Abstract
The emergence of the novel SARS coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in an unprecedented pandemic that has been accompanied by a global health crisis. Although the lungs are the main organs involved in COVID-19, systemic disease with a wide range of clinical manifestations also develops in patients infected with SARS-CoV-2. One of the major systems affected by this virus is the cardiovascular system. The presence of preexisting cardiovascular disease increases mortality in patients with COVID-19, and cardiovascular injuries, including myocarditis, cardiac rhythm abnormalities, endothelial cell injury, thrombotic events, and myocardial interstitial fibrosis, are observed in some patients with COVID-19. The underlying pathophysiology of COVID-19–associated cardiovascular complications is not fully understood, although direct viral infection of myocardium and cytokine storm have been suggested as possible mechanisms of myocarditis. In this Review, we summarize available data on SARS-CoV-2–related cardiac damage and discuss potential mechanisms of cardiovascular implications of this rapidly spreading virus.
Highlights
Coronavirus disease 2019 (COVID-19) has resulted in a global pandemic that emerged in 2019 and is the result of infection with the novel enveloped RNA beta coronavirus SARS coronavirus 2 (SARS-CoV-2)
Myocarditis documented by cardiac MRI (CMR) may present as a postacute sequela of SARS-CoV-2 infection in up to 19% of individuals [46], and isolated myocarditis without concomitant respiratory disease has been reported as an atypical presentation of COVID-19 [47, 48]
Since the emergence of COVID-19, multiple groups have reported cardiovascular complications associated with SARS-CoV-2 infection
Summary
Coronavirus disease 2019 (COVID-19) has resulted in a global pandemic that emerged in 2019 and is the result of infection with the novel enveloped RNA beta coronavirus SARS coronavirus 2 (SARS-CoV-2). In postmortem tissue analysis of COVID-19 patients, diffuse infiltration of mononuclear cells associated with endothelium and apoptosis of ECs were detected, and endothelitis and endothelial dysfunction in cardiac tissue were reported as consequences of SARS-CoV-2 infection [18]. These findings suggest that ECs may be the direct target of the virus via ACE2 [14, 18]. The recognition that COVID-19 may cause acute myocarditis may facilitate early diagnosis and possible prevention of myocarditis-related mortality, lack of an understanding of the mechanism(s) by which SARS-CoV-2 contributes to myocarditis and cardiac damage hinders thorough management of this condition. Another study that analyzed SARS-CoV RNA in postmortem tissue samples from 7 patients suggested
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