摘要
As more people become infected with SARS-CoV-2, we continue to learn about cardiac complications of the disease.Cardiac injury, commonly defined high-sensitivity troponin I level above the 99th percentile of the upper reference limit, is seen in >20% of hospitalized patients with coronavirus disease 2019 (COVID-19) and is associated with >3-fold in-hospital mortality compared with patients without myocardial injury. 1,2The etiology and significance of cardiac injury remains broad, ranging from arrhythmia to acute coronary syndrome to myocarditis. 2 With the logistical challenges that COVID-19 imposes, the first-line diagnostic test of choice for patients with myocardial injury is transthoracic echocardiography.Diastolic dysfunction is common in these patients, and ejection fraction is often preserved, with left ventricular ejection fraction notably declining with clinical deterioration. 3 While these findings are useful, the underlying etiology must still be defined.COVID-19-associated myocarditis is of particular interest given its variable presentation, encompassing most COVID-19-associated cardiac complications, and its potential for progression to heart failure.Cardiac magnetic resonance (CMR) imaging has been the primary modality by which COVID-19-associated myocarditis has been diagnosed in published reports.In one of the larger series of COVID-19 patients with myocardial injury, 13 of 29 patients with unexplained myocardial injury who underwent CMR were diagnosed with myocarditis by the Lake Louise criteria, though they had normal left ventricular ejection fraction by transthoracic echocardiogram and similar elevation of inflammatory markers in comparison to patients without myocarditis by the Lake Louise criteria. 4Long-term follow-up of these patients has not yet been reported.Meanwhile, a surprisingly large number of recovered COVID-19 patients with myocardial injury or persistent cardiac symptoms have variable CMR imaging patterns of increased T1 and T2 signals, delayed gadolinium enhancement, and increased extracellular volume fraction. 5,6 This raises the possibility of active, healing, or healed myocarditis, although the findings are difficult to interpret without pre-COVID or follow-up imaging.COVID-19-associated myocarditis has also been diagnosed, albeit less commonly, by endomyocardial biopsy (EMB).Case reports have shown a macrophage predominant infiltrate and cardiomyocyte damage, although the presence of direct viral involvement is still being studied. 7,8Intriguingly, a recent autopsy series reported SARS-CoV-2 RNA in the myocardial tissue of the majority of patients with COVID-19, with increased inflammatory cytokine expression associated with high viral load but no difference in inflammatory cell infiltration as compared with those without SARS-CoV-2 myocardial involvement. 9The deeper insights into car-