title: The efficacy of azimilide in the treatment of atrial fibrillation in the presence of left ventricular systolic dysfunction: results from the Azimilide Postinfarct Survival Evaluation (ALIVE) trial.
abstract: OBJECTIVE
  The purpose of this study was to assess the effect of oral azimilide dihydrochloride (AZ) 100 mg versus placebo on the onset, termination, and prevalence of atrial fibrillation (AF) in a subpopulation of patients in the Azimilide Postinfarct Survival Evaluation (ALIVE) trial.
  
  
  BACKGROUND
  Previous clinical trials have demonstrated the antiarrhythmic effects of AZ in patients with AF. Azimilide was investigated for its effects on mortality in patients with depressed left ventricular (LV) function after recent myocardial infarction (MI) and in a subpopulation of patients with AF.
  
  
  METHODS
  A total of 3,381 post-MI patients with depressed LV function were enrolled in this randomized, placebo-controlled, double-blind study of AZ 100 mg on all-cause mortality. A total of 93 patients had AF on the baseline 12-lead electrocardiogram (ECG). An additional 27 patients developed AF after initially being in sinus rhythm at randomization. These patients were identified through 12-lead ECGs obtained during routine visits at week 2, months 1, 4, 8, and 12.
  
  
  RESULTS
  Patients with AF at baseline had a higher mortality than those without AF (p = 0.0006). Among AF patients, there was no difference in mortality between AZ patients and placebo patients (p = 0.82). Fewer AZ patients developed AF than placebo patients (p = 0.04). More AZ patients than placebo patients converted to sinus rhythm, but this difference did not achieve statistical significance (p = 0.076). Over one-year follow-up, more AZ patients were in sinus rhythm than placebo patients (p = 0.04).
  
  
  CONCLUSIONS
  Azimilide was safe and effective AF therapy in patients with depressed LV function after an MI.
authors.affiliation: The Methodist DeBakey Heart Center and Department of Medicine, Section of Cardiology, Baylor College of Medicine, Houston, Texas 77030, USA. cpratt@bcm.tmc.edu
authors.forename: Craig M
authors.initials: CM
authors.lastname: Pratt
authors.forename: Steven N
authors.initials: SN
authors.lastname: Singh
authors.forename: Hussein R
authors.initials: HR
authors.lastname: Al-Khalidi
authors.forename: Jose M
authors.initials: JM
authors.lastname: Brum
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Holroyde
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Marcello
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Schwartz
authors.forename: A John
authors.initials: AJ
authors.lastname: Camm
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy*; D002121:Calcium Channel Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D004311:Double-Blind Method; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006827:Hydantoins; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology; D007093:Imidazoles / Q000009:adverse effects / Q000627:therapeutic use*; D048289:Imidazolidines; D008297:Male; D008875:Middle Aged; D009503:Neutropenia / Q000139:chemically induced; D010879:Piperazines / Q000009:adverse effects / Q000627:therapeutic use*; D015995:Prevalence; D013599:Systole / Q000187:drug effects; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D002121:Calcium Channel Blockers; D006827:Hydantoins; D007093:Imidazoles; D048289:Imidazolidines; D010879:Piperazines; C086123:azimilide