A Review of ST-Elevation Myocardial Infarction in Patients with COVID-19

Abstract

The Coronavirus disease 2019 (COVID-19) pandemic has led to a significant increase in worldwide morbidity and mortality. Patients with COVID-19 are at risk for developing a variety of cardiovascular conditions including acute coronary syndromes, stress-induced cardiomyopathy, and myocarditis. Patients with COVID-19 who develop ST-elevation myocardial infarction (STEMI) are at a higher risk of morbidity and mortality when compared with their age- and sex-matched STEMI patients without COVID-19. We review current knowledge on the pathophysiology of STEMI in patients with COVID-19, clinical presentation, outcomes, and the effect of the COVID-19 pandemic on overall STEMI care.

Keywords: COVID-19; SARS-COV 2; ST-Elevation myocardial infarction.

Fig. 1

Pathophysiology of STEMI in patients with COVID-19. COVID-19 induced hyperinflammatory state and thrombosis as mechanisms leading to acute myocardial infarction. COVID-19 enters alveolar epithelial cells via the angiotensin-converting enzyme-2 receptor. Once it gets replicated in these cells, then it exits the alveolar cells and stimulates a dysregulated immune response which leads to hyperinflammatory response with the elevation of multiple biomarkers such as TNF, Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), interleukin-2 (IL-2), and granulocyte monocyte colony-stimulating factor (GM-CSF). Parallel to this, there is upregulation of procoagulants and increased platelet activation which leads to thrombosis. Hyperinflammatory response and thrombosis are the main mechanisms behind STEMI in patients with COVID-19.