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818 respiratory syndrome coronavirus 2 binds to its target cells through angiotensin-converting enzyme 2 (ACE2)., which is expressed in the lungs, intestines, kidneys, blood vessels, and heart.6,7 In animal models, the upregulation of ACE2 expression in various organs resulted from ACEI and ARB treatment.8-10 Angiotensin-converting enzyme 2 turns angiotensin II to angiotensin 1-7, which has a protective role in the cardiovascular system and, potentially, a vasodilatory effect. Moreover, ACE2 prevents acute lung injury.11,12 Possible upregulation of ACE2 expression as a receptor for viral cell entry (with ACEIs or ARBs) may theoretically increase susceptibility to COVID-19. Interestingly, a contrasting hypothesis has also been postulated. Angiotensin receptor blockers have been suggested to act beneficially in patients with COVID-19 by ACE2 upregulation, thus increasing the concentration of vasodilating angiotensin 1-7 at the expense of angiotensin II causing vasoconstriction, which contributed to lung protection.13,14 Therefore, in the absence of firm evidence regarding beneficial or adverse outcomes of ACEI and ARB treatment in patients with COVID-19, the European Society of Cardiology (ESC) as well as the American College of Cardiology and American Heart Association do not recommend discontinuation or any modification of clinically indicated therapy. The risk of discontinuing drug use is well known: it may destabilize blood pressure control and consequently increase cardiovascular mortality in patients with COVID-19.15,16

Review of different clinical scenarios in patients with cardiovascular disease in the era of the coronavirus pandemic