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Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and
1Electrophysiology Laboratory, Milwaukee Heart Institute, Sinai Samaritan Medical Center, University of Wisconsin.
Background:
The presence of atrioventricular nodal dual-pathway physiology in patients with atrioventricular nodal reentrant tachycardia (AVNRT) provides an opportunity to characterize the effect of a selective slow-pathway ablation on the ventricular rate during atrial fibrillation (AF). This may have important clinical implications for the nonpharmacological management of AF with a rapid ventricular rate.
Methods And Results:
Selective radiofrequency catheter ablation of the atrioventricular nodal slow pathway was performed with a stepwise approach in patients with documented sustained AVNRT. The AV nodal conduction properties and refractoriness and the ventricular rate during induced AF were assessed at baseline and under autonomic blockade before and after a selective slow-pathway ablation in 18 patients (mean age, 34 +/- 8 years). Sustained AVNRT was induced with a mean cycle length of 339 +/- 58 ms. A slow-pathway ablation was successfully achieved with 5 +/- 4 applications of radiofrequency energy. The shortest cycle length of 1:1 AV conduction and the AV nodal effective refractory period significantly prolonged after ablation (367 +/- 53 versus 403 +/- 55 ms, P < .0001, and 258 +/- 55 versus 292 +/- 74 ms, P < .05, respectively). Selective slow-pathway ablation significantly prolonged the mean (526 +/- 93 versus 612 +/- 107 ms, P < .0001), the shortest (378 +/- 59 versus 423 +/- 73 ms, P < .0001), and the longest (826 +/- 150 versus 969 +/- 226 ms, P < .01) cycle lengths of the ventricular response to AF. Significant slowing of the ventricular rate during AF occurred in 13 patients (72%), including all eight patients in whom AV nodal dual-pathway physiology was abolished. Five patients did not have a significant change in the ventricular rate during AF; a persistent dual AV nodal pathway physiology was demonstrable in four of these patients. Loss of dual-pathway physiology after ablation had a sensitivity of 77%, specificity of 80%, and positive predictive value of 91% for slowing the ventricular rate during AF.
Conclusions:
In patients undergoing a slow-pathway ablation for control of AVNRT, selective slow-pathway ablation may cause a significant decrease in the ventricular rate during AF. These effects are primarily due to the prolongation of AV nodal conduction properties and refractory period of the residual AV nodal transmission system. These findings may have important therapeutic implications for the nonpharmacological treatment of AF, particularly in patients with underlying dual AV nodal physiology.