Although the effective refractory period (ERP) of the fast pathway is reported to be shortened after radiofrequency catheter ablation of the slow pathway in atrioventricular nodal reentrant tachycardia (AVNRT), whether the atrioventricular (AV) nodal physiology maintains the same condition over the long term is controversial. To assess the AV nodal physiology after catheter ablation of the slow pathway in AVNRT, the A-H interval and ERP of the fast pathway were measured before, immediately after and 3 months after catheter ablation in 12 patients. We compared these factors in 12 patients with left concealed accessory bypass tract to clarify the mechanism of the electrophysiological change in the AV node. Both the A-H interval and ERP of the fast pathway were significantly shortened from 111 +/- 18 to 96 +/- 17 ms and 365 +/- 68 to 261 +/- 52 ms immediately after catheter ablation (p < 0.01), and recovered to 128 +/- 44 and 372 +/- 80 ms 3 months after catheter ablation. There were no significant differences in the A-H interval of the fast pathway between the period immediately after and 3 months after catheter ablation following administration of atropine sulfate (99 +/- 52). There were no significant differences in the ERP of the fast pathway between the period immediately after and 3 months after catheter ablation following administration of atropine sulfate (248 +/- 33 ms). On the contrary, there were no significant changes in the A-H interval and ERP of the AV node at these two times in patients with Wolff-Parkinson-White (WPW) syndrome. The change in characteristics of AV nodal physiology was observed only immediately after catheter ablation in AVNRT, but not in WPW syndrome. The change in electrophysiology immediately after catheter ablation was similar to that following administration of atropine sulfate in AVNRT 3 months after catheter ablation. These findings suggest that catheter ablation does not cause a permanent change in AV nodal physiology and that the location of the ablated site plays an important role in AV nodal physiology.