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(BQ) Part 1 book Diagnostic imaging cardiovascular presents the following contents: Introduction and overview, congenital, shunts, valvular, pericardial, cardiomyopathy, neoplastic. Invite you to consult.
Diagnostic Imaging Cardiovascular Diagnostic Imaging Cardiovascular Contents Editors Dedication Foreword Preface 10 Acknowledgments 10 Section - Introduction and Overview 11 Cardiac CT: Acquisition and Postprocessing Indications and Interpretation .11 Cardiac MR: Acquisition and Imaging Protocols 19 Cardiac Anatomy 28 Section - 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 - 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 - 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 Diagnostic Imaging Cardiovascular Rheumatic Heart Disease 361 Left Ventricular Apical Aortic Conduit 367 Section - 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 - 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 - 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 - 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 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 - 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 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 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 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 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 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 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 10 Diagnostic Imaging Cardiovascular o Also frequently noted is thinning of LV wall, particularly involving apex, resulting in apical aneurysm (vortex lesion), a characteristic feature of Chagas heart disease Location o Apex and inferolateral segment of LV Morphology o 60-80% of infected cases not progress to clinical abnormalities Termed the indeterminate chronic stage Most will have preserved LV morphology and function, but 15-20% may show abnormal results on LGE MR o Progressive chronic disease is seen in 20-40% of cases Most common clinical manifestation: Chagas cardiomyopathy Dilated cardiomyopathy with global cardiac enlargement Imaging Recommendations Best imaging tool o LGE MR may demonstrate predominantly midwall and subepicardial hyperenhancement areas encompassing multiple coronary territories (nonischemic pattern) o Echocardiography, cine MR, and gated CTA (advanced clinical phase) show global biventricular dysfunction with segmental akinesis and aneurysms, usually involving LV apex and inferolateral walls Protocol advice o LGE MR should be included in any cardiac MR protocol for cardiomyopathy evaluation o Delayed-enhancement imaging patterns may provide specific diagnosis of cardiomyopathies Radiographic Findings Global cardiomegaly, pulmonary vascular congestion, pulmonary edema Echocardiographic Findings First-line tool for morphologic and functional evaluation Increased LV volumes Segmental or global wall motion abnormalities Apical aneurysm and intracavitary thrombus MR Findings MR cine o Cine imaging is useful in demonstrating location, extent, and severity of global and regional systolic dysfunction Dysfunction is often most severe in apex and lateral wall LGE enhancement o Extent of myocardial fibrosis shown on LGE MR correlates with global and regional function assessments and may reveal subclinical Chagas heart disease Prevalence of fibrosis on LGE MR images varies with disease severity Indeterminate/asymptomatic phase: 20% positive on LGE MR Symptomatic patients with cardiomyopathy: 85% positive on LGE MR Cardiomyopathy patients with ventricular tachycardia: 100% positive on LGE MR o Fibrosis is seen as abnormal enhancement on LGE MR Usually nonischemic pattern (midwall and subepicardial location in multiple coronary artery distributions) Subendocardial enhancement mimicking CAD may be seen in small percentage of cases o LGE MR imaging with long inversion time (˜ 600 milliseconds) is most sensitive and specific technique for evaluation of thrombus CT Findings Gated coronary CTA is occasionally useful in excluding significant coronary artery disease in selected Chagas patients with atypical chest pain Angiographic Findings Typical LV apical aneurysm (vortex lesion) Normal epicardial coronary arteries DIFFERENTIAL DIAGNOSIS Viral Myocarditis Serologic tests for Trypanosoma cruzi are negative Geographic history does not include endemic regions Imaging in viral myocarditis often occurs in acute phase and frequently shows T2 signal abnormalities (edema) 598 Diagnostic Imaging Cardiovascular Ischemic Cardiomyopathy May also produce apical aneurysm LGE MR findings usually follow ischemic wavefront pattern (beginning in subendocardium and extending toward epicardium) in coronary artery distribution Endocardial involvement is hallmark for ischemic lesions Apical Hypertrophic Cardiomyopathy Often complicated by formation of apical aneurysm, which usually shows delayed enhancement LV function is preserved Takotsubo Cardiomyopathy A form of nonischemic cardiomyopathy in which there is sudden temporary dysfunction of myocardium P.7:56 o Dysfunction is manifested as apical dilatation or “ballooning” Usually triggered by severe emotional stress Congenital Aneurysm Imaging pattern may be indistinguishable from that of Chagas disease, showing fibrotic apical aneurysms o LGE MR is abnormal in 70% Serologic tests for Trypanosoma cruzi are negative Geographic history does not include endemic regions PATHOLOGY General Features Etiology o Caused by flagellate protozoa Trypanosoma cruzi o Insect vectors of Chagas disease belong to Hemiptera order, Reduviidae family, and Triatominae subfamily (“kissing bugs”) Associated abnormalities o Megaesophagus and megacolon Gross Pathologic & Surgical Features Cardiomegaly with ventricular wall thinning/aneurysm formation Microscopic Features Intracellular parasite multiplication → rupture of infected cells → inflammatory response → fibrosis Cellular lesions mainly affect myocytes (causing myocytolysis) and nervous cells (leading to autonomic denervation) Arteriolar dilatation with organized thrombi and severe diffuse fibrosis in watershed myocardial regions (LV apex and basal inferior LV wall) CLINICAL ISSUES Presentation Most common signs/symptoms o Typically, arrhythmias, cardiac failure, thromboembolic phenomena, or sudden death o Atypical chest pain without evidence of coronary artery disease (15-20% of patients) o Chagas heart disease is the most frequent and serious manifestation of symptomatic chronic disease Demographics Age o Symptomatic acute phases mainly occur in newborns or young children o Chronic Chagas cardiomyopathy is generally detected in 3rd-5th decades of life Gender o Chronic cardiomyopathy occurs earlier and is more severe in males than in females Epidemiology o In USA, according to estimates, 100,000-675,000 immigrants from Latin America are infected with Trypanosoma cruzi o Internationally, estimated 8-10 million people are infected in Latin America 200,000 new cases per year Natural History & Prognosis Acute phase (1 week after initial infection) o Usually asymptomatic o Mortality in < 5% of cases Death results from acute myocarditis &/or meningoencephalitis 599 Diagnostic Imaging Cardiovascular Chronic phase o Indeterminate form: No symptoms; normal ECG; normal radiological study of heart, esophagus, and colon 60-80% of patients in indeterminate phase remain asymptomatic and never develop chronic lesions o Clinical forms: Cardiac, digestive, and mixed In endemic areas, Chagas heart disease is the most common cause of cardiomyopathy and is a leading cause of cardiovascular death of patients aged 30-50 years (21,000 deaths annually) o Independent prognostic factors in chronic Chagas disease Cardiomegaly with impaired LV function (New York Heart Association class III/IV) Nonsustained ventricular tachycardia Treatment Acute phase: Always requires treatment with benznidazole; cures 100% of children < years old and 60-70% of acutely infected older patients Chronic cardiac phase o Diuretics, digitalis, angiotensin-converting enzyme inhibitors, and other standard heart failure therapies o Class III antiarrhythmic drugs (sotalol and amiodarone) o Anticoagulant treatment is justified in patients at risk for thromboembolic complications DIAGNOSTIC CHECKLIST Consider Chagas disease in patients from endemic areas who present with new-onset heart failure Image Interpretation Pearls Look for apical aneurysm and abnormal enhancement on LGE MR SELECTED REFERENCES Peix A et al: Myocardial perfusion imaging and cardiac involvement in the indeterminate phase of chagas disease Arq Bras Cardiol 100(2):114-117, 2013 Buysschaert I et al: Stone heart or apical retraction and calcification in Chagas' cardiomyopathy Eur Heart J Cardiovasc Imaging 13(7):625, 2012 Mello RP et al: Delayed enhancement cardiac magnetic resonance imaging can identify the risk for ventricular tachycardia in chronic Chagas' heart disease Arq Bras Cardiol 98(5):421-30, 2012 Valdigem BP et al: Accuracy of epicardial electroanatomic mapping and ablation of sustained ventricular tachycardia merged with heart CT scan in chronic Chagasic cardiomyopathy J Interv Card Electrophysiol 29(2):119-25, 2010 Marcu CB et al: Chagas' heart disease diagnosed on MRI: the importance of patient “geographic” history Int J Cardiol 117(2):e58-60, 2007 P.7:57 Image Gallery 600 Diagnostic Imaging Cardiovascular (Left) Four-chamber view cine (left) and LGE MR images (right) in a patient with Chagas disease show apical thinning and ballooning on the systolic cine image Enhancement is seen in the apex on the LGE MR image, a typical finding in Chagas disease (Right) Two-chamber cine image (left) shows systolic apical ballooning in a patient with Takotsubo cardiomyopathy (Left) Short-axis (left) and 4-chamber (right) LGE MR images show nearly transmural lateral wall enhancement in a patient with Chagas disease The lateral wall is commonly involved in this disorder, particularly at the base There is also a small focus of enhancement of the anteroseptum (Right) Short-axis (left) and 4-chamber (right) LGE MR images of a patient with viral myocarditis demonstrate subepicardial lateral wall enhancement in a pattern commonly seen in this entity (Left) Four-chamber cine (top) and LGE (bottom) MR images of a Chagas aneurysm show systolic outpouching on the cine image & enhancement of the apex on the LGE MR (Right) Four-chamber view cine (top) and LGE (bottom) MR images of a patient with apical hypertrophic cardiomyopathy show an apical aneurysm Note there are hypertrophic changes in the adjacent segments that produce cavity obliteration in the systolic cine image (top), a finding not seen in Chagas aneurysms Iron Overload Syndromes Key Facts Terminology Iron overload syndromes Primary form: Hemochromatosis o Autosomal recessive genetic disorder resulting in abnormal uptake of dietary iron Secondary form: a.k.a transfusional siderosis, secondary hemochromatosis, or transfusional iron overload 601 Diagnostic Imaging Cardiovascular o Results from transfusion therapy of hereditary anemias characterized by ineffective erythropoiesis and hemolysis Thalassemia major and intermedia are most common worldwide o Imaging Low signal intensity of heart &/or liver on T2-weighted MR images should suggest diagnosis of iron overload Excess iron levels can be displayed qualitatively on T2- or T2*-weighted MR images by hypointense signal changes in affected organs T2* MR imaging can be used to quantify myocardial iron levels Top Differential Diagnoses Hemochromatosis o Normal appearance of spleen and bone marrow suggests hemochromatosis Transfusional iron overload o Abnormal amounts of iron accumulate 1st in reticuloendothelial system of liver, spleen, and bone marrow o Pancreas is initially spared but may be involved once reticuloendothelial system capacity is exceeded o Cardiac imaging findings are indistinguishable from those of hemochromatosis (Left) Vertical long-axis (2-chamber) MR cine image of a patient with iron overload cardiomyopathy demonstrates abnormally low signal intensity in both the myocardium and the liver The left ventricle is noted to be dilated, a finding commonly seen as the disease progresses (Right) Axial NECT shows diffusely increased attenuation throughout the myocardium , consistent with extensive myocardial iron deposition The left ventricular cavity is dilated, indicative of systolic dysfunction (Left) This SSFP MR cine image shows dark, amorphous artifact in the right ventricle , consistent with the dark banding artifact often seen with SSFP images It is accentuated by the field inhomogeneity induced by the extensive 602 Diagnostic Imaging Cardiovascular iron present in the patient's tissues due to iron overload (Right) Short-axis MR cine images (same patient) using SSFP (left) and GRE (right) sequences illustrate that the extensive banding artifact present on SSFP can often be circumvented by using GRE cine images P.7:59 TERMINOLOGY Abbreviations Iron overload syndromes (IOSs) Definitions Primary form: Hemochromatosis o Autosomal recessive genetic disorder resulting in abnormal uptake of dietary iron o Progressive increase in total body iron stores with abnormal multiorgan parenchymal iron deposition Not in reticuloendothelial system o Liver is primary site of abnormal iron deposition (leading to cirrhosis), although abnormal iron deposition can also occur in the heart (resulting in cardiomyopathy), pancreas (causing diabetes), or pituitary gland (resulting in hypogonadism) Cirrhosis and hepatocellular carcinoma are greatly increased in frequency, along with heart failure in untreated cases Secondary form: a.k.a transfusional siderosis, secondary hemochromatosis, or transfusional iron overload o Results from transfusion therapy used in treatment of hereditary anemias characterized by ineffective erythropoiesis and hemolysis Thalassemia major and intermedia are most common worldwide Commonly require 1-2 transfusions/month beginning in early infancy unit of packed cells contains 200-250 mg of iron (normal dietary uptake = 1-2 mg/d) Cardiac involvement is most common cause of death, with 50% of patients dying before age 35 o Excessive iron is initially localized to reticuloendothelial system, but when storage is overwhelmed, iron is deposited in multiple tissues in pattern similar to hemochromatosis Liver, spleen, and bone marrow are initially involved Pancreas is initially spared but may become involved later as iron overload progresses Cardiac involvement is most common cause of death IMAGING General Features Best diagnostic clue o Low signal intensity of heart &/or liver on T2-weighted MR images should suggest diagnosis of iron overload o Excess iron levels can be displayed qualitatively on MR by hypointense signal changes in affected organs on T2- or T2*-weighted images o Echocardiography or MUGA scan can depict heart failure from iron overload in later stages of disease but not identify etiology of disease Location o Diffuse involvement of myocardium is characteristic, but inhomogeneous involvement occasionally occurs Morphology o Although initially there may be restrictive cardiomyopathy produced, progressive cardiac iron loading results in dilated cardiomyopathy associated with systolic dysfunction Imaging Recommendations Best imaging tool o T2* MR imaging can be used to quantify myocardial iron levels Protocol advice o Breath-hold T2* GRE images with varying echo times (TEs) should be obtained to provide estimation of cardiac iron load o Standard short- and long-axis MR cine series should be obtained for evaluation of cardiac function CT Findings NECT o Global hyperdensity of myocardium &/or liver may be noted 603 Diagnostic Imaging Cardiovascular MR Findings T2* GRE o Can be done in a single breath-hold using GRE sequence with multiple TEs o Signal dropout with progressively longer TEs is greatly accelerated in patients with cardiac iron deposition o Iron deposition results in local field inhomogeneities that result in T2* shortening Degree of T2* shortening is closely correlated with degree of iron deposition Signal intensity measurements are typically obtained on short-axis midventricular images using region of interest positioned in the septum Postprocessing with dedicated software facilitates calculation of myocardial T2* values from a plot of signal intensity relative to changing TE T2* value < 10 milliseconds indicates severe iron loading (in study, ˜ 89% of thalassemia patients with new-onset failure had T2* < 10 milliseconds) T2* value of 10-20 milliseconds indicates mild to moderate iron loading T2* value > 20 milliseconds is in normal range (normal mean: ˜ 40 milliseconds) o Efficacy of iron reduction treatment is also best assessed in this way MR cine o Myocardial functional evaluations should show hyperdynamic contractility in unaffected anemic patients Apparently normal function is abnormal in these patients and may be an early marker of cardiac involvement Cine SSFP images may show reduced signal of the myocardium as they are relatively T2 weighted Significant iron loading may be present before function becomes abnormal o However, once functional abnormalities develop, rapid progression to severe failure, arrhythmia, or death occurs Ultrasonographic Findings Echocardiography may show restrictive physiology in initial stages and systolic dysfunction in later stages o Not recommended as screening tool (insensitive), because significant iron deposition may be present before echocardiographic abnormalities develop P.7:60 DIFFERENTIAL DIAGNOSIS Hemochromatosis Both primary and secondary forms of IOS produce dark liver on MR images o However, there is poor correlation between hepatic and cardiac iron loading in either disorder Normal appearance of spleen and bone marrow suggests hemochromatosis Pancreas and pituitary involvement is seen early in hemochromatosis Transfusional Iron Overload Abnormal amounts of iron accumulate 1st in reticuloendothelial system of liver, spleen, and bone marrow Pancreas is initially spared but may be involved once reticuloendothelial system capacity is exceeded Cardiac imaging findings are indistinguishable from those of hemochromatosis PATHOLOGY General Features Etiology o Excess unbound iron deposited in the myocardium is highly cardiotoxic Mitochondrial respiratory chain function is impaired, resulting in inadequate ATP production and eventual heart failure Genetics o Hemochromatosis is autosomal recessive genetic disorder characterized by excessive uptake of dietary iron 80% of cases are due to mutation in HFE gene, most commonly p.C282Y mutation Mutation leads to inadequate production of hepcidin, a protein that negatively modulates uptake of dietary iron There is no excretory pathway in humans to eliminate excess iron, and thus iron build-up ensues Patients homozygous for the gene show low penetrance for clinical disease, with probably < 3% developing significant disease 604 Diagnostic Imaging Cardiovascular o Beta-thalassemia is the most common worldwide hereditary anemia resulting in transfusional iron overload Homozygous patients will develop severe anemia early in life and require transfusions to survive Iron loading predominantly results from transfusions but may also reflect down-regulation of hepcidin production related to ineffective erythropoiesis This results in excessive dietary uptake of iron as well Associated abnormalities o Hemochromatosis Excessive liver deposition with development of cirrhosis, portal hypertension, and hepatocellular carcinoma Excessive pancreatic iron deposition can result in type diabetes mellitus Abnormal deposition in skin results in bronze skin color Pituitary hypogonadism o Transfusional iron overload/thalassemia Severe anemia may be present if transfusion is inadequate Frontal bossing (protuberance of frontal bones) may develop due to bone marrow expansion CLINICAL ISSUES Presentation Most common signs/symptoms o Congestive heart failure in setting of significant cardiac involvement Demographics Age o Hemochromatosis Patients often present in their 40s and 50s M>F o Transfusional siderosis Patients often have cardiac involvement by early adulthood Epidemiology o HFE-related primary form occurs predominantly in white populations of Northern European descent Prevalence of p.C282Y gene homozygosity is 1:200 in this population Natural History & Prognosis Once iron-related cardiac impairment has developed, the natural history is that of inexorable progression to heart failure and death Treatment Transfusional iron overload is treated by chelation therapy using deferoxamine (intravenous or subcutaneous) often coupled with deferiprone orally Hemochromatosis is treated by weekly phlebotomy until iron levels return to a normal range, and then bimonthly DIAGNOSTIC CHECKLIST Consider IOSs when low cardiac or hepatic signal intensity is noted on T2-weighted images SELECTED REFERENCES Siddique A et al: Review article: the iron overload syndromes Aliment Pharmacol Ther 35(8):876-93, 2012 Carpenter JP et al: On T2* magnetic resonance and cardiac iron Circulation 123(14):1519-28, 2011 Alexander J et al: HFE-associated hereditary hemochromatosis Genet Med 11(5):307-13, 2009 Kirk P et al: Cardiac T2* magnetic resonance for prediction of cardiac complications in thalassemia major Circulation 120(20):1961-8, 2009 Anderson LJ et al: Cardiovascular T2-star (T2*) magnetic resonance for the early diagnosis of myocardial iron overload Eur Heart J 22(23):2171-9, 2001 P.7:61 Image Gallery 605 Diagnostic Imaging Cardiovascular (Left) Short-axis MR cine image of a mild transfusional ion overload syndrome (IOS) shows normal cardiac signal but very dark liver and spleen signals, as they are part of the reticuloendothelial system Note that the pancreas is normal in signal intensity as expected early in transfusional IOS In contrast, hemochromatosis often shows pancreatic but not splenic involvement (Right) Short-axis MR cine of a severe transfusional IOS shows low pancreatic signal as well as cardiac and hepatic involvement (Left) Short-axis MR (left) and T2 FSE (right) images of a hemochromatosis patient show hepatic iron overload (low hepatic signal ) but normal cardiac signal intensity There can be significant discrepancy in the degree of iron loading between the liver and the heart (Right) Short-axis GRE images with varying echo times (4 ,7 , 10 , and 15 milliseconds) were obtained at a single slice location and show no signal dropout that would indicate abnormal iron deposition 606 Diagnostic Imaging Cardiovascular (Left) Short-axis GRE images with varying echo times (2.4 , 5.4 , 8.3 , and 11.3 milliseconds) were obtained at a single slice location and show extensive signal dropout, which indicates abnormal iron deposition (Right) Software analysis of the signal intensity of a selected region of the septum relative to the varying echo times allows calculation of the T2* value of the myocardium The T2* value of 5.7 milliseconds is consistent with severe iron loading in a patient with thalassemia Takotsubo Cardiomyopathy Key Facts Terminology Reversible left ventricular systolic dysfunction in absence of significant coronary artery stenosis Also known as stress cardiomyopathy or apical ballooning syndrome Classically described following periods of severe emotional or physical stress Imaging Initial imaging test is usually echocardiogram or left ventriculogram during cardiac catheterization Cardiac MR is best imaging modality to distinguish from other causes of left ventricular dysfunction, such as myocarditis or ischemic injury o Increased T2 signal (edema) in areas of hypokinesis o Areas of hypokinesis/akinesis can occur in various patterns o In large series using cardiac MR in stress cardiomyopathy, apical ballooning was seen in 82%, biventricular hypokinesis in 34%, midventricular hypokinesis in 17%, and basal hypokinesis in 1% Late gadolinium enhancement MR o Typically characterized by absence of significant late gadolinium enhancement o ˜ 9% can have minimal or subtle late gadolinium enhancement, particularly when lower signal intensity threshold is used Clinical Issues Initial presentation can closely resemble that of acute myocardial infarction or acute coronary syndrome In hospital, mortality range is 0-8% Most patients typically recover left ventricular function within weeks Most common complication is heart failure ± pulmonary edema Treatment is supportive using standard heart failure therapy 607 Diagnostic Imaging Cardiovascular (Left) Three-chamber view graphic shows the most common type of stress cardiomyopathy with severe hypokinesis of all apical segments resulting in apical ballooning This results in a left ventricular (LV) shape resembling the Japanese octopus trap (takotsubo), which gave the entity its name (Right) Vertical long-axis (2-chamber) MR cine image in systole shows a typical pattern of stress cardiomyopathy with akinesis of the mid to apical LV and normal contraction of the basal LV (Left) Vertical long-axis (2-chamber) late gadolinium enhancement (LGE) image of the LV shows no focal areas of abnormal LGE, which is typical in stress cardiomyopathy (Right) Axial T1-weighted spin-echo sequence after gadolinium contrast is shown The early global relative enhancement ratio is calculated by comparing pre- and postcontrast signal intensity in the myocardium normalized to skeletal muscle In this case of stress cardiomyopathy, the ratio was abnormal at P.7:63 TERMINOLOGY Synonyms Stress cardiomyopathy Apical ballooning syndrome Definitions Reversible dysfunction of left ventricle (LV) in absence of significant coronary artery stenosis o Classically described following periods of severe emotional or physical stress In recent prospective multicenter study, stressful trigger was identified in ˜ 70% of patients o Often accompanied by acute chest pain, ischemic ST segment abnormalities, and elevation of cardiac biomarkers 608 Diagnostic Imaging Cardiovascular IMAGING General Features Best diagnostic clue o Regional wall motion abnormalities in setting of recent emotional or physical stress o In its most common variant, LV during systole resembles Japanese octopus pot, which has narrow mouth and large round base Tako = octopus; tsubo = pot o Wall motion abnormalities often extend beyond a single coronary artery territory Location o Most common variant features distinct apical ballooning with hypokinesis of mid to apical LV with preserved or hyperdynamic function at the base o Other patterns of LV dysfunction include biventricular, midventricular, and basal Imaging Recommendations Best imaging tool o Initial imaging test is usually echocardiogram or left ventriculogram during cardiac catheterization o Cardiac MR is best imaging modality to distinguish from other causes of LV dysfunction, such as myocarditis or ischemic injury Protocol advice o SSFP cine images in horizontal long-axis, vertical long-axis, and short-axis views o Short-axis T2-weighted images, which typically show evidence of myocardial edema in areas of hypokinesis o Late gadolinium enhancement (LGE) images can help differentiate from other causes of cardiomyopathy Nuclear Medicine Findings Myocardial perfusion defects can be seen and may be related to microvascular dysfunction o Can be difficult to exclude ischemic heart disease on basis of nuclear myocardial perfusion CT Findings Cardiac gated CTA o Absence of obstructive epicardial coronary artery disease o Functional assessment on multiphase reconstructions can show patterns of wall motion abnormalities consistent with stress cardiomyopathy MR Findings T2WI FS o Increased T2 signal (edema) in areas of hypokinesis Can be quantified by normalizing to skeletal muscle (following same protocol as for myocarditis) MR cine o Areas of hypokinesis/akinesis can occur in various patterns Findings in large series using cardiac MR in stress cardiomyopathy Apical ballooning in 82% Biventricular hypokinesis in 34% Midventricular hypokinesis in 17% Basal hypokinesis in 1% o Pericardial effusion is seen in ˜ 40% of patients o LV thrombus is relatively uncommon finding LGE enhancement o ˜ 9% can have minimal or subtle LGE, particularly when lower signal intensity threshold is used Echocardiographic Findings Regional wall motion abnormalities (apical ballooning, biventricular, midventricular, and basal) Can be difficult to appreciate extent and severity of regional wall motion abnormalities if acoustic windows are limited Does not allow myocardial tissue characterization Angiographic Findings Absence of significant coronary artery disease Left ventriculogram shows typical regional wall motion abnormalities Rarely, multivessel epicardial spasm is evident, which may be spontaneous or induced by ergonovine or acetylcholine infusion Image-Guided Biopsy 609 Diagnostic Imaging Cardiovascular Endocardial biopsy shows nonspecific findings without evidence of myocardial necrosis DIFFERENTIAL DIAGNOSIS Acute Myocardial Infarction Given presentation of chest pain, ischemic ECG changes, and regional wall motion abnormalities, coronary artery disease should always be excluded o Anatomic assessment with coronary angiography or cardiac CT Ischemic pattern of LGE on cardiac MR o Subendocardial LGE in distribution of a coronary artery Acute Myocarditis Subepicardial or midmyocardial pattern of LGE Increase in T2 signal and increased early global relative enhancement can be seen in both stress cardiomyopathy and myocarditis Coronary Vasospasm Prinzmetal angina Due to focal coronary artery vasospasm May be associated with acute myocardial infarction, serious ventricular arrhythmias, and sudden death P.7:64 PATHOLOGY General Features Etiology o Precipitated by emotional or physical stress in most patients o Precise pathophysiology is not well established o Increased sympathetic activity has been suggested as central mechanism o Microvascular dysfunction o Cardiac MR shows evidence of myocardial edema and inflammation Microscopic Features Endomyocardial biopsy shows disorganized contractile proteins, increased collagen-1, and no evidence of cell necrosis CLINICAL ISSUES Presentation Most common signs/symptoms o Initial presentation can closely resemble that of acute myocardial infarction or acute coronary syndrome Chest pain and dyspnea Spectrum of ECG changes, including ST elevation, ST depression, T-wave inversion o Mild elevation of cardiac biomarkers (troponin I or T, CK-MB) Degree of elevation of biomarkers often does not correlate with extent of ventricular dysfunction o Congestive heart failure Elevated jugular venous pressure on exam Pulmonary edema Hypotension Other signs/symptoms o Patients may have more serious presentations, such as cardiogenic shock or ventricular fibrillation Demographics Age o Majority of cases are in postmenopausal females Gender o M:F = 1:6 Epidemiology o May account for 2% of patients presenting with acute coronary syndrome Natural History & Prognosis Mortality range in hospitals: 0-8% o Most patients recover LV function within weeks o Recurrence occurs in ˜ 10% of patients Most common complication is heart failure ± pulmonary edema 610 Diagnostic Imaging Cardiovascular o o o May have increased risk of thrombus formation in akinetic apex Tachy- and bradyarrhythmias Transient LV outflow tract obstruction has been described Treatment Supportive care with standard heart failure medications (β-blockers, angiotensin-converting enzyme [ACE] inhibitor, diuretics) o Optimal duration of therapy is unclear Intra-aortic balloon counterpulsation in cases of refractory shock Anticoagulation in cases of apical thrombus formation DIAGNOSTIC CHECKLIST Consider Echocardiogram &/or LV ventriculogram are often 1st imaging tests Cardiac MR can help distinguish between other causes of cardiomyopathy and allows for additional myocardial tissue characterization Image Interpretation Pearls On cardiac MR, both myocarditis and stress cardiomyopathy can present with myocardial edema and increased early global relative enhancement SELECTED REFERENCES Eitel I et al: Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy JAMA 306(3):277-86, 2011 King A: Cardiomyopathies: CMR sheds new light on the clinical profile of stress cardiomyopathy Nat Rev Cardiol 8(9):480, 2011 Hurst RT et al: Takotsubo cardiomyopathy: a unique cardiomyopathy with variable ventricular morphology JACC Cardiovasc Imaging 3(6):641-9, 2010 Sharkey SW et al: Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy J Am Coll Cardiol 55(4):333-41, 2010 Celik T et al: Stress-induced (Takotsubo) cardiomyopathy: a transient disorder Int J Cardiol 131(2):265-6, 2009 Rolf A et al: Immunohistological basis of the late gadolinium enhancement phenomenon in tako-tsubo cardiomyopathy Eur Heart J 30(13):1635-42, 2009 Dorfman TA et al: An unusual manifestation of Takotsubo cardiomyopathy Clin Cardiol 31(5):194-200, 2008 Arora S: Autonomic imbalance in patients with takotsubo cardiomyopathy: cause or association? QJM 100(9):5934; author reply 594-6, 2007 Cocco G et al: Stress-induced cardiomyopathy: a review Eur J Intern Med 18(5):369-79, 2007 10 Haghi D et al: Guidelines for diagnosis of takotsubo (ampulla) cardiomyopathy Circ J 71(10):1664; author reply 1665, 2007 11 Kawai S: Typical and atypical forms of takotsubo (ampulla) cardiomyopathy Circ J 71(10):1665, 2007 12 Kimura K et al: Images in cardiovascular medicine Rapid formation of left ventricular giant thrombus with Takotsubo cardiomyopathy Circulation 115(23):e620-1, 2007 13 Matsuzaki M: Stress ‘Takotsubo’ cardiomyopathy: questions still remain Nat Clin Pract Cardiovasc Med 4(11):577, 2007 14 Nanda S et al: Takotsubo cardiomyopathy—a new variant and widening disease spectrum Int J Cardiol 120(2):e34-6, 2007 15 Pilgrim TM et al: Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: A systematic review Int J Cardiol 2007 16 Gianni M et al: Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review Eur Heart J 27(13):1523-9, 2006 17 Iqbal MB et al: Stress, emotion and the heart: tako-tsubo cardiomyopathy Postgrad Med J 82(974):e29, 2006 18 Bybee KA et al: Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction Ann Intern Med 141(11):858-65, 2004 P.7:65 Image Gallery 611 Diagnostic Imaging Cardiovascular (Left) Three-chamber view echocardiogram image shows hypokinesis of the mid to apical LV in an elderly woman presenting with chest pain and anterior ST elevations shortly after learning of the death of a loved one (Right) Coronary angiography (same patient) shows absence of significant obstructive coronary artery disease of the left circumflex and left anterior descending coronary arteries The right coronary artery (not shown) was also normal (Left) Left ventriculography image was obtained during diastole in the cardiac catheterization lab via a pigtail catheter (Right) Left ventriculography image was obtained in the cardiac cath lab during systole Note severe hypokinesis of the mid to apical segments of the LV with preserved contractility of the basal segments This pattern of regional wall motion abnormality, coupled with the absence of obstructive coronary artery disease, is consistent with stress cardiomyopathy 612 ... 11 03 Acute Ischemic Stroke 11 08 Atherosclerosis, Extracranial 11 18 Carotid Stenosis, Extracranial 11 24 Carotid Dissection 11 29... Extracranial 11 35 Vertebral Dissection 11 40 Subclavian Steal Syndrome 11 46 Section 15 - Renal Vasculature 11 52 Approach to Renal Vasculature... Nodosa 11 76 Renal Arteriovenous Fistula 11 82 Renal Vein Thrombosis 11 88 Section 16 - Peripheral Vasculature 11 94 Introduction and