Coronavirus disease 2019, hypertension, and renin–angiotensin–aldosterone system inhibitors

Abstract

Purpose of reviewThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mostly uses the angiotensin-converting enzyme 2 (ACE-2) as cellular receptor for entering the host cells. Some, but not all, animal studies have shown that renin–angiotensin–aldosterone system (RAAS) inhibitors can increase ACE-2 expression. On that premise, it was hypothesized that these agents could make it more likely to develop coronavirus disease 2019 (COVID-19). On the other hand, there was also evidence that being on these agents could lessen the severity of the lung injury in patients with severe SARS-CoV-2 infection. Herein, we review the available evidence on the role of RAAS inhibitors on SARS-CoV-2 and COVID-19 development.Recent findingsRecent randomized controlled trials demonstrate that RAAS blockade or withdrawal does not influence the severity of COVID-19 in patients who are already on these medications. Currently, there is no evidence to support stopping RAAS inhibitors in patients hospitalized for COVID-19. Several questions still need to be addressed. Ongoing studies are currently evaluating the de novo use of RAAS inhibitors in patients with COVID-19. Another area that needs to be investigated is whether or not using these medications increase the risk of infection.SummaryThe wealth of evidence indicates that ACE inhibitors and angiotensin-receptor blocker administration has no harmful effects on hospitalizations and severity of COVID-19 in patients already on these medications and might even reduce mortality among hypertensive patients diagnosed with COVID-19. More evidence and data need to be collected, and at this time, these agents should not be discontinued.

Causal associations and shared genetics between hypertension and COVID‐19

“…The cell biology‐centered view of COVID‐19 emphasizes the direct interaction between its structural spike (S) protein and the angiotensin‐converting enzyme 2 (ACE2) receptor, which is an integral part of the renin–angiotensin–aldosterone system (RAAS) 24 . Nevertheless, the wealth of real‐world evidence indicates that ACE inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are safe in hypertensive patients infected with SARS‐CoV‐2 and might even reduce COVID‐19‐related mortality in this group 25 . Variations in RAAS genes were suggested as an explanation for the heterogeneous response to SARS‐CoV‐2 infection and have been associated both with the risk of developing hypertension 26 and with severe COVID‐19 27 …”

“…24 Nevertheless, the wealth of real-world evidence indicates that ACE inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are safe in hypertensive patients infected with SARS-CoV-2 and might even reduce COVID-19-related mortality in this group. 25 Variations in RAAS genes were suggested as an explanation for the heterogeneous response to SARS-CoV-2 infection and have been associated both with the risk of developing hypertension 26 and with severe COVID-19. 27 Previous studies have investigated the underlying molecular basis supporting severe COVID-19 and its common comorbidities.…”