Acute myocardial injury in patients with COVID-19: Possible mechanisms and clinical implications

Abstract

Severe acute respiratory syndrome coronavirus 2 infection affects not only the lungs, but also the cardiovascular system, having a major impact on patients' outcomes. Myocardial injury (MI) occurs in the context of coronavirus infectious disease 2019 (COVID-19) and is associated with a higher risk of severe clinical outcome and mortality. COVID-19-related MI can have various clinical manifestations, of which the main ones are myocarditis, stress cardiomyopathy, acute coronary syndrome, and pulmonary embolism. The exact mechanisms of how MI occurs in these patients are not yet fully known. Direct injury, through direct viral myocardial invasion, and indirect injury, through interaction with angiotensin I converting enzyme 2, increased inflammation, and thrombocyte and endothelial dysfunction, could be involved in acute MI in patients with COVID-19. A better understanding of these multiple potential mechanisms may help to develop new targeted therapeutic strategies. The purpose of this review is to provide the current understanding of the potential mechanisms involved in MI induced by COVID-19 and to discuss the current progress in the therapeutic strategies.

Keywords: Acute coronary syndrome; Coronavirus infectious disease; Myocardial injury; Myocarditis; Pulmonary embolism; SARS-CoV-2; Stress cardiomyopathy.

Figure 1

Schematic of the putative mechanisms of myocardial injury in severe acute respiratory syndrome coronavirus 2 infection. ACE2: Angiotensin I converting enzyme 2.