COVID-19 and renin-angiotensin system modulators: what do we know so far?

Angel de la Cruz1, Shoaib Ashraf1, Timothy J Vittorio2,3

  • 1Department of Internal Medicine, BronxCare Health System Bronx, NY, USA.

Insights

Physicians should continue renin-angiotensin system (RAS) inhibitors, such as ACE-inhibitors and ARBs, for patients with cardiovascular disease and COVID-19. Expert guidelines advise against altering these essential treatments based on clinical status.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Pharmacology

Background:

  • COVID-19, caused by SARS-CoV-2, poses a global health challenge.
  • Hypertension and cardiovascular disease increase COVID-19 mortality risk.
  • SARS-CoV-2 utilizes ACE2 for cell entry, raising concerns about RAS modulators.

Purpose of the Study:

  • To review literature on the association between RAS inhibitors and severe COVID-19.
  • To determine the appropriateness of continuing ACE-inhibitors and ARBs in active COVID-19 cases.

Main Methods:

  • Literature review of studies on RAS inhibitors (ACE-inhibitors, ARBs) and COVID-19 severity.
  • Analysis of recommendations regarding medication continuation in infected patients.

Main Results:

  • Concerns exist regarding RAS antagonists potentially increasing COVID-19 severity due to ACE2 upregulation.
  • Evidence synthesis to inform clinical decision-making.

Conclusions:

  • Major cardiology societies recommend against initiating or withdrawing RAS inhibitors for COVID-19 patients with cardiovascular disease.
  • Treatment decisions for ACE-inhibitors/ARBs should be individualized based on patient presentation and hemodynamics.
Abstract

Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.1K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
743
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.1K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.2K