Junctional tachycardia during radiofrequency ablation of the slow pathway in patients with AV nodal reentrant tachycardia: effects of autonomic blockade.

Abstract

The autonomic nervous system richly innervates the peri-AV nodal region and may be activated during radiofrequency (RF) ablation for AV nodal reentrant tachycardia, resulting in the generation of junctional tachycardia. The purpose of this prospective study was to determine the role of the autonomic nervous system in the genesis of junctional tachycardia. We compared the characteristics of junctional tachycardia in patients with (n = 10) and without (n = 10) autonomic blockade undergoing RF ablation for AV nodal reentrant tachycardia. Intravenous administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) were used to block the autonomic nervous system. There were no differences in clinical variables and baseline electrophysiologic characteristics between the two groups except for slightly longer effective refractory periods of the fast pathway and of the atrium in the autonomic blockade group. The autonomic blockade shortened the baseline sinus cycle length and effective refractory period of the ventricle only but not other electrophysiologic characteristics of the AV node. The junctional tachycardia was observed during ablation in each patient, but its occurrence and cycle length, as well as numbers of consecutive junctional beats, were not altered by the autonomic blockade. Our results indicate that the muscarinic and beta-adrenergic components of the autonomic nervous system play no role in the genesis of junctional tachycardia.