title: Impact of amiodarone on electrophysiologic properties of pulmonary veins in patients with paroxysmal atrial fibrillation.
abstract: BACKGROUND
  Pulmonary veins (PVs) are the predominant location of triggers for atrial fibrillation (AF), but little is known about the electrophysiologic properties of PVs. In addition, the influence of amiodarone on the electrophysiologic properties of PVs has not been elucidated.
  
  
  RESULTS
  Fifty-five patients with symptomatic and drug-resistant AF were divided into two groups: group 1 patients (n=29) without antiarrhythmic drug therapy at the time of electrophysiologic study (EPS), and group 2 patients (n=26) undergoing continuous long-term treatment with amiodarone. EPS including programmed stimulation of both atria and within the PVs was performed in both groups. In group 1, the effective refractory period (ERP) of all PVs (174 +/- 62 msec) was significantly shorter than the ERP of the left atrium ([LA] 254 +/- 30 msec, P=0.0001) and right atrium ([RA] 221 +/- 29 msec, P=0.0001). The same pattern was observed in group 2 (PV: 210 +/- 58 msec; LA: 259 +/- 35 msec, P=0.0001; RA: 246 +/- 37 msec, P=0.0255). The ERP of all stimulated PVs was significantly lower in group 1 (174 +/- 62 msec) than in group 2 (210 +/- 58 msec; P=0.0001). The ERP of the left superior and right superior PVs and RA but not the left inferior PV and LA were significantly increased in patients treated with amiodarone. Decremental conduction properties were observed in all stimulated PVs, and there were no significantly differences between the maximal decrement of both groups.
  
  
  CONCLUSIONS
  The distinctive electrophysiologic properties of PVs are emphasized by amiodarone therapy. Long-term amiodarone treatment is responsible for heterogeneous alteration of the PV electrophysiology, which may account for the individual antiarrhythmic responses in a subset of patients with paroxysmal AF.
authors.affiliation: Department of Cardiology, University Hospital Eppendorf, Hamburg, Germany. rostock@uke.uni-hamburg.de
authors.forename: Thomas
authors.initials: T
authors.lastname: Rostock
authors.forename: Helge
authors.initials: H
authors.lastname: Servatius
authors.forename: Tim
authors.initials: T
authors.lastname: Risius
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Ventura
authors.forename: Christian
authors.initials: C
authors.lastname: Weiss
authors.forename: Thomas
authors.initials: T
authors.lastname: Meinertz
authors.forename: Stephan
authors.initials: S
authors.lastname: Willems
mesh_terms: D000638:Amiodarone / Q000008:administration & dosage*; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology*; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D011667:Pulmonary Veins / Q000187:drug effects* / Q000503:physiopathology*; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D000889:Anti-Arrhythmia Agents; D000638:Amiodarone