Imaging Features of Arrhythmogenic Cardiomyopathies.

Arrhythmogenic cardiomyopathy (ACM) is a genetic disease characterized by replacement of ventricular myocardium with fibrofatty tissue, predisposing the patient to ventricular arrhythmias and/or sudden cardiac death. Most cases of ACM are associated with pathogenic variants in genes that encode desmosomal proteins, an important cell-to-cell adhesion complex present in both the heart and skin tissue. Although ACM was first described as a disease predominantly of the right ventricle, it is now acknowledged that it can also primarily involve the left ventricle or both ventricles. The original right-dominant phenotype is traditionally diagnosed using the 2010 task force criteria, a multifactorial algorithm divided into major and minor criteria consisting of structural criteria based on two-dimensional echocardiographic, cardiac MRI, or right ventricular angiographic findings; tissue characterization based on endomyocardial biopsy results; repolarization and depolarization abnormalities based on electrocardiographic findings; arrhythmic features; and family history. Shortfalls in the task force criteria due to the modern understanding of the disease have led to development of the Padua criteria, which include updated criteria for diagnosis of the right-dominant phenotype and new criteria for diagnosis of the left-predominant and biventricular phenotypes. In addition to incorporating cardiac MRI findings of ventricular dilatation, systolic dysfunction, and regional wall motion abnormalities, the new Padua criteria emphasize late gadolinium enhancement at cardiac MRI as a key feature in diagnosis and imaging-based tissue characterization. Conditions to consider in the differential diagnosis of the right-dominant phenotype include various other causes of right ventricular dilatation such as left-to-right shunts and variants of normal right ventricular anatomy that can be misinterpreted as abnormalities. The left-dominant phenotype can mimic myocarditis at imaging and clinical examination. Additional considerations for the differential diagnosis of ACM, particularly for the left-dominant phenotype, include sarcoidosis and dilated cardiomyopathy. ©RSNA, 2024 Test Your Knowledge questions for this article are available in the supplemental material.

Persistent Cardiac Magnetic Resonance Imaging Features of Myocarditis Detected Months After COVID-19 Infection.

Acute myocarditis is commonly caused by viral infections resulting from viruses such as adenovirus, enteroviruses, and, rarely, coronavirus. It presents with nonspecific symptoms like chest pain, dyspnea, palpitation, or arrhythmias and can progress to dilated cardiomyopathy or heart failure. Fulminant myocarditis is a potentially life-threatening form of the condition and presents as acute, severe heart failure with cardiogenic shock. In this report, we discuss a case of a 41-year-old female who presented with cough and chest pain of two days' duration. The patient had a new-onset atrial flutter. Her chest auscultation revealed bilateral crackles. Laboratory workup revealed elevated troponin levels, and the patient tested positive for coronavirus disease 2019 (COVID-19) by nasopharyngeal swab polymerase chain reaction (PCR). Transthoracic echocardiogram revealed a low left ventricular (LV) ejection fraction of 35-40% compared to 55% one year prior, as well as a granular appearance of LV myocardium. The patient's condition subsequently improved clinically and she was discharged home. Due to cardiac involvement and characteristic myocardial appearance on the echocardiogram, cardiac magnetic resonance (CMR) imaging was performed for further evaluation about two months from the date of admission. CMR showed extensive myocardial inflammation with a typical pattern of sub-epicardial and mid-wall delayed enhancement, confirming the diagnosis of myocarditis. This case highlights myocarditis as a potential complication of COVID-19 that requires early diagnosis and proper management to improve patients' quality of life. Additionally, we highlight the features of myocarditis on CMR in the acute phase and two months after clinical recovery.

Cardiac magnetic resonance imaging in heart failure: where the alphabet begins!

Cardiac Magnetic Resonance Imaging has become a cornerstone in the evaluation of heart failure. It provides a comprehensive evaluation by answering all the pertinent clinical questions across the full pathological spectrum of heart failure. Nowadays, CMR is considered the gold standard in evaluation of ventricular volumes, wall motion and systolic function. Through its unique ability of tissue characterization, it provides incremental diagnostic and prognostic information and thus has emerged as a comprehensive imaging modality in heart failure. This review outlines the role of main conventional CMR sequences in the evaluation of heart failure and their impact in the management and prognosis.

Quantitative relation of ST-segment depression during exercise to the magnitude of myocardial ischemia as assessed by single-photon emission computed tomographic myocardial perfusion imaging.

The mechanism of ST-segment depression during exercise electrocardiographic treadmill testing (ETT) is unknown. The relatively good correlation between the results of ETT and myocardial perfusion imaging suggests that ST-segment depression may be related to the magnitude of ischemia. Previous studies that investigated this relation have produced conflicting results. We evaluated 1,006 patients who underwent symptom-limited ETT and technetium-99m single-photon emission computed tomographic myocardial perfusion imaging at rest and during stress at a single institution. The magnitude, extent, and duration of ST-segment depression were each strongly associated with the magnitude of myocardial ischemia (p <0.001 for all). The magnitude, extent, and duration of ST-segment depression were highly correlated with each other and had similar relations to the magnitude of ischemia. After adjustment for significant clinical and ETT parameters, these relations remained highly significant. The location of myocardial ischemia was unrelated to ST-segment depression. This large study found that ST-segment depression during ETT is strongly associated with the magnitude of ischemia. These data support a causative role for the magnitude of ischemia in the generation of ST-segment depression.

Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction.

OBJECTIVES: The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion. METHODS: Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p < 0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p < 0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.