title: Blockade of the renin-angiotensin-aldosterone system (RAAS) for primary prevention of non-valvular atrial fibrillation: a systematic review and meta analysis of randomized controlled trials.
abstract: BACKGROUND
  The renin-angiotensin-aldosterone system is suggested to play a key role in the development of atrial fibrillation through structural and electrical remodeling. This review aims to assess the effectiveness of blockade of the renin-angiotensin-aldosterone system in the prevention of new onset atrial fibrillation.
  
  
  METHODS
  Electronic databases from 1984 onwards and previous systematic reviews were searched in addition to contacting experts in the field. Two reviewers independently selected eligible randomized controlled trials that reported on new onset atrial fibrillation, and that compared at least one of the following drugs: angiotensin-converting enzyme inhibitors, angiotensin II-receptor blockers, and aldosterone antagonists with conventional therapy or placebo.
  
  
  RESULTS
  Fourteen trials including 92,817 randomized patients met the inclusion criteria. RAAS inhibition compared with conventional therapy or placebo reduced new onset atrial fibrillation (RR=0.79; 95% CI; 0.69-0.90, p-value<0.001). ARBs showed a strong effect in the reduction of onset atrial fibrillation (RR=0.78; 95% CI: 0.66-0.92, p-value=0.009), whereas results for ACE inhibitors were not as clear but likely show no effect (RR=0.79, 95% CI: 0.62-1:00, p-value: 0.05). Aldosterone antagonists, did not appear to play a role in the prevention of new onset atrial fibrillation (RR=0.77, 95%CI: 0.55-1.08, p-value: 0.21). Risk reduction was highest among heart failure patients.
  
  
  CONCLUSIONS
  RAAS inhibition appears to reduce the risk of developing new onset atrial fibrillation in different patient groups with coronary artery disease. Yet these results were considered of low quality evidence and therefore further research with stronger quality trials is required to confirm current results.
authors.affiliation: Population Health Research Institute, Hamilton Health Sciences and McMaster University, Hamilton, ON, Canada. rasha.khatib@phri.ca
authors.forename: Rasha
authors.initials: R
authors.lastname: Khatib
authors.forename: Phillip
authors.initials: P
authors.lastname: Joseph
authors.forename: Matthias
authors.initials: M
authors.lastname: Briel
authors.forename: Salim
authors.initials: S
authors.lastname: Yusuf
authors.forename: Jeff
authors.initials: J
authors.lastname: Healey
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D011322:Primary Prevention / Q000379:methods*; D016032:Randomized Controlled Trials as Topic / Q000379:methods; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists