title: Effect of verapamil and procainamide on atrial fibrillation-induced electrical remodeling in humans.
abstract: BACKGROUND
  Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The purpose of this study was to determine the effect of verapamil and procainamide on these manifestations of AF-induced electrical remodeling.
  
  
  RESULTS
  In adult patients without structural heart disease, the atrial ERP was measured before and after AF after pharmacological autonomic blockade and administration of verapamil (17 patients), procainamide (10 patients), or saline (20 patients). AF was then induced by rapid pacing. Immediately on AF conversion, the post-AF ERP was measured at alternating drive cycle lengths of 350 and 500 ms. In the saline group, the pre-AF and first post-AF ERPs at the 350-ms drive cycle length were 206+/-19 and 179+/-27 ms (P<.0001), respectively, and at the 500-ms drive cycle length, the values were 217+/-16 and 183+/-23 ms, respectively (P<.0001). There was a similar significant shortening of the first post-AF ERP in the procainamide group. In the verapamil group, however, there was no difference between the pre-AF and the first post-AF ERP at the 350-ms (226+/-15 versus 227+/-22 ms, P=.8) or 500-ms (230+/-17 versus 232+/-20 ms, P=.6) drive cycle length. During determinations of the post-AF ERP, 105 secondary episodes of AF were unintentionally induced in 12% of verapamil patients compared with 90% and 80% of saline and procainamide patients (P<.01 versus verapamil).
  
  
  CONCLUSIONS
  Pretreatment with the calcium channel antagonist verapamil, but not the sodium channel antagonist procainamide, markedly attenuates acute, AF-induced changes in atrial electrophysiological properties. These data suggest that calcium loading during AF may be at least partially responsible for AF-induced electrical remodeling.
authors.affiliation: Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0022, USA.
authors.forename: E G
authors.initials: EG
authors.lastname: Daoud
authors.forename: B P
authors.initials: BP
authors.lastname: Knight
authors.forename: R
authors.initials: R
authors.lastname: Weiss
authors.forename: M
authors.initials: M
authors.lastname: Bahu
authors.forename: W
authors.initials: W
authors.lastname: Paladino
authors.forename: R
authors.initials: R
authors.lastname: Goyal
authors.forename: K C
authors.initials: KC
authors.lastname: Man
authors.forename: S A
authors.initials: SA
authors.lastname: Strickberger
authors.forename: F
authors.initials: F
authors.lastname: Morady
mesh_terms: D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D016275:Atrial Function; D002304:Cardiac Pacing, Artificial; D004594:Electrophysiology; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D011342:Procainamide / Q000627:therapeutic use*; D012008:Recurrence; D012032:Refractory Period, Electrophysiological; D013997:Time Factors; D014700:Verapamil / Q000627:therapeutic use*
chemical_list: D000889:Anti-Arrhythmia Agents; D014700:Verapamil; D011342:Procainamide