Myocarditis encompasses both primary and secondary processes causing inflammation of the myocardium. Viral infections are a common secondary cause of myocarditis with important clinical relevance. Viral myocarditis has a varied clinical presentation, potentially resulting in significant morbidity and mortality. Acutely, systolic dysfunction and sudden cardiac death may ensue; chronically, myocarditis may result in a dilated cardiomyopathy requiring heart transplantation. Myocarditis is thought to be one of the most common causes of myocardial infarction with nonobstructive coronary arteries (MINOCA), with important consequences for cardiovascular outcomes. Patients with myocarditis are currently underdiagnosed. Cardiac MRI has evolved as the noninvasive test of choice, with cardiac MRI‐specific diagnostic requirements defined in the Lake Louise Criteria (LLC). Detecting the presence of tissue edema, hyperemia, and necrosis in both acute and chronic stages form the foundation of the LLC. Cardiac MR for chronic myocarditis (greater than 8 weeks from symptom onset) has decreased sensitivity for diagnosis. Emerging sequences such as T1 and T2 parametric maps provide tissue characterization regarding inflammation without reliance on reference tissue, overcoming limitations of the LLC. Beyond diagnostic criteria, these imaging techniques have proven useful in further characterizing the diseased tissue, prognostication, and clinical decision‐making. This review describes the utility and evolving use of cardiac MRI in clinical practice. Level of Evidence: 1 Technical Efficacy Stage: 5 J. Magn. Reson. Imaging 2018;47:1061–1071.

Quantitative assessment of LV volumes and mass with inclusion of papillary muscles and trabeculae to myocardial mass resulted in significantly different values, while indexing to BSA and not height may miss LV hypertrophy in terms of overweight.

Introduction Wilson's disease (WD) is a rare autosomal recessive copper disorder with limited excretion of excess copper into the bile. Primary symptoms are hepatic or neurological. However, the clinical range of WD is wide and can result in cardiac symptoms as well. Previous studies revealed a higher incidence of heart failure in WD patients compared to the rest of the population. Purpose Cardiac magnetic resonance imaging (CMR) is used to identify the typical features of several systemic disorders with excessive myocardial deposition of substrates. The aim of this study was to perform a cardiac tissue characterization in WD patients by using CMR and to identify subgroups of WD patients with reduced ejection fraction (EF). Methods Patients with known WD using Ferenci-Score were included in this prospective study. WD patients were referred to 1.5 Tesla CMR. The following CMR protocol was performed; Cine-images, T1-, T2- and T2*-Mapping, fast-SENC strain and late gadolinium enhancement (LGE). Fast-SENC strain measurements were compared with values from healthy individuals scanned at the center. Results 43 patients (age 38.7±12.8 years, 20 female, BMI 23.80 (17.4–33.1)) with WD could be identified and were evaluated with CMR. CMR revealed normal left ventricular (LV) EF (62.4±5.4%) and right ventricular (RV) EF (64.4±7.1%) overall. However, three patients (7%), who suffered primarily from neurological symptoms, were found to have mildly reduced LV-EF (46.5%, 51%, and 53.5%). Strain analysis revealed significantly reduced LV global circumferential strain (GCS) overall compared to healthy individuals (WD (%): −19.2 2.7; control (%): −20.71±1.5, p<0.05). Patients with primarily hepatic symptoms (WD-h) did not show reduced strain measurements compared to the control group. Patients suffering from primarily neurological symptoms (WD-n) showed significantly reduced LV GCS compared to healthy individuals (WD-n (%): −18.3±3.1; control (%): −20.7±1.5, p<0.05) and RV GCS (WD-n (%): −17.5±3.0; control (%): −19.2±1.8, p<0.05). Also, LV GCS in WD-n was significantly reduced compared to WD-h (WD-n (%): −18.3±3.1; WD-h (%): −20.0±2.0). Furthermore, there were no significant differences between the two subgroups, besides a significant thicker lateral wall in patients with WD-n (WD-n (mm): 7 (5–9); WD-h (mm): 6 (5–8), p<0.05). T1-, T2- and T2*-Mapping did not show any pathological pattern and were overall in the normal range (T1: 1020±30ms; T2: 52.9±3.0ms; T2*: 38.4±5.6ms). Epicardial LGE was present in 1 patient. Conclusion Cardiac tissue characterization was performed in WD patients using CMR. Reduced EF, LV and RV GCS have been detected in patients with primarily neurological symptoms. Cardiovascular autonomic dysfunction in this subgroup could be a reason for the reduced biventricular strain. It is unknown if reduced circumferential strain influences the prognosis of WD patients, which should be investigated in further studies.

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