Author + information
- Agnieszka Brojakowska, BA,
- Jagat Narula, MD PhD,
- Rony Shimony, MD and
- Jeffrey Bander, MD∗ (, )@MountSinaiNYC
- ↵∗Address for correspondence: Jeffrey Bander. Mount Sinai West, 1000 10th Ave, New York, NY 10019 Tele: 646-556-5559 Fax: 212-656-1914
SARS-CoV2 host cell infection is mediated by the binding to angiotensin-converting enzyme 2 (ACE2). Systemic dysregulation observed in SARS-CoV was previously postulated to be due to ACE2/Ang1-7/Mas axis downregulation, increased ACE2 activity was shown to mediate disease protection. Since angiotensin II receptor blockers (ARBs), ACE inhibitors, and mineralocorticoid receptor antagonists (MRAs) increase ACE2 receptor expression, it has been tacitly believed that the use of these agents may facilitate viral disease, thus they should not be used in high-risk patients with cardiovascular disease. Based on the anti-inflammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefits of lung function improvement in SARS-CoV infections, we hypothesize that the benefits of treatment with renin-angiotensin system inhibitors in SARS-COV2 may outweigh the risks and at the very least should not be withheld.
- angiotensin converting anzyme-2
- ACE inhibitor
- angiotensin II receptor blockers
- mineralocorticoid receptor antagonist
- Received April 2, 2020.
- Revision received April 9, 2020.
- Accepted April 13, 2020.