Renin-angiotensin-system inhibition in the context of corona virus disease-19: experimental evidence, observational stud
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Renin-angiotensin-system inhibition in the context of corona virus disease-19: experimental evidence, observational studies, and clinical implications Filippos Triposkiadis 1,2
&
Randall C. Starling 3 & Andrew Xanthopoulos 1 & Javed Butler 4 & Harisios Boudoulas 5
Accepted: 27 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Coronavirus disease 2019 (COVID-19) is due to severe acute respiratory syndrome coronavirus (SARS-CoV)-2 which binds and enters the host cells through the angiotensin-converting enzyme (ACE)2. While the potential for benefit with the use of reninangiotensin-aldosterone system inhibitors (RAASi) and the risks from stopping them is more evident, potential harm by RAΑSi may also be caused by the increase in the activity of the ACE2 receptor, the inefficient counter regulatory axis in the lungs in which the proinflammatory prolyloligopeptidase (POP) is the main enzyme responsible for the conversion of deleterious angiotensin (ANG) II to protective ANG [1–7] and the proinflammatory properties of ACE2(+) cells infected with SARS-CoV-2. Acknowledging the proven RAΑSi benefit in patients with several diseases such as hypertension, heart failure, coronary disease, and diabetic kidney disease in the non-COVID-19 era, it is a reasonable strategy in this period of uncertainty to use these agents judiciously with careful consideration and to avoid the use of RAASi in select patients whenever possible, until definitive evidence becomes available. Keywords COVID-19 . Angiotensin . Proinflammatory prolyloligopeptidase . Hypertension . Heart failure
“Prudence is the footprint of Wisdom.” — Amos Bronson Alcott Coronavirus disease 2019 (COVID-19) is due to severe acute respiratory syndrome coronavirus (SARS-CoV)-2 which binds and enters the host cells through the angiotensinconverting enzyme (ACE)2. Therapy with renin-angiotensinaldosterone system (RAAS) inhibitors (ACE inhibitors [ACEi], angiotensin [ANG] II receptor blockers [ARB], and
mineralocorticoid receptor antagonists [MRA]) may increase ACE2 [1]. The concern, therefore, has been raised that a potential increase in ACE2 by these agents may facilitate development and increase severity of COVID-19. In this brief review, we contend that a potential harmful effect of RAΑS inhibitors cannot be excluded in the COVID-19 era and thus, caution required when prescribing these agents.
Lung renin angiotensin system * Filippos Triposkiadis [email protected] 1
Department of Cardiology, Larissa University General Hospital, PO Box 1425, 411 10 Larissa, Greece
2
University of Thessaly, Volos, Greece
3
Kaufman Center for Heart Failure and Recovery, Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA
4
Department of Medicine, University of Mississippi, Jackson, MS, USA
5
Department of Medicine/Cardiovascular Medicine, The Ohio State University, Columbus, OH, USA
The traditional view is that some of renin-angiotensin system intermediate products may be processed in alternative ways by A
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