The influence of cardiac autonomic nerve plexus on the electrophysiological properties in canines with atrial fibrillation.

Background: This study sought to examine the effect of the cardiac autonomic nerve plexus, which originates from the vagus nerve trunk, on atrial vulnerability.

Methods: Dogs in group I (n = 6) underwent ganglionated plexi (GP) sequential ablation following six hours of left atrial appendage rapid atrial pacing (RAP). The monophasic action potential duration at 90% of repolarization (APD90), effective refractory period (ERP), and the atrial fibrillation inducing rate of bilateral atria and pulmonary veins were recorded at baseline, l h, 3 h and 6 h after pacing, as well as after sequential ablation (RAGP + RIGP ablation, LSGP + RIGP ablation). Dogs in group II (n = 6) received vagus nerve stimulation following six hours of left atrial appendage RAP. APD90, ERP and atrial fibrillation inducing rate of bilateral atria and pulmonary veins were recorded at baseline, 1 h, 3 h and 6 h after pacing, as well as after GP sequential ablation (RAGP + RIGP ablation, LSGP + RIGP ablation).

Results: In group I, APD90 and ERP progressively shortened and atrial fibrillation inducing rate increased in various sites l h, 3 h and 6 h after RAP (P < 0.05). APD90 and ERP shortened significantly and atrial fibrillation inducing rate was significantly higher in the left atrial appendage and bilateral pulmonary veins than in other sites (P < 0.05). Following GP sequential ablation, APD90, ERP and atrial fibrillation inducing rate were not significantly different from baseline levels (P > 0.05). In group II, APD90 and ERP progressively shortened in various sites over pacing time period, and the atrial fibrillation inducing rate increased l h, 3 h and 6 h after RAP + VNS (P < 0.05). APD90 and ERP shortened significantly and atrial fibrillation inducing rate was significantly higher in the left atrial appendage and right superior/inferior pulmonary veins when compared with other sites (P < 0.05). After GP sequential ablation, APD90, ERP and atrial fibrillation inducing rate were not significantly different from baseline levels (P > 0.05). Compared with group I, APD90 and ERP shortened significantly, while atrial fibrillation inducibility increased significantly at baseline and l h, 3 h, and 6 h after pacing in group II (P < 0.05). After ablation of the four major cardiac GPs, no significant differences were observed in the two groups with respect to APD90, ERP and atrial fibrillation inducing rate (P > 0.05).

Conclusion: GP activation, as a result of vagal nerve stimulation, alters MAP90, ERP and atrial fibrillation inducing rate of the atrium and pulmonary veins and promotes the occurrence of RAF in the early stage of atrial fibrillation, resulting in increased atrial vulnerability and triggering the occurrence and maintenance of atrial fibrillation.