermeasures to either reduce or
ameliorate them.

A L I A S I NG

S OU RC E
Aliasing occurs when the field of view (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 direc-
tion (Figure 12.1). This can occur along 2 directions when
3-dimensional data are acquired, but it does not occur along
the frequency-encoding direction.

S OLU T ION S
• Increase the FOV along the phase-encoding axis. This will
solve this problem but will decrease the spatial resolution
along this direction.
• Enable no-phase-wrap or phase-oversampling features.
• Swap the readout and phase-encoding directions.
• Apply parallel imaging techniques to “unwrap” the Figure 12.1 Aliasing. A, Reduced-phase FOV 4-chamber image of
artifact. This will solve the problem but can decrease the heart demonstrating aliasing of the chest wall and arms into the
signal-to-noise ratio in the image. anatomical region of interest. B, Full-phase FOV image of the heart
with phase- and frequency-encoding directions swapped.

231
 232 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety
• Reposition the center of the FOV so that the aliased
regions 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 the region of interest.
G R A DI E N T DE C AY OR FA L L- OF F
S OU RC E
Gradient decay or fall-off is a result of the limited physical extent
of the spatial-encoding gradient fields, most notably along the
physical Z-axis of the MR scanner, which, in a cylindrical-bore
magnet, corresponds to the head-foot direction of the patient.
Along this axis, the gradient field is at a maximum at the physi-
cal ends of the coil but decreases to zero along this axis away
from the ends of the coil. Radiofrequency (RF) excitation and
reception of signal from tissue within the fall-off zone of these
gradient fields results in tissue within this region being spatially
mismapped on the reconstructed image (Figure 12.2). This
effect is due to aliasing, so it occurs along the phase-encoding
direction and can appear as different types of artifacts. Several
terms, including peripheral signal artifact, feather artifact, and
cusp artifact (also known as “annefact”) have been used.
S OLU T ION S
• For the coronal and sagittal imaging planes, select
the frequency-encoding direction to be along the
superior-inferior direction. If this causes flow and
breathing artifacts to propagate over the anatomy of
interest, then one of the other countermeasures should
be used.
• 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, select only the coils that cover the
region of interest.
• Place saturation bands over the regions in the fall-off zone
of the gradient fields.
• Use transmit-receive instead of receive-only coils. For
cardiac applications, this is usually not practical because
the body RF coil typically must be used for transmission.
R F Z I PPE R
S OU RC E
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 12.3). 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.
S OLU T IONS
• 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.
E C G G AT I N G M I S T R IG G E R S
S OU RC E
A poor quality (low-voltage) electrocardiographic (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,
ghosting, and signal loss. ECG-gated MR sequences typi-
cally 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 induce respiratory-induced 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 12.4).
S OLU T IONS
• 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.
 1 2 . C ommon M R I maging A rtifacts  • 233

Figure 12.2 Gradient decay or fall-off. A and B, Single-shot, fast spin echo, sagittal, 35-cm FOV localizer image with a superior-inferior (A) and
anterior-posterior (B) phase-encoding direction. Image A shows aliasing (wrap) of anatomy within the decay zone of the gradient and included within
the RF torso coil, with gradient fall-off contributing to the spatial distortion and hyperintensity in regions of the artifact. Switching phase and
frequency axes effectively eliminates the artifact in this instance. C, Sagittal spin-echo, T2-weighted spine image shows “feathering” (arrow) along the
superior-inferior direction at the position of the vertebral bodies, indicating the presence of annefact (cusp) artifact. An element of the multielement
RF coil is located within the fall-off region of the Z-axis gradient and is incorrectly spatially encoded, thereby producing the feathering along the
phase-encoding direction. D, Short-axis, balanced steady-state free precession (SSFP) image of the heart demonstrating both feathering and wrap
from anatomy outside the imaging plane. Although annefact artifact (arrows) is most commonly associated with multiecho spin echo sequences, this
image demonstrates that other pulse sequences can reproduce this effect. Due to fall-off of the gradients, fat signal in the aliased anatomy (arrowhead)
is brighter than other fat and is due to the collapse of this signal from anatomical regions that would normally be spatially encoded.
 234 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

Figure 12.3 RF Zipper. Four-chamber, balanced SSFP, gradient echo (A), perfusion (B), and late gadolinium-enhancement (C) images showing an
RF zipper propagated along the phase-encoding direction. The noise source that produced this artifact was an infusion pump in the MR scan room.
For imaging sequences with low signal-to-noise ratio, such as late gadolinium-enhancement imaging, the artifact can be particularly prominent.

• Increase the views per segment and, if necessary, decrease R E S PI R ATORY (B R E AT H I N G)

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 the ECG cable travels as closely as possible
to the center of the MR scanner bore as it exits.
• Choose peripheral pulse gating (eg, using a pulse
plethysmograph).
MO T ION A RT I FAC T
S OU RC E
Respiratory motion artifacts occur if patients are unable to
hold their breath and resume breathing during the data acqui-
sition process. Movement of the heart through the imaging
plane due to diaphragm motion induces blurring, ghosting,
 1 2 . C ommon M R I maging A rtifacts  • 235

Figure 12.4 ECG gating mistriggers. A, Four-chamber view of the

heart with gating mistriggers. Mixing of different cardiac views from
across the cardiac cycle produces motion blurring of the heart only. B,
Correctly gated 4-chamber view.

and volume averaging of the heart (Figure 12.5). These effects

can decrease image quality and the accuracy of 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.
S OLU T ION S
• Decrease the imaging time, if possible, so that the patient
can achieve a breath-hold throughout the imaging
acquisition. Parallel imaging techniques are useful in
Figure 12.5 Respiratory (breathing) motion. Short-axis images of the
heart during a free-breathing (A) and a breath-hold (B) ECG-gated
acquisition. Although ECG gating in this imaging sequence was
successful, respiratory motion severely degrades image quality.
Movement of the diaphragm results in movement of the cardiac anatomy
through the imaging slice, resulting in blurring and ghosting of the
cardiac anatomy.
 236 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

this regard. Another approach is to decrease the number F L OW-R E L AT E D A RT I FAC T S

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. Increasing
views per segment reduces acquisition time, but at the
expense of temporal resolution.
• In some instances, use navigator echoes or respiratory
bellows, which allow free breathing during data
acquisition, 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.
S OU RC E
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 modula-
tion produces replication and blurring of the signal along the
phase-encoding direction of the image (Figure 12.6). This
effect is most apparent for balanced steady-state free preces-
sion (SSFP) sequences and is exacerbated at increased pulse
repetition time (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.

Figure 12.6 Flow-related artifacts. A, Image shows fully magnetized blood in the aorta entering the imaging slice during a balanced SSFP gradient
echo imaging sequence. B, Image shows the same slice but during late diastole when flow is at a minimum.
 1 2 . C ommon M R I maging A rtifacts  • 237

S OLU T ION S
• 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).

S US C E P T I B I L I T Y-I N DUC E D
S IG N A L L O S S

S OU RC E
Differences in magnetic susceptibility of tissues or implanted
materials (eg, metals such as sternal wires or stents) distort the
magnetic field around the tissue interface or object, producing
image distortion and signal loss (Figure 12.7).

S OLU T ION S
• 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. Localized
shimming (eg, a manually selected shim box) is
particularly useful.
• Increase the receiver bandwidth of the imaging sequences
or choose spin echo–based sequences for imaging around
metal implants when appropriate.

B A N DI NG O N B A L A NC E D
S S F P I M AG E S

S OU RC E
Balanced SSFP 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
12.8). The source of this inhomogeneity can be the physi-
cal design limitations of the main magnetic field or sus-
ceptibility-induced field variations from different tissue
interfaces (eg, lung to liver to heart) or implanted devices
(eg, stents).

S OLU T ION S
• Minimize the TR. The spatial period of the banding
is proportional to the inhomogeneity of the main Figure 12.7 Susceptibility-induced signal loss. Multiple short-axis views of
magnetic field and the inverse of the TR of the imaging the heart showing signal loss and distortion around sternal wires (arrows).
 238 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

Figure 12.8 Banding on balanced SSFP images. A and C, Balanced SSFP gradient echo images demonstrating banding and signal loss (arrows) due
to magnetic field inhomogeneities. B and D, Spoiled gradient echo images without banding.

sequence. Decreasing the TR will increase the separation I M AG E-B A S E D PA R A L L E L I M AG I N G

of the bands and potentially shift these artifacts outside R E C ON S T RUC T ION A RT I FAC T
the anatomy of interest. This is especially important
at field strengths greater than 1.5T (eg, 3.0T). For
S OU RC E
field strengths of 3.0T, the TR should not exceed 3.5
milliseconds. Image-based parallel imaging methods such as SENSE reduce
the imaging FOV in the phase-encoding direction. This
• If decreasing the TR is not possible (ie, the TR is already at
decreases the total acquisition time by reducing the number of
its minimum value), improve the homogeneity of the main
phase-encoding steps but also causes image aliasing (ie, wrap-
magnetic field by linear or higher-order shimming over the
around artifact) (Figure 12.9). To unwrap the aliasing within the
localized volume of the heart to decrease the artifact.
image, a map of the RF coil sensitivity throughout the imaging
• Switch to another type of pulse sequence such as a spoiled volume must be used. This is often referred to as a calibration
gradient echo; however, signal-to-noise ratio may decrease. scan and is obtained before or during acquisition of the acceler-
ated image data (so-called autocalibration). Artifacts arise when:
• Change the resonant frequency of the receiver, thereby
shifting the banding artifact so that the region of
signal loss is outside the critical anatomical region of 1. The calibration scan does not cover the entire anatomy
interest. in the volume scanned. Regions of low signal in the
 1 2 . C ommon M R I maging A rtifacts  • 239

Figure 12.9 Image-based parallel imaging reconstruction artifact. Short-axis spoiled gradient echo images acquired with parallel imaging (SENSE)
techniques (A, C, and E), and full-acquisition short-axis views (B, D, and F). Insufficient coverage of the imaging volume by the calibration scan
results in reconstruction errors in the reconstructed, accelerated data (arrows).
 240 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

calibrated region, such as in the lungs, can produce similar

artifacts.
2. The reconstructed (ie, full) FOV is smaller than the
object. This is particularly problematic for autocalibrated
scans, which can derive their sensitivity maps from the
accelerated image data, thereby producing erroneous coil-
sensitivity maps.
3. The acceleration factor is too high (equal to or greater than
the number of coil elements in the phased-array RF coil).
In this case, the unwrapping algorithm is ill-conditioned
(number of aliases greater than the number of coil elements
in the phased-array RF coil) and the reconstruction
algorithm will also produce image artifacts.

S OLU T ION S
• Ensure that the calibration scan field more than covers the
object imaged.
• Ensure that the reconstructed (ie, full) FOV is greater than
the object’s extent in the phase-encoding direction.
• Decrease the acceleration factor to be equal to or less than
the number of RF coil elements.
• Acquire a fully sampled MR dataset but with a decreased
FOV (and scan time). This intentionally generates image
aliasing but with the aliased portions of the image being
outside the anatomy of interest (eg, the heart).
• Use properly designed RF coils with a higher number of
elements, and/or an MR system with an increased number
of channels, which allows the use of a higher acceleration
factor without serious artifacts.

k-S PAC E–B A S E D PA R A L L E L

I M AG I NG A RT I FAC T

S OU RC E
k-Space–based methods such as GRAPPA and ARC do not
require the use of a separate calibration scan. Scan times are
decreased by effectively skipping k-space lines, except for the
central portion of k-space. Missing k-space data are synthe-
sized from adjacent k-space lines using weighting functions
derived from the fully sampled portion of k-space. Artifacts
occur when synthesized (ie, missing) lines of k-space are incor-
rectly reconstructed because of errors in the weighting func-
tions (Figure 12.10). Incorrect weighting functions are the
result of an insufficient number of fully sampled, central lines
of k-space from which these functions are derived. Because Figure 12.10 k-Space–based parallel imaging artifact. A, Subtle aliasing
the weighting functions apply to all missing lines of k-space of the FOV in the phase-encoding direction (left-to-right) can be seen
data, artifacts appear as increased noise throughout the image in the center of the image (arrows) due to incorrect synthesis of skipped
k-space data. B, Short-axis, full-acquisition, balanced SSFP image.
and are not spatially localized, as is the case with sensitivity C, Highly accelerated k-space–based parallel imaging acquisition
maps in image-based approaches. Aliasing artifacts can also demonstrating noise amplification throughout the image introduced by
be observed due to incorrect reconstruction of missing data. synthesis of missing k-space lines.
 1 2 . C ommon M R I maging A rtifacts  • 241

S OLU T ION S
• Decrease the acceleration factor, thereby increasing
the number of sampled lines of k-space that are used
to generate the weighting functions used in the
reconstruction of missing k-space lines.
• Acquire a fully sampled MR dataset but with a
reduced FOV (and scan time), thereby intentionally
generating image aliasing but with the aliased portions
of the image being outside the anatomy of interest
(eg, the heart).
• Use properly designed RF coils with a higher number of
elements, and/or an MR system with an increased number
of channels, which allows the use of a higher acceleration
factor without serious artifacts.

PE R F US IO N DA R K-R I M
E N H A NC E M E N T A RT I FAC T

S OU RC E
Perfusion dark-rim enhancement is a loss of signal within
the myocardium during first-pass perfusion imaging that can
mimic myocardial perfusion defects (Figure 12.11). Several
possible sources have been identified, including Gibbs ringing,
motion, k-space sampling strategies, and a too-high concen-
tration of contrast agent resulting in susceptibility-induced
signal loss. The artifact is transient and typically disappears as
the peak of the bolus passes through the ventricles, as opposed
to a true perfusion defect, which will be present throughout
the first pass of the contrast agent. The artifact can be verified
by the lack of signal enhancement at the site of the signal void
on late gadolinium-enhancement (LGE) images, as shown in
Figure 12.11.

S OLU T ION S
• Decrease the injection rate of contrast agent. This
broadens the contrast bolus and decreases first-pass
image contrast.
• Increase the number of phase-encoding steps. This will
increase the spatial resolution, decreasing the potential
for Gibbs ringing and susceptibility-induced signal
loss. This will also increase the acquisition time, which
can then be decreased by using k-space–based parallel Figure 12.11 Perfusion dark-rim enhancement artifact. Example of
imaging approaches. the dark-rim enhancement artifact (arrows) on short-axis views of
the heart during first-pass perfusion imaging. The first 3 images show
• Zero-fill the k-space data before Fourier baseline (A), arrival of the bolus (B), and washout (C) of the contrast
transformation. This results in smaller pixel agent. During the peak bolus phase, the dark-rim enhancement artifact
dimensions by means of interpolation and can more is manifested as a dark line along the endocardial border of the septal
wall of the left ventricle and can be mistaken for a perfusion defect. D,
clearly depict Gibbs ringing artifacts, reducing The artifact is present for only a few cardiac phases and therefore is not
their dependence on the specific position of the present in the last perfusion image. The LGE image of the same slice
endocardial wall. does not show evidence of an infarction.
 242 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

L IG H T N I NG F L A S H A RT I FAC T

S OU RC E
Most MR imaging techniques require establishment of
the steady state (ie, the dynamic balance between longitu-
dinal signal recovery and the creation of transverse mag-
netization after an RF excitation pulse). Imaging under
non–steady-state conditions results in modulation of the
magnitude of the frequency (k-space) data and subsequent
image artifacts. For gradient echo cine sequences, tissues
with short T1 relaxation time will recover faster and contrib-
ute more signal under non–steady-state conditions. This typi-
cally occurs due to irregular heart rates. For cine acquisitions,
non–steady-state images will appear brighter (higher overall
signal) than images acquired under steady-state conditions.
When reviewed as a cine loop, non–steady-state images will
appear as a “flash” of increased signal in 1 portion of the cine
loop (Figure 12.12).

S OLU T ION S
• Use a pulse sequence that continuously applies RF pulses
during the entire R-R interval, including the window
when ECG triggers are detected. This maintains the
steady state throughout the data collection process. This
is particularly important if the patient has an irregular
heartbeat. If the patient’s heart rate is regular but the
imaging sequence is missing ECG triggers, then several
of the methods for improving gating reliability should
be implemented. The arrhythmia rejection window (if
applicable) should be increased to reject data outside the
average heart rate of the patient.

S US C E P T I B I L I T Y-I N DUC E D FAT

S AT U R AT ION FA I LU R E

S OU RC E
Chemical fat saturation techniques apply an RF pulse that
is tuned to the resonant frequency of lipids within the
imaging volume. Magnetic field inhomogeneities induced
by susceptibility differences alter the resonant frequency of
not only water but also lipids. If the susceptibility-induced
frequency shift is large enough, the resonant frequency of
the lipid signal can shift outside the pass band of the fat
Figure 12.12 Lightning flash artifact. Example of loss of the steady-state
saturation RF pulse. In certain circumstances the reso- condition during acquisition of a short-axis cine image series. Because
nant frequency of water can shift into the pass band of the of the short T1 of the lipid signal, ghosting artifacts are apparent and,
RF pulse. Under these conditions, the water signal is sup- when viewed as a cine loop, appear as a bright or lightning flash. A and
pressed and the fat signal remains unaffected. Figure 12.13 B, Short-axis views acquired during early systole before the steady state
demonstrates this effect in the thorax, with the sig- has been established. Ghostlike signal in the background and in the
lungs is an artifact due to the segmented nature of the data acquisition
nal from water being suppressed, creating a signal void scheme and the transition from non–steady state to steady state of the
about the ascending aorta, while the lipid signal remains signal. C, The steady state is established, and related artifacts are absent,
unaffected. in an image acquired at a later phase of systole.
 1 2 . C ommon M R I maging A rtifacts  • 243

Figure 12.13 Susceptibility-induced fat saturation failure. Images demonstrate susceptibility-induced alteration of the main magnetic field within
the thorax at the level of the aortic arch. A, In this fat-saturated, T1-weighted volumetric acquisition, susceptibility differences between the lungs,
anterior chest wall, and great vessels are large enough to shift the resonant frequency of tissue within the ascending aorta into the saturation band of
the fat saturation pulse, which results in signal loss within this vessel (arrow). The use of iterative Dixon-based methods results in water-only (B) and
fat-only (C) images, which are insensitive to off-resonance effects.
 244 • S ection I I I : T roubleshooting —M R I A rtifacts and S afety

Figure 12.14 Incomplete myocardial suppression on LGE imaging. This artifact is the effect of incorrect choice of inversion time. A, Single-shot,
long-axis, magnitude-only, LGE image. Incorrect inversion time results in incomplete suppression of normal myocardium and poor normal-to-infarcted
myocardial contrast. B, Phase-sensitive LGE image with the same inversion time demonstrates improved normal-to-infarcted myocardial contrast.
 1 2 . C ommon M R I maging A rtifacts  •
S OLU T ION S
• Image the anatomy of interest using iterative Dixon
imaging techniques. These techniques acquire image
data at 2 or 3 different echo times, followed by a special
iterative reconstruction that attempts to correct for
magnetic field inhomogeneities to improve the ability to
separate fat and water signals into fat-only and water-only
images. The separate fat and water images are absent of
any signal voids and accurately reproduce the anatomy of
interest.
• In the absence of Dixon-based fat-water imaging methods,
the homogeneity of the main magnetic field may be
improved by performing so-called small-volume linear
or higher-order shimming. Localized, small-volume
shimming allows a volume of interest to be identified
about the anatomy of interest that excludes the remainder
of the imaging volume. The spatial encoding gradients are
used to attempt to minimize the inhomogeneity within
the volume and hence reduce susceptibility-induced
off-resonance effects. Higher-order shimming involves
the use of special shimming coils and circuits that create
magnetic fields described by polynomial functions
of spatial position. This approach has not yet been
commonly used.
I N C OM PL E T E M YO C A R DI A L
S U PPR E S S ION ON
L G E I M AG I NG
S OU RC E
Incorrect choice of inversion time on LGE imaging results
in incomplete suppression of the signal from normal myo-
cardium. Incomplete suppression of normal myocardium
decreases overall image contrast and decreases conspicuity of
infarcted regions (Figure 12.14).
S OLU T ION S
• Check the inversion time by running T1 mapping
or T1 scout sequences. As a result of the wash-in and
wash-out of contrast agent into normal and infarcted
myocardium, a delay between running of the T1
mapping and LGE sequences can result in the choice of
an inversion time that is no longer accurate at the time
of imaging. Rechecking the inversion time by repeating
the mapping routine can correct this discrepancy, as
long as sufficient contrast is still within the blood pool
and myocardium.
• Use phase-sensitive LGE imaging methods. This method
preserves the sign of the MR signal, is less sensitive to
incorrect choice of inversion time, and provides improved
normal myocardium-to-infarction contrast. However,
phase-sensitive images have a lower signal-to-noise ratio
than magnitude-only methods.
245
S UG G E S T E D R E A DI N G
Anatomy and Physiology of the Heart
Marieb EN. Essentials of human anatomy and physiology. 7th ed. San
Francisco (CA): Benjamin Cummings; c2003.
Cardiac MR
Bogaert J, Dymarkowski S, Taylor AM. Clinical cardiac MRI: with
interactive CD-ROM. Berlin: Springer; c2005.
Lee VS. Cardiovascular MRI: physical principles to practical protocols.
Philadelphia (PA): Lippincott Williams & Wilkins; c2006.
ECG Physiology
Hobbie RK, Roth BJ. Intermediate physics for medicine and biology. 4th
ed. New York (NY): Springer; c2007.
Malmivuo J, Plonsey R. Bioelectromagnetism: principles and applica-
tions of bioelectric and biomagnetic fields. New York (NY): Oxford
University Press; c1995.
Gradient Decay or Fall-Off
Rangwala N, Zhou XJ. Reduction of fast spin echo cusp artifact using a
slice-tilting gradient. Magn Reson Med. 2010 Jul;64(1):220–8.
Miscellaneous
Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey
WK, et al; American Heart Association Writing Group on
Myocardial Segmentation and Registration for Cardiac Imaging.
Standardized myocardial segmentation and nomenclature for tomo-
graphic 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. Int J Cardiovasc
Imaging. 2002 Feb;18(1):539–42.
MR Acronyms
Boyle GE, Ahern M, Cooke J, Sheehy NP, Meaney JF. An interac-
tive taxonomy of MR imaging sequences. Radiographics. 2006
Nov-Dec;26(6):e24.
Brown MA, Semelka RC. MR imaging abbreviations, definitions, and
descriptions: a review. Radiology. 1999 Dec;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 Feb;15
Suppl 2:B10–6.
MR Physics and Pulse Sequences
Bernstein MA, King KF, Zhou XJ. Handbook of MRI pulse sequences.
Amsterdam: Elsevier Academic Press; c2004.
Haacke EM, Brown RW, Thompson MR, Venkatesan R. Magnetic reso-
nance imaging: physical principles and sequence design. New York
(NY): J Wiley & Sons; c1999.
Perfusion Dark-Rim Enhancement Artifact
Ferreira P, Gatehouse P, Kellman P, Bucciarelli-Ducci C, Firmin D.
Variability of myocardial perfusion dark rim Gibbs artifacts due to
sub-pixel shifts. J Cardiovasc Magn Reson. 2009 May 27;11:17.
Vector ECG Gating
Chia JM, Fischer SE, Wickline SA, Lorenz CH. Performance of QRS
detection for cardiac magnetic resonance imaging with a novel vec-
torcardiographic triggering method. J Magn Reson Imaging. 2000
Nov;12(5):678–88.
Fischer SE, Wickline SA, Lorenz CH. Novel real-time R-wave detection
algorithm based on the vectorcardiogram for accurate gated magnetic
resonance acquisitions. Magn Reson Med. 1999 Aug;42(2):361–70.
 13.
CAR DI AC MR I SAFET Y
Kiaran P. McGee, PhD, Robert E. Watson Jr, MD, PhD, and Eric E. Williamson, MD
T
he volumetric nature of magnetic resonance imag-
ing (MRI) data, the ability to acquire data in any
orientation, the wealth of anatomical and func-
tional information, and the lack of ionizing radiation make
MRI an extremely versatile imaging modality. However, the
MR scanner poses unique challenges with regard to patient
safety. Patient safety is further complicated by the presence
of various implantable medical devices, many of which have
the potential to interact with the MR environment, and by
the sometimes conflicting information regarding their MR
safety. The goal of this chapter is to provide an overview of
the potential risks faced by every patient undergoing an MRI
examination and to highlight the unique challenges associ-
ated with specific implanted devices and contrast agents. It
is important to appreciate that the information contained
herein is not definitive. The reader should also consult MRI
safety resources (see Suggested Reading) to obtain a more
in-depth review of the concepts and techniques necessary
to ensure the safety of patients undergoing MRI. We also
recommend seeking the advice of experts in the field of MR
scanning and safety.
C OM P O N E N T S OF T H E M R S C A N N E R
A N D A S S O C I AT E D S A F E T Y R I S K S
Figure 13.1 shows a schematic representation of a cylin-
drical, horizontal-bore, superconducting MR scanner and
identifies the major components of the system that work in
unison to generate an MR image. In the following sections,
the safety risks associated with these components will be
discussed.
M A I N M AG N E T IC F I E L D (B 0 )
Modern MR scanners maintain a large (≥0.5T) and perma-
nent magnetic field (B0) by passing a current through a super-
conducting circuit that forms a cylinder along the axis of the
MR scanner (Figure 13.1). Permanently magnetized materi-
als and materials with nonzero magnetic susceptibilities can
interact with the B0 field of the MR scanner by experiencing
both linear and rotational (ie, torque) forces. Both of these
forces pose a considerable safety risk to patients undergoing
246
MRI. One safety risk is the so-called projectile effect, which
occurs when a magnetized object experiences an attractive
force that is large enough to overcome both gravitational and
frictional forces. When this occurs, the object can become a
projectile, accelerating as it travels toward the bore of the MR
scanner. Depending on the mass of the object, its impact upon
a subject can be and has been catastrophic. Even if the object
does not hit a person, it can cause substantial damage to the
MR scanner, resulting in significant down time, repair costs,
and loss of revenue. The introduction of an object into the MR
environment which has the potential to become a projectile
should thus be avoided. Another risk occurs when a materi-
al’s magnetic susceptibility exhibits spatial anisotropy—that
is, the material is more easily magnetized in one direction
than another. The material will experience a torque that will
attempt to align the object’s net magnetization vector with
the applied field. These rotational forces are of most concern
for implanted devices, especially those whose susceptibility
is large and that exhibit significant spatial anisotropy. These
effects can also be amplified by the geometry of the implant; a
long thin rod in which the magnetization vector is orthogonal
to the main magnetic field will experience a large torque in
comparison to a sphere. For implanted devices located in and
around critical structures such as nerves and blood vessels,
their motion can be hazardous.
In general, the magnitude of the projectile force F is pro-
portional to the product of the net magnetism (m) of the
object, the magnetic field (B), and the spatial gradient of
this field as a function of the spatial field vector (r), or ∂B/∂r.
Mathematically this relationship is expressed as:
∂B
F ∝ mB
∂r
In MRI, B can include contributions from both B0 and
the spatial encoding gradients but due to differences in ampli-
tudes is more commonly used to describe only B0. Similarly,
∂B/∂r describes the spatial variation of B0, particularly as
the field decays away to zero beyond the bore of the scanner,
and is commonly referred to as the spatial gradient magnetic
field. This equation identifies the fact that the projectile force
is related to the product of both the strength of B0 and its
spatial variation. Within the bore of the MR scanner, ∂B/∂r
 13 . C ardiac M R I S afety  •
Figure 13.1 Schematic representation of a horizontal-bore superconducting MR scanner.
approaches a value of zero, and therefore the force experienced
by the object is small despite a large B0 field. In contrast, ∂B/∂r
is greatest beyond the bore of the magnet in the so-called B0
fringe field and, as such, objects with nonzero values of m
experience the largest force and undergo the greatest accel-
eration within these zones. The magnetization of an object is
determined by the magnetic class of the material, with ferro-
magnetic materials possessing the largest value of m, followed
by paramagnetic and diamagnetic materials. Diamagnetic
materials oppose the applied field and experience an oppos-
ing force, in comparison to ferromagnetic and paramagnetic
materials. In general, paramagnetic and diamagnetic materi-
als experience significantly lower forces of attraction.
The vast majority of patients undergoing MRI do not have
an implanted device, and thus the greatest risk to patient safety
is the B0 field and the potential for a foreign object entering
the MR environment and becoming a projectile. As a general
safety rule, any ferrous object should not be introduced into
the MR environment. Several implanted devices contain fer-
rous components or permanent magnets (eg, cochlear implants
and auditory brain stem devices). For these patients, extreme
247
caution should be exhibited; these devices are generally con-
sidered a contraindication to imaging. For MRI in patients
with implanted devices, it is recommended that guidelines on
MRI safety published by the American College of Radiology
(ACR) are followed (see Suggested Reading). Information on
the safety of a given implanted device can be obtained from
the manufacturer, in most cases, if the specific model number
and device description are known. Additionally, several MRI
safety websites and other reference materials describing the
MRI safety of a given device are available.
G R A DI E N T F I E L D S
Gradient magnetic fields are designed to provide a linearly
varying magnetic field across the imaging volume, thereby
enabling spatial encoding of the MR signal. Gradient fields
are specified in terms of their maximum amplitude (in mT/m)
and their switching or slew rate (in T/m/s). High-performance
gradient systems, commonly found on high-field MR scan-
ners (≥1.5T) have gradient specifications within the range of
40 to 50 mT/m and 150 to 200 T/m/s.
 248 • S ection I I I : T ro u b l eshootin g —M R I A rtifacts and S afety
Pulsed-gradient magnetic fields produce 2 bioeffects:
peripheral nerve stimulation and acoustic noise. Peripheral
nerve stimulation is most commonly manifested as pain,
uncontrolled muscle contraction, and tingling in the arms
and legs. Gradient-induced neurologic stimulation occurs
preferentially within peripheral nerves rather than the cen-
tral nervous system because the peripheral nerve fibers are
smaller and because of the relatively larger gradient fields that
occur away from the isocenter of the MR scanner. This effect
results from the associated electrical field that is induced by
a time-varying magnetic field (ie, slewing of the gradient), in
accordance with electromagnetic theory.
First promulgated by the US Food and Drug Adminis­
tration (FDA) and later adopted by international standards
organizations, restrictions are now imposed on the maximum
time rate of change (ie, dB/dt) of gradients to minimize the
potential for peripheral nerve stimulation. Note that this
value is the absolute value of the change in the magnetic field
with respect to time, as opposed to the rate of change of the
gradient field, or slew rate, previously described. This has
important implications regarding the physical length of the
gradient coil and the maximum slew rate. In advising manu-
facturers on premarket submissions, the FDA requires that
dB/dt values not exceed 20 T/s for a gradient pulse duration
longer than 120 microseconds. If a manufacturer wishes to
market an MR scanner with gradient performance in excess
of this value, limited human volunteer studies must be per-
formed to determine if peripheral nerve stimulation occurs.
Normal imaging can be performed with dB/dt values in
excess of the FDA recommendations as long as peripheral
nerve stimulation is avoided with an adequate safety margin.
The potential for inducing peripheral nerve stimulation
can also be determined according to an empirical model (see
Reilly, 1992) as a function of peak dB/dt versus pulse duration
for various waveform types. Manufacturers have adopted this
model as a method of predicting peripheral nerve stimulation
and by doing so provide a method to ensure that this level is
not reached. For example, under normal operating conditions,
pulse sequence gradient waveforms can be modified to ensure
that they operate within 66% of the stimulation threshold, on
the basis of the empirical model and specific pulse sequence
parameters.
Acoustic noise is generated by the MR scanner as a result
of the distortion of the cylindrical housing onto which the cir-
cuitry used to generate the gradient fields is wound. To gener-
ate the gradient magnetic fields, a current is passed through
the gradient coil circuit. Electrons flowing through the circuit
experience a force, known as the Lorentz force, due to their
movement through the B0 field, along a direction given by the
cross-product of the direction of motion and the magnetic
field vector. Macroscopically, this force distorts and twists
the gradient housing, which in turn mechanically interacts
with the inner bore of the magnet vessel, thus generating the
signature acoustic noise that occurs during imaging. In the
United States, manufacturers are required to limit the noise
generated by MR scanners to be less than 99 dB amplitude-
weighted and a peak unweighted sound pressure level of 140
dB. Although these limits are designed to reduce possible
noise-related hearing loss, scanners operating near these lim-
its often produce intolerable noise levels for many patients.
Therefore, we strongly advise, in accordance with the ACR
recommendations, providing to the patient and encouraging
the use of some form of noise abatement materials such as ear
plugs or headphones.
R A DIOF R E QU E NC Y F I E L D S
Generation of a detectable MR signal requires exposing the
patient to a radiofrequency (RF) field whose frequency is equal
to the Larmor frequency of hydrogen. With the exception of
localized transmit-receive coils such as head and extremity
(eg, knee and wrist) coils, most imaging studies generate this
field using a volumetric or body coil. The body coil is a large
cylindrical RF coil that fits inside of the gradient coil assem-
bly, extends over the majority of the inner bore of the MR
scanner, and is closest to the patient (Figure 13.1). Its design is
optimized to produce as uniform a magnetic field as possible
(also called a B1+ field), thereby ensuring image uniformity (by
generating a uniform flip angle throughout the imaging plane
or volume). RF power output by the body coil is absorbed by
the patient, which in turn causes heating by means of mag-
netic induction—the time-varying B1+ field induces an elec-
tromagnetic force, which results in the creation of electrical
currents. Currents generated in this manner produce Ohmic
heating due to the resistive properties of human tissue and,
if sufficiently high, can induce first-, second-, or third-degrees
burns. RF body coils also generate their own electric fields,
which are at a maximum at the coil surface and fall to zero
at the center of the coil. This electric field inhomogeneity can
also contribute to heating, especially in regions exposed to the
highest electrical field such as the arms and legs. If a conduct-
ing material is introduced into the MR scanner, the electric
field of the body coil can induce currents within the material
and produce associated heating. Because the electric field is
zero along the axis of the coil, conductors such as electrocar-
diographic (ECG) cables should be placed, as best as possible,
along the axis of the body coil.
The electromagnetic force induced by means of magnetic
induction produces eddy or circular currents. These current
loops follow any conducting pathway, such as that generated
when a patient’s arms or legs are crossed or when a conducting
material such as an ECG cable forms a closed loop. Implanted
conducting materials such as metal rods can serve as a conduit
for these currents, resulting in increased current density and,
hence, heating. Implanted or external conducting materials
such as deep-brain stimulators or pacemaker leads, if looped,
can also be a source of considerable heating, particularly at
the electrode tip due to the insulated length of these wires.
Loops in external conducting wires such as ECG leads should
similarly be avoided. For these reasons, it is commonly rec-
ommended to advise patients not to cross either their arms or
legs and to avoid any looping of conducting cables that are in
contact with the patient.
RF heating is typically quantified by the specific absorp-
tion rate (SAR), which is a measure of the amount of RF
power deposited per unit mass of tissue (in W/kg). Current
 13 . C ardiac M R I S afety  •
FDA regulations provide limits for SAR, and manufactur-
ers have implemented these into their scanners. However, it
is important to appreciate that the calculated values of SAR
for an individual patient and pulse sequence are based on
somewhat generic models of energy deposition in “typical”
patients. In addition, the SAR value reported represents an
estimated value averaged over the entire volume of tissue
exposed to the RF field, ignoring regional variations or SAR
“hot spots.”
As a general recommendation, the SAR value reported
on the MR scanner should be used as an additional safety
check to ensure that imaging is performed within safe lim-
its, particularly when a patient has an implanted device and
the device manufacturer has values of SAR that are below
the FDA-recommended nonsignificant risk values (ie, less
than those reported in Table 13.1). To reduce the risk of
RF-induced heating and the potential for burns, the patient
should not be in direct contact with the surface of the body
coil. This is easily achieved by the use of thin pads, either pro-
vided by the manufacturer or third-party suppliers or from an
in-house source, which provide some separation between the
patient and the inner surface of the scanner.
N AT IO N A L A N D
I N T E R N AT IO N A L S A F E T Y
S TA N DA R D S F OR M R I
In the United States, the FDA provides recommendations on
the use of MR scanners under conditions of nonsignificant
and significant risk. When operated under conditions of non-
significant risk, an MR scanner is considered a class II medi-
cal device, as defined by the US Code of Federal Regulations
Title 21 Chapter I Part 892 (21 CFR 892.1000). When
nonsignificant risk is exceeded, the US Federal Regulations
Table 13.1 US FDA CR ITER IA FOR SIGNIFICANT R ISK DUR ING MR I
PAR A METER SUBCLASSIFICATION/POPULATION
B0 Adults, children, and infants older than 1 mo
Neonates (infants younger than 1 mo)
Gradient fields dB/dt
Sound pressure level
Specific absorption rate (RF) Whole body
Head
Abbreviations: dB/dt, rate of change of gradient fields; rms, root mean square.
a
The FDA specifies that exceeding one of these parameter limits constitutes a transition from nonsignificant to significant risk. The FDA provides additional criteria
if MRI is performed when significant risk is established.
Adapted from Criteria for Significant Risk Investigations of Magnetic Resonance Diagnostic Devices. Guidance for Industry and Food and Drug Administration
Staff. US Department of Health and Human Services. Food and Drug Administration: 2014 June 20.
249
require that an investigational device exemption be obtained
from the FDA before patient imaging can be performed.
Imaging under conditions of significant risk also involves
additional requirements, as defined in the US Code of Federal
Regulations, that include institutional review board oversight
(21 CFR Part 56) and informed consent (21 CFR Part 50).
Modern MR scanners provide many software and hardware
checks to ensure that their devices comply with these recom-
mendations. However, it is also important to appreciate that
under certain conditions, and despite checks by the MR scan-
ner, the criteria of significant risk can be met under routine
imaging conditions.
The determination of significant risk by the FDA is based
on exceeding 4 operating parameters: main static magnetic
field, SAR, gradient field rate of change, and sound pressure
level (Table 13.1). Importantly, exceeding any one of these
parameters, for example imaging at an SAR value greater
than 3.2 W/kg over the head for 10 minutes or longer, would
mean that the MR examination is no longer of nonsignifi-
cant risk.
Recently, manufacturers have also started to accept
international standards promulgated by the International
Electrotechnical Commission (IEC). The IEC has estab-
lished the concept of operating modes that define limits for
several MRI-related parameters that should not be exceeded.
In particular, the IEC defines 3 operational modes—
normal, first level, and second level (Table 13.2). Each of
these modes has an associated safety level, as defined by SAR,
dB/dt, static magnetic field, and other parameters. Normal
mode describes the standard operating conditions for clinical
imaging in which exposure to the MR environment would not
be at a level sufficient to cause physiologic stress. First controlled
mode includes conditions that may cause physiologic stress
to the patient and in which medical supervision is required.
In addition, under this mode of operation, the MR scanner
LIMITa
>8T
>4T
If dB/dt is sufficient to produce severe discomfort or
painful nerve stimulation
Peak unweighted sound pressure level >140 dB
Weighted rms sound pressure level >99 dBA with
hearing protection in place
>4 W/kg over ≥15 min
>3.2 W/kg over ≥10 min
 250 • S ection I I I : T ro u b l eshootin g —M R I A rtifacts and S afety
Table 13.2 IEC MODES OF OPER ATION AND SELECTED PAR AMETER LIMITS FOR MR I
PAR A METER NOR M AL MODE
B 0, T <3
Gradient fields 80% of PNS threshold
SAR, W/kg
Volume transmit RF coils
Whole body 2 4
Partial body 2–10a
Head 3.2
Local transmit RF coils
Head 10
Trunk 10
Extremities 20
Body core temperature increase, °C 0.5
Abbreviations: IEC, International Electrotechnical Commission; PNS, peripheral nerve stimulation; SAR, specific absorption rate.
a
Scales with the ratio of exposed patient mass to total patient mass.
Adapted from Medical electrical equipment: Part 2-33. Particular requirements for the basic safety and essential performance of magnetic resonance equipment for
medical diagnosis. International Electrotechnical Commission; c2010. Reference No: IEC 60601-2-33:2010. Used with permission.
is required to indicate a software warning message (ie, dialog
box) at the operator console/computer and receive confirma-
tion from the user before proceeding. In the second controlled
mode, the patient is considered at significant risk, and, there-
fore, use of this mode requires approval by an institutional
review board. As a result, the IEC stipulates that users be
locked out of this mode under standard imaging conditions.
Under clinical imaging conditions, normal mode is pre-
ferred. However, for certain imaging sequences that require
optimized gradient performance, particularly with ultrashort
echo time and pulse repetition time values, as in the case of bal-
anced steady-state free precession imaging, first controlled mode
may be selected. In this mode, the MR scanner console will typi-
cally require some type of acknowledgement that the operator
has selected this mode. It is important to appreciate that while
operating under first controlled mode, an MRI examination is
still being performed in accordance with FDA regulations.
I M PL A N T E D DE V IC E S
PAC E M A K E R S A N D I M PL A N TA BL E
C A R DIOV E RT E R-DE F I BR I L L ATOR S
Pacemakers and implantable cardioverter-defibrillators (ICDs)
pose unique challenges for patients who need MRI. Initially, as a
result of several fatalities, a patient having either of these devices
was considered a contraindication to imaging. Recent research
and clinical experience has demonstrated that, with careful
patient selection and under specific imaging conditions—most
notably the avoidance of SAR values beyond a specific value
PAR A METER LIMITS
FIR ST CONTROLLED MODE SECOND CONTROLLED MODE
3–4 >4
100% of PNS threshold Beyond first level
>4
4–10a >4-10a
3.2 >3.2
20 >20
20 >20
40 >40
1.0 >1.0
and monitoring of the patient before, during, and after MR
examination by trained cardiology personnel—patients with
implanted cardiac pacemakers can be safely imaged. Although
it is beyond the scope of this work to describe the specific cir-
cumstances under which patients can be imaged, general guide-
lines followed within our institution are described below.
Patient Selection and Screening
The appropriateness of MRI for a patient with an implanted
cardiac device should be determined. If a patient is pace-
maker dependent, then MRI is not performed. In addi-
tion, the relative need for pacing (ie, the percentage of
heartbeats paced) is determined. Patients are also assessed
by pacemaker clinic personnel before imaging. This allows
important parameters such as battery status (gradient fields
are known to discharge the batteries of certain pacemaker
models), pacing and sensing thresholds, and lead imped-
ances to be quantified and documented.
Informed Consent
The increased potential risk associated with imaging of patients
with implanted cardiac devices must be discussed with the
patient and the referring physician. Obtaining informed con-
sent is essential and should be documented in the patient’s med-
ical record. In general, this is performed during assessment of
the patient in the pacemaker clinic. Referring physicians should
also be consulted to ensure that the examination is clinically
warranted and to determine if other imaging modalities or
diagnostic tests would answer the proposed clinical question.
 13 . C ardiac M R I S afety  •
Patient Monitoring
It is essential to monitor the patient before, during, and after
the MR examination. Monitoring before the MR examina-
tion establishes baseline values for the performance of the
pacemaker and allows pacemaker thresholds to be recorded.
In addition, the intrinsic heart rate of the patient should be
recorded and the pacemaker programmed to one of its asyn-
chronous modes, as established by the pacemaker technician
or cardiologist. All other diagnostic and therapeutic features
(eg, rate response, mode switch) should be programmed off.
During the MR examination, the patient should be moni-
tored by appropriately trained pacemaker or cardiology staff.
Monitoring should include, but not be limited to, pulse oxim-
etry, ECG, and oxygen saturation levels. Obtaining these
parameters during an MR examination requires the use of
specialized monitoring equipment designed to be compatible
with the MR environment. As a consequence, many institu-
tions may not have access to these critical patient monitoring
tools. In their absence, it is not recommended to proceed with
MRI. Additionally, a crash cart should be available in the MR
scanner console area but not in the MR scan room. Under
the extreme circumstance of cardiac arrest, the patient must
be removed from the MR scan room before performing any
intervention.
Imaging Methods
During an MR examination, the greatest risk posed is the risk
of lead tip heating from exposure to the RF field of the MR
scanner body coil. It is of the utmost importance to monitor
the amount of RF energy, as measured by the SAR, to ensure
it remains within levels known to be safe. The recommended
upper limit is 1.5 W/kg for up to 30 minutes of acquisition
time at a field strength of 1.5T. Imaging of patients at field
strengths exceeding 1.5T is not recommended.
Post-MRI Patient Assessment
After the MR examination is complete and the patient has been
removed from the MR scan room, the pacemaker should be inter-
rogated by a cardiologist or pacemaker technician. This allows
data to be recorded and compared with the values obtained
before MRI. The pacemaker should also be reprogrammed to its
appropriate pre-examination settings, unless directed otherwise
by the cardiologist. Finally, either the cardiologist or advanced
cardiac life support (ACLS)-trained pacemaker technologist
should examine the patient to ensure that his or her functional
status has not changed during the MR examination.
Personnel
At our institution, the personnel associated with MRI for
patients with implanted cardiac devices have specific roles and
responsibilities.
Pacemaker-trained MR technologists perform MRI of
patients with implanted cardiac devices and receive in-service
training by physicians and physicists. During this training,
251
the potential risks and benefits of the procedure are explained,
as are standard operating procedures during normal imaging
and emergencies.
MR physicists are present during all MR examinations of
patients with implanted cardiac devices. Their role is to ensure
that SAR limits are followed and to assist the technologist
with the technical details of each imaging series.
All examinations are monitored by an ACLS-trained
pacemaker technologist. The technologist monitors the patient
before, during, and after the MR examination in accordance
with the guidelines just described.
The supervising radiologist provides initial consultation
with the referring physician, advises on the appropriate imag-
ing to be performed, and provides physician oversight during
the imaging procedure.
A cardiologist assesses the patient before MRI to ensure
that the patient is able to undergo the MR examination, pro-
vides consultation services to the supervising radiologist and
referring physician, and can be present during the MR exami-
nation if specifically requested.
OT H E R DE V IC E S
The MR imaging of patients with either implanted (eg, drug
delivery, prosthesis, surgical clips, therapeutic) or external (eg,
infusion pumps, signal processors for cochlear implants) med-
ical devices is challenging. At our institution, information on
device compatibility and safety is overseen and maintained by
the MR safety committee within the department of radiol-
ogy. In general, the safety of a specific device is determined by
an MR physicist, either by literature review—which includes
peer-reviewed journal articles as well as information provided
by the manufacturer (if available)—or by direct measurement.
These measurements can include but are not limited to deflec-
tion testing to measure the associated force of attraction on
the device due to the B0 field, normal operation of the device
within the MR scanner environment, and temperature mea-
surements to test for RF-induced heating. Whenever appro-
priate, physical measurements are performed in accordance
with published testing methods, as defined by the American
Society for Testing and Materials (ASTM International).
Additional sources of information are available on the
Internet, most notably the MR safety website, http://www
.mrisafety.com. This site is dedicated to providing informa-
tion on the compatibility and safety of a range of devices and
maintains a searchable list. Whenever doubt exists about
the MR safety or compatibility of an external or implanted
device, the advice of a trained professional should be sought.
The specialist best suited for this is a clinical MR physicist.
G A D OL I N I U M-B A S E D C ON T R A S T
M E DI A A N D N E PH RO G E N IC
S Y S T E M IC F I B RO S I S
Nephrogenic systemic fibrosis (NSF) is a serious debilitating
disease characterized by skin and multisystem fibrosis that
occurs in patients with kidney disease. This disease is believed
 252 • S ection I I I : T ro u b l eshootin g —M R I A rtifacts and S afety
to reflect an “exaggerated healing response” mediated by
abundant fibrocytes. Clinically, involved skin and subcutane-
ous tissue in these patients is described as manifesting “woody
induration” (Figure 13.2). Visceral organ involvement, often
of the lungs, heart, and esophagus, is thought to be the mech-
anism underlying reported deaths with NSF.
In 2006, the first association of NSF with gadolinium-
based contrast media (GBCM) exposure in patients with
Figure 13.2 Photos showing the effects of NSF in a patient who received
gadolinium-based contrast media.
renal disease was proposed. This association led to an FDA
alert informing physicians of the potential risk of NSF with
GBCM and urging “caution” in administering these agents
to patients with advanced renal failure or to those on dialy-
sis. This discovery has resulted in a fundamental change in
patient screening practices before MRI, because it has become
imperative to prospectively identify patients with impaired
renal function. The radiology community has been remark-
ably successful in this endeavor, because no new cases of NSF
have been reported worldwide since 2009.
Currently, much still remains unclear about GBCM and
the etiology of NSF, including the role of potential additional
risk factors; for example, it is not clear why NSF has not devel-
oped in all at-risk patients with renal disease who were exposed
to GBCM. The pathologic mechanism underlying NSF is not
fully understood, although some data support a role of free gad-
olinium ion, liberated from its chelate. Additional data imply
that not all GBCM are associated with the same risk of NSF in
at-risk renal patients. This has led the ACR (see ACR manual on
Contrast Media, Version 7) and the FDA to stratify the various
contrast agents as “Group I” (agents associated with the great-
est number of NSF cases), “Group II” (agents associated with
few, if any, cases of NSF, unconfounded by exposure to multiple
GBCM), and “Group III” (agents that have appeared recently
on the US market and are not currently associated with any
cases of NSF) (Table 13.3). Group I agents are contraindicated
in patients with chronic, severe renal dysfunction. A potentially
confounding factor is that the incidence of NSF may reflect not
only the characteristics of an individual agent, but also its rela-
tive market share and the number of doses administered.
Because of the need to prevent NSF, radiologists must under-
stand how renal function is monitored. The National Kidney
Foundation describes 5 stages relative to renal insufficiency,
which are based on glomerular filtration rate (GFR) in units
of mL/min per 1.73 m2: Stage 1, normal or increased function,
GFR>90; Stage 2, mild decrease in function, GFR = 60-90;
Stage 3, moderate decrease in function, GFR = 30-59; Stage 4,
severe decrease in function, GFR = 15-29; and Stage 5, kidney
failure, GFR<15, or on dialysis.
Two distinct categories of patients are known to be at risk
for NSF. Although most NSF cases have occurred in patients
with chronic renal failure (Stage 5 disease), NSF has also been
reported in acutely ill patients believed to have sustained
acute renal injury. Unfortunately, serum creatinine value
does not always provide an accurate reflection of renal func-
tion in patients who are acutely ill, since a creatinine increase
can lag behind precipitously decreasing renal function in the
setting of acute renal injury. Factors influencing plasma cre-
atinine concentration are altered significantly in acutely ill
patients. Protein metabolism underlying creatinine produc-
tion is affected by nutrition and infection; the volume of dis-
tribution underlying creatinine concentration is altered in the
setting of edema; and renal excretion of creatinine is altered
by medication effects on tubular excretion, as well as prerenal
perfusion effects. Thus, the clinical need for GBCM must be
considered carefully in acutely ill persons, and if a GBCM is
to be administered, consideration must be given to the spe-
cific agent chosen.
 13 . C ardiac M R I S afety  • 253

Table 13.3 ACR-ASSIGNED NSF R ISK GROUPS FOR GBCM

Group I: Agents associated with the most NSF cases

Gadodiamide (Omniscan; GE Healthcare)
Gadopentetate dimeglumine (Magnevist; Bayer HealthCare Pharmaceuticals)
Gadoversetamide (OptiMARK; Covidien)
FDA-Reported Approximate Number of NSF Cases per Administered Doses (as of December 2009)
Agent Approximate Doses Given, in Millions Reported NSF Casesa
Gadodiamide 13 382
Gadopentetate dimeglumine 23 195
Gadoversetamide 4.7 35
Group II: Agents associated with few, if any, unconfounded cases of NSF
Gadobenate dimeglumine (MultiHance; Bracco Diagnostics)
Gadoteridol (ProHance; Bracco Diagnostics)
Gadoteric acid (Dotarem; Guerbet)
Gadobutrol (Gadavist; Bayer HealthCare Pharmaceuticals)
Group III: Agents that have only recently appeared on the US market
Gadofosveset (Ablavar; Lantheus Medical Imaging)
Gadoxetate disodium (Eovist; Bayer HealthCare Pharmaceuticals)
Data for these agents are limited, but to date, few, if any, unconfounded cases of NSF have been reported

a
Single agent (nonconfounded). Although various factors may have influenced the number of cases reported with each of these agents, investigators believe that
intrinsic properties of these 3 agents increase the relative likelihood of NSF developing after exposure in at-risk patients.
Reprinted with permission of the American College of Radiology. No other representation of this material is authorized without expressed, written permission from
the ACR. Note that the most current and complete document (Manual on Contrast Media v9) may be found at: http://www.acr.org/Quality-Safety/Resources/
Contrast-Manual.

Recommendations for NSF risk factor screening include
identifying patients with severe chronic kidney disease (GFR
<30 mL/min per 1.73 m2) and those at risk for acute kidney
injury. Screening should identify patients with a known his-
tory of renal disease (including solitary kidney, renal trans-
plant, renal neoplasm), those older than 60 years, and those
with a history of diabetes mellitus or hypertension. Patients
with risk factors for renal insufficiency should have direct
measurement of renal function before GBCM administra-
tion. If a patient is identified as having reduced renal function
or having sustained acute kidney injury, alternative studies
should be considered. If administration of GBCM is consid-
ered necessary, risk-benefit discussions should be conducted
with the patient and the referring clinician. The lowest possi-
ble dose of GBCM should be administered to at-risk patients,
and Group I agents should be avoided.
Currently, there is no evidence that Stage 1 or Stage 2
patients (GFR ≥60 mL/min per 1.73 m2) are at risk for NSF
after GBCM exposure. At our institution, these patients are
administered GBCM without restrictions, per protocol. Stage 3
patients, those with a GFR of 30 to 59 mL/min per 1.73 m2, are
administered a decreased (80%) dose of gadobenate dimeglu-
mine (MultiHance). The use of GBCM in Stage 4 and Stage
5 patients is carefully monitored and risk-benefit discussions
are conducted, as described above. Group I agents (gadodi-
amide [Omniscan], gadopentetate dimeglumine [Magnevist],
and gadoversetamide [OptiMARK]) are avoided in these
patients, as well as in patients believed to be at risk for acute
renal injury. Other available contrast agents, including gado-
fosveset (Ablavar), gadobutrol (Gadavist), gadoxetate (Eovist),
and gadobenate dimeglumine, can be administered to these
patients if the benefit is determined to outweigh the risks.
Exposure to GBCM is to be avoided during pregnancy
because the agents can accumulate in amniotic fluid, poten-
tially increasing fetal or maternal risk of NSF. Although no
fetal, neonatal, or maternal NSF has been reported in such
a setting, GBCM should not be administered in this group
unless the risk-benefit ratio and lack of clinically useful alter-
natives favor proceeding. Related issues, including GBCM
administration during breastfeeding and administration to
small children, have been reviewed.
PR E-E X A M I N AT ION M R I
S A F E T Y S C R E E N I NG
In accordance with the recommendations of the ACR, imag-
ing centers are encouraged to develop a screening procedure
for all patients about to undergo MRI. At our institution,
the patient is required to complete a 1-page questionnaire
that identifies key safety concerns, including the presence
of implanted devices, kidney disease, known drug allergies,
 254 • S ection I I I : T ro u b l eshootin g —M R I A rtifacts and S afety
pregnancy status for women, and a checklist of devices that
pose a high safety risk or are contraindications to MRI.
Patients or appropriate family members or legal guardians
are required to complete these forms before entering the MR
environment. MR technologists review the screening form
and then provide a verbal review of the questionnaire with
the patient or representative. Once both written and verbal
screening has been performed and it is determined that MRI
is safe for the patient, the patient is then escorted into the MR
scanner room.
PROF E S S ION A L M R S O C I E T I E S
I N T E R N AT ION A L S O C I E T Y FOR M AG N E T IC
R E S ON A NC E I N M E DIC I N E (I S M R M)
This is the official society associated with research and clini-
cal MRI. The ISMRM holds an annual meeting located
throughout the world to discuss various MR-related topics.
In addition, the ISMRM organizes workshops throughout
the year focusing on a range of topics, including MR safety.
Details of these and other issues concerning MR safety can
be obtained from the society’s official website at http://www.
ismrm.org.
EU ROPE A N S O C I E T Y FOR M AG N E T IC
R E S ON A NC E I N M E DIC I N E A N D
BIOL O G Y (E S M R M B)
This is a professional MR society serving the European
MR community whose mission closely matches that of the
ISMRM. Similar information can also be obtained from their
website at http://www.esmrmb.org/.
OT H E R PROF E S S ION A L S O C I E T I E S
A range of national and international societies with ties to
the MR community exist. These groups can provide spe-
cific information such as highly specialized workshops and
up-to-date information relevant to their area of expertise.
The ISMRM maintains a comprehensive list of these groups,
which can be obtained from the ISMRM website at http://
www.ismrm.org.
S UGG E S T E D R E A DI N G
International Electrotechnical Commission (IEC)
Medical electrical equipment: Part 2-33. Particular requirements for
the basic safety and essential performance of magnetic resonance
equipment for medical diagnosis. International Electrotechnical
Commission; c2010. Reference No: IEC 60601-2-33:2010.
MR Safety
Kanal E, Barkovich AJ, Bell C, Borgstede JP, Bradley WG Jr, Froelich
JW, et al; ACR Blue Ribbon Panel on MR Safety. ACR guidance
document for safe MR practices: 2007. AJR Am J Roentgenol. 2007
Jun;188(6):1447–74.
Magnetic Resonance Diagnostic Device, 21 C.F.R. Sect. 892.1000
(2012).
Schaefers G. Testing MR safety and compatibility: an overview of the
methods and current standards. IEEE Eng Med Biol Mag. 2008
May-Jun;27(3):23–7.
Schaefers G, Melzer A. Testing methods for MR safety and compat-
ibility of medical devices. Minim Invasive Ther Allied Technol.
2006;15(2):71–5.
Shellock FG. Magnetic resonance procedures: health effects and safety.
Boca Raton (FL): CRC Press; c2001.
Nephrogenic Systemic Fibrosis
ACR Committee on Drugs and Contrast Media. ACR manual on contrast
media, Version 7. Reston (VA): American College of Radiology; c2010.
ACR Committee on Drugs and Contrast Media. ACR manual on contrast
media, Version 9. Reston (VA): American College of Radiology; c2013.
Cowper SE. Nephrogenic systemic fibrosis [ICNSFR Website]. 2001–
2009. [cited 2013 Feb 5]. Available from: http://www.icnsfr.org.
Grobner T. Gadolinium: a specific trigger for the development of neph-
rogenic fibrosing dermopathy and nephrogenic systemic fibrosis?
Nephrol Dial Transplant. 2006 Apr;21(4):1104–8. Epub 2006 Jan
23. Erratum in: Nephrol Dial Transplant. 2006 Jun;21(6):1745.
Kalb RE, Helm TN, Sperry H, Thakral C, Abraham JL, Kanal E.
Gadolinium-induced nephrogenic systemic fibrosis in a patient
with an acute and transient kidney injury. Br J Dermatol. 2008
Mar;158(3):607–10. Epub 2007 Dec 11.
Marckmann P, Skov L, Rossen K, Dupont A, Damholt MB, Heaf JG,
et al. Nephrogenic systemic fibrosis: suspected causative role of gado-
diamide used for contrast-enhanced magnetic resonance imaging. J
Am Soc Nephrol. 2006 Sep;17(9):2359–62. Epub 2006 Aug 2.
Sadowski EA, Bennett LK, Chan MR, Wentland AL, Garrett AL, Garrett
RW, et al. Nephrogenic systemic fibrosis: risk factors and incidence
estimation. Radiology. 2007 Apr;243(1):148–57. Epub 2007 Jan 31.
Sundgren PC, Leander P. Is administration of gadolinium-based con-
trast media to pregnant women and small children justified? J Magn
Reson Imaging. 2011 Oct;34(4):750–7.
Tremblay E, Therasse E, Thomassin-Naggara I, Trop I. Quality initia-
tives: guidelines for use of medical imaging during pregnancy and lacta-
tion. Radiographics. 2012 May-Jun;32(3):897–911. Epub 2012 Mar 8.
Pacemakers and ICDs
Faris OP, Shein M. Food and Drug Administration perspective:
magnetic resonance imaging of pacemaker and implantable
cardioverter-defibrillator patients. Circulation. 2006 Sep 19;114(12):
1232–3.
Gimbel JR, Bailey SM, Tchou PJ, Ruggieri PM, Wilkoff BL. Strategies
for the safe magnetic resonance imaging of pacemaker-dependent
patients. Pacing Clin Electrophysiol. 2005 Oct;28(10):1041–6.
Gimbel JR, Wilkoff BL, Kanal E, Rozner MA. Safe, sensible, saga-
cious: responsible scanning of pacemaker patients. Eur Heart J. 2005
Aug;26(16):1683–4. Epub 2005 Jun 9.
Irnich W, Irnich B, Bartsch C, Stertmann WA, Gufler H, Weiler G.
Do we need pacemakers resistant to magnetic resonance imaging?
Europace. 2005 Jul;7(4):353–65.
Levine GN, Gomes AS, Arai AE, Bluemke DA, Flamm SD, Kanal E,
et al; American Heart Association Committee on Diagnostic
and Interventional Cardiac Catheterization; American Heart
Association Council on Clinical Cardiology; American Heart
Association Council on Cardiovascular Radiology and Intervention.
Safety of magnetic resonance imaging in patients with cardiovas-
cular devices: an American Heart Association scientific statement
from the Committee on Diagnostic and Interventional Cardiac
Catheterization, Council on Clinical Cardiology, and the Council
on Cardiovascular Radiology and Intervention: endorsed by the
American College of Cardiology Foundation, the North American
Society for Cardiac Imaging, and the Society for Cardiovascular
Magnetic Resonance. Circulation. 2007 Dec 11;116(24):2878–91.
Epub 2007 Nov 19.
 13 . C ardiac M R I S afety  •
Luechinger R, Duru F, Candinas R, Boesiger P. Safety considerations
for magnetic resonance imaging of pacemaker and ICD patients.
Herzschrittmacherther Elektrophysiol. 2004;15(1):73–81.
Sommer T, Naehle CP, Yang A, Zeijlemaker V, Hackenbroch M, Schmiedel
A, et al. Strategy for safe performance of extrathoracic magnetic reso-
nance imaging at 1.5 tesla in the presence of cardiac pacemakers in
non-pacemaker-dependent patients: a prospective study with 115 exami-
nations. Circulation. 2006 Sep 19;114(12):1285–92. Epub 2006 Sep 11.
Reilly Curve Estimation for Peripheral Nerve Stimulation
Reilly JP. Principles of nerve and heart excitation by time-varying mag-
netic fields. Ann N Y Acad Sci. 1992 Mar 31;649:96–117.
255
Relevant Federal and International Standards
and Guidelines FDA
Guidance for industry and FDA staff: criteria for significant risk
investigations of magnetic resonance diagnostic devices. Rockville
(MD): US Department of Health and Human Services, Food and
Drug Administration; 2003 Jul 14.
Guidance for industry: guidance for the submission of premarket
notifications for magnetic resonance diagnostic devices. Rockville
(MD): Department of Health and Human Services (US), Food and
Drug Administration; 1998 Nov 14.
Institutional Review Boards, 21 C.F.R. Sect. 56 (1980).
Protection of Human Subjects, 21 C.F.R. Sect. 50 (1981).
SEC T ION I V
R E V I E W QU E S T ION S
 14.
BOAR D-T Y PE QUESTIONS A ND A NSW ER S

QU E S T IO N S

Multiple Choice (choose the best answer)

14.1. The magnetohydrodynamic effect in cardiac magnetic 14.2. Figure 14.Q2 shows a 4-chamber late gadolinium-
resonance imaging (MRI): enhancement (LGE) image. A rim of hyperintense signal
a. Is manifested as electrocardiographic (ECG) T-wave encapsulating a region of hypointense signal can be seen at the
swelling (amplification) when a patient is placed inside apex of the left ventricle (LV). What is the underlying process
the magnetic resonance (MR) scanner that produces this signal pattern?
b. Can be ignored because it is a physical phenomenon
a. Normal myocardium
that is independent of magnet field strength
b. Mural thrombus
c. Increases the heart rate of the person when placed
c. Microvascular obstruction
inside the MR scanner
d. Subendocardial perfusion defect
d. Can be ignored at MR field strengths of 3.0T or less
e. Myocarditis
e. Relates to change in blood flow after an external
stimulus such as finger tapping

Figure 14.Q2

259
 260 • S e c tion I V: R eview Q uestions

Figure 14.Q3

14.3. Figure 14.Q3 shows 4 sequential 4-chamber, long-axis, d. T1 only

LGE views of the heart. What is the most likely diagnosis of e. T2 only
the mass in the LV apex?
14.5. A 40-year-old man was evaluated for mild exertional
a. Metastasis chest pressure. Echocardiography findings included LV
b. Thrombus outflow tract gradient <30 mm Hg at rest and with provo-
c. Angiosarcoma cation. Figure 14.Q5, from a follow-up cardiac MRI exami-
d. Myxoma nation, shows 3-chamber, long-axis, balanced SSFP images
e. Fibrosis from prior infarction at 2 different phases of the cardiac cycle. Which of the fol-
lowing is the most likely diagnosis?
14.4. Which best describes the contrast produced by a bal-
anced steady-state free precession (SSFP) gradient echo pulse a. Cardiac sarcoidosis
sequence? b. Cardiac amyloidosis
c. Long-standing hypertension
a. T1/T2
d. Hypertrophic cardiomyopathy (HCM)
b. T2/T1
e. Mitral valve prolapse
c. T1/T2*
 14 . B oa r d -T y pe Q uestions a n d Answers  • 261

Figure 14.Q5

14.6. Pericardial thickness has been recommended as a bio- 14.8. The short-axis, balanced SSFP image in Figure 14.Q8
marker for diagnosis of constriction. What is the threshold is from a patient with tetralogy of Fallot who has undergone
for a positive diagnosis of pericardial constriction? surgical repair with a transannular patch. Which of the
following is the most common postoperative complication in
a. 4 mm
patients who have undergone complete repair for tetralogy of
b. <4 mm
Fallot?
c. None
d. Any thickness a. Pulmonic valvular regurgitation
e. Unable to measure pericardial thickness by cardiac MRI b. Pulmonic valvular stenosis
c. Infundibular stenosis
14.7. Which of the following will increase the temporal reso-
d. Aortic valvular stenosis
lution of a segmented-acquisition, cine, gradient echo image?
e. Aortic valvular regurgitation
a. Decreasing the phase-encoding matrix from 160 to 128
14.9. Which of the following prostheses is unsafe for cardiac
b. Decreasing the number of views per segment from 25 to 16
MRI performed on a 1.5T system?
c. Increasing the flip angle from 40° to 60°
d. Increasing the number of reconstructed phases from a. St. Jude bileaflet valve
20 to 30 b. Starr-Edwards caged-ball valve
e. Increasing the pulse repetition time (TR) of the pulse c. Medtronic-Hall monoleaflet valve
sequence d. Ferrous (steel) aneurysm clip
e. Prosthetic hip replacement
14.10. Which of the following will not decrease the total
imaging time of a segmented cine gradient echo image
acquisition?
a. Decreasing the phase-encoding matrix from 256 to 128
b. Increasing the number of views per segment from 16 to
24
c. Decreasing the phase field of view (FOV) from 1.0 to 0.75
d. Decreasing the number of signal averages from 1 to 0.5
e. Decreasing the number of interpolated cardiac phases
from 30 to 20
14.11. A certain gradient echo pulse sequence produced a
banding artifact in the reconstructed image. In the absence
of wraparound or aliasing artifact, in which type of gradient
echo sequence will the artifact be seen?
a. Both spoiled and balanced gradient echo images
b. Only spoiled gradient echo images
c. Only balanced gradient echo images
d. Neither spoiled nor balanced gradient echo images
e. Multiecho gradient echo images
Figure 14.Q8
 262 • S e c tion I V: R eview Q uestions

Figure 14.Q12

14.12. The images in Figure 14.Q12 show 4-chamber bal- 14.14. To assess for LV hypertrophy, wall thickness is mea-
anced SSFP (A and B) and LGE (C) views of the heart. Based sured at which point in the cardiac cycle?
on these images, what are the clinical findings from this
a. End systole
study?
b. End diastole
a. Akinesis of the LV apex c. Both end systole and end diastole
b. Myocardial iron deposition d. Mid diastole
c. Diffuse myocardial fibrosis e. Mid systole
d. Subendocardial late enhancement
14.15. Which is the simplest way to shift, but not elimi-
e. Amyloid heart disease
nate, the off-resonance banding artifact in balanced SSFP
14.13. What is an advantage of MRI over echocardiography imaging?
for imaging of pericardial disease?
a. Perform B0 shimming over the region of interest
a. Improved temporal resolution b. Use a lower field-strength magnet
b. Decreased acquisition time c. Change pulse sequences to non–SSFP-based imaging
c. Decreased ionizing radiation exposure to the patient d. Turn on chemical fat suppression
d. Identification of pericardial inflammation e. Adjust the resonant frequency of the digital signal
e. Identification of pericardial fluid receiver
 14 . B oa r d -T y pe Q uestions a n d Answers  • 263

14.16. What is the Larmor frequency of protons (1H) at 1.5T 14.18. What is the primary role of cardiac MRI in the assess-
and 3.0T? ment of patients with tetralogy of Fallot after repair?
a. 64.8 kHz and 127.7 MHz a. Assessment of right ventricular (RV) volumes
b. Depends on the manufacturer b. Quantification of aortic regurgitation
c. 63.8 MHz and 127.7 MHz c. Quantification of RV mass
d. Cannot be calculated d. Assessment of LV function
e. 127.7 MHz and 48 MHz e. Quantification of Qp/Qs
14.19. Only collecting MRI data from the center of k-space
will produce images that:
a. Are flow (ie, motion) sensitized
b. Have a low signal-to-noise ratio (SNR)
c. Have low temporal resolution
d. Have low spatial resolution
e. Have a small FOV
14.20. Blood is bright on a spoiled gradient echo image of the
heart because of:
a. The T2-weighted nature of this pulse sequence
b. T2/T1 contrast of the pulse sequence
c. Inflow of freshly magnetized blood
d. High lipid content within the blood pool
e. Saturation and therefore T1 shortening of blood
14.21. How does increasing the B-field strength from 1.5T to
3.0T affect the theoretical SNR?
a. SNR is halved
b. SNR is quadrupled
c. SNR is doubled
d. SNR is quartered
e. SNR is unaffected
Figure 14.Q17 14.22. Which of the following provides the strongest evi-
dence of significant aortic insufficiency?
a. Aortic valve area = 0.9 cm2
b. Peak systolic velocity in the ascending aorta = 5 m/s
14.17. Figure 14.Q17 shows a short-axis LGE image with a c. Regurgitant volume = 100 mL
region of hyperintense signal within the septal wall indicat- d. Ascending aorta diameter = 5.0 cm
ing the presence of myocardial infarction. Which coronary e. Bicuspid aortic valve
artery is most likely to be occluded in this patient?
14.23. What is the most common cause of an LV apical
a. Left anterior descending thrombus?
b. Circumflex
c. Right a. Nonischemic cardiomyopathy
d. Posterior descending b. Atrial fibrillation
e. Diagonal branch c. Apical myocardial infarction
d. Myocarditis
e. Sarcoidosis
14.24. What are the typical echo time (TE) and TR values
of a T1-weighted, spin echo, black blood imaging sequence?
a. TE<100 ms, TR = 1 R-R interval
b. TE<40 ms, TR = 1 R-R interval
c. TE>200 ms, TR > 2 R-R intervals
d. TE<100 ms, TR > 2 R-R intervals
e. TE>100 ms, TR = 1 R-R interval
 264 • S e c tion I V: R eview Q uestions

Figure 14.Q25

14.25. A 54-year-old man with a recent history of flulike 14.26. What is the effect of performing view sharing on car-
symptoms comes to the emergency department with acute diac image acquisition?
chest pain. His cardiac biomarker levels are increased, and
a. Increases absolute temporal resolution
the coronary arteries are normal. Cardiac MRI, shown in
b. Decreases imaging time in cine data
Figure 14.Q25, reveals no wall-motion abnormalities on
c. Allows acquisition of static (noncine) data
cine imaging (A and B). Fat-suppressed black blood (C)
d. Reduces gradient-induced image distortion
and LGE images (D) are acquired. What is the most likely
e. Increases the conspicuity of vessels
diagnosis?
14.27. A patient with stroke symptoms is found to have a
a. Cardiac sarcoidosis
left atrial mass by transthoracic echocardiography. Cardiac
b. Myocardial infarction
MRI was obtained. Axial balanced SSFP (A) and LGE (B)
c. Coronary embolism
images are shown in Figure 14.Q27. What is the most likely
d. Myocarditis
diagnosis?
e. Apical ballooning cardiomyopathy
 14 . B oa r d -T y pe Q uestions a n d Answers  • 265

Figure 14.Q27

a. Thrombus 14.29. Which imaging finding is a risk factor for sudden car-
b. Papillary fibroelastoma diac death in patients with HCM?
c. Angiosarcoma
a. Midcavity obliteration
d. Metastasis from undiagnosed primary
b. Myocardial thickness >30 mm
e. Myxoma
c. Systolic anterior motion of the mitral valve
14.28. What information can T2-weighted black blood imag- d. Flow dephasing in the LV outflow tract
ing provide in pericardial imaging? e. Left atrial enlargement
a. Assessment of associated myocardial inflammation
(myopericarditis)
b. Assessment of ventricular function
c. Assessment of regional wall-motion abnormalities
d. Assessment of myocardial perfusion
e. Identification of coronary artery anatomy
 266 • S e c tion I V: R eview Q uestions

Figure 14.Q30

14.30. A 30-year-old man with a heart murmur was found 14.31. What is the most common cause or causes of zipper
to have a dilated RV by echocardiography. Cardiac MRI artifacts in cardiac MR images?
was ordered. Multislice, oblique coronal, balanced SSFP
a. Metal on the patient’s clothing (eg, a zipper) or jewelry
images are shown in Figure 14.Q30. What is the most likely
b. Acoustic noise resulting from the rapid switching of
diagnosis?
spatial encoding (gradient) fields
a. Secundum atrial septal defect c. Aliasing due to anatomy outside of the imaging FOV
b. Sinus venosus septal defect d. Nonlinearity of the spatial encoding magnetic
c. Pulmonary hypertension (gradient) fields
d. Anomalous drainage of the left upper pulmonary vein e. A pulse sequence error, an external radiofrequency (RF)
e. Pulmonic valve stenosis noise source, or a leak in the Faraday cage (RF screen)
 14 . B oa r d -T y pe Q uestions a n d Answers  • 267

Figure 14.Q32

14.32. An 18-year-old man with a history of dyspnea was 14.33. Which of the following cardiac MRI sequences pro-
noted to have RV dilation on echocardiography. The axial vides the best view for assessment of aortic valve morphology?
balanced SSFP image and volume-rendered, 3D, gadolinium-
a. Three-chamber cine balanced SSFP
enhanced, MR angiograms shown in Figure 14.Q32 identify
b. Coronal oblique cine balanced SSFP
an enlarged RV. What is the most likely cause of the enlarged
c. Axial double inversion recovery black-blood spin echo
ventricle?
d. Axial oblique cine balanced SSFP
a. A left superior vena cava (SVC) e. A short-axis view during diastole
b. A dilated duct of Kommerell
c. Aortic dissection
d. Anomalous pulmonary drainage
e. Unroofed coronary sinus
 268 • S e c tion I V: R eview Q uestions

Figure 14.Q34

14.34. The images in Figure 14.Q34 show magnitude (A) and a. Flow will be encoded into a direction orthogonal to
velocity (ie, flow) information at 2 phases of the cardiac cycle (B the true flow direction.
and C). Which of the following information can be derived from b. Flow will be overestimated due to the overestimation
these data for evaluation of patients with tetralogy of Fallot? with the phase.
c. Flow will be underestimated due to aliasing of the
a. Assessment of RV function and volumes
high-velocity flow values.
b. Quantification of pulmonic valvular regurgitation
d. Aliasing in the phase image will occur but will not
c. Assessment for myocardial edema
affect the quantitative analysis of these data.
d. Identification of areas of late gadolinium enhancement
e. There will be no effect on the reported flow
(ie, fibrosis)
since phase-contrast imaging is independent
e. Quantification of vessel wall compliance
of flow.
14.35. If the velocity-encoding value (VENC) in a phase-ontrast
14.36. Selected images from a cardiac MRI examination of
imaging sequence is less than the highest velocity of tissue mov-
a 16-year-old boy are shown in Figure 14.Q36. What is the
ing along the direction of encoding, how will this affect the mea-
most likely diagnosis?
surement of flow (flow = velocity × area) in this direction?
 14 . B oa r d -T y pe Q uestions a n d Answers  • 269

Figure 14.Q36
 270 • S e c tion I V: R eview Q uestions

a. Severe aortic stenosis

b. LV noncompaction cardiomyopathy
c. Dilated cardiomyopathy
d. Congenitally corrected transposition of the great
arteries
e. Anomalous pulmonary drainage
14.37. By which method does image-based parallel imaging
attempt to decrease scan time or increase resolution?
a. Increasing the number of coil elements in phased-
arrays coils to compensate for signal loss when
imaging at decreased FOV in the phase-encoding
direction
b. Undersampling higher-order k-space data followed by
reconstruction of the missing lines of k-space in the
frequency domain
c. Doubling the FOV and halving the number of
acquisitions (excitations) to keep imaging time within
reasonable limits
d. Doubling the signal by requiring that parallel imaging
techniques are performed at 3.0T as opposed to 1.5T
Figure 14.Q39
e. Decreasing the FOV in the phase-encoding direction
by decreasing the number of phase-encoding
steps, followed by unwrapping aliasing after image 14.41. Which types of imaging do not require ECG gating in
reconstruction cardiac MRI?
14.38. What type of enhancement is characteristic of a a. Images that require temporal sorting (cine) of data
thrombus? b. Images that require acquisition of a specific cardiac phase
a. No enhancement c. Sequences that acquire data in real-time mode
b. Intense early enhancement d. Black blood spin echo–based imaging
c. Faint patchy late enhancement e. Cardiac sequences when the patient is free-breathing
d. Intense late enhancement
e. Enhancing ring with nonenhancing core 14.42. In cardiac MRI, what is the most common reason for
altering the phase FOV from a full to partial (rectangular)
14.39. Figure 14.Q39 shows a short-axis LGE image with a FOV?
region of hyperintense signal within the LV lateral free wall
indicating the presence of myocardial infarction. The LGE a. To increase the slice thickness
pattern in this patient is: b. To decrease the temporal resolution
c. To decrease the RF pulse flip angle
a. Subendocardial d. To increase the contrast-to-noise ratio
b. Subepicardial e. To decrease the breath-hold time
c. Midmyocardial
d. Transmural 14.43. In a 3D acquisition such as contrast-enhanced MR angi-
e. Mural thrombus ography, aliasing can occur in how many encoding directions?
14.40. A 26-year-old woman with atypical chest pain at a. 1
rest and normal cardiac biomarkers underwent a cardiac b. 2
MRI examination for further evaluation. Fat-suppressed (A c. 3
and B) and non–fat-suppressed (C and D) axial black blood d. 4
images are shown in Figure 14.Q40. What is the most likely e. 5
diagnosis?
14.44. The findings in the LV outflow tract seen in Figure
a. Loculated pericardial effusion 14.Q44 are due to:
b. Pericardial cyst a. Apical hypertrophy
c. Serous pericardial effusion b. Mitral valve regurgitation
d. Hepatic hemangioma c. Left atrial enlargement
e. Small cell lung cancer d. Systolic anterior motion of the mitral valve
e. Aortic stenosis
 14 . B oa r d -T y pe Q uestions a n d Answers  • 271

Figure 14.Q40

Figure 14.Q44
 272 • S e c tion I V: R eview Q uestions

14.47. On a routine cardiac MR examination, breath-hold,

multiecho spin echo images appear grainy. Which pulse
sequence parameter modification will improve image quality?
a. Decrease the FOV
b. Decrease the number of signal averages
c. Use parallel imaging
d. Increase the slice thickness
e. Increase the number of slices
14.48. Two common methods of acquiring fat-suppressed
images include using an inversion recovery–based prepulse or
applying a frequency-selective presaturation pulse followed by
gradient-induced signal spoiling. What advantages do inver-
sion recovery–based approaches offer over frequency-selective
methods?
a. Higher contrast-to-noise ratio
b. Lower specific absorption rate (SAR)
c. Shorter acquisition time
d. Decreased sensitivity to B0 field inhomogeneities
e. Higher SNR

Figure 14.Q45

14.45. Figure 14.Q45 is an example of a gadolinium-enhanced

MR angiogram in a patient who had previously undergone
surgery for tetralogy of Fallot. What is the clinical utility of
performing MR angiography in this setting?
a. To delineate the pulmonary arterial tree and to assess
for obstructive lesions
b. To delineate the pulmonary venous anatomy to assess
for anomalous pulmonary venous drainage
c. To delineate the systemic venous anatomy to assess for
anomalous systemic venous drainage
d. To delineate the systemic arterial anatomy to assess for
coarctation of the aorta
e. To identify the presence of peripheral vascular disease
14.46. What is the reason for signal distortion and loss
around a foreign, particularly metal, object on MR images?
a. Intravoxel phase incoherence and B0 distortion due to
the differences in magnetic susceptibility of the object
Figure 14.Q49
of interest and the surrounding tissue
b. Attenuation of the RF signal and hence signal loss by
the material whose magnetic susceptibility is different 14.49. Figure 14.Q49 shows a T1-weighted, black blood, axial
from that of surrounding tissue MR image of the heart acquired before the administration of
c. Local heating due to eddy currents generated in the gadolinium contrast. What is the abnormality depicted in
material whose magnetic susceptibility differs from this MR image?
that of surrounding tissue
d. Chemical shift of the first kind resulting in shifting of a. A primary cardiac malignancy
the signal from the implant into adjacent tissue regions b. A cardiac metastasis
e. Chemical shift of the second kind as a result of the c. Atrial myxoma
difference in magnetic susceptibilities between the d. Infection with vegetation
object of interest and surrounding tissue e. Lipomatous hypertrophy of the interatrial septum
 14 . B oa r d -T y pe Q uestions a n d Answers  • 273

14.50. Which statement regarding bicuspid aortic valve

(BAV) is true?
a. BAV is the most common cause of aortic stenosis.
b. BAV is the least common congenital cardiac anomaly.
c. BAV is associated with coarctation of the aorta.
d. BAV requires contrast media injection to completely
evaluate valve morphology.
e. MRI is less successful than transthoracic
echocardiography in identifying BAV.
14.51. As a rule, T1, T2, and T2* relaxation times follow which
order:
a. T2<T2*<T1
b. T2>T2*>T1
c. T1<T2<T2*
d. T2*>T1>T2
e. T1>T2>T2*
14.52. You are asked to describe the cardiac MRI findings on
an LGE image in a patient with typical myocarditis. Which
of the following best describes the pattern of late gadolinium
enhancement? Figure 14.Q55

a. Basal lateral subepicardial enhancement

b. Basal septal subendocardial enhancement 14.55. Figure 14.Q55 shows a T2-weighted, short-axis, fat-
c. Global diffuse subendocardial enhancement suppressed, black blood image. The subtle increased signal in
d. Global diffuse subepicardial enhancement the inferolateral wall (arrow) is due to:
e. Enhancement of RV insertion points
a. Myocardial fibrosis
14.53. The spacing between the maxima (or minima) of off- b. Myocardial enhancement
resonance banding artifacts in balanced SSFP gradient echo c. Myocardial edema
imaging sequences is: d. Pericardial enhancement
e. Pericardial effusion
a. Proportional to the TE
b. Proportional to the TR 14.56. Why is tamponade rarely imaged with MRI?
c. Inversely proportional to the flip angle
a. Tamponade-induced pericardial rupture cannot be
d. Inversely proportional to the TR
visualized on MRI.
e. Independent of both TE and TR
b. Tamponade is an emergency requiring urgent
14.54. A 70-year-old woman was referred for a cardiac MRI intervention.
stress perfusion scan for progressive exertional dyspnea. c. Pericardial effusions are poorly visualized by cardiac MRI.
Which of the following is a contraindication to adenosine d. Quantitative assessment (ie, ejection fraction) cannot
stress cardiac MRI? be performed during tamponade.
e. Tamponade requires use of contrast media.
a. Mild chronic obstructive pulmonary disease
b. First-degree atrioventricular block on resting 12-lead
ECG
c. A history of severe shellfish allergy
d. One half-cup of decaffeinated coffee 8 hours before the
examination
e. Treatment with dipyridamole
 274 • S e c tion I V: R eview Q uestions
Figure 14.Q57
14.57. A 57-year-old man with exertional shortness of breath
and a heart murmur is referred for cardiac MRI for further
assessment. Based on the images in Figure 14.Q57, what is the
most likely diagnosis?
a. Recurrent metastatic breast cancer
b. Dilated cardiomyopathy secondary to chemotherapy
myocardial toxicity
c. Pericardial constriction
d. Severe aortic stenosis
e. Restrictive cardiomyopathy
14.58. Chemical shift of the second kind can be exploited to
create images that contain which of the following?
a. In-phase and out-of-phase data that can be processed
to generate images in which out-of-phase images
highlight fat-banded structures
b. Images in which the fat and water are spatially
misregistered along the frequency-encoding direction
c. Spectroscopic information on the distribution of
metabolites within the myocardium
d. Improved visualization of anatomy surrounding
materials with differing magnetic susceptibilities, such
as implants
e. Information on flow, including visualization of
nonlaminar flow and vortices within vessels
14.59. Respiratory motion during cardiac MR data acquisi-
tion is undesirable because it:
a. Requires the use of dedicated hardware to allow for
respiratory triggering of cardiac MRI sequences
b. Prolongs the cardiac data acquisition process
by requiring reacquisition of those data with
motion-induced artifacts
c. Changes the location of the RF coil and hence affects
image uniformity
d. Creates the potential for the patient to hyperventilate
and thereby results in a nonsignificant-risk
examination
e. Introduces phase errors that result in blurring and
ghosting artifacts that can obscure cardiac anatomy
14.60. A 29-year-old woman with a history of hemophilia
and an abnormal echocardiography result is sent for MRI
of the heart for further evaluation. Figure 14.Q60 shows
short-axis views of the heart obtained using a gradient echo
imaging sequence with 2 separate echo times of 1.32 and
11 milliseconds. Based on these images, what is the correct
diagnosis?
a. Restrictive cardiomyopathy
b. Dilated cardiomyopathy
c. Myocardial iron deposition
d. Pericarditis
e. Amyloid heart disease
14.61. Which is true of pericardial effusion?
a. A small amount of pericardial fluid is physiologically
normal.
b. Pericardial effusions should almost always be followed
with serial imaging.
c. Pericardial effusions are always associated with
pericardial enhancement.
d. Pericardial fluid is always bright on spin echo–based
black blood imaging.
e. Pericardial fluid is typically accompanied by pericardial
thickening.
14.62. Figure 14.Q62 shows adenosine stress perfusion (A),
rest perfusion (B), and LGE (C) short-axis images at the mid
ventricle. On the basis of these images, what is the clinical
diagnosis in this patient?
 14 . B oa r d -T y pe Q uestions a n d Answers  • 275

Figure 14.Q60

Figure 14.Q62
 276 • S e c tion I V: R eview Q uestions

Figure 14.Q64

a. Normal myocardium a. Fabry disease

b. Ischemic myocardium b. Amyloid heart disease
c. Infarcted myocardium c. Muscular dystrophy
d. Stress-induced cardiomyopathy (apical ballooning) d. Myocardial infarction
e. Myocarditis e. Healed myocarditis
14.63. Which describes the method by which spin echo black 14.65. What is the most likely cause of a rapidly expanding
blood imaging techniques suppress the signal from the blood white cloud within the MR scan room?
pool?
a. Humidity levels set too high within the MR scan room
a. Inversion of the blood pool signal and inflow-outflow b. The uncontrolled release of helium from the
effects containment vessel of the MR scanner
b. Spectrally selective RF pulses tuned to the resonant c. Smoke from a possible fire within the MR scan room
frequency of blood or elsewhere
c. Spatially selective RF pulses on the inflow side of the d. Escape of medical gases from faulty equipment within
imaging slice the MR scan room
d. The use of adiabatic RF pulses to spoil the blood pool e. Poor ventilation within the MR scan room resulting
signal from the recirculation of room air
e. Use of a gadolinium contrast agent to shorten the T1
14.66. A 54-year-old man with an abnormal echocardiogra-
relaxation of the blood pool
phy result is referred for cardiac MRI for further assessment.
14.64. A 55-year-old woman with an abnormal echocar- Systolic (A) and diastolic (B) balanced SSFP images; black
diography result is referred for cardiac MRI for further blood, fat-suppressed (C) and non–fat-suppressed (D) images;
assessment. LGE and balanced SSFP images from the and LGE images (E and F) from the MRI examination are
study are shown in Figure 14.Q64. What is the most likely shown in Figure 14.Q66. Based on these data, what is the most
diagnosis? likely diagnosis?
 14 . B oa r d -T y pe Q uestions a n d Answers  • 277

Figure 14.Q66
 278 • S e c tion I V: R eview Q uestions

a. Fabry disease 14.69. A 35-year-old man with an abnormal echocardiog-

b. Amyloid heart disease raphy result is referred for cardiac MRI for further assess-
c. Muscular dystrophy ment. Figure 14.Q69 shows 3-chamber (A and B) and
d. Myocardial infarction and hibernation 2-chamber (C and D) balanced SSFP views of the LV dur-
e. Hemochromatosis ing diastole (A and C) and systole (B and D), along with
short-axis, fat-suppressed, black blood (E), and 2-chamber
14.67. Which of the following statements regarding mitral
LGE images (F) from the MRI examination. Based on these
insufficiency is true?
data, what is the most likely diagnosis?
a. The most common cause of mitral insufficiency is
a. Fabry disease
mitral valve prolapse.
b. Amyloid heart disease
b. Acute mitral insufficiency is most often caused by
c. Hypertrophic cardiomyopathy
rheumatic heart disease.
d. Myocardial infarction and hibernation
c. Ischemic mitral regurgitation does not affect the
e. Healed myocarditis
prognosis in patients with myocardial infarction.
d. Acute pulmonary edema is a common manifestation of 14.70. What is the main safety risk associated with the RF
chronic mitral insufficiency. field generated within the MR scanner?
e. Acute mitral valve regurgitation is not identifiable by
a. A ferrous metal object becoming a projectile if brought
MRI.
too close to the scanner
b. Induced stimulation of nerves, particularly peripheral
nerves, resulting in pain and paraesthesia
c. Heating as a result of electrical currents generated in
conducting materials, including tissue and implanted
devices
d. Dielectric resonances producing inhomogeneous
signal within the imaging FOV, resulting in signal loss,
particularly within the center of the image
e. Noise-related discomfort associated with physical
interaction between the RF body coil and the inner
bore of the magnet

Figure 14.Q68

14.68. What is the most appropriate diagnosis for the abnor-

mality shown in the non–fat-saturated, T1-weighted, black
blood, axial image (Figure 14.Q68) acquired before adminis-
tration of gadolinium?
a. Lipomatous hypertrophy of the interatrial septum
b. Prominent crista terminalis
c. Prominent eustachian valve
d. Myocardial infarction
e. Atrial myxoma
 14 . B oa r d -T y pe Q uestions a n d Answers  • 279

Figure 14.Q69
 280 • S e c tion I V: R eview Q uestions

c. Atrioventricular discordance and ventriculoarterial

concordance
d. Atrioventricular concordance and ventriculoarterial
discordance
e. Right-sided aorta along with a persistent left-sided vena
cava
14.73. A 35-year-old man with abnormal echocardiography
results is referred for cardiac MRI for further assessment.
Representative LGE and systolic and diastolic balanced SSFP
images are shown in Figure 14.Q73. What is the most likely
diagnosis?
a. Fabry disease
b. Amyloid heart disease
c. Muscular dystrophy
Figure 14.Q71 d. Myocardial infarction and hibernation
e. Myocarditis
14.74. Figure 14.Q74 shows a 3-chamber balanced SSFP
14.71. A 51-year-old man with chest pain, mildly increased image (A) and an LGE view (B) of the heart. Which of the
cardiac biomarkers, and nonspecific T-wave changes is following imaging features is present on these images?
admitted to the hospital. Coronary angiography results a. Apical pouch
are reported as normal, and cardiac MRI is performed. b. Mitral regurgitation
Representative balanced SSFP and LGE images are shown c. Flow dephasing in the LV outflow tract
in Figure 14.Q71. What is the most likely diagnosis? d. Asymmetric septal hypertrophy
a. Healed myocarditis e. Systolic anterior motion of the anterior leaflet of the
b. Amyloid heart disease mitral valve
c. Muscular dystrophy 14.75. What is the most common primary cardiac
d. Subendocardial myocardial infarction malignancy?
e. Acute myocarditis
a. Lymphoma
14.72. What does the term transposition of the great arteries b. Hemangioma
refer to? c. Angiosarcoma
a. Atrioventricular concordance and ventriculoarterial d. Fibroma
concordance e. Melanoma
b. Atrioventricular discordance and ventriculoarterial
discordance
 14 . B oa r d -T y pe Q uestions a n d Answers  • 281

Figure 14.Q73

Figure 14.Q74
 282 • S e c tion I V: R eview Q uestions
Figure 14.Q78
14.76. In which of the following situations is cardiac MRI
useful for evaluation of transposition complexes?
a. Assessment of atrioventricular valve function
b. Assessment of intra-atrial baffle leak in the setting of a
prior Mustard procedure
c. Assessment of intra-atrial baffle stenosis in the setting
of a prior Jatene procedure
d. Assessment of pulmonic valve regurgitant flow
e. Evaluation of an intracardiac shunt after a
percutaneous device closure procedure
14.77. According to the American College of Radiology,
what is the safest method of delivering care if a patient has a
cardiac arrest in the MR scanner room?
a. First quench the magnet and then allow all staff into
all MR zones (I-IV).
b. Immediately allow all staff into zone IV (MR
scan room), where all medical assistance will be
administered to the patient.
c. Have the MR technologist screen emergency
personnel, then admit them into zone IV, from which
emergency care will be administered.
d. Bring the patient and/or MR table to the door
separating zones IV and III, and allow emergency
personnel to administer care.
e. Administer basic cardiopulmonary resuscitation
(airway, breathing, chest compressions) during
transportation of the patient from zone IV into
zone III or lower where definitive care can be
administered.
14.78. A patient was sent for evaluation of aortic stenosis.
Cine phase-contrast images were acquired with the velocity
encoding factor (VENC) set to 250 cm/s, encoding flow per-
pendicular to the imaging plane. The magnitude and phase
(velocity) images are shown in Figure 14.Q78. What is the
most likely explanation for the appearance of the valve?
a. The velocities are greater than 250 cm/s
b. The velocities are less than 150 cm/s
c. The velocities are equal to 250 cm/s
d. The velocities are approaching 500 cm/s
e. The velocities are 125 cm/s
14.79. Which of the following measurements can be used
to determine cardiac output in a patient with mitral valve
insufficiency?
a. LV stroke volume minus systolic flow in the ascending
aorta
b. Mitral inflow minus systolic flow in the ascending
aorta
c. LV minus RV stroke volumes
d. LV ejection fraction
e. Cardiac output cannot be estimated by MRI
14.80. A 41-year-old man with chest pain, mildly increased
cardiac biomarkers, and nonspecific T-wave changes is
admitted to the hospital. Coronary angiography indicates
that the patient is without obstructive coronary artery dis-
ease. Cardiac MRI is performed, with representative LGE
(A and B) and balanced SSFP images (C and D) shown in
Figure 14.Q80. What is the most likely diagnosis?
a. Healed myocarditis
b. Amyloid heart disease
c. Apical ballooning (takotsubo) or stress
cardiomyopathy
d. A subendocardial myocardial infarction
e. Acute myocarditis
14.81. Figure 14.Q81 shows axial balanced SSFP images in
diastole (A) and systole (B). Which clinical finding do these
images indicate?
a. Tricuspid valve regurgitation
b. Myocardial late gadolinium enhancement
c. Aneurysms of the RV free wall
d. Fibrofatty replacement of the RV myocardium
 14 . B oa r d -T y pe Q uestions a n d Answers  • 283

Figure 14.Q80

Figure 14.Q81
 284 • S e c tion I V: R eview Q uestions

basis of these images, is the administration of gadolinium a

requirement for the evaluation of transposition complexes?
a. No, non–contrast-enhanced white blood techniques
can be used.
b. Yes, only gadolinium-enhanced images provide
sufficient blood pool signal.
c. No, gadolinium is a contraindication in these cases.
d. Yes, gadolinium-enhanced MR angiography is the only
useful imaging method.
e. No, gadolinium is not used because of the likelihood of
nephrogenic systemic fibrosis in these patients.
14.84. Which of the following imaging features is
required to establish the diagnosis of arrhythmogenic RV
cardiomyopathy?
Figure 14.Q83 a. RV dyskinesis
b. RV free wall aneurysms
c. Late gadolinium enhancement
14.82. According to the American College of Radiology, d. Fibrofatty infiltration of the RV
what do the 4 MR safety zones—designated I, II, III and e. RV wall hypertrophy
IV—describe? 14.85. Which of the following is true regarding the tricuspid
a. I, MR equipment room; II, patient waiting area; III, valve?
scan room; and IV, operator console area a. Primary disease is more common than secondary
b. I, MR patient waiting area; II, scan room; III, general causes of tricuspid insufficiency.
patient access area; and IV, patient change rooms b. Carcinoid syndrome generally spares the tricuspid valve.
c. I, MR patient waiting area; II, scanner operator c. Ebstein anomaly results in apical displacement of the
console area; III, MR scan room; and IV, MR septal and posterior leaflets.
equipment room d. The tricuspid annulus is contiguous with the pulmonic
d. I, General access area; II, MR patient waiting area; III, valve.
operator console area; and IV, MR scan room e. Right-sided valve disease is difficult to visualize using
e. I, Operator console; II, MR scanner computer MRI.
room; III, MR scan room; and IV, radiology
administrator office
14.83. The images in Figure 14.Q83 are balanced SSFP
acquisitions of 3 separate transposition complexes. On the
 14 . B oa r d -T y pe Q uestions a n d Answers  • 285

d. Decreasing the TR
e. Increasing the main magnetic field strength
14.88. In acute pericarditis, which of the following is true?
a. Patients typically have fatigue and shortness of breath.
b. Pericardial enhancement is typically pronounced.
c. Free-breathing respirophasic changes are necessary to
make the diagnosis.
d. Pericardial thickness is almost always normal.

14.89. What is the LeCompte maneuver?

a. A surgical technique in which an intra-atrial baffle

connects the morphologic right atrium to the morphologic
LV in transposition of the great arteries
b. A surgical technique in which the pulmonary arteries
Figure 14.Q90 are placed posterior to the aorta
c. A surgical technique in which the pulmonary arteries
are placed anterior to the aorta
d. A surgical technique to increase pulmonary arterial
14.86. What is the specific risk to the patient associated with flow through a systemic-to-pulmonary arterial shunt
executing a high SAR pulse sequence? e. A surgical technique in which an MR-compatible stent
a. Tissue heating is placed in one of the coronary arteries
b. Radiation burns 14.90. Figure 14.Q90 shows a 2-chamber balanced SSFP
c. Decreased image SNR image (A), a 4-chamber balanced SSFP image (B), and a
d. Decreased spatial resolution 4-chamber LGE image (C) of the heart. What is the most
e. Decreased temporal resolution important imaging finding seen in this case?
14.87. For balanced SSFP imaging, which of the following a. Hypertrabeculation of the LV
does not increase the SAR? b. Fibrosis of the interventricular septum
a. Changing the number of receive-only RF coils c. Late gadolinium enhancement of the RV free wall
b. Increasing the RF pulse flip angle d. Asymmetric thickening of the basal interventricular septum
c. Adding RF preparation pulses e. Apical aneurysm with a mural thrombus
 286 • S e c tion I V: R eview Q uestions

Figure 14.Q94

Figure 14.Q96
 14 . B oa r d -T y pe Q uestions a n d Answers  • 287

Figure 14.Q98

14.91. Use of gadolinium for LGE images results in which of c. Pulmonary arteries
the following? d. Pulmonary veins
e. Left ventricle
a. Gadolinium-induced T1 shortening
b. Gadolinium-induced T1 lengthening 14.96. What are the 4 anatomical structures identified by
c. No change in T1 labels A through D on the MR image in Figure 14.Q96?
d. Gadolinium-induced T2 shortening 14.97. Cardiovascular MRI is often used in the setting of
e. Gadolinium-induced T2 lengthening HCM. Of the following, which is its best utility?
14.92. LGE imaging relies on choosing an accurate inversion a. Assessing dynamic LV outflow tract gradients
time that optimally nulls normal myocardium. Which of the b. Assessing the severity of mitral regurgitation
following will not affect the inversion time? c. Evaluating coronary artery anatomy
d. Identifying reversible perfusion defects
a. The dose of the contrast agent administered to the patient e. Measuring LV wall thickness
b. The time elapsed between injection of contrast and imaging
14.98. A 22-year-old man with no significant past medical
c. The time delay between the inversion and imaging pulses
history came to the emergency department with sud-
d. An increase in signal averages from 1 to 3
den onset of nonexertional and nonpositional chest pain.
e. Imaging at a field strength of 3.0T instead of 1.5T
Creatine kinase-MB and troponin-T values were mildly
14.93. A 45-year-old woman is referred for cardiac MRI to increased. ECG revealed sinus tachycardia, and echocardiog-
evaluate for partial anomalous pulmonary venous connec- raphy results were normal. MRI was performed, with repre-
tion. In addition to identifying the anomalous pulmonary sentative triple inversion recovery and LGE images shown
veins, what is the most important goal of imaging with MRI? in Figure 14.Q98. On the basis of these images, what is the
clinical finding?
a. Assessment of LV size and function
b. Assessment of left atrial size a. Moderate LV chamber dilatation
c. Assessment of RV size and function b. Edema in the posterolateral LV wall
d. Assessment of pulmonic valvular regurgitation c. Asymmetric myocardial hypertrophy
e. Assessment of aortic valvular regurgitation d. Subendocardial gadolinium enhancement
e. Iron deposition
14.94. The 2 axial balanced SSFP images in Figure 14.Q94
show the heart at different phases of the cardiac cycle. What is 14.99. Which is the most common anomalous pulmonary
the most likely diagnosis in this case? venous return pathway in patients with partial anomalous
pulmonary venous return?
a. RV lipoma
b. RV myocardial infarction a. Right lower pulmonary vein directly into the right atrium
c. Benign fatty infiltration of the RV b. Right upper pulmonary vein directly into the right
d. Arrhythmogenic RV cardiomyopathy atrium
e. RV thrombus c. Right upper pulmonary vein into the SVC
d. Left upper pulmonary vein into the SVC
14.95. What is the most common anatomical location of car- e. Left lower pulmonary vein into the right atrium
diac myxomas?
a. Right atrium
b. Left atrium
 288 • S e c tion I V: R eview Q uestions

Figure 14.Q100

Figure 14.Q101
 14 . B oa r d -T y pe Q uestions a n d Answers  • 289

14.100. What are the 4 anatomical structures identified by 14.103. Which of the following should be reported in a
labels A through D on the MR image in Figure 14.Q100? patient with repaired tetralogy of Fallot with pulmonic valve
regurgitation?
14.101. The images in Figure 14.Q101 show 4-chamber
balanced SSFP (A and B) and LGE (C) views of the heart. a. Indexed RV end-diastolic volume
What is the most likely diagnosis? b. Pulmonic regurgitation fraction
c. Indexed LV end-diastolic volume
a. Cardiac siderosis
d. LV end-diastolic volume
b. Apical ballooning syndrome
e. LV end-diastolic mass
c. Hypertrophic cardiomyopathy
d. Chronic myocardial infarction 14.104. In total anomalous pulmonary venous connection,
e. Cardiac hemosiderosis the pulmonary veins converge on a pulmonary venous conflu-
ence before entering the heart. What is the most common site of
14.102. The so-called India ink artifact describes a dark band
drainage of the blood from this pulmonary venous confluence?
that circumscribes the border of organs and masses. Which of
the following masses will exhibit the India ink artifact at the a. The SVC or innominate vein (supracardiac)
interface of the mass and blood pool? b. The right atrium (cardiac)
c. The coronary sinus
a. Myxoma
d. The inferior vena cava or hepatic veins (infracardiac)
b. Angiosarcoma
e. The fundus of the left atrium
c. Lipoma
d. Fibroma 14.105. What are the 3 anatomical structures identified by
e. Thrombus labels A through C on the MR image in Figure 14.Q105?

Figure 14.Q105
 290 • S e c tion I V: R eview Q uestions

Figure 14.Q106

Figure 14.Q108
 14 . B oa r d -T y pe Q uestions a n d Answers  • 291

c. Myocardial infarction
d. Endomyocardial fibrosis
e. Microvascular obstruction
14.107. Scimitar syndrome includes which of the following
imaging features?
a. Connection of all the right-sided pulmonary veins to
the SVC
b. Hypoplasia of the ipsilateral lung
c. Connection of all the left-sided pulmonary veins to the
inferior vena cava
d. Supply of the lower part of the right lung by
pulmonary arteries
e. Regurgitant flow jets characterized by signal voids on
balanced SSFP imaging
14.108. What are the 7 anatomical structures identified by
Figure 14.Q110
labels A through G on the MR image in Figure 14.Q108?
14.109. What criteria are used to classify hemangiomas?
14.106. A 40-year-old woman from El Salvador with no
significant history was evaluated for chest pain, shortness a. Size of the vascular channels
of breath, and watery diarrhea. Complete blood count b. Location of the mass
revealed eosinophilia, and troponin value was mildly c. Size of the mass
increased. ECG showed LV hypertrophy. Echocardiography d. First-pass perfusion contrast kinetics
confirmed hypertrophy and revealed severe LV diastolic e. Amount of late gadolinium enhancement
dysfunction and a large apical LV thrombus. Representative 14.110. Figure 14.Q110 shows 2-chamber balanced SSFP (A),
MR images shown in Figure 14.Q106 include 4-chamber 4-chamber balanced SSFP (B), and 4-chamber LGE (C) images
balanced SSFP (A), 4-chamber perfusion (B), and LGE (C) of the heart. What is the most likely diagnosis in this case?
images. On the basis of the clinical presentation and char-
acteristic trilayer appearance (bright, dark, bright) of the a. Cardiac sarcoidosis
LV on LGE imaging, what is the diagnosis? b. LV noncompaction
c. RV myocardial infarction
a. Myocarditis d. Hypertrophic obstructive cardiomyopathy
b. Amyloidosis e. Cardiac sarcoidosis
 292 • S e c tion I V: R eview Q uestions

Figure 14.Q112

14.111. What percentage of patients with coarctation of the

aorta also have a bicuspid aortic valve?
a. 0%-5%
b. 15%-25%
c. 25%–45%
d. 85%–95%
e. 95%–100%

14.112. What are the 6 anatomical structures identified by

labels A through F on the MR image in Figure 14.Q112?

Figure 14.Q113
 14 . B oa r d -T y pe Q uestions a n d Answers  •
Figure 14.Q115
14.113. A 42-year-old man with dyspnea is sent for MRI
of the heart after abnormal results on echocardiography.
Representative LGE (A and B) and balanced SSFP (C)
images are shown in Figure 14.Q113. Which of the follow-
ing correctly identifies the disease illustrated?
a. Healed myocarditis
b. Dilated cardiomyopathy
c. Amyloid heart disease
d. A subendocardial myocardial infarction
e. Acute myocarditis
14.114. What is the role of cardiac MRI in patients with a
new diagnosis of coarctation of the aorta?
a. Assessment of the presence of LV eccentric
hypertrophy
b. Assessment of the presence of systemic venous
collateral vessels using MR venography
c. Assessment of the presence of pulmonary arterial
collateral vessels using MR angiography
d. Assessment of the presence of retrograde flow in the
intercostal vessels proximal to the site of coarctation
using phase-contrast imaging
e. Assessment of fibrosis using LGE imaging
293
14.115. What are the 5 anatomical structures identified by
labels A through E on the MR image in Figure 14.Q115?
14.116. What is the role of cardiac MRI in patients who have
undergone repair of a coarctation of the aorta?
a. Assessing for restenosis or aneurysm at the site of the
initial coarctation
b. Assessing for regression of collateral vessels
c. Assessing for RV hypertrophy
d. Assessing for bicuspid aortic valve
e. Assessing for laminar flow distal to the repair using
phase-contrast MRI
14.117. What are the characteristic cardiac MRI findings of
Ebstein anomaly?
a. RV dysplasia or the so-called parchment heart
b. Apical displacement of the septal and posterior leaflets
of the tricuspid valve
c. Ventricularization of the right atrium
d. Tricuspid stenosis with or without tricuspid
regurgitation
e. Patchy, diffuse, hyperintense signal in the LV
myocardium on LGE imaging
 294 • S e c tion I V: R eview Q uestions

Figure 14.Q118

Figure 14.Q120
 14 . B oa r d -T y pe Q uestions a n d Answers  • 295

14.118. What are the 2 features identified by labels A and B

on the MR image in Figure 14.Q118?
14.119. Which imaging plane provides the most accurate
data for quantifying RV volumes?
a. Axial imaging plane
b. Coronal imaging plane
c. Short-axis imaging plane
d. Vertical long-axis (inflow/outflow) imaging of the RV
e. Any plane as long as the full volume of the RV is covered
14.120. Figure 14.Q120 shows balanced SSFP (A), LGE
(B), and non–fat-suppressed, T1-weighted, black blood
(C) images identifying a rounded mobile mass in the right
atrium. Based on these images, what is the most likely
diagnosis?
a. Thrombus
b. Metastasis
c. Myxoma
d. Papillary fibroelastoma
e. Myocardial infarction
14.121. Which is true regarding pulmonic valve disease?
a. Most cases of pulmonic stenosis are acquired.
b. Most cases of pulmonic insufficiency are congenital.
c. Dilatation of the left main pulmonary artery is often
seen in pulmonic stenosis.
d. MRI measurements are not sufficiently accurate for use
in pulmonic valve replacement surgery.
e. Pulmonic stenosis is usually associated with rheumatic
heart disease.
 296 • S e c tion I V: R eview Q uestions
A NSW ER S
14.1. Answer a.
The magnetohydrodynamic effect is a well-known phenom-
enon that occurs when a conducting fluid moves through a
magnetic field, resulting in the generation of an electric field
and subsequent current within the conductor. Blood flow, in
the presence of a magnetic field such as the field of a high-field
MR scanner, will produce a time-varying electric field, mod-
eled as an electric dipole moment whose magnitude is pro-
portional to the volume of blood flowing into and out of the
chambers of the heart. This induces a time-varying signal that
is detected by the ECG leads placed close to the heart on the
patient’s chest wall. Because the electrical activity of the heart
precedes the flow of blood from the left side of the heart, there
is a delay between the QRS complex and the detected signal
resulting from the magnetohydrodynamic effect. This delay
is typically equal to the duration of the ST interval, which
results in the superposition of this signal onto the T wave of
the ECG signal, producing an increase of the T-wave signal,
or T-wave swelling.
14.2. Answer c.
The bright-dark-bright signal pattern seen in the figure is
characteristic of microvascular obstruction. In diagnos-
ing microvascular obstructions it is important to determine
whether the abnormality is within the myocardium or in
the cavity. The band of low signal intensity at the apex and
in the septum is in the subendocardial myocardium. This is
caused by lack of contrast enhancement secondary to micro-
vascular obstruction (lack of blood flow in the microvessels
in the region). The region is surrounded by avidly enhanc-
ing infarcted myocardium. Normal myocardium should
be dark on this type of image if done properly, but normal
myocardium will not be present along the subendocardial
myocardium in a patient with an infarction. Although mural
thrombus will not enhance, the thrombus should be located
in the cavity, not in the myocardium. This patient may have a
perfusion abnormality; however, this image is from an LGE
acquisition after injection of contrast, not a dynamic perfu-
sion scan. Myocarditis shows subepicardial late gadolinium
enhancement.
14.3. Answer b.
Although not of optimal image quality, these LGE images
identify the presence of a mass at the apex of the LV. The
mass is circumscribed by an area of enhancement and a cen-
tral nonenhancing region. The lack of enhancement indicates
that this region is not perfused and is representative of a solid
(ie, thrombolytic) mass. Intracardiac thrombi are the most
common imitators of a cardiac mass. They are most com-
monly found at the LV apex in the setting of apical myocar-
dial infarction and in the left atrial appendage in the setting
of atrial fibrillation. Note that these figures highlight 2 key
clinical findings: 1) transmural late gadolinium enhance-
ment of the LV apex indicating the presence of an infarction
and 2) a nonenhancing thrombus at the LV apex, adjacent to
the infarction. The lack of enhancement is characteristic of a
thrombus.
14.4. Answer b.
The balanced SSFP signal is the combination of echoes with
both T2 and T1 weighting. In general, the contrast is propor-
tional to the ratio of these 2 signals, or T2/T1. This explains
why blood (without gadolinium-based contrast agents on
board), which is typically dark on gradient echo imaging
sequences, is bright and why blood pool–myocardial contrast
is so high.
14.5. Answer d.
HCM is characterized by variable thickening (hypertrophy) of
the myocardium. LV outflow tract obstruction occurs in ≈25%
of these patients during rest and occurs in ≈70% under stress.
The features of HCM can be well visualized on cardiac MRI.
Cardiac amyloidosis is characterized by diffuse amyloid depo-
sition, which usually causes diffuse myocardial thickening.
Hypertension also typically produces concentric, rather than
regional, thickening of the myocardium. Cardiac sarcoidosis
does not result in regional myocardial thickening but abnor-
mal areas of late gadolinium enhancement on postcontrast
imaging.
14.6. Answer d.
Pericardial thickness correlates imprecisely with the risk of
pericardial constriction. Although various authors have pro-
posed using 2 mm or 4 mm as a cutoff for “normal” thickness
for diagnosing pericardial constriction, constriction has been
shown to occur even when pericardial thickness is normal on
histopathologic investigation.
14.7. Answer b.
In segmented cine acquisitions, temporal resolution (ie, the
time between successive cine phases) is the product of the
views per segment and repetition time. Decreasing this value
will improve temporal resolution. This will, however, require
more heartbeats to acquire the desired number of phase-
encoding steps and, therefore, will result in an increase in
acquisition time. For a fixed heart rate, decreasing the number
of phase-encoding steps will decrease overall image acquisi-
tion time and will decrease spatial resolution but not tempo-
ral resolution. Increasing or decreasing the flip angle will not
affect the temporal resolution. Increasing the TR will increase
overall acquisition time and decrease the number of views per
segment acquired.
14.8. Answer a.
The most common postoperative complication in patients
who have undergone complete repair for tetralogy of Fallot is
pulmonic valvular regurgitation. This is more frequently seen
after transannular patch repair, in which case the patient will
be left with free pulmonic regurgitation, as in the image asso-
ciated with this question. For this reason, one of the major
 14 . B oa r d -T y pe Q uestions a n d Answers  •
indications for cardiac MRI in this setting is to assess the
amount of pulmonic regurgitation either as regurgitant frac-
tion or regurgitant volume using phase-contrast imaging and
to assess its effect on RV function.
14.9. Answer d.
It is generally appreciated that currently available valve pros-
theses are safe to scan on 1.5T systems. Most device manufac-
turers recommend delaying elective MRI for approximately 6
weeks after valve replacement surgery to allow scar formation
and to minimize any potential magnetic field–induced move-
ment. Prosthetic orthopedic replacements are usually safe. In
general, any device that contains ferrous components is not
considered compatible with MRI. However, depending on the
type of device, its location within the body (ie, not near any
critical structures), and the amount of ferrous metal within
the device, the manufacturer may have performed testing to
verify that the device is safe to scan at a given field strength. It
is recommended that the MR safety of every implanted device
be verified before the patient is placed in the MR scanner.
14.10. Answer e.
Decreasing the number of phase-encoding steps will decrease
the amount of data acquired and therefore total imaging
time. Increasing the views per segment means that more data
can be acquired within a given R-R interval, decreasing the
total number of R-R intervals over which data are acquired
and hence total imaging time. Decreasing the phase FOV
decreases the number of phase-encoding steps and hence total
imaging time. Decreasing the number of signal averages or
excitations to 0.5 decreases the number of phase-encoding
steps and imaging time by a factor of 2. Additional cardiac
phases can be reconstructed by interpolation and additional
view-sharing schemes, but this occurs after data acquisition
and therefore does not decrease acquisition time.
14.11. Answer c.
The signal from balanced gradient echo imaging is the sum
of 2 separate echoes. Off-resonance effects including poor B0
shimming destroy phase coherence between the 2 echoes, thus
producing varying degrees of signal cancellation and resulting
in the characteristic banding artifacts. Gradient echo images
resulting from only 1 type of echo, for example spoiled gra-
dient echo images, are not the result of multiple echoes and
thus do not exhibit the typical off-resonance banding evi-
dent in balanced gradient echo images. Multiecho gradient
echo sequences produce increasing signal loss as a function of
increasing TE, but this is a result of T2* effects and does not
produce the characteristic banding or “zebra stripe” artifacts
produced in balanced gradient echo images. An exception can
occur when a wraparound artifact is present in the image and
signal from 2 different spatial locations overlaps.
14.12. Answer a.
Balanced SSFP 4-chamber views of the heart show noncon-
centric contraction of the LV during systole (B), as identified
297
by thickening of the base of the ventricle compared with the
apex. The LV blood pool also exhibits a balloonlike appear-
ance. No regions of hyperenhancement are seen on the LGE
images that would suggest the presence of a myocardial
infarction.
14.13. Answer d.
MRI has lower temporal resolution and generally longer
acquisition time than echocardiography. Neither echocar-
diography nor MRI uses ionizing radiation, and both are able
to identify pericardial fluid. MRI is able to identify pericar-
dial inflammation. In addition, extended anatomical coverage
and simultaneous tissue characterization of myocardial tissue
are relative advantages.
14.14. Answer b.
Accurate measurements are essential for cardiac MRI.
Measuring wall thickness should be done at end diastole.
Imaging at other points in the cycle will not lead to accurate
measurements.
14.15. Answer e.
Banding in balanced SSFP imaging is due to shifts in the
frequency of tissue across the imaging FOV, most com-
monly a result of B 0 inhomogeneities. The dark band rep-
resents a specific shift in the resonant frequency of the
imaging sequence. Modifying the resonant frequency of the
digital RF receiver that is used to acquire the MR signal by
this amount results in those dark band regions now being
“on resonance,” effectively eliminating the dark band. Those
regions initially on resonance will be off resonance and will
produce regions of signal loss or banding. Thus, the appear-
ance within the image will be the effective shifting of the
banding across the FOV. Although it does not eliminate
the artifact, it is a simple and effective method for moving
the effect outside of the region of interest, which for cardiac
imaging is often relatively small compared with the overall
FOV.
14.16. Answer c.
The Larmor frequency ƒL in units of hertz is defined by the
equation ƒL = γ/2π B(r), where B is the net magnetic field at
position r and γ the gyromagnetic ratio, which for protons
equals 42.57 MHz/T. Substitution of these values into the
Larmor equation results in the values given by option c in
units of MHz. Importantly, the Larmor frequency and field
strength are linearly related.
14.17. Answer a.
Abnormal gadolinium enhancement can be seen on this image
in the mid ventricular septum. This pattern of enhancement is
typical of infarction in the left anterior descending coronary
artery territory. A circumflex territory myocardial infarction
typically involves the lateral wall at the base and mid ven-
tricle. A right coronary artery territory myocardial infarction
typically involves the inferior wall (with possible extension
 298 • S e c tion I V: R eview Q uestions
into the adjacent inferoseptum and inferolateral wall) at the
base and mid ventricle. The RV can also be involved. A pos-
terior descending artery territory myocardial infarction typi-
cally involves the inferior wall. A diagonal branch occlusion
will result in infarction of the anterior or anterior lateral wall
and usually spares the septum and apex.
14.18. Answer a.
One of the major indications for cardiac MRI in patients with
tetralogy of Fallot after repair is to assess RV function. One of
the postoperative issues that needs to be monitored in these
patients is the presence and severity of pulmonic regurgitation.
The RV responds to volume overload with dilation, whereas
the RV response to pressure is hypertrophy. Since pulmonic
regurgitation is predominantly a volume overload problem,
RV dilation will be the primary response. Therefore, one of the
goals of surveillance imaging is to assess the degree of dilation
so that optimal timing of pulmonic valve replacement can be
planned.
14.19. Answer d.
Low spatial frequencies (low k-space numbers) contain infor-
mation regarding the contrast within the image. High spatial
frequencies (high k-space numbers) contain edge informa-
tion. If only low spatial frequency information (ie, low k-space
or central portion of the k-space spectrum) is acquired, the
image will appear blurry because there is no information to
distinguish between boundaries. The other options do not
affect the frequency content of the image.
14.20. Answer c.
Spoiled gradient echo pulse sequences are heavily T1 weighted
because of the spoiling of stimulated echoes. (In non–spoiled
gradient echo images such as balanced SSFP images, these
echoes combine to provide additional T2 weighting). Blood,
which has a long T1 and T2 will typically be dark or isoin-
tense due to the significantly decreased contribution of this
tissue when exposed to multiple RF pulses (ie, steady state).
However, in cardiac imaging in which blood is flowing into
and out of the imaging slice, the signal from the blood pool
is significantly greater because the blood is in a non–steady
state and is effectively fully magnetized, thus contributing the
maximum amount of signal.
14.21. Answer c.
The MR signal theoretically increases or decreases lin-
early with field strength. Assuming that the noise content
remains the same, a doubling of field strength from 1.5T to
3.0T will increase the signal by a factor of 2. Thus, the SNR
will effectively double, although the actual increase is less
than 2-fold.
14.22. Answer c.
Aortic valve area and peak systolic velocity are criteria for aor-
tic stenosis rather than aortic insufficiency. Dilatation of the
ascending aorta can be associated with aortic insufficiency;
however, it can also be seen with aortic stenosis or can be inde-
pendent of aortic valve disease. Bicuspid aortic valves can be
either stenotic or regurgitant.
14.23. Answer c.
The most common cause of a left apical thrombus is myocar-
dial infarction that interrupts the microvascular distribution
of blood to the myocardium. Ischemia-induced injury results
in cellular damage and platelet accumulation within the myo-
cardium. Extensive ischemic damage results in the accumula-
tion of platelets and other cellular debris, thereby producing a
thrombus or clot.
14.24. Answer b.
In general, black blood imaging is performed with spin echo–
based pulse sequences. These sequences are performed with
short TE and TR values. For cardiac imaging, this translates
to TRs well below 1000 ms, or more commonly 1 ECG R-R
interval, assuming a heart rate of 60 beats per minute. In addi-
tion, TE values are commonly chosen to be less than 50 ms,
with specific values being chosen based on which phase of the
cardiac cycle is imaged.
14.25. Answer d.
The pattern of subepicardial late gadolinium enhancement
along with the clinical history is most consistent with myo-
carditis. A myocardial infarction would produce subendo-
cardial late gadolinium enhancement, as would a coronary
embolism leading to an infarction. Apical ballooning cardio-
myopathy has been described as having no late gadolinium
enhancement.
14.26. Answer b.
A straightforward method for acquiring cine cardiac data is
to divide the cardiac cycle into n discrete time intervals. Each
interval represents the data acquisition window for a given
cardiac phase. The total scan time is equal to the R-R inter-
val times the ratio of the number of k-space lines per image
to the number of k-space lines or views acquired per cardiac
phase. In this scenario, k-space lines are grouped into discrete
and independent bins of data associated with a given cardiac
phase. In view sharing, this restriction is relaxed, thereby
allowing views to be shared between adjacent cardiac phases.
This effectively increases the number of views acquired for a
given cardiac phase per R-R interval, which decreases both
the number of R-R intervals necessary to collect a complete
set of k-space data and overall scan time. This method has the
additional advantage of blurring out rapid temporal changes
in cardiac volume, thus creating a smoother representation of
the heart as it beats throughout the cardiac cycle.
14.27. Answer e.
Cardiac myxomas, the most common benign cardiac tumors,
typically have an appearance of that illustrated in this case
example. They usually are attached to the interatrial septum
by a stalk and are often highly mobile. They are isointense on
 14 . B oa r d -T y pe Q uestions a n d Answers  •
T1-weighted images, hyperintense on T2-weighted images,
and have heterogeneous enhancement. A thrombus should
not perfuse and is typically completely black on LGE images.
Angiosarcomas are the most common primary cardiac
tumor. They are classically a bulky, heterogeneous tumor that
infiltrates into the right atrium. Papillary fibroelastomas,
the second most common benign cardiac tumor, are small
tumors and are usually found on valve surfaces. This exam-
ple does not have an appearance of an undiagnosed primary
metastasis.
14.28. Answer a.
Black blood T2-weighted imaging can demonstrate myocar-
dial, as well as pericardial, inflammation, potentially adding
diagnostic value. This imaging sequence can be used with and
without fat suppression. Images are acquired at a single phase
of the cardiac cycle and therefore are static or “snap shot”
views of the heart. Ventricular function, regional wall-motion
abnormalities, coronary artery anatomy, and perfusion are
not demonstrated with this type of imaging and require cine
sequences that reproduce the motion of the heart throughout
its cardiac cycle.
14.29. Answer b.
Although a minority of patients with HCM have a myocar-
dial thickness measuring 30 to 50 mm, myocardial thick-
ness greater than 30 mm is a major risk factor for sudden
cardiac death. Other high-risk features for sudden cardiac
death in patients with HCM are a family history of sudden
death in a first-degree family member, unexplained syncope,
sustained ventricular tachycardia, nonsustained ventricu-
lar tachycardia on Holter monitoring, and an abnormal
blood pressure response during exercise testing. Midcavity
obliteration, systolic anterior motion of the anterior leaflet
of the mitral valve, and flow dephasing in the LV outflow
tract seen on balanced SSFP images are imaging findings of
hypertrophic obstructive cardiomyopathy but are not spe-
cific risk factors for sudden cardiac death in patients with
HCM.
14.30. Answer b.
The sinus venosus atrial septal defect is often difficult to image
by other modalities. The wide FOV and multiplanar ability of
MRI make it an obvious choice to visualize this abnormality.
A secundum atrial septal defect is usually in the middle of the
atrial septum, and a primum defect is often lower and involves
the area closer to the crux of the heart.
14.31. Answer e.
Zipper artifacts can arise from various sources. Stimulated
echoes and reception of a spurious signal from a refocusing
pulse by the receiver coil are 2 examples of zipper artifacts that
can arise from pulse sequence–related errors. External noise
sources from within the MR scan room, such as from patient
monitoring equipment or patient pumps, can also produce
zipper artifacts. Finally, RF noise from sources external to the
299
scan room can also be detected and digitized into the MR sig-
nal due to RF leaks in the Faraday cage (screen room) of the
MR scanner.
14.32. Answer d.
This is the typical appearance of the so-called scimitar defect
with anomalous pulmonary drainage into the inferior vena
cava. A persistent left SVC would be seen immediately to the
left of the aorta. An aortic diverticulum (or Kommerell diver-
ticulum) is a rare aortic congenital anomaly that is produced
as a result of the aberrant origin of the left subclavian artery.
An aortic dissection or unroofed coronary sinus would not
have this appearance.
14.33. Answer d.
An axial, oblique, balanced SSFP acquisition through the
aortic valve plane prescribed from previous 3-chamber
and coronal oblique views provides optimal visualization
of valve morphology and function and can also be used to
estimate the valve area in aortic stenosis. Three-chamber
and coronal, oblique, balanced SSFP acquisitions are useful
for visualization of stenotic and regurgitant flow jets but do
not permit complete assessment of valve morphology. Axial,
double inversion recovery, spin echo (ie, non–fat-suppressed
black blood) images may visualize the valve leaflets, but this
technique is less reliable than cine balanced SSFP images.
Systole is the best time to identify aortic valve morphology.
14.34. Answer b.
A cardiac MRI examination in patients with tetralogy of
Fallot is usually straightforward and in most cases does not
require the administration of intravenous gadolinium con-
trast agents. The main goal of the examination is to assess
cardiac volumes and ventricular function and to qualify
and quantify the extent of valvular abnormalities. Figures
A and B demonstrate the magnitude and phase image,
respectively, in systole, that is used in regurgitant volume
quantification using phase-contrast imaging. Figure C is
a phase image during diastole; note the bright signal in
the main pulmonary artery just above the pulmonic valve
due to retrograde (caudal) flow caused by pulmonic valve
regurgitation.
14.35. Answer c.
The velocity-encoding value (VENC) represents the maxi-
mum velocity encoded into the phase value of π (3.14159)
radians within the phase of the MRI sequence. Velocities cor-
rectly encoded into the phase of the phase-contrast MR sig-
nal are all values between +VENC and −VENC. This range
of velocities can be considered to be the velocity-encoding
dynamic range. If the VENC is less than the highest veloc-
ity of moving tissue, then the phase value will be aliased to a
value between −π and + π (−3.14159) and the peak velocity
will no longer correspond to a unique phase shift. For a vessel
in which some pixels are aliased, the net flow (sum of velocity
× area of pixel) within the vessel will be decreased due to the
 300 • S e c tion I V: R eview Q uestions
negative velocity, and hence flow values, of the aliased pixels.
When the VENC is set too high, the sensitivity for measure-
ment of relatively small velocities is decreased, and therefore
flow may be underestimated. The VENC determines the
velocities corresponding to phase shifts of ±π radians, and
therefore should be set to a value slightly above the expected
peak velocity, not the expected average velocity.
14.36. Answer d.
The images shown are classic examples of corrected transposi-
tion of the great arteries. There are no views suggesting severe
aortic stenosis, noncompaction, cardiomyopathy, or anoma-
lous pulmonary drainage.
14.37. Answer e.
The spacing between k-space lines in the frequency domain
is inversely proportional to the imaging FOV. A decrease
of FOV in the phase-encoding direction with an equiva-
lent decrease in the number of phase-encoding steps main-
tains spatial resolution, while decreasing acquisition time
by a factor equal to the decrease in phase-encoding steps
(ie, a 20-cm FOV with 128 phase-encoding steps decreased
to a 10-cm FOV and 64 phase-encoding steps maintains
a pixel resolution of 1.56 mm, while decreasing scan time
by a factor of 2). Image-based MR parallel-imaging tech-
niques use this phenomenon by intentionally decreas-
ing the FOV and reconstructing the original, larger FOV
image. Reconstruction of the larger FOV image is achieved
by using RF multicoil data in combination with individual
spatial sensitivity maps of each coil element within the mul-
tielement RF coil.
14.38. Answer a.
Thrombi consist of consolidated blood products and there-
fore do not contain an intact vascular network. These tumors
are not perfused, so there is no way in which gadolinium
can perfuse into the mass. This is manifested as a lack of
signal on LGE images and on dynamic contrast enhance-
ment (ie, perfusion) imaging. The region circumscribing
the thrombus is typically perfused and includes regions of
inflammation, which is visualized by hyperintense signal on
LGE imaging.
14.39. Answer d.
There is increased signal in the lateral wall involving the
entire myocardial thickness (transmural) on this LGE image.
The location and extent of enhancement is typical of a trans-
mural infarction in the circumflex coronary artery territory.
There is a low likelihood of functional recovery in myocar-
dial segments with transmural enhancement after myocar-
dial infarction. Subendocardial enhancement can be seen
with nontransmural myocardial infarction. The likelihood
of functional recovery decreases with increasing thickness of
enhancement. Subepicardial and midmyocardial late gado-
linium enhancement are patterns that should not typically
be seen with ischemic heart disease but can be seen with
other types of heart disease such as myocarditis and non-
ischemic cardiomyopathy. Mural thrombus would be dark
on LGE images and involves the endocardial surface of the
myocardium.
14.40. Answer b.
This is the typical appearance of a pericardial cyst. It is impor-
tant to recognize this as a benign finding. Because of their
high fluid content, cysts will appear hyperintense on both T2-
weighted and SSFP images. Fluid on balanced SSFP images
will be hyperintense because the signal is proportional to the
ratio T2/T1.
14.41. Answer c.
Knowledge of the point within the cardiac cycle at which
a given line of k-space is acquired as determined from the
ECG waveform is typically needed to reconstruct a single (ie,
static) or a series of cine images throughout the cardiac cycle.
Free-breathing sequences typically involve respiratory gat-
ing but also typically require ECG gating if cardiac images
are being acquired. The purpose of real-time data acquisition
is to acquire images at a rate of several images per second. To
achieve this goal, real-time data are often relatively low resolu-
tion and continuously acquired. There is no need to segment
data acquisition across multiple R-R intervals or at a given
point of the cardiac cycle. Under these real-time acquisition
conditions, cardiac (ECG) gating is not used.
14.42. Answer e.
Partial-phase FOV imaging, also known as rectangular
FOV imaging, decreases the number of phase-encoding
steps while reducing the FOV in this direction. Fewer
phase-encoding steps decreases the overall acquisition
time and, as a result, breath-hold acquisition times, assum-
ing that all other parameters are held constant. Temporal
resolution is affected by the number of lines of k-space
acquired per cardiac phase (views per segment) and is not
affected by a partial-phase FOV. Contrast is affected by
pulse sequence choice, TE, and TR. Slice thickness is unre-
lated to the FOV.
14.43. Answer b.
In MR sampling, the readout of data in the frequency-encod-
ing direction can be filtered so that aliasing does not occur.
Aliasing therefore occurs only along the phase-encoding
direction(s) and is manifested as the so-called wraparound
artifact, in which signal that falls outside of the imaging FOV
along the phase-encoding direction is wrapped around to the
opposite side. In a 3D acquisition, phase encoding occurs
along 2 orthogonal directions, 1 within the imaging slice or
plane and 1 along the slice or slab-encoding direction.
14.44. Answer d.
This set of balanced SSFP images in end diastole (A) and
end systole (B) demonstrate asymmetric LV basal antero-
septal hypertrophy with a signal flow void in the LV outflow
 14 . B oa r d -T y pe Q uestions a n d Answers  •
tract during systole. This finding indicates turbulent flow,
which is consistent with dynamic LV outflow tract obstruc-
tion in this patient with HCM. Systolic anterior motion of
the anterior leaflet and chordae of the mitral valve and the
posteromedial papillary muscle contribute to LV outflow
tract obstruction.
14.45. Answer a.
Tetralogy of Fallot is delineated by the presence of a
malaligned ventricular septal defect, an overriding aorta, pul-
monic stenosis, and RV hypertrophy. The pulmonic stenosis
can occur at several levels: subvalvular, valvular, or supraval-
vular. In extreme cases, there can be atresia of the pulmonic
valve. In all cases, the role of MR angiography is to delineate
the pulmonary arterial vasculature to ensure that the periph-
eral branching pattern is normal and to assess for the presence
of peripheral pulmonary arterial stenoses.
14.46. Answer a.
Magnetic susceptibility is a constant of proportionality that
describes the amount of magnetization M that will be induced
in a material when exposed to an applied magnetic field B.
This constant, or χ (commonly referred to as the magnetic
susceptibility of the material), is given by χ = M/B. Across
the range of tissue types, the variation in χ is relatively small
and as a consequence, the perturbation of the main magnetic
field of the MR scanner (B0) will be relatively small and often
neglected. If χ differs significantly, for example due to a for-
eign implanted object such as a sternal wire or hip prosthesis,
a significant perturbation of B0 can result. In addition, the
size of the object and its orientation also affect the perturba-
tion field. Because spatial position in MR is mapped according
to a linear relationship between magnetic field and position,
nonlinear perturbations of B0 due to susceptibility differences
result in geometric distortion of the object. Additionally, if
the perturbation within a local region (ie, a voxel) is large,
intravoxel phase dispersion will occur, destroying phase
coherence of the spins within the voxel and ultimately signal
cancellation or loss. This phenomenon is the basis for gradi-
ent-induced spoiling that is used to destroy residual transverse
signal in ultrafast imaging sequences. Chemical shift of the
second kind describes the decrease in signal in voxels that
contain both fat and water when an TE is chosen such that
the spins from both species are 180° out of phase with respect
to one another. Unless the voxel contains equal parts fat and
water, there will not be complete signal loss. Additionally, this
effect is restricted to voxels that contain both fat and water.
14.47. Answer d.
A grainy appearance of an MR image is most commonly
associated with increased image noise. Although a smaller
FOV will help with shimming and decrease flow artifact in
many cases, it also decreases the dimensions of the pixel and
overall signal without decreasing image noise. Decreasing
the number of signal averages will also decrease the MR
signal but without decreasing the noise in the MR image.
301
Parallel imaging will decrease acquisition time but will also
amplify noise, making the image appear even grainier. An
increase in slice thickness will increase the MR signal by
increasing the voxel dimensions of the image. Increasing the
number of slices, in general, will not affect the amount of
noise in each slice.
14.48. Answer d.
Fat has a very short T1 relaxation time, which produces a
high signal on most T1-weighted sequences. Spectral satura-
tion, or FAT-SAT, takes advantage of the difference in reso-
nant frequencies between water and fat. The saturation pulse
is applied to the entire imaging volume but it will only work
if the frequencies of the RF pulse coincide with the resonant
frequency of fat. A nonuniform B0 field throughout the imag-
ing volume will induce resonant frequency shifts of both fat
and water. If the shifts are large enough, the resonant fre-
quency of fat can shift out of the bandwidth of the RF fat-
suppression pulse, thus resulting in incomplete suppression of
the fat signal. STIR (Short TI Inversion Recovery) sequences
use an inversion pulse and time delay (TI) to null longitudi-
nal magnetization so that fat will not contribute signal in any
subsequent signal-generation routine. Inversion recovery–
based fat-suppression techniques are less sensitive to B0 field
inhomogeneities.
14.49. Answer e.
The 4-chamber long-axis view of the heart identifies a hyper-
intense lesion within the interatrial septum. Because gado-
linium has not been administered, the signal enhancement
cannot be due to gadolinium-induced T1 shortening. The
lesion’s signal intensity is similar to that of surrounding peri-
cardial fat and it spares the fossa ovalis, which suggests that
the lesion is benign. These are characteristic imaging features
of lipomatous hypertrophy of the interatrial septum.
14.50. Answer c.
Degeneration of a morphologically normal valve is the most
common cause of aortic stenosis, although patients with BAV
generally become symptomatic 1 to 2 decades earlier. BAV is
the most common congenital cardiac anomaly, with an esti-
mated prevalence of 1% to 2%, and has been associated with
aortic coarctation in at least 20% of patients. A few studies
have shown that MRI may be superior to transthoracic echo-
cardiography for identification of valve morphology.
14.51. Answer e.
Spin-lattice (T1) relaxation describes the ability of the pro-
ton to exchange energy with the lattice or other surrounding
molecular structures of the material. Because solids and semi-
solids have relatively low vibrational frequencies in relation
to the resonant frequency of the proton, the exchange rate is
relatively low, resulting in long T1 values. Spin-spin (T2) relax-
ation describes the loss of phase coherence as a result of local
perturbations of the magnetic field induced by individual
protons in proximity to one another. For semisolids, T2 is less
 302 • S e c tion I V: R eview Q uestions
than T1. Finally, T2* relaxation describes the effects of both
microscopic (ie, T2) and macroscopic perturbations of the
main magnetic field, so T2* is shorter than both T1 and T2.
14.52. Answer a.
A basal lateral distribution of subepicardial late gado-
linium enhancement is consistent with myocarditis.
Subendocardial late gadolinium enhancement is most
consistent with a myocardial infarction. Global, diffuse,
subendocardial late gadolinium enhancement has been
described in patients with amyloidosis, although the late
gadolinium distribution in amyloidosis can be quite vari-
able. Late gadolinium enhancement involving the RV
insertion points has been described in several disease states
including HCM and severe pulmonary hypertension.
Global diffuse subepicardial late gadolinium enhancement
would be quite unusual and not directly correlated with a
specific disease state.
14.53. Answer d.
The signal generated by a balanced SSFP pulse sequence is the
coherent sum of 2 constituent echoes. The complex nature
(ie, magnitude and phase) of the MR signal means that the
echoes must have zero phase relative to one another to ensure
that their signals combine constructively. B0 inhomogeneities
perturb this coherence, thereby producing signal cancellation.
The spacing between regions of maximum signal cancellation
(ie, dark bands) is constant for a given balanced SSFP pulse
sequence. The spacing, measured in units of hertz, is equal to
1/TR where TR is the pulse repetition time of the balanced
SSFP pulse sequence. Thus, a shorter TR will result in a larger
off-resonance bandwidth so that for a fixed B0 inhomogeneity
within the FOV, a shorter TR will produce a larger spacing
between dark bands.
14.54. Answer e.
Adenosine can lead to many adverse effects, including chronic
obstructive pulmonary disease and heart block. In general,
and depending on their severity, the pre-existence of these is
not considered a contraindication. Dipyridamole will worsen
and prolong these adverse effects and is the best answer of
the choices. Shellfish allergy is not an issue in cardiac MRI.
Caffeine can interfere with adenosine, but drinking decaf-
feinated coffee more than 8 hours before the examination is
not an absolute contraindication.
14.55. Answer c.
T2 weighting provides image contrast in which tissues with
long T2 values are bright and those with short T2 values are
dark. The imaging sequence is less sensitive to T1 effects,
and therefore tissues of different T1 values do not necessar-
ily contribute to image contrast. Fluids are characterized by
long T2 values and therefore appear bright on T2-weighted
images. The use of black blood imaging suppresses the signal
from moving blood. Thus, tissues with high fluid content will
appear bright on a T2-weighted image. Myocardial edema,
which shows high fluid content, can be detected as regions
of myocardium with increased signal relative to the remain-
der of the myocardium. In ischemic heart disease, myocar-
dial T2 signal can increase within 30 minutes of the onset of
ischemia. This patient had acute onset of chest pain and was
found to have a distal circumflex coronary artery occlusion
on catheterization, which was treated with a drug-eluting
stent the day before the MRI. The area of increased T2 sig-
nal was significantly greater than the area of enhancement
on LGE images. This discordant area of increased T2 signal,
but without enhancement, may represent myocardium spared
due to stenting.
14.56. Answer b.
Tamponade generally presents emergently and requires
urgent intervention. Pericardial rupture, effusions, and quan-
titative assessment of cardiac MR cine data are all relatively
straightforward to visualize and calculate. Contrast media is
not required for a diagnosis of tamponade physiology.
14.57. Answer d.
Cardiac MRI can accurately evaluate severe aortic stenosis.
The balanced SSFP images acquired through the aortic valve
plane illustrate an abnormal aortic valve with a flow distur-
bance suggestive of severe stenosis. No masses are identified.
In addition, cardiac MRI can identify other cardiac causes
of exertional dyspnea, such as constrictive and restrictive
cardiomyopathy.
14.58. Answer a.
Chemical shift of the first kind produces a misregistration
between voxels that contain only fat or water. Because fat
resonates at a lower frequency than water, voxels containing
only fat will be shifted relative to water along the frequency-
encoding direction. This produces dark and bright bands,
most notably at the border of organs that contain extraorgan
fat layers, such as the kidneys. Chemical shift of the second
kind occurs when a voxel contains both fat and water and
results in either constructive or destructive interference of the
signal from the 2 species, depending on the TE of the imag-
ing sequence. Judicious choice of TE can produce an image
in which the 2 signals are 180° out of phase or in phase. The
out-of-phase images display destructive interference between
fat and water, which outlines water-containing structures sur-
rounded by fat.
14.59. Answer e.
Free-breathing cardiac acquisitions eliminate the need for
breath holding and are therefore easily tolerated by patients.
However, unless accounted for by either prospective or retro-
spective motion correction methods, respiratory motion will
introduce artifacts into the reconstructed image. Although
most cardiac imaging planes are double oblique in their orien-
tation, the frequency-encoding axis is typically oriented along
the superior-inferior direction, with the phase-encoding
direction along the anterior-posterior axis, especially in
 14 . B oa r d -T y pe Q uestions a n d Answers  •
short-axis acquisitions. Under these conditions, the chest
wall moves more or less along the phase-encoding axis, pro-
ducing ghosting artifacts. Prospective motion-correction
methods include respiratory gating using either respiratory
bellows strapped to the patient’s chest or navigator echoes,
both of which are designed to monitor the breathing and trig-
ger data acquisition only during a given phase of the respira-
tory cycle. Retrospective methods involve processing the raw
image data to correct for translations and/or rotations during
the acquisition. The presence of respiratory motion–induced
artifacts, while undesirable, does not necessitate repeating
the image acquisition process. These artifacts are a function
of the magnitude of the motion and the location of the arti-
facts, especially if they are not within the anatomy of interest.
Finally, the movement of a surface coil on the anterior chest
of a patient in the supine position due to respiratory motion
will result in variations in the sensitivity profile of that coil
element in relation to the imaged anatomy, but artifacts aris-
ing from these effects are often secondary compared with
motion-induced ghosting.
14.60. Answer c.
Signal loss within the myocardium, as seen on late echo, gra-
dient echo images is characteristic of hemochromatosis effects
on the heart. Associated iron overload decreases the T2* of the
myocardium and produces increased signal loss as the echo
time of the gradient echo image increases. Multiecho gradi-
ent echo (ie, T2*-weighted) sequences are provided by most
MR scanner manufacturers and should be used when iron
overload is suspected. Amyloid heart disease has a different
appearance, of which abnormal nulling of the myocardium
is a hallmark feature. Restrictive cardiomyopathies, dilated
cardiomyopathies, and pericarditis do not have this appear-
ance. The global black appearance of both the myocardium
and liver are indicative of iron deposition.
14.61. Answer a.
The pericardium normally contains 15 to 50 mL of fluid;
therefore, it is normal to visualize a small amount of fluid
within the pericardium on cardiac MRI. It is not always
associated with pericardial thickening or inflammation.
Pericardial fluid is not always bright on black blood spin echo
imaging because of the potential for “sloshing” fluid to create
a flow void and appear black. Pericardial effusions can have
multiple causes and usually do not result in hemodynamic
compromise. Therefore, follow-up or sampling is not gener-
ally required unless the fluid is rapidly accumulating, hemor-
rhagic, or associated with a primary malignancy.
14.62. Answer b.
The images show a subendocardial perfusion defect on
adenosine stress images predominantly involving the sep-
tum. There is no corresponding perfusion defect with
rest nor enhancement on LGE images. These findings are
characteristic of myocardial ischemia. Normal myocar-
dium and myocardium with stress-induced cardiomyopa-
thy should have normal perfusion with stress and rest and
303
no enhancement on LGE images. Infarcted myocardium
should have matched perfusion defects with stress and rest
perfusion images and matched areas of enhancement on
LGE images. Myocarditis would not involve the subendo-
cardial surface.
14.63. Answer a.
Using as an example a double inversion-recovery, spin-echo,
black blood imaging sequence, suppression of the blood pool
signal is achieved by application of 2 180° inversion pulses
before the beginning of the data acquisition component of the
sequence. The first 180° RF pulse is a non–slice-selective or
hard RF pulse that effectively inverts all of the magnetization
of the tissue within the imaging volume. The pulse is known
as a hard pulse because no slice-selection gradient waveforms
are simultaneously applied during the application of the RF
pulse. A second slice-selective RF pulse is then applied to
reinvert magnetization of the tissue within the imaging vol-
ume such that the magnetization of the static tissue is now
at a state similar to that before the application of the initial
RF pulse. After a delay determined by the patient’s heart rate
and the T1 of the blood pool, a conventional multiecho spin
echo imaging sequence is applied to acquire the data from the
static tissue. The delay between the 2 180° RF pulses and the
imaging segment of the pulse sequence is chosen such that
the longitudinal magnetization component of the blood pool
signal is zero and does not see any of the RF pulses that are
part of the imaging component. The absence of any transverse
magnitude means that there will be no signal from the blood
pool in the image data. Adiabatic RF pulses are used because
of their improved slice-selection profiles.
14.64. Answer d.
Subendocardial late gadolinium enhancement is most con-
sistent with a myocardial infarction. Subepicardial distribu-
tion late gadolinium enhancement is the typical appearance
of myocarditis. Fabry disease has been described as having a
lateral wall subepicardial late gadoliniumenhancement pat-
tern. Amyloid heart disease is not described by any of these
features, having a different appearance, of which abnormal
nulling of the myocardium is a hallmark feature. The appear-
ance on LGE images is variable.
14.65. Answer b.
Under normal operating conditions, an increase in room air
humidity would not be detected by the naked eye. Although
smoke from a fire within the scan room or the facility is possi-
ble, it would most likely not be characterized by a rapid expan-
sion within the scan room. Superconducting MR scanners are
maintained in their superconducting state by the use of liquid
helium. The expansion ratio of liquid helium is approximately
1:700, meaning that 1 L of helium liquid will expand to 700
L of gas. If the temperature within the dewar containing the
liquid helium increases (eg, as a result of failure of the cryo-
gen cooling system), the liquid helium can transition from a
liquid to gas and expand accordingly. Modern MR scanners
are designed to exhaust this gas to the outside environment
 304 • S e c tion I V: R eview Q uestions
by means of a ventilation stack, but failure of this system
can result in the release of this gas into the scan room itself.
Although gaseous helium is colorless, the very low tempera-
ture of the gas will result in rapid condensation of water vapor
within the room air, producing the so-called white cloud.
14.66. Answer a.
Subendocardial late gadolinium enhancement is most con-
sistent with a myocardial infarction. In those with severe
coronary artery obstruction and LV dysfunction, the
absence of late gadolinium enhancement is indicative of
hibernating myocardium. Late gadolinium enhancement
in a subepicardial distribution is a typical appearance of a
nonischemic distribution. This appearance is not unique
to Fabry disease, but the pattern in Fabry disease has been
described as subepicardial late gadolinium enhancement in
the basal lateral wall. Amyloid heart disease has a different
appearance, of which abnormal nulling of the myocardium
is a hallmark feature; the appearance on LGE images is
variable.
14.67. Answer a.
Mitral valve prolapse is the most common cause of mitral
insufficiency and is estimated to occur in 2% to 3% of the
population. Acute mitral insufficiency generally occurs as a
result of endocarditis or rupture of the papillary muscles or
chordae tendineae, often in the setting of myocardial infarc-
tion. The presence of ischemic mitral regurgitation worsens
the prognosis of infarction. Pulmonary edema is a common
symptom in acute mitral insufficiency due to the sudden vol-
ume overload on the left atrium and LV.
14.68. Answer a.
In the absence of contrast-induced signal enhancement, lip-
ids appear hyperintense on T1-weighted, non–fat-suppressed,
black blood imaging. The lesion is most likely essentially
fat, providing the diagnosis of lipomatous hypertrophy.
Lipomatous hypertrophy of the interatrial septum is a benign
normal variant caused by hyperplasia of fat cells in the inter-
atrial septum. Patients are usually asymptomatic but can have
associated atrial tachyarrhythmias. Lipomatous hypertrophy
of the interatrial septum is typically a dumbbell-shaped mass
that spares the fossa ovalis and follows the signal characteris-
tics of fat on all imaging sequences.
14.69. Answer b.
Amyloid heart disease has a unique appearance on LGE
images, with abnormal nulling of the myocardium being
a hallmark feature. The appearance on LGE imaging is
variable but classically has been described as diffuse sub-
endocardial late gadolinium enhancement in a ringlike
pattern. Subendocardial late gadolinium enhancement is
most consistent with a myocardial infarction. In those with
severe coronary artery obstruction and LV dysfunction,
the absence of late gadolinium enhancement is indicative
of hibernating myocardium. Subepicardial distribution late
gadolinium enhancement is typical of myocarditis. Fabry
disease has been described as having a lateral wall subepi-
cardial late gadolinium enhancement pattern.
14.70. Answer c.
Ferrous objects can become projectiles by interaction with the
main (ie, B0) magnetic field if they are brought too close to
the MR scanner. The force of attraction between the object
and the B0 field is not influenced by the RF field. Artificial
stimulation of nerves, most notably peripheral nerves, can
result from the rapid switching of imaging gradients, which
is also not a factor of the RF field. Dielectric resonances can
produce nonuniform signal within the imaged anatomy, par-
ticularly at higher field strengths as the wavelength of the
RF electromagnetic wave approaches the dimensions of the
imaged anatomy. However, this is not a safety risk but rather
an image-quality concern. The oscillating electric and mag-
netic field components of the RF field can induce small cur-
rents in conducting materials such as tissue and implanted
devices. This in turn can induce resistive heating and, poten-
tially, burning. The amount of RF energy deposited from the
RF coil is quantified by the SAR; this parameter is used as
the most common measure of the potential for RF-induced
heating. Noise generated from the MR scanner is a result of
physical interaction between the gradient coils and inner bore
of the MR scanner, not the RF field.
14.71. Answer d.
Subendocardial late gadolinium enhancement is most con-
sistent with a myocardial infarction. A subepicardial distri-
bution of hyperintense signal on LGE imaging is the typical
appearance of myocarditis. Chronic myocarditis can be dis-
tinguished from acute myocarditis by the use of T2-weighted
edema sequences, which are often abnormally bright in the
acute phase. Amyloid heart disease has a different appearance,
of which abnormal nulling of the myocardium is a hallmark
feature; the appearance on late gadolinium enhancement is
variable.
14.72. Answer d.
Transposition of the great arteries describes the condition
in which the aorta arises from the morphologic RV and
the pulmonary artery arises from the morphologic LV. This
arrangement represents ventriculoarterial discordance. The
morphologic right atrium returns systemic venous blood to
the morphologic RV; similarly, the morphologic left atrium
returns pulmonary venous blood to the morphologic LV.
This arrangement represents atrioventricular concordance.
The pulmonary and systemic circulations are therefore in
parallel rather than in series, and unless there is a connection
between the 2 circuits, this arrangement is not compatible
with life.
14.73. Answer e.
A subepicardial distribution late gadolinium-enhancement pat-
tern is the typical appearance of myocarditis. Old myocarditis
 14 . B oa r d -T y pe Q uestions a n d Answers  •
can be distinguished from acute myocarditis by the use of T2-
weighted edema sequences, which are often abnormally bright
in the acute phase. Subendocardial late gadolinium enhance-
ment is most consistent with a myocardial infarction. Fabry dis-
ease has been described as having a lateral wall subepicardial late
gadoliniumenhancement pattern. Amyloid heart disease has a
different appearance, of which abnormal nulling of the myocar-
dium is a hallmark feature; the appearance on LGE images is
variable.
14.74. Answer a.
The balanced SSFP and LGE images in end systole show
LV apical myocardial hypertrophy with near-obliteration of
the mid cavity. There is a tiny apical pouch with associated
rimlike late enhancement (B), but no apical thrombus. No
features of LV outflow tract obstruction are present, such as
flow dephasing in the LV outflow tract, or systolic anterior
motion of the anterior leaflet of the mitral valve.
14.75. Answer c.
Angiosarcoma is the most common primary cardiac malig-
nancy. The most common appearance is a vascular mass in the
right atrioventricular groove. Although fibromas can occur
within the heart, they are benign tumors.
14.76. Answer b.
The evaluation of patients with transposition of the great
arteries includes assessment of biventricular function, assess-
ment of baffle function, and determination of either leaks or
obstruction. The Mustard procedure is an atrial switch pro-
cedure in which a baffle is placed to both redirect systemic
venous blood to the morphologic LV and then to the pulmo-
nary artery and also to redirect pulmonary venous blood to
the RV and then to the aorta. The Jatene procedure is an arte-
rial switch procedure and does not use baffles in the repair.
Although advancements in cardiac MRI have increased its
utility for assessment of valvular function, standard echo-
cardiography remains the primary imaging procedure for
assessing valvular function, and cardiac MRI would not be
indicated in this setting.
14.77. Answer e.
According to an American College of Radiology white paper
on safe MR practices, the procedure described in option e is
the correct method. Definitive care should not be adminis-
tered in the MR scan room because of the high probability
of non-MR personnel with potential projectiles entering the
scan room. In the case of a cardiac arrest, defibrillator equip-
ment is most likely not MR compatible.
14.78. Answer a.
The VENC is a parameter that encodes the maximum veloc-
ity within the imaging slice. If this value is too low, veloci-
ties greater than the VENC value will be aliased in the phase
image, mapping to the opposite sign phase angle. This is seen
305
as a bright-dark transition or banding in the phase image. A
larger VENC value can be set to avoid this problem but with
a subsequent loss of velocity sensitivity due to the larger range
of encoded velocities.
14.79. Answer d.
Methods described in a through c can be used to estimate the
mitral regurgitant volume, assuming that a second valvular
lesion is not present. Direct measurement of regurgitant flow
across the mitral valve with cine phase-contrast images could
also be performed but is often technically difficult because
of the prominent anterior-posterior excursion of the mitral
valve, as well as the frequent eccentric orientation of the
regurgitant jets. For the left side of the heart, cardiac output
is most commonly measured by calculation of the LV ejection
fraction.
14.80. Answer c.
Subendocardial late gadolinium enhancement is most con-
sistent with a myocardial infarction. A subepicardial distri-
bution of hyperintense signal on LGE imaging is the typical
appearance of myocarditis. Old myocarditis can be distin-
guished from acute myocarditis by the use of T2-weighted
edema sequences, which are often abnormally bright in the
acute phase. Amyloid heart disease has a different appearance,
of which abnormal nulling of the myocardium is a hallmark
feature; the appearance on LGE imaging is variable. This case
illustrates an unusual presentation of the so-called “midwall
variant” of apical ballooning (or takotsubo) cardiomyopathy.
This patient recovered to normal function without recurrence
at follow-up.
14.81. Answer c.
The axial balanced SSFP images show a dilated RV with
dyskinesis and associated aneurysmal outpouching of the
basal RV free wall. Late gadolinium enhancement is not
pictured here (and was not present in this case), and the tri-
cuspid valve is not visualized on these images.
14.82. Answer d.
The 4 MR safety zones are as follows: Zone I, regions that
are freely accessible to the general public; Zone II, interface
between the publicly accessible uncontrolled Zone I and the
strictly controlled Zone III; Zone III, restricted zone with
access controlled by and under the supervision of MR person-
nel; Zone IV, MR scanner room itself.
14.83. Answer a.
Although administration of intravenous gadolinium con-
trast may be useful in delineating the systemic arterial and
pulmonary arterial tree, as well as the systemic and pulmo-
nary venous return, contrast is not required in every situ-
ation. Balanced SSFP sequences can be useful to delineate
the anatomy and the baffle pathways using off-axis imag-
ing planes that are developed during the examination.
 306 • S e c tion I V: R eview Q uestions

The images are from a patient with D-transposition of the
great arteries after an interatrial baffle (Mustard) proce-
dure. The entire examination was performed using bal-
anced SSFP imaging sequences in different planes and
allowed assessment of biventricular size and function and
of the integrity of the interatrial baffle.
14.84. Answer a.
The diagnostic criteria for arrhythmogenic RV cardio-
myopathy require the presence of dyskinesis or dyssyn-
chrony of the RV. Additional diagnostic criteria include
RV dilatation and decreased contractility; however, these
are not required to make the diagnosis. Although RV late
gadolinium enhancement has been reported to correlate
with fibrofatty replacement on histopathologic analysis
of endomyocardial biopsy, the presence of late gadolinium
enhancement is not included in the current diagnostic
criteria.
14.85. Answer c.
Secondary causes of tricuspid insufficiency are most com-
mon and include pulmonary hypertension and intrinsic RV
abnormalities. Carcinoid syndrome results in plaque deposi-
tion on right-sided heart valves. The right side of the heart is
predominantly affected because of its close proximity to the
liver, which is the source of the 5-hydroxytryptamine thought
to be responsible for the valvular manifestations of carcinoid
syndrome. Ebstein anomaly is a rare congenital lesion with
apical displacement of septal tricuspid valve leaflets leading to
atrialization of the RV and severe tricuspid insufficiency. The
mitral annulus is contiguous with the aortic valve apparatus,
but the tricuspid annulus is distinct from the pulmonic valve
apparatus. Cardiac MRI is often the best method to visualize
right-sided cardiac structures, including valvular heart disease.
Decreasing the TR interval increases the duty cycle of the
pulse sequence, effectively increasing the SAR since the
units of SAR are Joules per kilogram-second. Since time is
in the denominator, a lower TR will increase SAR. SAR
also is proportional to the square of the magnetic field
strength so that a doubling of the B 0 field from 1.5T to 3.0T
will result in a theoretical quadrupling of the amount of
SAR deposited in the patient.
14.88. Answer b.
Patients with acute pericarditis typically have chest pain and
demonstrate considerable pericardial thickening and enhance-
ment as a result of pericardial inflammation. Constriction
may not be present, and respirophasic changes may therefore
be absent. Fatigue and shortness of breath are more typical of
patients with pericardial constriction.
14.89. Answer c.
The LeCompte maneuver is a surgical technique used in the
arterial switch operation for transposition of the great ves-
sels. It involves placing the pulmonary arteries anterior to the
aorta. Figure 14.A89 shows a patient with D-transposition of
the great arteries who has undergone an arterial switch proce-
dure with the LeCompte maneuver.

14.86. Answer a.
SAR is a measure of RF power delivered to the body. RF
energy deposited in the body is dissipated in the form of
Ohmic heating due to the resistive properties of human tis-
sue. RF energy is below the ionization threshold of elements
and is therefore, by definition, a form of nonionizing radia-
tion. Spatial resolution, temporal resolution, and SNR are
not directly related to SAR.

14.87. Answer a.
SAR is a measure of the amount of absorbed RF power in
a given mass of tissue and is directly proportional to the
amount of RF power transmitted into the patient. Receive-
only RF coils do not supply RF energy to the patient and
therefore do not contribute to SAR. Increasing the RF
flip angle increases the amount of power transmitted to
the patient and hence SAR. The addition of RF prepara-
tion pulses such as fat saturation or inversion pulses will
increase the SAR with all other parameters being equal.
Figure 14.A89
14.90. Answer a.
Both short- and long-axis balanced SSFP images show
hypertrabeculation in the LV. There is a region of increased
signal enhancement within the septal wall of the LV on the
4-chamber LGE image. However, the most prominent fea-
ture in this image is also the trabeculation of the LV.
 14 . B oa r d -T y pe Q uestions a n d Answers  • 307

14.91. Answer a. 14.97. Answer e.

Gadolinium chelate is a T1-shortening agent. For concentra-
tions typically used in routine MRI (0.1-0.2 mmol/kg body
weight), perfusion of gadolinium contrast agent into the myo-
cardium from the blood pool will decrease the T1 of this tissue.
At concentrations of 0.1 to 0.2 mmol/kg, T2 relaxation values
are not generally affected by the uptake of gadolinium con-
trast. Excessive amounts of contrast can result in T2*-induced
signal loss. However, these concentrations are not used in rou-
tine diagnostic imaging.
14.92. Answer d.
Signal averaging affects the SNR of the image and not the
inversion time (TI) of the tissue and is therefore independent
of TI choice. Gadolinium contrast medium is a T1-shortening
agent; therefore, an increased dose will alter the T1 of tissue in
which contrast is present. This will directly affect the choice
of the optimal TI value. The concentration of contrast agent
is directly affected by the kinetics of the wash-in and wash-out
of the agent, which is a function of time. If the TI is too short,
the null point of normal myocardium may not be reached,
resulting in incomplete signal suppression and poor infarct-
to-normal myocardial contrast. An increase in field strength
from 1.5T to 3.0T will increase the T1 of gadolinium contrast
agents and most tissues. TI values must therefore be modi-
fied (increased) to account for T1 lengthening with increasing
field strength.
14.93. Answer c.
Partial anomalous pulmonary venous connection refers to
the connection of at least 1 but not all of the pulmonary
veins to the right-sided chamber. This situation leads to a
left-to-right-sided shunt at the atrial level. If the size of
the shunt is substantial, this can lead to right-sided cham-
ber enlargement. Therefore, in addition to identifying the
number and location of the anomalous pulmonary veins, it
is also important to interrogate RV function and quantify
RV volumes.
Cardiovascular MRI is most useful for accurately measur-
ing myocardial wall thickness. Reversible defects evaluated by
nuclear imaging, but not cardiac MRI, have prognostic value in
HCM. Cardiac MRI is able to accurately assess valvular pathol-
ogy and coronary artery anatomy, but its best utility in HCM
is in the assessment of wall thickness and the identification of
myocardial fibrosis.
14.98. Answer b.
Triple inversion recovery imaging sequences generate fat-
suppressed, typically T2-weighted contrast. Regions of high
signal intensity are indicative of fluid. In this instance, the
hyperintense signal in the posterolateral LV wall in the tri-
ple inversion recovery image is due to an acute infarction.
Hyperintense signal on the LGE image indicates a region of
infarction (ie, ischemia).
14.99. Answer c.
The most common arrangement in patients with anomalous
pulmonary venous return is drainage of the right upper pulmo-
nary vein into the SVC. Therefore, a successful MRI examina-
tion must include appropriate imaging of this pathway. It is also
important to assess for other congenital anomalies. In particu-
lar, sinus venosus atrial septal defect is associated with anoma-
lous pulmonary venous drainage of the right upper pulmonary
vein into the SVC in 80% to 90% of cases. The importance of
imaging this vessel structure is shown in Figure 14.A99, a bal-
anced SSFP image in a coronal plane at the level of the SVC
demonstrating partial anomalous pulmonary venous drainage
of the right upper and right middle lobe pulmonary veins to
the SVC.

14.94. Answer d.
The RV dilatation, dyskinesis, and associated RV free wall
aneurysms seen in this case are characteristic of arrhythmo-
genic RV cardiomyopathy.

14.95. Answer b.
Myxomas account for approximately 50% of primary cardiac
masses. They typically occur in adults aged 30 to 60 years and
are more common in women. Most myxomas (75%) occur in
the left atrium, and another 15% to 20% occur in the right
atrium.

14.96. Answers:
a. Ascending aorta
b. Sinus of Valsalva
c. Aortic valve
d. Stomach Figure 14.A99
 308 • S e c tion I V: R eview Q uestions
14.100. Answers:
a. Superior vena cava
b. Brachiocephalic artery
c. Left common carotid artery
d. Left subclavian artery
14.101. Answer b.
End-diastolic (A) and end-systolic (B) 4-chamber long-axis
balanced SSFP images show biventricular basal and mid
hyperkinesis and apical akinesis and dilation. The 4-cham-
ber long-axis LGE image (C) shows no enhancement to sug-
gest myocardial fibrosis. These findings are characteristic of
apical ballooning syndrome, also known as stress-induced
cardiomyopathy or takotsubo cardiomyopathy.
14.102. Answer c.
The appearance of a dark line identifying the boundary
of both organs and masses is a result of the chemical shift
effect of the second kind. The dark line occurs in voxels that
contain both fat and water (ie, tissue) and is a result of sig-
nal cancellation between the 2 signal species. Lipomas are
smooth, homogeneous, encapsulated fatty masses. They have
high signal on T1-weighted images and should demonstrate
signal drop-out when fat saturation is applied. Lipomas will
have high signal intensity on balanced SSFP images, similar
to the adjacent epicardial fat. Due to the finite size of each
voxel, voxels along the periphery of the lipoma will contain
signal from both the mass and the surrounding tissue. For
lipomas, these voxels are most likely to contain both fat and
water, resulting in the occurrence of the chemical shift of the
second kind, which is manifested as a dark rim around the
homogeneous mass.
14.103. Answer a.
Pulmonic regurgitation is the most common complication
after repaired tetralogy of Fallot. The degree of RV volume
Figure 14.A107
overload can be accurately and serially assessed and quanti-
fied by cardiac MRI. This can be used to determine when to
replace the pulmonic valve before RV dysfunction becomes
irreversible.
14.104. Answer a.
In total anomalous pulmonary venous connection, the
pulmonary veins converge on a pulmonary venous conflu-
ence that is usually located superior and posterior to the
left atrium. In most cases, this blood drains into the SVC
or innominate vein (supracardiac drainage). Supracardiac
drainage of the pulmonary veins occurs in approximately
36% of cases, drainage directly into the coronary sinus
occurs in 15% of cases, drainage directly into the right
atrium occurs in 14% of cases, and drainage into the infe-
rior vena cava or hepatic veins (infracardiac) occurs in 13%
of cases.
14.105. Answers:
a. Either left superior vena cava or left upper pulmonary
vein
b. Main pulmonary artery
c. Superior vena cava
14.106. Answer d.
Four-chamber, long-axis, end-diastolic, balanced SSFP (A),
perfusion (B), and LGE images (C) show diffuse myocar-
dial thickening, diffuse subendocardial enhancement, and
a large LV thrombus that does not enhance. These findings
are consistent with endomyocardial fibrosis in a patient
with eosinophilic myocardial disease.
14.107. Answer b.
Scimitar syndrome is a rare anomaly characterized by con-
nection of all the right pulmonary veins to the inferior
 14 . B oa r d -T y pe Q uestions a n d Answers  • 309

vena cava. Usually also present is hypoplasia of the ipsilat-
eral lung and pulmonary artery. The term scimitar refers to
radiographic shadow that resembles the shape of a Turkish
sword. The lower part of the right lung is perfused by sys-
temic arteries from the abdominal aorta. Scimitar syn-
drome rarely involves the left lung. An example of scimitar
syndrome is shown in Figure 14.A107: volume-rendered
images obtained from gadolinium-enhanced MR angiog-
raphy. Note that all the right pulmonary veins coalesce to
drain into the inferior vena cava, which appears as the shape
of a scimitar.
14.108. Answers:
a. Superior vena cava
b. Right pulmonary artery
c. Azygous vein
d. Ascending aorta
e. Main pulmonary artery
f. Descending thoracic aorta
g. Spinal cord with surrounding spinal fluid
14.109. Answer a.
Hemangiomas are benign vascular tumors that can occur
in any cardiac chamber and can be endocardial, epicar-
dial, or intramural. They are classified by the size of their
vascular channels as capillary, cavernous, or arteriovenous
hemangiomas.
14.110. Answer b.
The 2- and 4-chamber long-axis balanced SSFP images in
end diastole show left ventricular noncompaction (LVNC)
with sparing of the basal inferolateral and basal and mid sep-
tal segments. The 4-chamber, long-axis, LGE image shows
subepicardial and midmyocardial enhancement of the mid
anteroseptal and inferoseptal wall. LVNC is newly recog-
nized as a primary genetic cardiomyopathy. However, some
authorities consider LVNC an unclassified cardiomyopathy
and possibly a phenotypic variant of other cardiomyopa-
thies, including HCM. Although different imaging criteria
are used for diagnosing LVNC by cardiac MRI, a ratio of
noncompacted-to-compacted myocardium of greater than
2.3 during diastole is generally accepted as establishing the
diagnosis.
c. Right inferior pulmonary vein
d. Left atrium
e. Left superior pulmonary vein
f. Left inferior pulmonary vein
14.113. Answer b.
Subendocardial late gadolinium enhancement is most
consistent with a myocardial infarction. A subepicardial
distribution of hyperintense signal on LGE imaging is
the typical appearance of myocarditis. Old myocarditis
can be distinguished from acute myocarditis by the use
of T 2 -weighted edema sequences, which are often abnor-
mally bright in the acute phase. Amyloid heart disease
has a different appearance, of which abnormal nulling
of the myocardium is a hallmark feature; the appearance
on LGE imaging is variable. This case illustrates a severe
dilated cardiomyopathy without abnormal late gadolin-
ium enhancement.
14.114. Answer d.
The role of cardiac MRI in the assessment of patients
with coarctation of the aorta is to locate the site of coarc-
tation and then to assess its functional significance. The
functional significance of a coarctation refers to its effects
on the heart and vasculature. A significant coarctation is
associated with pressure overload of the LV, leading to con-
centric LV hypertrophy. In a hemodynamically significant
coarctation, the only way blood can be received distal to

14.111. Answer c.
In patients with bicuspid aortic valve, 5% will have coarcta-
tion of the aorta. However, in patients with coarctation of
the aorta, 25%-45% will have a bicuspid aortic valve. In some
series, up to 80% of patients with coarctation of the aorta have
been reported to have bicuspid aortic valve. However, no stud-
ies have reported coarctation in more than 90% of patients
with bicuspid aortic valve.

14.112. Answers:
a. SVC and right atrial junction
b. Right superior pulmonary vein Figure 14.A114
 310 • S e c tion I V: R eview Q uestions
the site of coarctation is via systemic arterial collateral ves-
sels. These are usually provided by the internal mammary
artery, the intercostal arteries, or directly from the sub-
clavian artery; these can all be delineated with the use of
MR angiography. The presence of retrograde flow in these
vessels (ie, flow in the opposite direction than expected),
as demonstrated by phase-contrast imaging, can allude to
the presence of a hemodynamically significant coarctation.
Formation of venous collaterals is not associated with the
pathophysiology of this lesion. Figure 14.A114—a gadolin-
ium-enhancement MR angiography data set that has been
postprocessed to produce a volume-rendered image—illus-
trates these effects. A severe coarctation at the juxtaductal
location can be seen. Note the enlarged intercostal and
internal mammary arteries due to collateral blood flow.
14.115. Answers:
a. Tricuspid annulus
b. Right atrium
c. Coronary sinus
d. Left ventricle
e. Descending thoracic aorta
14.116. Answer a.
Surveillance imaging in patients who have undergone
repair for coarctation of the aorta is focused on the evalu-
ation of complications of the procedure that may require
further surgical intervention. Such complications include
restenosis with concomitant hemodynamic effects, as dem-
onstrated by persistence or development of concentric LV
Figure 14.A119
hypertrophy or new systemic arterial collateral arteries.
Aneurysmal dilation at the site of repair can be seen as a
postoperative complication. The type of complication is
predicated by the type of repair. As such, part of the compre-
hensive MRI approach for these patients includes a review
of the exact surgical procedure performed. Assessment for
the presence or absence of a bicuspid aortic valve should
be achieved on the index imaging study (ie, the first MRI
examination) and should not be performed as part of sur-
veillance imaging. It is, however, important to assess aor-
tic valve function in the setting of a bicuspid aortic valve
because hemodynamically significant stenosis or regurgita-
tion will influence clinical management.
14.117. Answer b.
Ebstein anomaly is a primary abnormality of the tricuspid
valve. A failure of the delamination of the tricuspid valve leaf-
lets leads to apical displacement of the septal and posterior
leaflets. The anterior leaflet is variably mobile and is classically
described as sail-like. The consequence of this arrangement is
variable atrialization of the RV. Most patients have significant
tricuspid insufficiency.
14.118. Answers:
a. Sternal wires
b. Left pleural effusion
14.119. Answer a.
The RV has a complicated geometric arrangement. The
major issues with using the short-axis imaging plane, as
 14 . B oa r d -T y pe Q uestions a n d Answers  •
is traditionally done for assessment of LV volumes, is iden-
tification of the atrioventricular annular plane. This is espe-
cially important in the setting of congenital heart diseases
that show atrialization of the RV such as Ebstein anomaly,
which makes delineation of the annular plane in the short
axis extremely difficult and fraught with error. For this rea-
son, when the primary indication for a cardiac MRI exami-
nation is to assess the RV, the convention is to use a standard
axial plane. Identifying the tricuspid annular plane is easier
in this arrangement. More importantly, setting up the imag-
ing plane will be consistent on serial follow-up examinations,
thereby reducing sources of potential measurement errors.
In these patients, the RV volume measurements and changes
over time are used to make crucial management decisions, so
it is additionally important that all tracings of the current
and prior studies be reviewed to ensure that they are being
performed systematically in the same way. These points are
illustrated in Figure 14.A119, a balanced SSFP axial image
in a patient with Ebstein anomaly. Note that this plane is
easily reproducible, and for the purposes of measurement of
RV volumes, the annulus is easily identified.
14.120. Answer c.
Based on the signal characteristics of the mass in these images,
the mass is a myxoma. Myxomas are typically rounded atrial
masses that arise from the interatrial septum, usually near
311
the fossa ovalis, in the left atrium, but they can be found
in any chamber. Myxomas are generally isointense on T1-
weighted images but may be heterogeneous due to calcifica-
tion or hemorrhage. On T2-weighted imaging, myxomas are
typically hyperintense due to their myxoid stroma. Balanced
SSFP cine images are typically hyperintense compared with
myocardium but hypointense compared with the blood pool.
Late gadolinium-enhancement also can be homogeneous and
intense.
14.121. Answer c.
Pulmonic stenosis is congenital in more than 95% of cases,
whereas most cases of pulmonic insufficiency result from
prior intervention (repair of tetralogy of Fallot or valvotomy
for pulmonic stenosis). Dilatation of the left pulmonary
artery is a classic finding of pulmonic stenosis and is thought
to occur more commonly than right pulmonary artery
dilatation because of the direct path from the pulmonic
valve toward the left pulmonary artery. RV size and func-
tion measurements are slightly more difficult and slightly
less reproducible than LV volumetrics; however, MRI is the
standard for assessment of both RV and LV size and func-
tion, and this information can be very useful when consid-
ering pulmonic valve replacement surgery. Rheumatic heart
disease typically involves the left-sided valves, although any
valve can be involved.

t denotes table; b denotes box; f denotes figure
A k-space-based parallel imaging
ACR. See American College of Radiology
ACR-assigned NSF risk groups for
GBCM, 253t
acute flare of chronic pericarditis, 150f
acute flare of chronic recurrent pericarditis
(case study), 150–151
acute myocarditis, 128f
acute myocarditis with fibrosis (case study),
130–131
acute myopericarditis (case study),
148–149
aliasing, 47–50, 61, 231–233, 238, 240,
241
American College of Cardiology, 83, 199
American College of Radiology (ACR),
247, 248, 252, 253
American Heart Association, 199
American Heart Association Writing
Group on Myocardial Segmentation
and Registration for Cardiac
Imaging, 17
aneurysm with thrombus, 90–93
angiosarcoma (case study), 178–179
aorta
coronal view, 38–39f
described, 26
aortic arch, 26
aortic imaging, 38–44
aortic insufficiency with bicuspid
aortic valve, 204f
case study, 205
aortic insufficiency with LV enlargement,
206f
case study, 207
aortic stenosis with dilation of
ascending aorta, 208f
case study, 209
aortic valve (AV), 23–24, 42–44
aortic valve disease, 203
aortic valve plane, 43–44
apical ballooning cardiomyopathy. 132f
case study, 133
apical HCM (case study), 116–117
apical obstructive HCM, 116f
arrhythmogenic right ventricular
cardiomyopathy, 118f
case study, 119
artifacts
aliasing, 231–232. See also aliasing
banding on balanced SSFP, 237–238f
ECG gating mistriggers, 232, 234, 235
flow-related artifacts, 236–237
gating during chemical stress, 14
gradient decay or fall-off, 232, 233
gradient switching, 12, 13
image-based parallel imaging
reconstruction artifact, 238–240
incomplete myocardial suppression on
LGE imaging, 244f, 245
I NDE X
bicuspid aortic valve (case study), aortic insufficiency with bicuspid aortic
artifact, 240–241, 240f 196–197 valve, 204–205
lightning flash artifact, 242 bicuspid aortic valve with ascending aortic aortic insufficiency with LV
magnetohydrodynamic effect, 8–10 dilation and aortic regurgitation (case enlargement, 206–207
MR-induced ECG artifacts, 7–14 study), 200–201 aortic stenosis with dilation of the
perfusion dark-rim enhancement bicuspid aortic valve without ascending ascending aorta, 208–209
artifact, 241 aortic dilation (case study), apical ballooning cardiomyopathy,
peripheral photo-pulse sensor, 14 198–199 132–133
radiofrequency (RF) body coil blood inversion time (sequence-specific apical HCM, 116–117
switching, 11–12 variable), 54–56 arrhythmogenic right ventricular
respiratory (breathing) motion artifact, blood pool, 45, 48 cardiomyopathy/dysplasia, 118–119
234–236 bright (blood pool signal), 48 bicuspid aortic valve, 196–197
RF zipper, 232, 234 bright-exogenous contrast agent (blood bicuspid aortic valve with ascending
sternal wires/clips, 12, 14 pool signal), 48 aortic dilation and aortic
susceptibility-induced fat saturation regurgitation, 200–201
failure, 242–243, 245 C bicuspid aortic valve without ascending
susceptibility-induced signal loss, 237 “candy cane” (sagittal oblique) view, aortic dilation, 198–199
triboelectric effect, 10 40, 43 cardiac amyloidosis, 134–135
assignment of 17 myocardial segments cardiac amyloidosis, 134f cardiac amyloidosis with mitral
to territories of LAD, RCA, and case study, 135 and tricuspid regurgitation,
LCX, 83f cardiac amyloidosis with mitral and 218–219
atria tricuspid regurgitation, 218f cardiac sarcoidosis, 140–141
described, 18 case study, 219 cardiac siderosis, 136–137
identifying and distinguishing of by cardiac anatomy, 16–26 coarctation of the aorta,
MRI, 18b cardiac cycle 194–195
AV. See aortic valve components of, 7 congenitally corrected transposition of
axial, coronal, and sagittal localizer planes, events of (left heart), 3–4 the great arteries, 189
29f MRI characteristics of, 5 constrictive pericarditis, 146–147,
axial balanced SSFP image demonstrating cardiac function, pulse sequences for 152–153
small, low-signal, rounded mass, 166f imaging of, 59–72 constrictive physiology on
axial cine images, 35 cardiac imaging modules, free-breathing imaging, 147
axial images demonstrating thickening of 74–80 DCM with fibrosis, 126–127
interatrial septum, 164f cardiac masses DCM without fibrosis, 124–125
axial view of RV, 37f case studies, 163–181 Ebstein anomaly, 192–193,
imaging of, 79 222–223
B cardiac mass protocol, 79 endomyocardial fibrosis, 138–139
B0 fringe field, 247 cardiac morphology, pulse sequences for false aneurysm, 92–93
balanced gradient echo, 46, 47, imaging of, 51–59 findings of infarction, 100–101
62, 76, 237 cardiac MRI, advantages of, 16 findings of ischemia, 102–103
balanced gradient echo (balanced SSFP) cardiac phases (sequence-specific variable), hemangioma, 176–177
cine, 52–53 47, 53, 62, 63 intracardiac thrombus,
balanced gradient echo image, short-axis cardiac physiologic waveforms, 4 170–171
view, 53f cardiac sarcoidosis, 140f ischemic cardiomyopathy, 94–97
balanced SSFP images case study, 141 isolated LV noncompaction,
axial multislice of tetralogy of Fallot, cardiac siderosis, 136f 120–121
184f case study, 137 left anterior descending artery territory,
of congenitally corrected transposition cardiac valve planes, 43 transmural extent with microvascular
of great arteries, 188f–189f cardiac valves, 23–24 obstruction, 84–85
demonstrating prominent eustachian cardiomyopathies, 94–97, 105, lipoma, 174–175
valve, 168f 132–133 lipomatous hypertrophy of the
multislice through bicuspid aortic valve, case studies interatrial septum, 164–165
196f acute flare of chronic recurrent LV noncompaction with decreased
of transposition of great arteries after pericarditis, 150–151 systolic function, 122–123
Mustard procedure, 186f acute myocarditis with fibrosis, mitral insufficiency, 210–211
balanced steady-state free precession 130–131 mitral stenosis, 214–215
(SSFP), 74, 145, 184, 191, 203 acute myopericarditis, mitral valve prolapse, 212–213
ballooning syndromes, 105. See also apical 148–149 myocardial ischemia and infarction,
ballooning cardiomyopathy aneurysm with thrombus, 85–103
banding on balanced SSFP images, 238f 90–93 myocarditis, 128–129
case study, 237 angiosarcoma, 178–179 myoxma, 172–173
313

case studies (Cont.)
neoplasms, 172–181
normal variants of cardiac masses,
164–169
parachute mitral valve with mitral
stenosis, 216–217
partial anomalous pulmonary venous
return, 190–191
pericardial abscess, 160–161
pericardial constriction, 158–159
pericardial cyst, 156–157
pharmacologic stress testing, 98–99
prominent crista terminalis,
166–167
prominent eustachian valve,
168–169
pulmonic stenosis, 226–227
recurrent constriction after subtotal
pericardiectomy, 154–155
reverse curve HCM, 108–109
right coronary artery territory,
transmural infarction with MVO,
edema, and right ventricular
infarction, 88–89
severe pulmonic regurgitation and
pulmonary artery aneurysm, 224–225
sigmoid nonobstructive HCM, 114–115
sigmoid obstructive HCM, 112–113
sigmoid obstructive HCM with SAM,
110–111
simple pericardial effusion, 144–145
subepicardial and circumflex artery
territories, 86–87
tetralogy of Fallot, 184–185
transposition of the great arteries,
186–187
tricuspid insufficiency, 220–221
true aneurysm, 90–91
centric view order encoding
(sequence-specific variable), 59–60
cine (imaging mode), 48
cine phase contrast, 60–62, 195
classification and subtypes of nonischemic
myocardial disease, 106
coarctation of the aorta, 194f
case study, 194–195
sagittal oblique (“candy cane”) view used
for evaluation of, 40
congenital heart disease
case studies, 183–201
imaging of, 80
congenital heart disease protocol, 80
congenitally corrected transposition of the
great arteries (case study), 189
constrictive pericarditis (case study),
146–147, 152–153
constrictive physiology on free-breathing
imaging (case study), 147
constructive pericarditis,
146f, 152f
conventional axial right ventricular cine
view, 35, 38
D FDA. See US Food and Drug
dark (blood pool signal), 48
data acquisition
components of for image reconstruction,
47
segmented data acquisition, 3, 47
volumetric nature of, 246
DCM. See dilated cardiomyopathy
DCM with fibrosis, 126f
case study, 127
DCM without fibrosis, 124f
case study, 125
decision tree for determining cardiac mass
type, 163
314
dilated cardiomyopathy (DCM). See also
DCM with fibrosis; DCM without
fibrosis
case study, 124–127
imaging of, 105
Dixon, Thomas, 72
Dixon-based data reconstruction method,
72
Dixon fat and water separation, 72
dobutamine stress testing, 14, 83, 99
double inversion recovery, 53–54, 56, 76
double inversion recovery image, short-axis
view, 56f
dynamic perfusion short-axis images, 100f
E pericardial effusion, 178f
Ebstein anomaly, 222f
case studies, 192–193, 222–223
diagnosis of, 35
of tricuspid valve, 193f
ECG (electrocardiogram), 7
ECG gating
defined, 3
patient preparation for, 6–7
purposes in using, 3b
segmented data acquisition and, 3
ECG gating mistriggers, 232, 234, 235
ECG lead placement, 7, 8, 11
ECG noise, sources of in MR imaging, 9t
ECG reference signal, 9
ECG waveform from healthy volunteer,
10, 11
ECG waveform from lead II, 7, 9
echocardiography, 16, 27, 95, 99, 105, 121,
141, 145, 183, 185, 191, 193, 199, 201,
203, 211
echo formation, 45, 46–47
echo trains (data acquisition), 47
effects of NSF in patient who received
gadolinium-based contrast media,
252f
Einthoven, Willem, 6
Einthoven configuration, 6
Einthoven lead arrangement, 5–6
Einthoven's triangle, 6
electrical activity, measurement of, 5–6
end-diastolic and end-systolic balanced
SSFP long-axis images, 90
endomyocardial fibrosis, 138f
case study, 139
European Society for Magnetic Resonance
in Medicine and Biology (ESMRMB),
254
examples from patients with and without
hemocromatosis, 71f
F schematic representation of in
false aneurysm (case study), 92–93
fat inversion time (sequence-specific
variable), 56
fat saturation, 45, 242
fat-suppressed, T1-weighted axial
image, 59
Administration
fibrosis along midmyocardial septum,
127f
field of view (FOV), for imaging
parameters, 16, 50
findings of infarction (case study),
100–101
findings of ischemia (case study), 102–103
first controlled mode (MR scanner
operational mode), 249–250
flow encoding (phase contrast), 45
flow-encoding direction (sequence-specific
variable), 61
• I n de x
flow-related artifacts, 236f
described, 236–237
4-chamber images
balanced steady-state, gradient echo,
perfusion, and late gadolinium-
enhancement, 234f
demonstrating mass in right atrium, 170f
long-axis and short-axis views
demonstrating mass in lateral wall of
LV, 180f
long-axis cine series, 5f
long axis views acquired with 3 separate
imaging sequences, 174f
long-axis views demonstrating presence
of bulky right atrial mass and small
long-axis views demonstrating round
left atrial mass attached to interatrial
septum, 172f
of LV, long-axis, 27, 28f, 29, 31f, 33f,
34f–36f
valve panes, 43f
with wide FOV, 19f
FOV. See field of view
G implanted devices, 250–251
gadolinium-based contrast media
(GBCM), 251–253
gadolinium contrast-enhanced MR
angiography of bicuspid aortic valve,
200f
gating during chemical stress, 14
GBCM. See gadolinium-based contrast
media
GFR. See glomerular filtration rate
glomerular filtration rate (GFR), 252
grade of mitral valve regurgitation vs
regurgitant volume derived from
MRI, 213t
gradient decay or fall-off, 233f
described, 232
gradient echo, 47
gradient echo (balanced and spoiled)
cine, 59
gradient fields, 247–248
gradient switching, 9, 12–14
gradient switching interference in ECG
waveforms, 13f
GRAPPA (rapid imaging), 48
great vessels, 26
H isolated LV noncompaction, 120f
HCM. See hypertrophic cardiomyopathy
heart
images of with selected anatomical
landmarks identified, 20f–22f
cross-section, 16
hemangioma (case study), 176–177
hemochromatosis, 70, 71, 125, 137
hybrid (spatial-temporal) (rapid imaging),
48
hypertrophic cardiomyopathy (HCM),
105–108
I late gadolinium enhancement (LGE), 53,
ICDs. See implantable cardioverter
defibrillators
IEC. See International Electrotechnical
Commission
IEC modes of operation and selected
parameter limits for MRI, 250t
image-based parallel imaging (SENSE)
(rapid imaging), 47–48, 238
image-based parallel imaging
reconstruction artifact, 238–240
imaging components
balance gradient echo cine, 52
cine phase contrast, 61
double inversion recovery, 56
late gadolinium enhancement, 55
perfusion, 63
quantification of T1 relaxation
time, 66
quantification of T 2* relaxation
time, 70
quantification of T 2 relaxation
time, 68
spin echo T1 weighted, 58
spoiled gradient echo cine, 54
tagging, 65
3D MR angiography, 59
triple inversion recovery, 57
imaging mode, 48
imaging parameters, 48–51
imaging planes
standard ones in cardiac MR imaging,
27–44
used to characterize LV, 28f
used to characterize RV, 36f
implantable cardioverter-defibrillators
(ICDs), 250–251
incomplete myocardial suppression on
LGE imaging, 244f
described, 245
infarction, findings of (case study),
100–101
infarction short-axis views,
67, 69
infarction within lateral wall of LV
(short-axis view), 67, 69
inferior vena cava, 26
infiltrative cardiomyopathy, 105
interference, sources of, 7, 9
International Electrotechnical
Commission (IEC), 249–250
International Society for Magnetic
Resonance in Medicine (ISMRM),
254
intervalvular fibrosa, 23, 25
intracardiac thrombus (case study),
170–171
inversion recovery, 45
ischemia, findings of (case study),
102–103
ischemic cardiomyopathy,
94–97
case study, 121
K
k-space-based parallel imaging
(SMASH and GRAPPA) (rapid
imaging), 48
k-space-based parallel imaging artifact,
240f
described, 240–241
kt-BLAST (rapid imaging), 48
L
LA. See left atrium
55, 72
late gadolinium-enhancement images,
long-axis balanced SSFP and, 92f
late gadolinium-enhancement images
with Dixon-based data reconstruction, 73f
imaging key points, 77b
long-axis balance SSFP, 92f
of normal and infarcted
myocardium, 55
short-axis images, 84f, 86f, 88f
viability module, 74, 76t, 77

left anterior descending artery territory,
transmural extent with microvascular
obstruction (case study), 84–85
left atrium (LA), 18
left heart, 3–4
left ventricle (LV)
described, 21–23
imaging of, 27–35
LV noncompaction, 122f
LV noncompaction with decreased
systolic function (case study),
122–123
LVOT balanced SSFP images at end
systole and diastole, 96f
in short-axis view, 32f
left ventricular noncompaction (case
study), 120–124
left ventricular outflow tract
(LVOT), 105
LGE. See late gadolinium enhancement
lightning flash artifact, 242f
described, 242
lipoma (case study), 174–175
lipomatous hypertrophy of the interatrial
septum (case study), 164–165
localizer module, 74–75
localizer module sequences, 75t
long-axis balanced SSFP and late
gadolinium-enhancement images, 92f
LV. See left ventricle (LV)
LV noncompaction, 122f
LV noncompaction with decreased systolic
function (case study), 123
LVOT. See left ventricular outflow tract
M of increased activity, 180f
magnetization preparation, 45–46
magnetohydrodynamic effect, 8–11
maximum-intensity projection
images, 61f
Mayo Configuration, 7, 8
metastases (case study), 180–181
microvascular obstruction (MVO), 85
midventricular dynamic perfusion short-
axis images, 102f
midventricular stress and resting perfusion
short-axis images, 98f
mitral insufficiency (case study),
210–211
mitral stenosis (case study), 214–215
mitral valve, 24, 25, 43, 44
mitral valve insufficiency, 210f
mitral valve prolapse, 212f
case study, 213
mitral valve stenosis, 214f
modified Look-Locker imaging (MOLLI),
63, 66, 67
modular cardiac MR imaging protocols,
74–80
MOLLI. See modified Look-Locker
imaging
MRI metrics for mitral valve evaluation,
213b
MR scanner
as class II medical device, 249
safety of, 247–249
schematic representation
of, 247
multiple oblique balanced SSFP
image of bicuspid aortic
valve, 198f
multiple-spin echo, 46
multishot (data acquisition), 47
Mustard procedure, 186, 187
MVO. See microvascular obstruction
myocardial inversion time
(sequence-specific variable), 53
I n de x
myocardial ischemia and infarction
case studies, 83–103
imaging of, 78
myocardial ischemia and infarction
protocol, 78
myocarditis (case study), 129
myopericarditis, 148f
myoxma (case study), 173
N for cardiac mass, 79
National Kidney Foundation, 251
neoplasms (case study), 172–181
nephrogenic systemic fibrosis (NSF),
251–253
noise spikes in ECG waveform, 12
nonischemic myocardial disease, 78,
105–141
nonischemic myocardial disease
protocol, 78
nonischemic pattern of myocardial fibrosis
suggestive of myocarditis, 130
normal mode (MR scanner operational
mode), 249, 250
normal variants of cardiac masses (case
studies), 164–169
NSF. See nephrogenic systemic fibrosis
number of echoescardiac phases
(sequence-specific variable), 69
number of TEs (sequence-specific
variable), 70
number of TI values (sequence-specific
variable), 66
O pulse sequences
octreotide study demonstrating area
P 59–72
pacemakers, 250–251
parachute mitral valve with mitral stenosis,
216f
case study, 217
parallel imaging, 74
parametric assessment, 63, 65
partial anomalous pulmonary
venous return,190f
case study, 191
partial fourier (k-space) (rapid
imaging), 48
perfusion, 62–64
perfusion dark-rim enhancement
artifact, 241
perfusion model, 74, 76–77
perfusion module, 76t
perfusion sequence at time delays after
administration of gadolinium-based
contrast agent, 64
pericardial abscess, 160f
case study, 161
pericardial constriction, 158f
case study, 159
pericardial cyst, 156f
case study, 157
pericardial disease, 143–161
pericardial effusion, 144
pericarditis, 78
pericarditis protocol, 78
pericardium, 25–26, 143
peripheral photo-pulse sensor, 14
pharmacologic stress testing (case study),
98–99
phase and magnitude images
of ascending and descending
aorta, 63f
phase contrast (flow encoding), 45
phases per slice (sequence-specific
variable), 62
• 315
pre-examination MRI safety screening,
253–254
professional MR societies, 254
prominent crista terminalis (case study),
166–167
prominent eustachian valve (case study),
168–169
protocoling, 74
protocols
for congenital heart disease, 80
for imaging left side of heart, 36
for imaging right side of heart, 36
for myocardial ischemia and
infarction, 78
for nonischemic myocardial
disease, 78
for performing chemical stress testing
for diagnosis of coronary artery
disease, 103
for pericarditis, 78
for pulmonary vein, 79
for valvular heart disease, 79
pulmonary artery, 26
pulmonary vein, 79
pulmonic stenosis, 226f
case study, 227
pulmonic valve, 23, 24, 41
pulmonic valve disease, 203
pulmonic valve plane, 43
pulse repetition time (TR), 45–50, 51,
57–59, 75, 236–238
pulse sequence diagrams, 46
anatomy of cardiac MR imaging pulse
sequence, 45–51
for imaging cardiac function,
for imaging cardiac morphology,
51–59
Q sequence-specific variables, 45, 51, 53, 54,
quantification of aortic insufficiency, 205t
quantification of aortic stenosis, 209t
R 17-segment model, 17, 18, 83
RA. See right atrium
radiofrequency (RF)
body coil switching, 9, 11
field from body coil, 9
fields, 248–249
rapid imaging, 47–48
reconstruction type (sequence-specific
variable), 62
rectangular (fractional)-phase FOV (rapid
imaging), 48
recurrent constriction after subtotal
pericardiectomy (case study),
154–155
reference values of T 2* and [FE] for
normal myocardium and moderate
and severe myocardial iron
overload, 70t
regurgitant volume, 203
respiratory (breathing) motion, 235
respiratory (breathing) motion artifact,
234, 235–236
reverse curve HCM, 108f
case study, 109
RF. See radiofrequency
RF zipper, 232, 234
right atrium (RA), 18
right coronary artery territory,
transmural infarction with MVO,
edema, and right ventricular
infarction (case study), 88–89
right heart, 3
right ventricle (RV)
axial view of, 37
described, 18, 21
imaging of, 35–38
inflow tract long-axis view, 35–36f
long-axis view, 38f
outflow tract view, 38f, 39f
sagittal view, 39f
risk, US FDA criteria for during
MRI, 249
R-R intervals
as data acquired over multiple cardiac
cycles, 3
as sequence-specific variable, 63, 69, 70
RV. See right ventricle
R wave, of ECG waveform, 3, 9, 10,
14, 232
S
safety
components of MR scanner, 246–249
gadolinium-based contrast media
(GBCM), 251
implanted devices, 250–251
main magnetic field (B 0), 246–247
national and international standards,
249–250
other devices, 251
pre-examination MRI safety screening,
253–254
professional MR societies, 254
sagittal oblique (“candy cane”) view, 40,
40f, 43
SAR. See specific absorption rate
saturation recovery, 45
scout images, 27
second controlled mode (MR scanner
operational mode), 250
segmented data acquisition, 3, 47
SENSE (image-based parallel imaging)
(rapid imaging), 47–48, 238
56–64, 66, 69, 70, 72
sequential view order encoding
(sequence-specific variable), 60
severe pulmonic regurgitation and
pulmonary artery aneurysm, 224f
case study, 225
short-axis balanced SSFP images
from healthy volunteer, 49f
with varying bandwidth, 50f
with varying FOV, 50f
with varying matrix size, 51f
with varying signal averages, 49f
with varying slice thickness, 51f
short-axis images
demonstrating presence of large
epicardial mass, 176f
late gadolinium-enhancement, 84f,
86f, 88f
of LV, 31–33f
short-axis SSFP images at base in end
diastole and end systole, 94f
sigmoid HCM, 110f
sigmoid HCM with SAM, 110f
sigmoid morphologic subtype obstructive
HCM, 112f
sigmoid nonobstructive HCM, 114f
case study, 115
sigmoid obstructive HCM (case study),
112–113
sigmoid obstructive HCM with SAM (case
study), 110–111
signal-to-noise ratio (SNR), 48
simple pericardial effusion (case study),
144–145

single echo (data acquisition), 47
single frame (static) (imaging mode), 48
single shot (data acquisition), 47
sinus of Valsalva, 26
SMASH (rapid imaging), 48
SNR. See signal-to-noise ratio
specific absorption rate (SAR),
248–249
spin echo, 46–47
spin echo T1 weighted, 58–59
spoiled gradient echo, 46, 47,
53–54
SSFP. See balance steady-state free
precession
sternal wires/clips, 12
stress testing, 14, 83, 98–99,
101, 103
structure and function module, 74
structure and function module
sequences, 75t
subepicardial and circumflex
artery territories (case study),
85–86
subtotal pericardiectomy, 154
superior vena cava, 26
susceptibility-induced fat saturation
failure, 243f
described, 242–243, 245
susceptibility-induced signal loss, 237f
described, 237
316
T transthoracic echocardiography, 203
T1 relaxation time, 63, 66
T2* relaxation time, 69–70, 72
T2 relaxation time, 66, 68
tagged short-axis images at systole, mid
diastole, and late diastole, 66f
tagging, 45, 62–63, 65
tag spacing (sequence-specific variable), 62
tag type (sequence-specific variable), 62
TE/2 (sequence-specific variable), 58
TEs, number of (sequence-specific
variable), 70
tetralogy of Fallot (case study), 184–185
thoracic cavity, 18f
3-chamber images
of aortic valve, 42f
of LV, 33
of LV, long axis, 33f
mitral annulus, 43f
3D (imaging mode), 48
3D MR angiography, 59–60
three-lead ECG configuration, 6
3-plane localizer, 27, 29, 35, 74
tissue characterization module,
74–76, 76t
TI values, number of (sequence-specific
variable), 66
TR. See pulse repetition time
transposition of the great arteries
(case study), 186–187
• I n de x
triboelectric effect, 9, 10–12
TRICKS (rapid imaging), 48
tricuspid insufficiency (case study),
220–221
tricuspid valve, 24, 25, 43, 44
tricuspid valve insufficiency, 220f
trigger delay, 3
trigger point, 3
triple inversion recovery, 56–58
triple inversion recovery image,
short-axis view, 58f
true aneurysm (case study),
90–91
true axial plane, images in, 26f
T-wave swelling/T-wave elevation,
9, 10
2-chamber images
of LV, 29, 30
of LV, long-axis, 28, 30f, 32f,
34f, 36f
mitral annulus, 43f
short-axis cine series, 5f
2D (imaging mode), 48
typical VPS versus heart rate, 53t, 62t,
63t, 70t
U
UNFOLD (rapid imaging), 48
US Code of Federal Regulations, 249
US Food and Drug Administration (FDA),
248, 249, 251, 252
criteria for significant risk during MRI,
249t
V
valves, 23–25
valvular heart disease
case studies, 203–227
protocol, 79
vascular and flow module, 74, 77, 77t
vasodilator stress testing, 14
VCG configuration, 10
vector ECG (VCG), 6
vector ECG lead placement, 11
velocity encoding (VENC)
(sequence-specific variable), 61
velocity encoding parameters, 61t
VENC. See velocity encoding
ventricles. See also left ventricle (LV); right
ventricle (RV)
ventricles, identifying and distinguishing
of, 22b
view sharing (data acquisition), 47
views per segment (VPS) (sequence-specific
variable), 47, 51, 53, 62–63, 69, 70,
234, 236
W
Waller, Augustus Desiré, 5