Cardiac Involvement of COVID-19: A Comprehensive Review

Abstract

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Multimodality Imaging for Cardiac Evaluation in Patients with COVID-19

“…The forms of COVID-19-related CV injury generally fall into the following categories: primary damage resulting from direct viral effect; secondary damage as a consequence of other organ or systemic dysfunction; and importantly, exacerbation of baseline CV disease by either primary or secondary causes [ 10 ]. The reported CV complications have included clinical and subclinical myocardial dysfunction, heart failure, myocarditis, cardiac arrhythmias, myocardial infarction, stress cardiomyopathy, pericarditis, vasculitis, circulatory shock, pulmonary hypertension, and thromboembolism [ 2 , 11 – 13 ].…”

“…Similar processes additionally lead to platelet dysfunction and heightened thrombosis [ 25 , 26 ]. Furthermore, indirect cellular damage is hypothesized to occur by widespread immune activation and cytokine release [ 11 , 25 , 27 – 29 ]. Significant elevations in proinflammatory cytokines such as interleukin-6, C-reactive protein, tumor necrosis factor alpha, and ferritin in patients with COVID-19 are frequently reported [ 30 – 32 ].…”

“…Significant elevations in proinflammatory cytokines such as interleukin-6, C-reactive protein, tumor necrosis factor alpha, and ferritin in patients with COVID-19 are frequently reported [ 30 – 32 ]. These circulating molecules may then release reactive oxygen species, acutely depress myocardial contractility, trigger cardiac arrhythmias, cause localized arterial inflammation, and lead to secondary CV damage via cardiomyopathy, acute coronary syndrome, and thrombosis [ 11 , 25 , 27 ]. Other secondary mechanisms of injury include electrolyte imbalance, hypoxia, medication effect, catecholamine surge, and overall increased cardiometabolic demand [ 25 ].…”

Cardiovascular Imaging Evaluation in COVID-19 Heart and Vascular Non-Ischaemic Involvement

“…The high inflammatory burden due to cytokine release can significantly hit the patients' cardiovascular systems [37][38][39][40]; it can induce arrhythmias, myocarditis, coagulation abnormalities with venous thromboembolism, Takotsubo cardiomyopathy, Kawasaki-like disease and multisystemic inflammatory syndrome, [41] leading directly or indirectly to cardiogenic shock [42]. SARS-CoV-2 uses the ACE2 as the receptor to enter the host cell [43,44], that requires its binding to the viral spike protein (Fig.…”

“…The entry of SARS-CoV-2 into the lungs and heart could be facilitated by an underlying renin-angiotensin system (RAS)-related, pathophysiology of the cardiovascular disorders and chronic use of pharmacologic RAS inhibitors which both induce an increase of the ACE2 levels [48]. Thus, the infection may have a direct impact on cardiovascular diseases [41]. However, ACE2 reduces the levels of angiotensin II, a potent proinflammatory agent in the lungs, which can contribute to lung injury.…”