title: Ventricular rate during atrial fibrillation before and after slow-pathway ablation. Effects of autonomic blockade and beta-adrenergic stimulation.
abstract: BACKGROUND
  Radiofrequency catheter modification of AV conduction can be used to control the ventricular rate during atrial fibrillation both in the baseline state and during exercise. Slow-pathway ablation has been suggested to be the mechanism for this response. The purpose of this study was to determine the effect of slow-pathway ablation on the ventricular rate in atrial fibrillation during autonomic blockade and sympathetic stimulation in patients with AV nodal reentrant tachycardia (AVNRT).
  
  
  RESULTS
  Thirty-five patients undergoing slow-pathway radiofrequency ablation for AVNRT were assigned to autonomic blockade (0.2 mg/kg propranolol and 0.04 mg/kg atropine; n = 14) or isoproterenol (2 micrograms/min; n = 21). Atrial fibrillation was induced before and after slow-pathway radiofrequency ablation. During autonomic blockade, the mean ventricular cycle length (448 +/- 34 versus 525 +/- 103 ms, P < .01) and maximum ventricular cycle length (640 +/- 105 versus 798 +/- 226 ms, P = .04) were prolonged after ablation, whereas the minimum ventricular cycle length did not change significantly (361 +/- 42 versus 403 +/- 83 ms, P = .05). During isoproterenol infusion, the mean ventricular cycle length (375 +/- 52 versus 390 +/- 61 ms, P = .2), maximum ventricular cycle length (520 +/- 88 versus 537 +/- 106 ms, P = .3), and minimum ventricular cycle length (307 +/- 59 versus 298 +/- 33 ms, P = .4) did not change significantly after slow-pathway ablation.
  
  
  CONCLUSIONS
  Slow-pathway ablation slows the ventricular rate during atrial fibrillation under conditions of autonomic blockade but not during sympathetic stimulation. Therefore, slow-pathway ablation alone cannot account for the clinical results obtained with radiofrequency modification of AV conduction in patients with atrial fibrillation.
authors.affiliation: Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109, USA.
authors.forename: S A
authors.initials: SA
authors.lastname: Strickberger
authors.forename: R
authors.initials: R
authors.lastname: Weiss
authors.forename: E G
authors.initials: EG
authors.lastname: Daoud
authors.forename: R
authors.initials: R
authors.lastname: Goyal
authors.forename: F
authors.initials: F
authors.lastname: Bogun
authors.forename: K C
authors.initials: KC
authors.lastname: Man
authors.forename: F
authors.initials: F
authors.lastname: Morady
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000601:surgery; D001285:Atropine / Q000494:pharmacology; D017115:Catheter Ablation; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010276:Parasympatholytics / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D013565:Sympatholytics / Q000494:pharmacology*
chemical_list: D010276:Parasympatholytics; D011943:Receptors, Adrenergic, beta; D013565:Sympatholytics; D001285:Atropine; D011433:Propranolol; D007545:Isoproterenol