Ventricular rate during atrial fibrillation before and after slow-pathway ablation. Effects of autonomic blockade and beta-adrenergic stimulation.

Abstract

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). 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. 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.