Abstract

: Coronavirus disease 2019 (COVID-2019) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may affect the cardiovascular system in multiple ways causing acute cardiac injury, cardiac ischemia, arrhythmias and sudden cardiac deaths. Fulminant SARS-CoV-2 viral myocarditis have been reported, though it is likely relatively rare. In both children and adults, COVID-19 may also cause a Kawasaki-like multisystem inflammatory syndrome with heart involvement being a prominent feature. Possible mechanisms of cardiovascular injury in COVID-19 include hypoxia from lung disease, direct viral infection of cells in the cardiovascular system, down-regulation of angiotensin converting enzyme 2 (ACE2), dysregulated immune response, endothelial dysfunction, and thrombosis. Medications used to treat COVID-19 may also have cardiac side effects including QT-prolongation and arrhythmias. Troponin elevation or acute cardiac injury may be used to risk-stratify patients with severe COVID-19. The dysregulated immune response in COVID-19 can be targeted with glucocorticoids and possibly immunomodulators. Anticoagulation may be indicated in select COVID-19 patients to prevent or treat thrombotic complications. The relationship between angiotensin-converting-enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs) and COVID-19 is not completely understood and major societies have recommended that patients who were otherwise benefiting from ACEIs or ARBs continue to take it.

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