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. 2020 May 14;41(19):1801-1803.
doi: 10.1093/eurheartj/ehaa235.

SARS-CoV2: should inhibitors of the renin-angiotensin system be withdrawn in patients with COVID-19?

Gabriela M Kuster  1   2 , Otmar Pfister  1   2 , Thilo Burkard  1   3 , Qian Zhou  1 , Raphael Twerenbold  1   4 , Philip Haaf  1 , Andreas F Widmer  5 , Stefan Osswald  1
Affiliations

SARS-CoV2: should inhibitors of the renin-angiotensin system be withdrawn in patients with COVID-19?

Gabriela M Kuster et al. Eur Heart J. .
No abstract available

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Figures

Take home figure
Take home figure
Conceptual figure highlighting the central role of ACE2 in the potentially deleterious (red) and protective (green) effects of the RAAS and its inhibition in the development of severe acute respiratory syndrome (SARS). ACE-Is and ARBs increase ACE2 expression and activity (grey) as shown by a few animal and human studies,6,7 but the mechanism has yet to be identified. Although there is currently no evidence, this could theoretically increase viral load and worsen outcome (red). In a reverse causality, ACE2 acts as a gatekeeper of the RAAS by degrading AngII to Ang1-7, hence diminishing its Ang II receptor 1-mediated deleterious effects. Therefore, ACE-I or ARB treatment could theoretically mitigate lung injury (green). Evidence for this mainly stems from animal studies.9,10 Providing soluble recombinant (r)ACE2 (blue) addresses both mechanisms by cell independent binding of SARS-CoV2 and degrading AngII to Ang 1-7. This concept is currently being tested in a pilot study in patients with COVID-19.13
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