Renin-Angiotensin-Aldosterone System (RAAS) Inhibitors and Coronavirus Disease 2019 (COVID-19)

Ahmed Abdalazim Dafallah Albashir, MBBS, MSc

Disclosures

South Med J. 2021;114(1):51-56. 

In This Article

Abstract and Introduction

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the virus responsible for the coronavirus disease 2019 (COVID-19) pandemic. The angiotensin-converting enzyme 2 (ACE2) has been proven to be used by SARS-CoV-2 for host cell entry. Considering that angiotensin receptor blockers and ACE inhibitors (ACEIs) upregulate the expression of ACE2 in animal studies, there may be a concern about whether these drugs may increase COVID-19 susceptibility and severity. Recently, there has been a debate among clinicians about whether to continue or to stop ACEIs and angiotensin receptor blockers in the context of COVID-19. Also, some media outlets and health systems have called for the discontinuation of these drugs in the context of suspected COVID-19. This has necessitated an urgent release of guidance on the use of such medications in COVID-19 patients. To date, multiple theories relating to the pure effects of renin-angiotensin-aldosterone system (RAAS) inhibitors on COVID-19 infections have been postulated. Favorable effects include blocking the ACE2 receptors, preventing viral entry into the heart and lungs, and protecting against lung injury in COVID-19. Adverse effects include a possible retrograde feedback mechanism that upregulates ACE2 receptors. This review provides greater insight into the role of the RAAS axis in acute lung injury and the effects of RAAS inhibitors on SARS-CoVs. The hypothesis that RAAS inhibitors facilitate viral insertion and the alternative hypothesis of the beneficial role of these drugs are discussed. Up-to-date published data concerning the RAAS inhibitors and COVID-19 are summarized.

Introduction

Coronavirus disease 2019 (COVID-19) is a pandemic disease caused by a novel coronavirus called severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). It is an enveloped RNA virus found in wildlife and humans. It was discovered for the first time in Wuhan City, Hubei Province, China. On December 31, 2019, the disease was initially reported to the World Health Organization.[1] The disease has a clinical spectrum ranging from asymptomatic upper respiratory tract infections to severe pneumonia linked with acute respiratory distress syndrome (ARDS).[2] On January 30, 2020, the World Health Organization declared the COVID-19 epidemic a global health emergency.[3]

The early reports from China revealed that old age, diabetes mellitus, hypertension, and cardiovascular disease were prevalent in COVID-19-infected patients, and patients with these comorbid conditions seemed to have higher case fatality rates.[4,5] Patients with these comorbidities were admitted into intensive care units, required mechanical ventilation, and died more often than patients without these comorbidities. In a study that included 1099 patients with confirmed COVID-19 infection, many of the 173 individuals who developed severe disease had comorbidities, including hypertension (23.7%), diabetes mellitus (16.2%), coronary artery disease (5.8%), and cardiovascular diseases (2.3%).[6] In another study, many of the 140 patients admitted to the hospital with COVID-19 infection had hypertension (30%) or diabetes mellitus (12%).[7] In a third study done by Zhou et al, 191 confirmed COVID-19 cases in Wuhan, China were enrolled in a retrospective, multicenter cohort study that found that hypertension was associated with a hazard ratio of 3.05 for in-hospital mortality.[8] This has raised concerns about the influence of hypertension and antihypertensive medications on the infectivity and severity of COVID-19.

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