title: Therapy with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins: no effect on ablation outcome after ablation of atrial fibrillation.
abstract: BACKGROUND
  The renin-angiotensin-aldosterone system and inflammation are supposed to play a key role in the pathogenesis of atrial fibrillation (AF). This retrospective clinical study was intended to assess the influence of drugs with antiinflammatory and/or renin-angiotensin-aldosterone system-modulating properties, namely angiotensin-converting enzyme inhibitors (ACE-Is), angiotensin II receptor blockers (ARBs), and statins, on AF-free survival after AF ablation.
  
  
  METHODS
  The study included 234 patients (23-80 years; 71.8% men) with drug-resistant paroxysmal (n = 165) or persistent AF (n = 69) who either underwent a Lasso-guided segmental pulmonary vein isolation (n = 83) or a CARTO-guided left atrial circumferential ablation (n = 151). Treatment with statins (n = 113), ACE-Is, or ARBs (n = 124), or a combination of a statin and an ACE-I or ARB (n = 75) was started >3 months before ablation and was continued during follow-up.
  
  
  RESULTS
  After a median follow-up of 12.7 months, 64% of patients with paroxysmal and 45% of patients with persistent AF were free of AF. Statin use (hazard ratio [HR], 1.06; P = .79), ACE-I or ARB use (HR, 1.12; P = .59), and their combined use (statin + ACE-I/ARB; HR, 1.17; P = .54) did not significantly influence ablation outcome as assessed by Cox regression analysis. In addition, after multivariate adjustment for potential confounders, the examined drugs did not significantly affect ablation outcome. Ablation induced an acute up-regulation of C-reactive protein levels (preablation vs 48 hours postablation, 5.9 +/- 8.1 vs 33.7 +/- 30 mg/L; P < .001) and other inflammatory markers. The examined drugs did not significantly alter baseline levels or ablation-induced up-regulation of inflammatory markers.
  
  
  CONCLUSIONS
  The routine use of statins, ACE-Is, or ARBs did not result in an improved outcome of AF ablation.
authors.affiliation: Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Austria. bernhard.richter@meduniwien.ac.at
authors.forename: Bernhard
authors.initials: B
authors.lastname: Richter
authors.forename: Michael
authors.initials: M
authors.lastname: Derntl
authors.forename: Manfred
authors.initials: M
authors.lastname: Marx
authors.forename: Peter
authors.initials: P
authors.lastname: Lercher
authors.forename: Heinz D
authors.initials: HD
authors.lastname: Gössinger
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery*; D017115:Catheter Ablation; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000187:drug effects; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators