title: Verapamil reduces tachycardia-induced electrical remodeling of the atria.
abstract: BACKGROUND
  Prolonged periods of atrial fibrillation or rapid atrial pacing induce shortening of the atrial effective refractory period (AERP), which is thought to be related to the lower success rates of various antifibrillatory treatments when the arrhythmia has lasted for a longer period of time.
  
  
  RESULTS
  To investigate whether an increase in intracellular calcium could be the stimulus for electrical remodeling, the effects of verapamil on shortening of the AERP in response to 24 hours of rapid atrial pacing (300 bpm) were studied in five chronically instrumented conscious goats during infusion of saline or verapamil. During rapid atrial pacing, the ventricular rate was kept constant by ventricular pacing (150 bpm). The AERP was measured by programmed electrical stimulation at basic cycle lengths of 430, 300, and 200 ms. Verapamil had no effects on the AERP before rapid atrial pacing. However, in the course of 24 hours of rapid atrial pacing, the AERP shortened significantly less (27% to 58%) in the presence of verapamil compared with control (at 430, 300, and 200 ms, P < .001, P < .01, and P < .01, respectively). Also, after cessation of pacing, complete recovery of the AERP during verapamil infusion occurred much sooner than in the control experiments. Despite a significant reduction in electrical remodeling, there was only a minimal reduction in inducibility of atrial fibrillation by verapamil (34% versus 39% in the control experiments, P = .03).
  
  
  CONCLUSIONS
  Electrical remodeling of the atrium during rapid atrial pacing was significantly attenuated by verapamil. This suggests that electrical remodeling of the atrium is triggered by the high calcium influx during rapid atrial pacing rates.
authors.affiliation: Department of Cardiology, University Hospital Groningen, Netherlands.
authors.forename: R G
authors.initials: RG
authors.lastname: Tieleman
authors.forename: C
authors.initials: C
authors.lastname: De Langen
authors.forename: I C
authors.initials: IC
authors.lastname: Van Gelder
authors.forename: P J
authors.initials: PJ
authors.lastname: de Kam
authors.forename: J
authors.initials: J
authors.lastname: Grandjean
authors.forename: K J
authors.initials: KJ
authors.lastname: Bel
authors.forename: M C
authors.initials: MC
authors.lastname: Wijffels
authors.forename: M A
authors.initials: MA
authors.lastname: Allessie
authors.forename: H J
authors.initials: HJ
authors.lastname: Crijns
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D006041:Goats; D006325:Heart Atria / Q000187:drug effects* / Q000473:pathology; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects*; D013610:Tachycardia / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D014700:Verapamil / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D002121:Calcium Channel Blockers; D014700:Verapamil; D002118:Calcium