Prevention of atrial fibrillation by Renin-Angiotensin system inhibition a meta-analysis

Markus P Schneider1, Tsushung A Hua, Michael Böhm

  • 1Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Erlangen, Germany.

Abstract

Insights

Renin-angiotensin system (RAS) inhibition effectively prevents atrial fibrillation (AF) in primary and secondary prevention settings. RAS inhibition shows significant benefits for heart failure and hypertension patients, and when combined with antiarrhythmic drugs for AF recurrence.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Clinical Trials

Background:

  • Controversial results exist regarding the effectiveness of renin-angiotensin system (RAS) inhibition for atrial fibrillation (AF) prevention.
  • Individual studies have yielded conflicting data on RAS inhibition's role in AF prevention.

Purpose of the Study:

  • To review published clinical trial data on the effects of RAS inhibition for AF prevention.
  • To determine the optimal timing and patient populations for RAS inhibition in AF prevention.

Main Methods:

  • Systematic review and meta-analysis of published randomized controlled trials (RCTs).
  • Included trials focused on angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for primary or secondary AF prevention.
  • Analyzed data from 23 RCTs involving 87,048 patients.

Main Results:

  • RAS inhibition reduced the overall odds ratio for AF by 33% (p < 0.00001), with significant heterogeneity.
  • Effective in primary prevention for heart failure and hypertension with left ventricular hypertrophy patients.
  • In secondary prevention, RAS inhibition reduced AF recurrence by 45% post-cardioversion and 63% in medically treated patients.

Conclusions:

  • RAS inhibition is an emerging treatment for both primary and secondary AF prevention.
  • Effectiveness noted in specific patient subgroups, particularly those with heart failure and hypertension.
  • Further research needed on specific RAS inhibitors and interactions with antiarrhythmic drugs.

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,...
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...
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...
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...