Mechanism of the conversion of a pulmonary vein tachycardia to atrial fibrillation in normal canine hearts: Role of autonomic nerve stimulation

Introduction: The role of the autonomic nervous system in inducing pulmonary vein (PV)-triggered atrial fibrillation (AF) and the termination mechanism of the AF are unknown. The purpose of this study was to elucidate the mechanism of the conversion of a tachycardia within a PV into AF under autonomic stimulation and the termination mechanism of the AF in normal canine hearts. Methods and Results: In open-chest dogs, the electrophysiologic parameters were measured under vagal stimulation (VS) or an isoproterenol administration. The effects of the VS or isoproterenol on the PV tachycardias (PVTs), which were created by burst pacing from a PV or the application of aconitine onto the PV, were evaluated. Pilsicainide, a Na channel blocker, was administered during the induced AF. VS and isoproterenol shortened the atrial and PV effective refractory periods. In the pacing model, the VS converted the PV rapid activations into sustained AF in 9 of 12 dogs during pacing cycle lengths <= 120 msec, but the isoproterenol did not cause any sustained AF. In the aconitine model, the VS increased the rate of the aconitine-induced PVTs and transformed them into sustained AF in all 14 dogs, whereas the isoproterenol did not induce AF, and decreased the PVT rate. In all 14 dogs the sustained AF was terminated by pilsicainide, which had suppressive effects on the PVT as well as atria and PV-atrial junction. Conclusions: These findings indicate that the vagal effects affecting the PVT and atria facilitate the onset and maintenance of PV-triggered AF in normal canine hearts.