Cardiovascular Manifestations of COVID-19 Infection

Abstract

SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus's pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.

Keywords: COVID-19; SARS-CoV-2; angiotensin converting enzyme-2; cardiovascular disease; cytokine storm and inflammation; myocardial injury.

Figure 1

The potential risk factors and the cardiovascular complications in COVID-19. The possible risk factors are old age, immunosuppressive diseases, hypertension, CVD, chronic respiratory disease, obesity, renal abnormalities, diabetes mellitus, coagulation aberrations, and tumor. COVID-19-induced cardiovascular complications can be myocardial infarction, cytokine storm, heart failure, systemic inflammation, myocarditis, arrhythmia, myocardial injury, cardiac arrest, thrombotic events, and cardiotoxicity.

Figure 2

The hypothetical mode of action on heart in COVID-19. COVID-19 can induce cardiovascular complications through different mechanisms, including direct myocardial infection or injury, cytokine storm, hypoxemia or lung failure, systemic inflammation, DIC, and stress-induced cardiomyopathy.

Figure 3

ACE2 expression and SARS-CoV-2 infection of heart cells. The potential SARS-CoV-2 direct infection in heart will be through ACE2-expressing cells, like cardiomyocytes and pericytes (high level expression of ACE2), while cardio-fibroblast, endothelial cells, epicardial adipose cells, and immune cells (low level expression of ACE2) may also be infected.