Cardiac complications, including clinically suspected myocarditis, have been described in Coronavirus Disease 2019 (COVID-19). Here, we review current data on suspected myocarditis in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Hypothetical mechanisms to explain the pathogenesis of troponin release in patients with COVID-19 include direct virus-induced myocardial injury (i.e. viral myocarditis), systemic hyper-inflammatory response (i.e. cytokine storm), hypoxemia, downregulation of angiotensin-converting enzyme 2, systemic virus-induced endothelialitis, and type 1 and type 2 myocardial infarction. To date, despite the fact that millions of SARS-CoV-2 infections have been diagnosed worldwide, there is no definitive proof that SARS-CoV-2 is a novel cardiotropic virus causing direct cardiomyocyte damage. Diagnosis of viral myocarditis should be based on the molecular assessment of endomyocardial biopsy (EMB)/autopsy by polymerase chain reaction/in-situ hybridization. Blood, sputum or nasal/throat swab virology testing are insufficient and do not correlate with the myocardial involvement of a given pathogen. Data from EMB/autopsy in clinically suspected SARS-CoV-2 myocarditis are scarce. Overall, current clinical epidemiological data do not support the hypothesis that viral myocarditis is caused by SARS-CoV-2, or that it is common. More EMB/autopsy data are also needed for better understanding of pathogenesis of clinically suspected myocarditis in the course of SARS-CoV-2 infection, which may include virus-negative immune-mediated or already established subclinical autoimmune forms, triggered or accelerated by the hyper-inflammatory state of severe COVID-19.
Clinically suspected myocarditis in the course of SARS-CoV-2 infection: fact or fiction?