Key result
Continuing ACEIs or ARBs in COVID-19 appears safe and may offer protective cardiovascular effects.
Why the study?
The safety and impact of RAS inhibitors on ACE2 expression and SARS-CoV-2 entry in COVID-19 patients were uncertain and needed investigation.
Hypothesis-generating for RAS inhibitor continuation in COVID-19; extends preclinical ACE2 upregulation data to potential clinical signals.
Angiotensin-converting enzyme 2 (ACE2) is the leading player of the protective renin-angiotensin system (RAS) pathway but also the entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). RAS inhibitors seemed to interfere with the ACE2 receptor, and their safety was addressed in COVID-19 patients. Pedrosa et al. (Clin. Sci. (Lond.) (2021), 135, 465-481) showed in rats that captopril and candesartan up-regulated ACE2 expression and the protective RAS pathway in lung tissue. In culture of pneumocytes, the captopril/candesartan-induced ACE2 up-regulation was associated with inhibition of ADAM17 activity, counterbalancing increased ACE2 expression, which was associated with reduced SARS-CoV-2 spike protein entry. If confirmed in humans, these results could become the pathophysiological background for justifying RAS inhibitors as cornerstone cardiovascular protectives even during COVID-19 pandemic.
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Šimko et al. (2021) conducted a review in COVID-19 and cardiovascular conditions. Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) was evaluated. Continuing ACEI or ARB therapy in COVID-19 patients appears safe and may offer protective effects by counterbalancing SARS-CoV-2-induced renin-angiotensin system dysregulation.
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