title: Role of oral amiodarone in patients with atrial fibrillation and congestive heart failure.
abstract: BACKGROUND
  Amiodarone is recognized as the most effective therapy for maintaining sinus rhythm (SR) post cardioversion in patients with atrial fibrillation (AF). It is also recommended for controlling AF in patients with congestive heart failure (CHF). We retrospectively examined the efficacy and safety of oral amiodarone in patients with AF and CHF.
  
  
  METHODS
  Forty-eight consecutive AF patients whose left ventricular ejection fraction (LVEF) was less than 50% and B-type natriuretic peptide (BNP) was higher than 100 pg/ml were investigated retrospectively, and divided into 3 groups: paroxysmal AF, 16 patients; persistent AF, 9 patients; and permanent AF, 23 patients.
  
  
  RESULTS
  The permanent AF group had a longer history of AF, larger left ventricular end-diastolic diameter (LVDd) and left atrial diameter (LAD) than paroxysmal and persistent AF groups (p<0.05). After median follow-up of 265 days, amiodarone suppressed paroxysms in 88% of paroxysmal AF patients, while SR was maintained in all persistent AF patients, and 35% of permanent AF patients. Of the 32 persistent and permanent AF patients, 12 (71%) out of 17 maintained SR after successful electrical cardioversion, and conversion to SR occurred spontaneously in 5 (33%) out of 15. The effective group had significantly smaller LVDd and LAD than the ineffective group. In the effective group, BNP decreased significantly from 723±566 pg/ml to 248±252 pg/ml, (p<0.0005) and LVEF increased significantly from 33±7% to 50±13% (p<0.0005) during follow up, while no changes were observed in the ineffective group. The patients with low LVEF (≤30%) benefited comparably from amiodarone to the patients with LVEF >30%. Complications occurred in 24 (50%) patients leading to discontinuation of amiodarone in 11 (23%).
  
  
  CONCLUSIONS
  Oral amiodarone helped restore SR in paroxysmal and persistent AF patients with CHF. The successful rhythm control by amiodarone resulted in the improvement of LV function and the decrease of BNP levels.
authors.affiliation: Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. mihoko kawabata.cvm@tmd.ac.jp
authors.forename: Mihoko
authors.initials: M
authors.lastname: Kawabata
authors.forename: Kenzo
authors.initials: K
authors.lastname: Hirao
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Hachiya
authors.forename: Kouji
authors.initials: K
authors.lastname: Higuchi
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Atsuhiko
authors.initials: A
authors.lastname: Yagishita
authors.forename: Osamu
authors.initials: O
authors.lastname: Inaba
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Isobe
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000638:Amiodarone / Q000008:administration & dosage*; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage*; D001281:Atrial Fibrillation / Q000188:drug therapy*; D004554:Electric Countershock; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D012189:Retrospective Studies; D013318:Stroke Volume; D016896:Treatment Outcome
chemical_list: D000889:Anti-Arrhythmia Agents; D020097:Natriuretic Peptide, Brain; D000638:Amiodarone