Potential harmful effects of discontinuing ACE-inhibitors and ARBs in COVID-19 patients

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Abstract

The discovery that SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) binds to the angiotensin converting enzyme (ACE)-2, which is highly expressed in the lower airways, explained why SARS-CoV-2 causes acute respiratory distress syndrome (ARDS) and respiratory failure. After this, news spread that ACEis and ARBs would be harmful in SARS-CoV-2-infected subjects. To the contrary, compelling evidence exists that the ACE-1/angiotensin(Ang)II/ATR-1 pathway is involved in SARS-CoV-2-induced ARDS, while the ACE-2/Ang(1-7)/ATR2/MasR pathway counteracts the harmful actions of AngII in the lung. A reduced ACE-1/ACE-2 ratio is, in fact, a feature of ARDS that can be rescued by human recombinant ACE-2 and Ang(1-7) administration, thus preventing SARS-CoV-2-induced damage to the lung. Based on the current clinical evidence treatment with ACE-inhibitors I (ACEis) or angiotensin receptor blockers (ARBs) continues to provide cardiovascular and renal protection in patients diagnosed with COVID-19. Discontinuing these medications may therefore be potentially harmful in this patient population.

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Gian Paolo Rossi

Department of Medicine-DIMED - Hypertension Unit, University of Padova, Padova, Italy

For correspondence
gianpaolo.rossi@unipd.it

Competing interests
No competing interests declared.

"This ORCID iD identifies the author of this article:" 0000-0002-7963-0931
Viola Sanga

Department of Medicine-DIMED - Hypertension Unit, University of Padova, Padova, Italy

For correspondence
sangaviola.md@gmail.com

Competing interests
No competing interests declared.
Matthias Barton

University of Zurich, Zurich, Switzerland

For correspondence
barton@access.uzh.ch

Competing interests
Matthias Barton, Senior Editor, eLife.

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The authors declare that there was no funding for this work.

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This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.