Transient ST-segment elevation in coronavirus disease-2019.

Cardiovascular involvement in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections may contribute to morbidity and mortality. Acute myocardial injury, defined by increased high-sensitivity troponin I (hs-TnI) levels, is the most common finding. Clinical phenotypes associated with high levels of hs-TnI include myocarditis, arrhythmias, acute coronary syndromes (ACS) and heart failure. The underlying pathogenetic mechanisms are still unclear. Early reports suggest cytokine storm and widespread endothelial damage as the most relevant causes but conflicting data emerged from clinical and pathology studies. Contributing to the interpretation of available evidence, we describe two cases of transient ST-segment elevation and mild increase in hsTnI of probable vasospastic etiology in laboratory-confirmed coronavirus disease-2019 (COVID-19).

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