LAUSR

Myocardial injury is a common phenomenon in coronavirus disease 2019 (COVID-19).1 Initial clinical studies in China and later in the United States found that >30% of hospitalized patients with COVID19 had myocardial injury as evidenced by elevated cardiac troponin I levels,2–4 and the elevation of troponin was associated with a higher risk of mortality.2–4 Although several mechanisms have been hypothesized, including direct infection of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) to cardiomyocytes5–7 leading to fulminant myocarditis, hypercoagulable state in a cytokine storm leading to vascular injuries such as coronary artery occlusion or microvascular thrombi,8 stress-induced cardiomyopathy,1,9,10 or type II myocardial infarction by supply-demand mismatch,1,9,10 the precise mechanisms are unclear and therapeutic targets to prevent or alleviate myocardial injury in COVID-19 are unknown.