Antwi-Amoabeng D, Beutler BD, Moody AE, Kanji Z, Gullapalli N, Rowan CJ. Management of hypertension in COVID-19. World J Cardiol 2020; 12(5): 228-230 [PMID: 32547717 DOI: 10.4330/wjc.v12.i5.228]
Corresponding Author of This Article
Bryce D Beutler, MD, Department of Internal Medicine, Reno School of Medicine, University of Nevada, 1155 Mill Street, W-11, Reno, NV 89052, United States. bbeutler@med.unr.edu
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Letter To The Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. May 26, 2020; 12(5): 228-230 Published online May 26, 2020. doi: 10.4330/wjc.v12.i5.228
Management of hypertension in COVID-19
Daniel Antwi-Amoabeng, Bryce D Beutler, Alastair E Moody, Zahara Kanji, Nageshwara Gullapalli, Christopher J Rowan
Daniel Antwi-Amoabeng, Bryce D Beutler, Zahara Kanji, Nageshwara Gullapalli, Christopher J Rowan, Department of Internal Medicine, Reno School of Medicine, University of Nevada, Reno, NV 89052, United States
Alastair E Moody, Department of Anesthesiology, University of Utah, Salt Lake City, UT 84132, United States
Christopher J Rowan, Renown Institute for Heart and Vascular Health, Reno, NV 89512, United States
Author contributions: Antwi-Amoabeng D, Beutler BD, and Moody AE wrote the letter to the editor and associated literature review; Kanji Z revised the letter; and Gullapalli N and Rowan CJ supervised the project from initiation to completion.
Conflict-of-interest statement: The authors declare no potential conflicts of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Bryce D Beutler, MD, Department of Internal Medicine, Reno School of Medicine, University of Nevada, 1155 Mill Street, W-11, Reno, NV 89052, United States. bbeutler@med.unr.edu
Received: April 19, 2020 Peer-review started: April 19, 2020 First decision: May 5, 2020 Revised: May 8, 2020 Accepted: May 12, 2020 Article in press: May 12, 2020 Published online: May 26, 2020
Core Tip
Core tip: The pathogenic mechanisms of severe acute respiratory syndrome coronavirus 2 remain under investigation, but data suggest that the ACE2 receptor plays a central role in infection. It is therefore possible that drugs known to increase ACE2 expression, such as angiotensin converting enzyme inhibitors and angiotensin receptor blockers, could promote viral proliferation. Data from animal studies have shown that carvedilol and verapamil attenuate inflammation in viral myocarditis. We are in agreement with the recommendation of major medical societies to maintain angiotensin converting enzyme inhibitor or angiotensin receptor blocker therapy in individuals who are already receiving treatment. However, in the age of coronavirus disease-19, alternative agents should be considered for patients with a new diagnosis of hypertension.
