COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors

The clinical manifestations of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for coronavirus disease 2019 (COVID-19) commonly include dyspnoea and fatigue, and they primarily involve the lungs. However, extra-pulmonary organ dysfunctions, particularly affecting the cardiovascular system, have also been observed following COVID-19 infection. In this context, several cardiac complications have been reported, including hypertension, thromboembolism, arrythmia and heart failure, with myocardial injury and myocarditis being the most frequent. These secondary myocardial inflammatory responses appear to be associated with a poorer disease course and increased mortality in patients with severe COVID-19. In addition, numerous episodes of myocarditis have been reported as a complication of COVID-19 mRNA vaccinations, especially in young adult males. Changes in the cell surface expression of angiotensin-converting enzyme 2 (ACE2) and direct injury to cardiomyocytes resulting from exaggerated immune responses to COVID-19 are just some of the mechanisms that may explain the pathogenesis of COVID-19-induced myocarditis. Here, we review the pathophysiological mechanisms underlying myocarditis associated with COVID-19 infection, with a particular focus on the involvement of ACE2 and Toll-like receptors (TLRs).

Automated summary

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for COVID-19 commonly leads to dyspnea and fatigue, primarily affecting the lungs. However, it can also result in dysfunction of extra-pulmonary organs, particularly the cardiovascular system. Cardiac complications such as hypertension, thromboembolism, arrhythmia, and heart failure have been observed in COVID-19 patients, with myocardial injury and myocarditis being the most frequent. Understanding the mechanisms of COVID-19-induced myocarditis, including changes in ACE2 expression and immune responses, is crucial.