CORRESPONDENCE levels were 23.0 ng/L (19.0–32.8). Patients had lymphopenia (lymphocyte count 0.76±0.37× 109/L) and elevated C-reactive protein (227.8±126.5 mg/L) during admission. On CMR, 20 (69%) patients had residual lung parenchymal changes. Four (14%) had pleural effusions and 2 (7%) had pericardial effusions. Mean biventricular systolic function for the overall cohort was normal (left ventricular ejection fraction 67.7±11.4%, right ventricular ejection fraction 63.7%±9.5%); 1 patient had mild left ventricular dysfunction, and 1 had severe biventricular dysfunction. With the use of the LGE technique and (where possible) stress perfusion imaging, 20 patients (69%) had an identifiable mechanism of myocardial injury (Figure), classified as nonischemic heart disease–related (11 patients, 38%), ischemic heart disease–related (5, 17%), or dual ischemic and nonischemic pathology (4, 14%).

A nonischemic cause of elevated hsTnT was conferred by the presence of noninfarct pattern LGE (not corresponding to a coronary territory and sparing the endocardium). The LGE patterns were myocarditis-like in 13 patients (45%) by international criteria, 5 with 2 other patients having nonspecific midwall LGE only. These patients all had normal left ventricular function (left ventricular ejection fraction 70.4±6.9%) with no regional wall motion abnormalities. The median extent of the myocarditis-pattern LGE was 2 (1–2.5) segments with no significant residual myocardial edema in the overall cohort (peak myocardial T2 51.0 ms [49–54] in patients with myocarditis-like LGE versus 51.0 ms [48–53] nonmyocarditis, P= 0.68). Peak C-reactive protein (211±103 versus 255±150 mg/L, P= 0.35) and hsTnT (25.0 [18.5–37.5] versus 27.0 ng/L [20.3–47.0], P= 0.48) were not significantly elevated in comparison