Published online Jan 21, 2022. doi: 10.12998/wjcc.v10.i3.762
Peer-review started: April 27, 2021
First decision: June 15, 2021
Revised: June 15, 2021
Accepted: December 21, 2021
Article in press: December 21, 2021
Published online: January 21, 2022
Processing time: 262 Days and 19.6 Hours
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.
Core Tip: Myocardial injury (MI) has been described in coronavirus infectious disease 2019 patients and is associated with a higher risk of severe clinical outcome and mortality, but the exact mechanisms involved are not completely elucidated. Multiple potential mechanisms have been proposed, such as direct viral infection and indirect injury through inflammation, angiotensin I converting enzyme 2 interaction and hemostatic anomalies. Understanding the mechanisms underlying MI is needed to guide effective therapeutic strategies in these patients.