Ebook Diagnostic imaging cardiovascular (2nd edition): Part 1

Diagnostic Imaging Cardiovascular

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Diagnostic Imaging Cardiovascular

Contents
Editors ........................................................................................................................................................................ 6
Dedication .............................................................................................................................................................. 9
Foreword ................................................................................................................................................................ 9
Preface ..................................................................................................................................................................10
Acknowledgments..................................................................................................................................................10
Section 1 - Introduction and Overview........................................................................................................................11
Cardiac CT: Acquisition and Postprocessing Indications and Interpretation .............................................................11
Cardiac MR: Acquisition and Imaging Protocols ......................................................................................................19
Cardiac Anatomy ....................................................................................................................................................28
Section 2 - Congenital ................................................................................................................................................73
Approach to Congenital Heart Disease....................................................................................................................73
Coarctation of Aorta...............................................................................................................................................84
Double Aortic Arch .................................................................................................................................................93
Right Aortic Arch .................................................................................................................................................. 102
Persistent Fifth Arch ............................................................................................................................................. 111
Pulmonary Sling ................................................................................................................................................... 114
D-Transposition of Great Arteries ......................................................................................................................... 123
L-Transposition of Great Arteries .......................................................................................................................... 129
Truncus Arteriosus ............................................................................................................................................... 135
Pulmonary Atresia................................................................................................................................................ 141
Hypoplastic Left Heart Syndrome ......................................................................................................................... 147
Heterotaxia Syndromes ........................................................................................................................................ 153
Ebstein Anomaly .................................................................................................................................................. 162

Cor Triatriatum .................................................................................................................................................... 171
Tetralogy of Fallot ................................................................................................................................................ 174
Tetralogy of Fallot Palliation: BT Shunt ................................................................................................................. 183
Tetralogy of Fallot: Definitive Repair..................................................................................................................... 186
Proximal Interruption of Pulmonary Artery ........................................................................................................... 194
Section 3 - Shunts .................................................................................................................................................... 200
Approach to Shunts .............................................................................................................................................. 200
Patent Ductus Arteriosus ...................................................................................................................................... 203
Atrial Septal Defects ............................................................................................................................................. 212
Ventricular Septal Defects .................................................................................................................................... 221
Endocardial Cushion Defect .................................................................................................................................. 230
Scimitar Syndrome ............................................................................................................................................... 236
Total Anomalous Pulmonary Venous Return ......................................................................................................... 242
Partial Anomalous Pulmonary Venous Return ....................................................................................................... 248
Section 4 - Valvular .................................................................................................................................................. 251
Approach to Valvular Disease ............................................................................................................................... 251
Aortic Stenosis ..................................................................................................................................................... 259
Transcatheter Aortic Valve Replacement .............................................................................................................. 265
Aortic Regurgitation ............................................................................................................................................. 270
Bicuspid Aortic Valve ............................................................................................................................................ 276
Mitral Stenosis ..................................................................................................................................................... 282
Mitral Valve Prolapse ........................................................................................................................................... 288
Mitral Regurgitation ............................................................................................................................................. 294
Mitral Annular Calcification .................................................................................................................................. 300
Pulmonary Stenosis .............................................................................................................................................. 306
Pulmonary Regurgitation...................................................................................................................................... 312
Tricuspid Stenosis................................................................................................................................................. 317
Tricuspid Regurgitation ........................................................................................................................................ 321
Infective Endocarditis ........................................................................................................................................... 326
Valvular Prosthesis ............................................................................................................................................... 332

Prosthetic Valve Complications............................................................................................................................. 341
Carcinoid Syndrome ............................................................................................................................................. 347
Multivalvular Disease ........................................................................................................................................... 353
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Diagnostic Imaging Cardiovascular
Rheumatic Heart Disease ..................................................................................................................................... 361
Left Ventricular Apical Aortic Conduit ................................................................................................................... 367
Section 5 - Pericardial............................................................................................................................................... 372
Approach to Pericardial Disease ........................................................................................................................... 372
Pericardial Anatomy ............................................................................................................................................. 380
Infectious Pericarditis ........................................................................................................................................... 388
Uremic Pericarditis ............................................................................................................................................... 395
Neoplastic Pericarditis .......................................................................................................................................... 398
Constrictive Pericarditis........................................................................................................................................ 404
Pericardial Cyst .................................................................................................................................................... 410
Absent Pericardium .............................................................................................................................................. 416
Pericardial Effusion .............................................................................................................................................. 419
Pericardial Tamponade......................................................................................................................................... 428
Section 6 - Neoplastic............................................................................................................................................... 434
Approach to Neoplastic Disease ........................................................................................................................... 434
Metastatic Disease ............................................................................................................................................... 443
Tumor Extension Into the Atria ............................................................................................................................. 449
Atrial Myxoma ..................................................................................................................................................... 455
Cardiac Lipoma..................................................................................................................................................... 461
Cardiac Thrombus ................................................................................................................................................ 467
Cardiac Sarcoma .................................................................................................................................................. 476
Tumor Mimics ...................................................................................................................................................... 485
Hemangioma........................................................................................................................................................ 490

Papillary Fibroelastoma ........................................................................................................................................ 496
Fibroma ............................................................................................................................................................... 499
Lipomatous Hypertrophy, Interatrial Septum ........................................................................................................ 505
Lymphoma ........................................................................................................................................................... 514
Section 7 - Cardiomyopathy ..................................................................................................................................... 520
Imaging of Cardiomyopathies: The Evidence ......................................................................................................... 520
Hypertrophic Cardiomyopathy ............................................................................................................................. 528
Ischemic Cardiomyopathy .................................................................................................................................... 537
Nonischemic Dilated Cardiomyopathy .................................................................................................................. 543
Restrictive Cardiomyopathy ................................................................................................................................. 549
Myocarditis .......................................................................................................................................................... 555
Arrhythmogenic RV Dysplasia/Cardiomyopathy .................................................................................................... 561
Endomyocardial Fibrosis....................................................................................................................................... 567
Hypereosinophilic Syndrome ................................................................................................................................ 573
Cardiac Sarcoidosis............................................................................................................................................... 579
Cardiac Amyloidosis ............................................................................................................................................. 584
Left Ventricular Noncompaction ........................................................................................................................... 590
Chagas Disease..................................................................................................................................................... 596
Iron Overload Syndromes ..................................................................................................................................... 601
Takotsubo Cardiomyopathy.................................................................................................................................. 607
Section 8 - Coronary Artery Disease.......................................................................................................................... 613
Approach to Coronary Heart Disease .................................................................................................................... 613
Coronary Anatomy ............................................................................................................................................... 615
Anomalous Left Coronary Artery, Malignant ......................................................................................................... 628
Anomalous Left Coronary Artery, Benign .............................................................................................................. 631
Anomalous LCX .................................................................................................................................................... 636
Anomalous RCA.................................................................................................................................................... 639
Bland-White-Garland Syndrome ........................................................................................................................... 642
Coronary Embolism .............................................................................................................................................. 644
Coronary Artery Aneurysm ................................................................................................................................... 647

Coronary Calcification .......................................................................................................................................... 650
Coronary Atherosclerotic Plaque .......................................................................................................................... 655
Coronary Thrombosis ........................................................................................................................................... 664
Coronary Artery Stenosis ...................................................................................................................................... 673
Ischemia RCA Stenosis .......................................................................................................................................... 681
Left Main Coronary Stenosis ................................................................................................................................. 687
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Diagnostic Imaging Cardiovascular
Coronary Artery Dissection ................................................................................................................................... 693
Acute Myocardial Infarction ................................................................................................................................. 699
Chronic Myocardial Infarction .............................................................................................................................. 705
Infarction LAD Distribution ................................................................................................................................... 711
Papillary Muscle Rupture...................................................................................................................................... 717
Right Ventricular Infarction .................................................................................................................................. 723
Nonatherosclerosis Myocardial Infarction ............................................................................................................ 729
Nontransmural Myocardial Infarction ................................................................................................................... 735
Post-Infarction LV Aneurysm ................................................................................................................................ 743
Post-Infarction LV Pseudoaneurysm ..................................................................................................................... 749
Post-Infarction Mitral Regurgitation ..................................................................................................................... 754
Left Ventricular Free Wall Rupture ....................................................................................................................... 757
Ventricular Septal Rupture ................................................................................................................................... 763
Post-Angioplasty Restenosis ................................................................................................................................. 766
In-Stent Restenosis............................................................................................................................................... 769
Post-CABG Thrombosis......................................................................................................................................... 777
Post-CABG Atherosclerosis ................................................................................................................................... 783
Myocardial Bridge ................................................................................................................................................ 789
Coronary Fistula ................................................................................................................................................... 792
Section 9 - Heart Failure ........................................................................................................................................... 797

Approach to Heart Failure .................................................................................................................................... 797
Right Heart Failure ............................................................................................................................................... 803
Left Heart Failure ................................................................................................................................................. 808
Heart Transplant .................................................................................................................................................. 814
Ventricular Assist Devices ..................................................................................................................................... 820
Left Ventricular Hypertrophy ................................................................................................................................ 827
Right Ventricular Hypertrophy .............................................................................................................................. 830
PVH/Pulmonary Edema (Cardiogenic) ................................................................................................................... 833
Cor Pulmonale...................................................................................................................................................... 842
Section 10 - Electrophysiology .................................................................................................................................. 845
Imaging Before and After Electrophysiology Procedures ....................................................................................... 845
Pulmonary Vein Mapping ..................................................................................................................................... 848
Pulmonary Vein Stenosis ...................................................................................................................................... 853
Pacemakers/ICDs ................................................................................................................................................. 859
Cardiac Vein Mapping .......................................................................................................................................... 865
Left Atrial Thrombus............................................................................................................................................. 868
Section 11 - Pulmonary Vasculature ......................................................................................................................... 873
Approach to Pulmonary Vasculature..................................................................................................................... 873
Pulmonary Arteriovenous Malformation .............................................................................................................. 878
Pulmonary Artery Pseudoaneurysm ..................................................................................................................... 881
Pulmonary Artery Aneurysm ................................................................................................................................ 884
Acute Pulmonary Embolism.................................................................................................................................. 890
Chronic Pulmonary Embolism ............................................................................................................................... 896
Pulmonary Sequestration ..................................................................................................................................... 902
Branch Pulmonary Artery Stenosis........................................................................................................................ 908
Pulmonary Arterial Hypertension ......................................................................................................................... 914
Pulmonary Venoocclusive Disease ........................................................................................................................ 921
Section 12 - Arterial ................................................................................................................................................. 924
Introduction and Overview ................................................................................................................................... 924
Approach to Congenital and Acquired Diseases of the Aorta ............................................................................. 924

Approach to Acute Aortic Syndrome ................................................................................................................. 927
Thoracic Aorta and Great Vessels ......................................................................................................................... 935
Thoracic Aorta and Great Vessel Anatomy ........................................................................................................ 935
Thoracic Aortic Aneurysm ................................................................................................................................. 946
Mycotic Aneurysm............................................................................................................................................ 955
Chronic Post-Traumatic Pseudoaneurysm ......................................................................................................... 961
Aortic Intramural Hematoma ............................................................................................................................ 967
Penetrating Atherosclerotic Ulcer ..................................................................................................................... 973
Aortic Dissection .............................................................................................................................................. 979
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Diagnostic Imaging Cardiovascular
Takayasu Arteritis ............................................................................................................................................. 988
Giant Cell Arteritis ............................................................................................................................................ 991
Marfan Syndrome............................................................................................................................................. 997
Pseudocoarctation.......................................................................................................................................... 1002
Traumatic Aortic Laceration ............................................................................................................................ 1008
Ductus Diverticulum ....................................................................................................................................... 1014
Abdominal Aorta and Visceral Vasculature ......................................................................................................... 1020
Abdominal Aorta and Visceral Vasculature Anatomy ....................................................................................... 1020
Abdominal Aortic Aneurysm ........................................................................................................................... 1027
AAA With Rupture .......................................................................................................................................... 1037
Aortic Graft Complications.............................................................................................................................. 1043
Abdominal Aortic Occlusion ............................................................................................................................ 1046
Section 13 - Venous ............................................................................................................................................... 1052
Approach to Venous Conditions ......................................................................................................................... 1052
Venous Anatomy................................................................................................................................................ 1054
Superior Vena Cava Syndrome............................................................................................................................ 1061
Inferior Vena Cava Anomalies ............................................................................................................................. 1068

Inferior Vena Cava Occlusion .............................................................................................................................. 1074
Left Superior Vena Cava ..................................................................................................................................... 1080
Azygos Continuation of the IVC........................................................................................................................... 1085
May-Thurner Syndrome ..................................................................................................................................... 1091
Nutcracker Syndrome......................................................................................................................................... 1097
Section 14 - Extracranial Cerebral Arteries .............................................................................................................. 1103
Approach to Extracranial Cerebral Arteries ......................................................................................................... 1103
Acute Ischemic Stroke ........................................................................................................................................ 1108
Atherosclerosis, Extracranial .............................................................................................................................. 1118
Carotid Stenosis, Extracranial ............................................................................................................................. 1124
Carotid Dissection .............................................................................................................................................. 1129
Carotid Pseudoaneurysm, Extracranial ............................................................................................................... 1135
Vertebral Dissection ........................................................................................................................................... 1140
Subclavian Steal Syndrome ................................................................................................................................. 1146
Section 15 - Renal Vasculature ............................................................................................................................... 1152
Approach to Renal Vasculature........................................................................................................................... 1152
Renal Vasculature Anatomy................................................................................................................................ 1160
Renal Artery Atherosclerosis .............................................................................................................................. 1164
Fibromuscular Dysplasia, Renal .......................................................................................................................... 1170
Polyarteritis Nodosa ........................................................................................................................................... 1176
Renal Arteriovenous Fistula ................................................................................................................................ 1182
Renal Vein Thrombosis ....................................................................................................................................... 1188
Section 16 - Peripheral Vasculature ........................................................................................................................ 1194
Introduction and Overview................................................................................................................................. 1194
Approach to Peripheral Vasculature................................................................................................................ 1194
Lower Extremity Vasculature Anatomy ........................................................................................................... 1196
Vasculature of the Trunk .................................................................................................................................... 1201
Subclavian Artery Stenosis/Occlusion ............................................................................................................. 1201
Subclavian Vein Thrombosis ........................................................................................................................... 1207
Iliac Artery Occlusive Disease .......................................................................................................................... 1213

Iliac Artery Aneurysmal Disease ...................................................................................................................... 1220
Lower Extremity Vasculature .............................................................................................................................. 1226
Lower Extremity Aneurysms ........................................................................................................................... 1226
Acute Lower Extremity Ischemia ..................................................................................................................... 1232
Femoropopliteal Artery Occlusive Disease ...................................................................................................... 1238
Cystic Adventitial Disease ............................................................................................................................... 1244
Persistent Sciatic Artery .................................................................................................................................. 1250
Arteriovenous Fistula...................................................................................................................................... 1253
Deep Vein Thrombosis.................................................................................................................................... 1259
Index ..................................................................................................................................................................... 1266

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Diagnostic Imaging Cardiovascular

Editors
Editors
Suhny Abbara MD, FSCCT
Professor of Radiology
Chief, Division of Cardiac and Thoracic Imaging
Director, 3D Image
Processing Laboratory University of Texas Southwestern Medical Center
Dallas, Texas
Authors
Stephan Achenbach, MD
Chairman
Department of Cardiology
University of Erlangen
Erlangen, Germany

Brett W. Carter, MD
Assistant Professor of Radiology
The University of Texas MD Anderson Cancer Center
Houston, Texas
Christopher M. Walker, MD
Assistant Professor of Radiology
Saint Luke's Hospital of Kansas City
University of Missouri-Kansas City
Kansas City, Missouri
Jonathan D. Dodd, MD, MSc, MRCPI, FFR(RCSI)
Associate Professor of Radiology
University College Dublin
Director of Radiology
St. Vincent's University Hospital
Dublin, Ireland
Raymond J. Kim, MD
Director, Duke Cardiovascular Magnetic Resonance Center
Professor of Medicine and Radiology
Duke University Medical Center
Durham, North Carolina
T. Gregory Walker, MD, FSIR
Assistant Professor of Radiology
Harvard Medical School
Associate Director, Fellowship
Division of Interventional Radiology
Massachusetts General Hospital
Boston, Massachusetts
Jonathan Hero Chung, MD
Associate Professor, Department of Radiology
Director of Radiology Professional Quality Assurance

Director of Cardiopulmonary Imaging Fellowship
National Jewish Health
Denver, Colorado
John D. Grizzard, MD
Associate Professor of Radiology
Section Chief, Non-Invasive Cardiovascular Imaging
VCU Health Systems
Richmond, Virginia
Sanjeeva P. Kalva, MBBS, MD, FSIR
Associate Professor of Radiology
Chief, Division of Interventional Radiology
University of Texas Southwestern Medical Center
Dallas, Texas
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Diagnostic Imaging Cardiovascular
Santiago Martínez-Jiménez, MD
Associate Professor of Radiology
University of Missouri-Kansas City
Saint Luke's Hospital of Kansas City
Kansas City, Missouri
Carol C. Wu, MD
Instructor of Radiology
Harvard Medical School
Assistant Radiologist
Massachusetts General Hospital
Boston, Massachusetts
John P. Lichtenberger, III, MD
Chief of Cardiothoracic Imaging

David Grant Medical Center
Travis Air Force Base, California
Assistant Professor of Radiology
Uniformed Services University of the Health Sciences
Bethesda, Maryland
Sanjeev A. Francis, MD
Director, Cardio-Oncology Program
Cardiac MRI/CT Program
Instructor in Medicine
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Suvranu “Shoey” Ganguli, MD
Assistant Professor of Radiology
Harvard Medical School
Vascular & Interventional Radiology
Massachusetts General Hospital
Boston, Massachusetts
P.vi

Contributing Authors
Bronwyn E. Hamilton, MD
Associate Professor of Radiology
Associate Director of Neuroradiology Fellowship
Neuroradiology Division
Oregon Health & Science University
Portland, Oregon
Carlos A. Rojas, MD
Assistant Professor of Radiology
University of South Florida

Associate Director
Cardiothoracic Imaging Fellowship
Tampa, Florida
C. Douglas Phillips, MD, FACR
Professor of Radiology
Director of Head and Neck Imaging
Weill Cornell Medical College
NewYork-Presbyterian Hospital
New York, New York
Daniel W. Entrikin, MD
Associate Professor
Departments of Radiology and Internal Medicine
Section on Cardiology
Wake Forest University School of Medicine
Winston-Salem, North Carolina
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Diagnostic Imaging Cardiovascular
Gudrun Feuchtner, MD
Associate Professor of Radiology
Innsbruck Medical University
Innsbruck, Austria
Gerald F. Abbott, MD
Associate Professor of Radiology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Darragh Brady, MD, MRCPI
Research Fellow

University College Dublin
Dublin, Ireland
Lowie M.R. Van Assche, MD
Post Doctoral Research Fellow
Duke Cardiovascular Magnetic Resonance Center
Duke University Medical Center
Durham, North Carolina
Kathryn M. Olsen, MD
Assistant Professor of Radiology
Virginia Commonwealth University School of Medicine
VCU Medical Center
Richmond, Virginia
Michael T. Lu, MD
Fellow, Cardiac and Thoracic Imaging
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Naveen M. Kulkarni, MD
Fellow, Cardiac and Thoracic Imaging
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
P.vii

Roy Bryan, MD, MBA
Clinical Fellow, Radiology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Andrew J. Gunn, MD

Clinical Fellow, Radiology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Cameron Hassani, MD
Assistant Professor of Radiology
Keck Medical Center of USC
University of Southern California
Los Angeles, California
Rahul Sheth, MD
Fellow, Division of Abdominal Imaging and Interventions
Department of Radiology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Ali Devrim Karaosmanoglu, MD

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Diagnostic Imaging Cardiovascular
Clinical Fellow, Cardiac Imaging
Department of Radiology
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Terrance T. Healey, MD
Director, Thoracic Radiology
Assistant Professor of Diagnostic Imaging
Department of Diagnostic Imaging

Warren Alpert Medical School of Brown University
Providence, Rhode Island
Jeffrey P. Kanne, MD
Associate Professor
Chief of Thoracic Imaging
Vice Chair of Quality and Safety
Department of Radiology
University of Wisconsin School of Medicine and Public Health
Madison, Wisconsin
Melissa L. Rosado-de-Christenson, MD, FACR
Section Chief, Thoracic Imaging
Saint Luke's Hospital of Kansas City
Professor of Radiology
University of Missouri-Kansas City
Kansas City, Missouri
Rebecca S. Cornelius, MD, FACR
Professor of Radiology and Otolaryngology—
Head and Neck Surgery
University of Cincinnati College of Medicine
University of Cincinnati Medical Center
Cincinnati, Ohio
Tyler H. Ternes, MD
Chest Imaging Fellow
Saint Luke's Hospital of Kansas City
University of Missouri-Kansas City
Kansas City, Missouri

Dedication
Dedication
To Amanda, Tyler, Marlene, Yasser, Mona, and Susu. SA

Foreword
Cardiovascular imaging continues to evolve. Cardiac computed tomography and cardiac magnetic resonance imaging
are widely available and have expanded appropriate use, flexibility and popularity. Traditional imaging modalities such
as echocardiography, nuclear cardiology and digital fluoroscopy are also morphing into new technologies, with new
applications including preoperative planning of transcatheter valve replacement and transcutaneous treatment of
many congenital diseases.
Radiologists are challenged today to embrace the complexity of cardiovascular pathologic anatomy and physiology as
never before. Conversely, cardiologists have had to reorient their thinking and expand their knowledge to include the
entire range of thoracic anatomy and pathology, rather than restrict their attention to the heart alone. For the
patient, this more holistic viewpoint can only be beneficial. For the physician, embracing the breadth of our
responsibilities can be intimidating, particularly at advanced imaging facilities that receive referrals of the most
difficult and unusual cases.
As a cardiologist who directs a combined radiology/cardiology advanced cardiovascular imaging teaching program, I
found the first edition of Diagnostic Imaging: Cardiovascular to be a uniquely successful resource, both for physiciansin-training and for our attending physicians, due to its lucid organization, fine illustrations, extensive clinical images,
and the uniform excellence of its text.
The organization and presentation of the material is successful because it is so clear. This derives from the talents of
the authors, the publisher, and the artists, who collaborate to present a visually appealing and highly readable style.
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Diagnostic Imaging Cardiovascular
Separate boxes on terminology, imaging findings, differential diagnosis, pathology, and clinical issues all complement
the image gallery for each disease entity. The authors go beyond traditional didactic texts by integrating clinical
features, alternative diagnoses, and potential diagnostic pitfalls. The result concisely summarizes a vast amount of
diagnostic expertise with a clarity that is hard to duplicate.
The second edition has incorporated entirely new clinical images, which is a major undertaking but vitally important in
such a rapidly changing field. There are expanded sections on diagnostic anatomy, additional material on imaging
technique and introductory text on the role of imaging in clinical management.
In summary, Diagnostic Imaging: Cardiovascular is a key textbook for our clinical cardiovascular imaging practice and

teaching service, with radiologists, cardiologists, residents, and fellows working collaboratively in a high-volume
environment. It is an outstanding book and highly recommended.
Gilbert L. Raff, MD
Director, Advanced Cardiovascular Imaging
Florine and J. Peter Ministrelli
Endowed Chair in Cardiovascular Research
Oakland University William Beaumont School of Medicine
Rochester, Michigan

Preface
Since the publication of the first edition of Diagnostic Imaging: Cardiovascular, there have been a number of
significant advancements in the field of cardiovascular medicine. New treatments have become available, imaging
methods have further developed, the published scientific evidence related to cardiovascular imaging has doubled. As
a result, new complex guidelines on the management of patients with cardiovascular disorders have been published.
The role of cardiovascular imaging is at the heart of many of these guidelines, illuminating the evolution of imaging
and its critical role in patient management.
In this second edition of Diagnostic Imaging: Cardiovascular, we were fortunate to attract some of the top world
experts in cardiac CT and MR as well as several rising stars in the fields of cardiac and vascular imaging, both from
radiology and cardiology backgrounds. I am immensely grateful to the many authors who have made this work
possible.
Several aspects of this edition are new. First, the imaging content is nearly 100% new. Virtually every figure has been
replaced with one or several new, high-quality illustrative figures, 2,473 in total. More than 1,000 additional figures
from the first edition are made accessible to the reader in the eBook version of this work. The illustrations have been
updated, and new tables have been added where useful.
Additionally, there are 18 new section introductions that review the “how to” technical aspects of cardiac MR and CT
imaging as well as introductions that review the approach to patients with a suspected type of pathology. Eight new
detailed anatomy modules with several drawings and illustrative imaging studies have been created.
In total, this edition has 203 chapters, of which 32 are new and 171 have been extensively revised and updated from
the first edition.
Creating this text has been an incredible effort for a large group of wonderful people. I am very grateful for the

tremendous support and encouragement from the publishing and art and design teams at Amirsys as well as the
senior leadership at Amirsys. The exquisite creative talents of all the authors and the contributions of their associates,
trainees, and their patients have made this work possible, and I am most grateful for that.
I truly hope you will find this second edition of Diagnostic Imaging: Cardiovascular informative, enjoyable, and useful
in everyday practice.
Suhny Abbara, MD, FSCCT
Professor of Radiology
Chief, Division of Cardiac and Thoracic Imaging
Director, 3D Image Processing Laboratory
University of Texas Southwestern Medical Center
Dallas, Texas

Acknowledgments
Text Editing
Dave L. Chance, MA, ELS
Arthur G. Gelsinger, MA
Lorna Kennington, MS
Rebecca L. Hutchinson, BA
Angela M. G. Terry, BA
Sarah J. Connor, BA
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Diagnostic Imaging Cardiovascular
Image Editing
Jeffrey J. Marmorstone, BS
Lisa A. M. Steadman, BS
Medical Editing
Bobak Heydari, MD, MPH
Umesh C. Sharma, MD

Illustrations
Richard Coombs, MS
Laura C. Sesto, MA
Lane R. Bennion, MS
Art Direction and Design
Laura C. Sesto, MA
Lisa A. M. Steadman, BS
Lead Editor
Kalina K. Lowery, MS
Production Lead
Katherine Riser, MA

Section 1 - Introduction and Overview
Cardiac CT: Acquisition and Postprocessing
Indications and Interpretation
> Table of Contents > Section 1 - Introduction and Overview > Cardiac CT: Acquisition and Postprocessing Indications
and Interpretation
Cardiac CT: Acquisition and Postprocessing Indications and Interpretation
Stephan Achenbach, MD
Introduction
Due to the rapid technical evolution of computed tomography (CT), cardiac imaging has become reliably possible, and
CT has assumed a new clinical role for the work-up of cardiac disease. Noninvasive coronary CT angiography in
particular has tremendous clinical potential for detecting or ruling out coronary artery stenoses in some patients.
Imaging of cardiac structure and function, potentially even perfusion, can be useful in selected patients. However, the
spatial resolution, and especially the temporal resolution of CT imaging, even in the latest scanner generations, still
possesses certain restrictions and can lead to artifacts and imaging limitations that must be taken into account during
data acquisition and interpretation.
Diagnostic accuracy is impaired when image quality is reduced. In turn, image quality is influenced by many factors,
such as the patient's heart rate, body weight, ability to cooperate, and, for coronary CT angiography, the extent of
coronary calcification. Therefore, the clinical utility of cardiac CT significantly depends both on the specific clinical

situation and on the patient under investigation. The specific advantages and disadvantages of cardiac CT and
coronary CT angiography must be carefully considered before using either method in the work-up of a patient with
known or suspected coronary artery disease or other cardiovascular disorders.
Imaging Protocol
Currently, 64-slice CT imaging is considered a state-of-the-art modality for coronary artery studies. Newer
technologies, such as dual-source CT and scanners that allow simultaneous acquisition of 256 or 320 cross sections,
provide further improved image quality and are less susceptible to artifacts.
Patient Preparation
Even slight respiratory motion during data acquisition will cause substantial artifact on cardiac CT. Therefore, patients
must be able to follow breath-hold commands and hold their breath for approximately ten seconds. For most imaging
purposes, heart rate should be regular, and if coronary CT angiography is attempted, heart rate should be < 65
beats/min and, optimally, < 60 beats/min. Patients therefore usually receive pre-procedure medication with shortacting β-blockers that can be administered orally approximately one hour prior to scanning or intravenously
immediately before the scan. In order to achieve coronary dilatation on CT angiography and thus substantially
improve image quality, nitrates should be given to all patients who have no contraindications.
Contrast Injection
For contrast-enhanced imaging of the heart, 50-100 mL of iodine-based high-concentration contrast agent is injected
intravenously. Recommended flow rates are 4-7 mL/s, and the contrast bolus should be followed by saline solution or
a mixture of saline and contrast to improve right heart visualization. Synchronization of contrast injection and data
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Diagnostic Imaging Cardiovascular
acquisition can be achieved either through a bolus tracking method or by using a separate “test bolus” acquisition. For
visualization of the coronary veins, the delay between contrast injection and the start of image acquisition must be
prolonged by about six to ten seconds.
Data Acquisition
Subsequent data acquisition can follow various principles. Reconstructed images need to be synchronized with the
heart beat, and this can be achieved through either retrospective ECG gating or prospective ECG triggering.
Retrospectively gated scans are acquired in spiral mode and usually provide for high image quality, flexibility to
choose the cardiac phase during which images are reconstructed, as well as ability to reconstruct functional data sets

throughout the cardiac cycle in order to analyze cardiac function. To limit radiation exposure, the output of the x-ray
tube can be modulated during the acquisition, with lower output in systole and higher output in diastole. The most
relevant image reconstructions are usually performed in diastole.
Prospectively triggered scans are associated with substantially lower radiation exposure. Less flexibility to reconstruct
data at different time instants is the trade-off for the advantage of lower dose. Heart rate must be low so that artifactfree images can be guaranteed at the time instant of radiation exposure.
Image Reconstruction and Postprocessing
Typical data sets for coronary artery visualization by CT consist of approximately 200-300 thin (0.5-0.75 mm) transaxial
cross sections. Useful postprocessing tools include maximum-intensity projections and multiplanar reconstructions.
3D renderings may be impressive but are not accurate for stenosis detection and play no role in data interpretation.
Coronary CT Angiography
Most cardiac CT investigations are performed to detect or rule out significant coronary artery stenosis. On CT, stenosis
severity can appear to be less or more than seen on invasive angiography; the typical limits of agreement are
approximately ± 20%. Thus, stenoses that appear to be < 50% on CT can be assumed to be < 70% on invasive
angiography with a very high degree of certainty. In most cases, however, there is a tendency to overestimate, rather
than underestimate, the degree of luminal stenosis on coronary CT angiography as compared with catheter-based
invasive coronary angiography.
False-positive findings are frequent when image quality is reduced. Insufficient image quality is most frequently the
consequence of motion artifact (secondary to either coronary movement or, less often, respiration), high image noise,
or a combination of both. Severe calcification can cause additional problems. In some cases, artifacts render some
coronary segments, or even the entire data set, unevaluable. This has become less frequent with modern scanners
but can still occur, especially if patients are not adequately prepared or data acquisition is not carefully performed.
Coronary CT angiography has a high sensitivity and a very high negative predictive value for the identification of
coronary stenosis. Severe coronary lesions are very infrequently missed, and CT angiography is extremely reliable to
rule out coronary artery stenosis. Specificity and positive predictive value may be lower because of the tendency to
overestimate stenosis because of artifacts and because coronary artery stenosis, even if detected with high image
quality, does not always lead to myocardial ischemia.
P.1:3

The very high negative predictive value makes coronary CT angiography an especially clinically useful tool in
symptomatic patients who have a lower or intermediate likelihood of coronary disease but require further work-up to

rule out significant coronary stenoses. This applies both to patients with stable chest pain and to patients with acute
chest pain and a suspected acute coronary syndrome. A negative coronary CT angiography scan will render further
testing unnecessary. Indeed, several observational trials have clearly demonstrated that when coronary CT
angiography was negative, symptomatic patients had a very favorable clinical outcome even without further
additional testing and that downstream healthcare costs may be lower than with other diagnostic procedures.
Coronary CT Angiography and Ischemia
Coronary CT angiography, like invasive angiography, is a purely morphologic imaging modality and cannot
demonstrate the functional relevance of stenoses (i.e., ischemia). Especially in the case of lesions with a borderline
degree of stenosis, poor correlation of CT findings with myocardial ischemia may limit the clinical application of CT
angiography.
Several methods are under evaluation to improve the ability of coronary CT angiography to predict ischemia. They
include the combination with CT-based myocardial perfusion and specific analysis methods, such as CT-based
determination of the fractional flow reserve. Based on the anatomic CT data set, computational fluid dynamics are
applied to model the flow and resistance pattern under adenosine stress and to obtain the fractional flow reserve
value for all segments of the coronary artery tree. Publications of initial studies show that this is feasible and has
potential to improve the specificity of CT to identify ischemia causing lesions over a purely anatomic assessment
alone. However, further validation is necessary.
Coronary CT angiography, like invasive angiography, should not be performed in an unselected patient population or
for “screening” purposes. A positive CT scan taken by itself does not strongly predict the need for revascularization.
12


Diagnostic Imaging Cardiovascular
However, a negative coronary CT angiography result is extremely reliable to rule out the presence of coronary artery
stenoses and the need for revascularization.
Imaging of Patients With Bypass Grafts and Stents
Coronary CT angiography has relevant limitations in patients with previous coronary revascularization. In patients who
have undergone bypass surgery, the accuracy of the detection of graft stenosis and occlusion is extremely high.
However, assessing the native coronary arteries can be extremely difficult because of their often small diameter and
severe calcification. Consequently, the accuracy of detecting and ruling out stenoses in nongrafted and runoff vessels

is substantially lower.
Imaging of Coronary Atherosclerotic Plaque
Coronary Calcification
Using cardiac CT, calcium in the coronary arteries can be detected and quantified in low-radiation, nonenhanced
image acquisition protocols. Tissue within the vessel wall with a CT number of ≥ 130 Hounsfield units is defined as
calcified. For qualification, the Agatston score, which takes into account the area and the CT density of calcified
lesions, is used.
Coronary calcifications, with the possible exception of calcifications in patients with renal failure, are always due to
coronary atherosclerotic plaque. The correlation between calcium and stenosis is poor. The lack of calcium therefore
does not reliably eliminate the possibility of coronary artery stenosis in symptomatic individuals. On the other hand,
even substantial amounts of coronary calcium are not necessarily associated with the presence of hemodynamically
relevant luminal narrowing. Therefore, the detection of coronary calcium alone, even when very pronounced, should
not prompt invasive coronary angiography in otherwise asymptomatic individuals.
Coronary calcium is associated with individual coronary artery disease risk. In asymptomatic individuals, the absence
of coronary calcium is associated with very low (< 1% per year) risk of major cardiovascular events over the next three
to five years. Note, however, that a significantly increased risk of major cardiac events has been reported in
asymptomatic subjects with extensive coronary calcification in numerous trials. For risk stratification, coronary
calcium is superior to other measures of risk, such as C-reactive protein or intimamedia thickness tests.
A potential clinical role of coronary calcium for further risk stratification is assumed for patients who have an
intermediate risk as assessed by traditional risk factors. Coronary calcium imaging therefore can be used when a
decision regarding risk-modifying treatment, such as statin therapy, hinges on additional information beyond
conventional risk factor analysis. Unselected screening or patient self-referral is not recommended.
Plaque in Coronary CT Angiography
Coronary CT angiography allows visualization of nonstenotic coronary atherosclerotic plaque if image quality is good.
With some limitations, and again under the prerequisite of excellent image quality, plaque quantification and
characterization are possible. Some parameters that are readily available from CT might contribute to the detection of
vulnerable plaques at an increased risk for near-term rupture.
Several studies and data based on large registries have demonstrated a prognostic value of atherosclerotic lesions
detected by coronary CT angiography both in symptomatic and asymptomatic individuals. An analysis of a clinical
registry including > 23,000 patients confirmed the prognostic value of coronary CT angiography in cases where the

presence of coronary stenoses and the presence of nonobstructive plaque were associated with an increased risk of
mortality. However, the hazard ratio for nonobstructive plaque was relatively low (i.e., hazard ratio of 1.6 with 95%
confidence interval of 1.2-2.2). Furthermore, another analysis of the same registry was unable to demonstrate, for this
mostly symptomatic patient group, an incremental prognostic value of contrast-enhanced coronary CT angiography
over coronary calcium measurements. Therefore, coronary CT angiography for the identification of coronary
atherosclerotic plaque is currently not recommended for risk assessment purposes in asymptomatic individuals.
P.1:4

Noncoronary Cardiac CT
Cardiac CT permits high-resolution functional and morphologic imaging of the heart. Although cardiac CT is most
frequently utilized for coronary artery imaging, it can also be useful for other applications.
Cardiac CT is highly accurate in assessing left and right ventricular function. Even parameters of diastolic dysfunction
can be derived from CT. Clinically, however, it will only be used if echocardiography and magnetic resonance imaging
fail.
Morphologic imaging of the heart has applications in congenital heart disease and in the follow-up of cardiac surgery.
Again, however, CT will typically be used only when echocardiography and magnetic resonance imaging are unable to
yield the desired results.
Cardiac CT can be used to assess left-sided cardiac valves (adequate contrast enhancement is often a problem for
imaging of right-sided cardiac valves). It has been shown that both the degree of stenosis and the degree of
regurgitation can be estimated by CT.

13


Diagnostic Imaging Cardiovascular
Another application of major importance is the use of CT imaging in the evaluation of patients who are candidates for
transcatheter aortic valve replacement. CT imaging permits assessment of the femoral and iliac access vessels, and CT
angiography provides detailed measurement of aortic annulus dimensions. In fact, it has been shown that procedure
success is increased and complication rates are reduced when CT imaging is incorporated into the pre-transcatheter
aortic valve replacement work-up for prosthesis size selection and identification of suitable candidates.

Selected References
1. Taylor CA et al: Computational fluid dynamics applied to cardiac computed tomography for noninvasive
quantification of fractional flow reserve: scientific basis. J Am Coll Cardiol. 61(22):2233-41, 2013
2. Achenbach S et al: SCCT expert consensus document on computed tomography imaging before transcatheter aortic
valve implantation (TAVI)/transcatheter aortic valve replacement (TAVR). J Cardiovasc Comput Tomogr. 6(6):366-80,
2012
3. Hoffmann U et al: Coronary CT angiography versus standard evaluation in acute chest pain. N Engl J Med.
367(4):299-308, 2012
4. Litt HI et al: CT angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med.
366(15):1393-403, 2012
5. Min JK et al: Age- and sex-related differences in all-cause mortality risk based on coronary computed tomography
angiography findings results from the International Multicenter CONFIRM (Coronary CT Angiography Evaluation for
Clinical Outcomes: An International Multicenter Registry) of 23,854 patients without known coronary artery disease. J
Am Coll Cardiol. 58(8):849-60, 2011
6. Erbel R et al: Coronary risk stratification, discrimination, and reclassification improvement based on quantification
of subclinical coronary atherosclerosis: the Heinz Nixdorf Recall study. J Am Coll Cardiol. 56(17):1397-406, 2010
7. Min JK et al: The present state of coronary computed tomography angiography a process in evolution. J Am Coll
Cardiol. 55(10):957-65, 2010
8. Pflederer T et al: Aortic valve stenosis: CT contributions to diagnosis and therapy. J Cardiovasc Comput Tomogr.
4(6):355-64, 2010
9. Taylor AJ et al: ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac
computed tomography. A report of the American College of Cardiology Foundation Appropriate Use Criteria Task
Force, the Society of Cardiovascular Computed Tomography, the American College of Radiology, the American Heart
Association, the American Society of Echocardiography, the American Society of Nuclear Cardiology, the North
American Society for Cardiovascular Imaging, the Society for Cardiovascular Angiography and Interventions, and the
Society for Cardiovascular Magnetic Resonance. J Am Coll Cardiol. 56(22):1864-94, 2010
10. Abbara S et al: SCCT guidelines for performance of coronary computed tomographic angiography: a report of the
Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr. 3(3):190-204,
2009
11. Motoyama S et al: Computed tomographic angiography characteristics of atherosclerotic plaques subsequently

resulting in acute coronary syndrome. J Am Coll Cardiol. 54(1):49-57, 2009
12. Raff GL et al: SCCT guidelines for the interpretation and reporting of coronary computed tomographic
angiography. J Cardiovasc Comput Tomogr. 3(2):122-36, 2009
13. Sayyed SH et al: Use of multidetector computed tomography for evaluation of global and regional left ventricular
function. J Cardiovasc Comput Tomogr. 3(1 Suppl):S23-34, 2009
14. Budoff MJ et al: Diagnostic performance of 64-multidetector row coronary computed tomographic angiography
for evaluation of coronary artery stenosis in individuals without known coronary artery disease: results from the
prospective multicenter ACCURACY (Assessment by Coronary Computed Tomographic Angiography of Individuals
Undergoing Invasive Coronary Angiography) trial. J Am Coll Cardiol. 52(21):1724-32, 2008
15. Detrano R et al: Coronary calcium as a predictor of coronary events in four racial or ethnic groups. N Engl J Med.
358(13):1336-45, 2008
16. Meijboom WB et al: Diagnostic accuracy of 64-slice computed tomography coronary angiography: a prospective,
multicenter, multivendor study. J Am Coll Cardiol. 52(25):2135-44, 2008
17. Miller JM et al: Diagnostic performance of coronary angiography by 64-row CT. N Engl J Med. 359(22):2324-36,
2008
18. Ferencik M et al: Diagnostic accuracy of image postprocessing methods for the detection of coronary artery
stenoses by using multidetector CT. Radiology. 243(3):696-702, 2007
19. Meijboom WB et al: 64-slice computed tomography coronary angiography in patients with high, intermediate, or
low pretest probability of significant coronary artery disease. J Am Coll Cardiol. 50(15):1469-75, 2007
20. McClelland RL et al: Distribution of coronary artery calcium by race, gender, and age: results from the Multi-Ethnic
Study of Atherosclerosis (MESA). Circulation. 113(1):30-7, 2006
P.1:5

14


Diagnostic Imaging Cardiovascular
Image Gallery

(Left) Axial cardiac CTA, 5 mm maximum-intensity projection at the level of the left main coronary artery, shows

proximal segments of the left anterior descending coronary artery
and left circumflex coronary artery
. (Right)
Axial cardiac CTA maximum-intensity projection image, several millimeters more caudally, shows cross sections of the
left anterior descending coronary artery
, the diagonal branch
, and the left circumflex coronary artery
.

(Left) Axial cardiac CTA thin maximum-intensity projection image at the level of the right coronary ostium shows the
proximal right coronary artery
. Cross sections of the left anterior descending artery, the diagonal branch
,
and the left circumflex artery end branches
are also seen. (Right) Axial cardiac CTA image at the level of the mid
right coronary artery
shows the right coronary artery in cross section. The end branches of the left anterior
descending
and left circumflex
arteries are also shown.

15


Diagnostic Imaging Cardiovascular

(Left) Axial coronary CT maximum-intensity projection image (7 mm thickness) shows the distal right coronary artery
, the posterior descending artery
, and an acute marginal branch
. (Right) Cardiac CT curved multiplanar

reconstruction shows the entire course of the right coronary artery
.
P.1:6

(Left) Invasive coronary angiography shows a high-grade stenosis
of the distal left anterior descending coronary
artery after the 2nd diagonal branch. (Right) Coronary CT angiography maximum-intensity projection (7 mm thickness)
in a curved plane in the same patient shows a corresponding stenosis
of the left anterior descending coronary
artery. Note absence of calcium at the stenosis site.

16


Diagnostic Imaging Cardiovascular

(Left) High-threshold 3D reconstruction in the same patient shows the stenosis
. The value of 3D reconstructions
for stenosis assessment is extremely limited because the visualization of stenoses depends strongly on manually
chosen window and level settings. (Right) As this 3D reconstruction image shows, the stenosis is not detectable
with a lower threshold.

(Left) This typical visualization of coronary artery stenoses in a coronary CT angiography maximum-intensity projection
(7 mm thickness) of the proximal left anterior descending coronary artery demonstrates a stenosis in the mid left
anterior descending coronary artery segment
. (Right) Invasive coronary angiogram in the same patient can be
used to confirm the stenosis
initially detected in cardiac CTA.
P.1:7

17


Diagnostic Imaging Cardiovascular

(Left) Bypass graft stenosis in coronary CT angiography, curved multiplanar reconstruction, shows a venous bypass
graft to the left anterior descending coronary artery with a high-grade stenosis
. The inset shows invasive
coronary angiography. (Right) 3D model shows simulated fractional flow reserve within the coronary tree. The color
coding represents fractional flow reserve values for the respective coronary artery branch.

(Left) Nonenhanced CT demonstrates coronary calcifications
of the proximal left anterior descending coronary
artery. (Right) Contrast-enhanced CT shows noncalcified plaque components. Here, a partially calcified plaque
without significant luminal stenosis in the proximal left anterior descending coronary artery is present. The inset
shows a cross-sectional view of the lesion.

18


Diagnostic Imaging Cardiovascular

(Left) Functional imaging via contrast-enhanced CT shows (top) left ventricular function with a regional wall motion
abnormality
in systole and (bottom) normal function of the aortic valve. (Right) Aortic annulus is shown before
(left) and after (right) transcatheter aortic valve replacement
. Note the oval shape prior to transcatheter aortic
valve replacement, which becomes round after a valve prosthesis has been placed.

Cardiac MR: Acquisition and Imaging Protocols

Introduction
Over the last several years, cardiovascular magnetic resonance (CMR) imaging has undergone rapid evolution, and
tremendous advances in pulse sequence design, scanner hardware, and coil technology have resulted in progressive
expansion of the clinical applications. In particular, new pulse sequences such as the late gadolinium enhancement
(LGE) technique have leveraged the inherently superior soft tissue contrast provided by MR to enable superb in vivo
viability imaging. These improvements have led to the recognition of CMR as the reference standard for the
assessment of regional and global systolic function, the detection of myocardial infarction and viability, and the
evaluation of pericardial disease and cardiac masses. This chapter provides a brief overview of the common
techniques used in CMR. Suggested protocols for imaging common disorders will be presented in a tabular format at
the end of this section.
CMR Techniques
A unique characteristic of MR imaging is that a variety of information can be obtained simply by selecting different
software sequences to probe the tissue characteristics of the organ in question.
Morphologic Images: Dark Blood Imaging
Morphologic black blood imaging is performed with single-shot double inversion-recovery fast spin-echo (IR-FSE) and
half-Fourier acquisition single-shot turbo spin-echo (HASTE) techniques. These result in still-frame images and are
acquired in the standard orthogonal imaging planes (i.e., axial, sagittal, or coronal). The repetition time is typically set
at 90% of the R-R interval and adjusted to null the signal from blood. The rapidity of acquisition is such that breath
holding is not required. These resulting images produce an excellent depiction of the overall myocardial structure and
the relationships of the great vessels.
Occasionally, segmented FSE images are acquired when higher spatial resolution &/or improved T1 or T2 weighting is
desired, such as when characterizing cardiac masses. These acquisitions take approximately 7-10 seconds per image
and require breath holding. They can be performed either with or without fat saturation. T2-weighted images are
helpful in demonstrating an edema, a finding useful in determining if an infarct is acute or chronic, and in diagnosing
myocarditis. Some evidence suggests that T2-weighted imaging may allow the depiction of the area at risk (but not
infarcted) from an acute ischemic injury, but the evidence is controversial.
T2* imaging using a multiecho gradient recall echo (GRE) sequence has proven to be an extremely accurate and useful
technique for quantifying cardiac iron deposition and is now considered the reference standard for monitoring and
managing cardiac iron overload syndromes (including thalassemia).
Morphologic Images: Bright Blood Imaging

The steady-state free precession (SSFP) sequence is now the standard sequence for bright blood imaging. With this
sequence, image contrast is not dependent on inflow effects (as with the older GRE sequences) but rather on the
T2/T1 ratio of the tissue being imaged. The result is a bright signal for intracavitary blood and a relatively dark
appearance for myocardium. Images can be rapidly acquired (typically in < 300-400 milliseconds per image). These
19


Diagnostic Imaging Cardiovascular
sequences do not require breath holding and are also a form of single-shot imaging. One image is typically acquired
during each heartbeat (at the same cardiac phase), and a stack of 30 images can be acquired in approximately 30
seconds. SSFP sequences are very useful in the evaluation of disorders producing intraluminal abnormalities (such as
aortic dissection).
Cine Imaging
The SSFP technique can be adapted for cine acquisition in which multiple images are obtained at a single-slice location
in rapid succession during different phases of the cardiac cycle and can be displayed as a continuous movie loop.
Typically, 20-30 frames per cycle are reconstructed. Cine imaging allows evaluation of ventricular wall motion
abnormalities, assessment of dynamic changes in wall thickness, and measurement of chamber sizes.
The standard cine sequence is a segmented, retrospectively gated acquisition in which the data are acquired
throughout the cardiac cycle and “time stamped” to allow assignment to the proper cardiac phase. The 6-8 mm slices
are acquired at 1 cm intervals in the short-axis plane from the mitral valve to the apex, and standard long-axis views
(2-, 3-, and 4-chamber views) are also obtained. A matrix of 256 × 200 is typically used, with a resultant spatial
resolution of 1-1.6 mm, and with a temporal resolution of < 45 milliseconds. The segmented acquisition indicates that
data from several heartbeats are combined to yield the image. Hence, irregularities in the patient's heart rate and
rhythm may degrade image quality.
In cases of arrhythmia, prospectively triggered acquisitions may be helpful. In this technique, images are acquired
beginning with the R wave and for a predetermined length of time (usually up to early or mid diastole). This can
remove some of the artifacts that result from irregular cycle lengths, as changes in heart rate predominately affect the
length of diastole rather than systole. Unfortunately, prospectively triggered acquisitions often result in the loss of the
terminal phase of diastole, and measurements of ventricular ejection fraction and chamber volumes from these
acquisitions may be slightly imprecise. If gating is unsuccessful, the arrhythmia is severe, or the patient cannot breathhold adequately, real-time cine acquisitions may be necessary. These acquisitions also employ SSFP sequences in a

single-shot rather than segmented fashion. Although these acquisitions have lower spatial and temporal resolution,
they may provide sufficient information for diagnosis. In addition, real-time cine acquisitions can be helpful in the
detection of dynamic processes because they can be acquired during inspiratory and expiratory maneuvers.
Perfusion Imaging
Perfusion imaging sequences are designed to demonstrate contrast media passage through the myocardium in a
manner that reliably reflects myocardial blood flow. It is desirable to have multiple slices during each heartbeat to
ensure sufficient ventricular coverage with high temporal resolution. The sequences used by various manufacturers
differ, but the general strategy is to acquire heavily T1-weighted images of the myocardium and to accurately depict
the passage of a T1-shortening contrast agent such as gadolinium.
Perfusion imaging is most often used for the detection of obstructive coronary artery disease, where
P.1:9
it is performed with pharmacological vasodilation (e.g., adenosine or regadenoson). During adenosine infusion,
myocardial blood flow increases approximately fourfold downstream of normal coronary arteries but does not
normally increase downstream of severely diseased arteries, because the arteriolar beds are already maximally
vasodilated. MR perfusion imaging is a first-pass imaging study that directly images the passage of contrast; therefore,
it is performed using an abbreviated adenosine protocol (approximately 3 minutes). MR perfusion imaging has higher
spatial resolution than nuclear techniques; thus, it can depict small subendocardial perfusion defects that may be
inapparent on nuclear techniques. Although research studies often emphasize complex postprocessing of the
perfusion data, recent reports using visual analysis demonstrate comparable sensitivity and specificity. Perfusion
imaging can also be used in the evaluation of suspected intracardiac shunts as well as in the characterization of
cardiac masses.
Viability Imaging (LGE Imaging)
Normal, infarcted, and scarred myocardia will all demonstrate contrast enhancement. However, they have different
contrast kinetics in that contrast will wash out of normal myocardium at a much more rapid rate than it will from
infarcted or scarred myocardium. In addition, areas of infarction, whether acute or chronic, will have a larger amount
of extracellular space and a greater volume of distribution for gadolinium contrast than will normal myocardium.
Accordingly, areas of prior infarction will have higher concentrations of contrast on delayed images (5-10 minutes
after intravenous administration). The LGE sequences used for infarct detection are designed to maximize the
differential signal intensity between normal myocardium and infarcted myocardium.
The standard LGE imaging sequence incorporates a segmented GRE read-out and an inversion prepulse to produce

heavy T1 weighting. The inversion pulse serves to flip the magnetization 180 degrees. The recovery of magnetization
back to baseline in areas that have a higher gadolinium concentration will be more rapid (as they have a lower T1
value) than in those with a lower concentration of gadolinium, such as normal myocardium. Therefore, the increased
concentration of gadolinium in an area of scar will be reflected by more rapid return above the zero-crossing line and
back to baseline longitudinal magnetization. The time after the inversion pulse at which normal myocardium is at the
20


Diagnostic Imaging Cardiovascular
zero-crossing line will result in maximum suppression of signal from a normal myocardium (the myocardium is said to
be “nulled”) and will result in maximum conspicuity of the area of infarction. At this time point, infarcted regions will
be well above the zero-crossing line and will therefore appear bright on these images. A phase-sensitive variant may
be used that can correct for errors in choosing the inversion time.
The standard LGE sequences are segmented acquisitions, acquired at every other heartbeat in order to allow normal
myocardial regions to recover longitudinal magnetization before the next inversion pulse is applied. Therefore, they
are constructed from the data of multiple heartbeats. Acquisition typically takes approximately 8-12 seconds. For
patients with significant arrhythmia or difficulty with breath holding, single-shot LGE images using an SSFP IR
sequence can provide a reasonable alternative in a fraction of the imaging time. These images are slightly lower in
contrast to noise ratio and have a mildly reduced sensitivity for the detection of infarction. Nevertheless, they provide
a satisfactory option in these circumstances. Single-shot LGE sequences may also be obtained with a long inversion
time (550-600 milliseconds). These are quite useful in the detection of thrombi. On these images, thrombi will appear
dark in contrast to normal myocardium and infarcted myocardium, which will be gray and bright in image intensity,
respectively.
Although predominately used for assessment of myocardial infarction and viability, the same LGE sequences can also
be helpful in a variety of other circumstances, such as the detection of viral myocarditis and cardiac involvement by
sarcoidosis.
Flow-Sensitive Imaging Using Velocity-Encoded Sequences (Phase-Contrast Imaging)
In this form of imaging, velocity-encoding phase shifts result from the sequential application of bipolar magnetic field
gradients, which are composed of two lobes with opposite polarities. These opposed gradients will produce a phase
shift with the first pulse that will be reversed by the second pulse. Therefore, stationary spins will acquire equal and

opposite phases in the two gradients and will have no net phase at the end of the sequence. However, flowing spins
passing through the imaging plane will acquire a net phase change, which will be dependent on their velocity in the
direction of the flow-encoding gradients.
These sequences are typically used in two situations: For quantification of gradients across stenotic valves and for
measurement of blood flow. The peak gradient across a stenotic valve can be calculated using the Bernoulli equation,
which is ΔP = 4V2, where velocity (V) is in meters per second and the pressure gradient (ΔP) is given in mm Hg. Flow is
simply the sum of the velocities through a given area over time. These measurements are typically performed during
postprocessing using a dedicated workstation.
Standard CMR Examination
At a minimum, a standard cardiac MR examination should provide a comprehensive evaluation of the structure and
function of the heart. Additionally, in the vast majority of patients, myocardial tissue characterization, with an
assessment of infarction, scarring, and viability, provides substantial clinical value at minimal time and cost. Therefore,
in most centers, a standard exam includes cine images in the short-axis plane from above the mitral valve through the
cardiac apex as well as in the standard orthogonal long-axis views (2-chamber, 4-chamber, and 3-chamber) or left
ventricular outflow tract views. LGE images spatially matched to the cine images are also typically obtained. Many
centers also obtain a stack of axial morphologic images throughout the chest. Additional sequences are added as
needed for specific clinical indications, such as flow studies in cases of suspected valvular disease, T2 sequences for
suspected myocarditis, etc.
The following pages include suggested acquisition protocols for various indications in a tabular format and images
demonstrating how to acquire the proper imaging planes in a step-by-step fashion.
P.1:10

Tables
Suggested Protocols by Indication

Indication

Left Ventricular Late
Morphologi Perfusion
Structure/Functio Gadolinium c Images

Images
n Cines
Enhanceme
nt
Ischemic heart disease Standard
Segmented
(chronic)
IR-FSE with
inversion
time set to
null
myocardium

21

Other
Modification
s
Single-shot
IR-SSFP with
long
inversion
time to
exclude
thrombus


Diagnostic Imaging Cardiovascular

Ischemic heart disease Standard

(acute myocardial
infarction)

Ischemic heart disease Standard (may
(stress testing)
perform after
stress perfusion)

Cardiomyopathy
Standard
(hypertrophic
cardiomyopathy,
amyloid, Fabry disease)

Myocarditis/sarcoid

As above; Pre-contrast
single-shot T2 is
IR SSFP mayoptional (to
be necessary look for
in ill or
edema, area
arrhythmic at risk)
patients
Done after
rest
perfusion
images

Segmented

IR-FSE with
inversion
time set to
null
myocardium

Segmented
IR-FSE with
inversion
time set to
null
myocardium
Arrhythmogenic right Standard + stack Inversion
ventricular
of 4-chamber
time of right
dysplasia/cardiomyopat cines through
ventricle
hy
right ventricular may be ˜ 30outflow tract;
40
right ventricular milliseconds
2-chamber view earlier than
for left
ventricle
Iron overload
Standard
Segmented
syndromes
IR-FSE with

inversion
time set to
null
myocardium
Valvular disorders

Standard (postcontrast cines are
sometimes
helpful)

To look for
Single-shot
microvascular IR-SSFP with
obstruction
long
inversion
time to
exclude
thrombus
3-4
images/beat
during
infusion of
adenosine (140
µg/kg/min) or
regadenoson,
with rest
images 10
minutes later
Hypertrophic Inversion

cardiomyopath time scout
y patients may series
show
(modified
abnormal
Look-Locker)
perfusion
has
despite normal characteristic
coronaries
abnormal
pattern in
amyloidosis
Pre-contrast Normal (as
Early
T2 images opposed to in enhancement
for edema acute coronary imaging for
quantificatio syndrome
global
n
patients)
relative
enhancement
Looking for
Fatfat is likely
suppressed
not useful
LGE is
sometimes
recommende

d

Multiecho
short-axis
GRE images
to evaluate
T2*

Standard + high- Segmented Aorta should
resolution cine
IR-FSE with be evaluated
images through inversion
in patients
22

Postprocessin
g allows
calculation of
T2* from
multiecho
GRE
sequence
Velocityencoded
images


Diagnostic Imaging Cardiovascular

affected valve

time set to with aortic
null
valve
myocardium pathology

Congenital heart disease Standard + stack
of 4-chamber and
short-axis cine
images through
atria

Segmented
IR-FSE with
inversion
time set to
null
myocardium

Mass

Standard

Tailored to
mass

Pericardium

Standard + realtime cine images
can show
abnormal septal

motion during
provocative
maneuvers

Segmented
IR-FSE with
inversion
time set to
null
myocardium

through the
affected valve
to measure
gradient
Axial,
May be helpfulVelocitysagittal, and in
encoded
coronal
demonstrating images
images
shunts
through the
throughout
proximal
chest
aorta and
pulmonary
artery to
quantify

Qp:Qs
T1 and T2 Very helpful inSingle-shot
images are assessing
IR-SSFP with
often
lesion
long
helpful, with vascularity
inversion
fattime to
suppression
exclude
as needed
thrombus
FSE images
Tagged
may show
images may
pericardial
confirm
thickening
abnormal
more clearly
adherence of
than HASTE
pericardial
or SSFP
layers
images

Diagnostic Findings in Specific Cardiomyopathies

Suspected Diagnosis
Amyloid

Arrhythmogenic right
ventricular
dysplasia/cardiomyopathy
Fabry disease

Hypertrophic
cardiomyopathy

Myocarditis

Structure/Function
LGE Module
Module
Thick ventricles, dilated Diffuse
atria
subendocardial
enhancement
Large right ventricle with2/3 of patients
poor function, regional show right
wall motion
ventricular
abnormalities
enhancement
Concentric hypertrophy Midwall
enhancement of

inferolateral basal
wall
Asymmetric, concentric, Positive at right
or apical forms
ventricular
insertion
sites/thickened
areas
Focal thickening, wall Lateral epicardial
motion abnormality
or midseptal
patterns common

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Other
Difficulty finding null
point on inversion time
scout series
Null point of right
ventricle may be slightly
earlier than for left
ventricle
Predominantly men

Extent of LGE
correlates with risk
factors for sudden death

T2-weighted images

may show edema; early
relative global
hyperenhancement


Diagnostic Imaging Cardiovascular

Sarcoid

Focal thickening, wall
motion abnormality

Patchy uptake with Mediastinal/hilar
basal/septal
adenopathy is often
predominance
noted

P.1:11

Image Gallery

(Left) Axial low-resolution SSFP scout image is used to begin scan planning. To acquire the scout 2-chamber long-axis
view, a line is placed bisecting the left ventricular (LV) apex and the mitral valve. (Right) Vertical long-axis (2-chamber)
scout SSFP view is then used to obtain the 4-chamber scout view. The imaging plane is acquired by placing a line
paralleling the long axis of the LV through the LV apex and left atrium as shown. This results in the low-resolution 4chamber scout SSFP image.

(Left) Four-chamber view scout SSFP image is used to obtain the short-axis scout image for planning the stack of shortaxis cine images. The imaging plane is placed perpendicular to the septum and lateral wall and parallels the mitral
valve as shown. (Right) Short-axis scout SSFP image is then copied using the standard, high-resolution cine SSFP
technique after assuring that no wrap artifact has been produced and that the image is appropriately centered.

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Diagnostic Imaging Cardiovascular

(Left) Short-axis stack of SSFP cine images is then acquired from the mitral valve plane through the LV apex using their
positions on the 4-chamber view to assure proper coverage. A diastolic image is used as the plane of the mitral valve
may move toward the apex in systole. (Right) Short-axis SSFP cine image is used to plan the 3-chamber or left
ventricular outflow tract view (LVOT) by placing an imaging plane through the mitral valve and aortic valve as seen on
the basilar short-axis view.
P.1:12

(Left) Short-axis MR cine image is used to plan the high-resolution 4-chamber cine view by placing a line through the
basal septum that is roughly perpendicular to the septum and parallel to the inferior margin of the heart. Care should
be taken to avoid the inferior aspect of the aortic valve, which can be confused with a septal defect if included. (Right)
Short-axis MR cine is used to plan the 2-chamber view by placing an imaging plane to bisect the anterior and inferior
LV walls.

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