An experimental study on the site dependency and mechanism of vagal denervation following radiofrequency catheter ablation for supraventricular arrhythmias including atrial fibrillation.

Radiofrequency catheter ablation (RFCA) for supraventricular arrhythmias results in parasympathetic nervous damage. Recently, RFCA around the pulmonary veins (PVs) has become a standardized curative therapy for atrial fibrillation (AF). The aim of the present study was to elucidate the relationship between the degree of vagal denervation and RFCA sites, including the PV areas. In 21 dogs, RFCA was performed at the ostium of the right PV (n = 7), ostium of the left PV (n = 7), and posteroseptal site of the right atrium (n = 7). Electrical stimulation of the cervical vagal trunk (ESCV) was performed and the resultant increase in the P-P interval (PPI) observed on the ECG was measured. The PPI was compared between the different RFCA sites. In another 7 animals, the vagal ganglia located in the fat pads that innervate the sinoatrial (SA) node were also stimulated (ESFP), testing the degree of postganglionic damage. The PPI after RFCA was decreased with right PV RFCA whereas there was no change with left PV RFCA. The ESFP yielded a significantly greater decrease in the PPI than the ESCV. The PPI during ESFP was completely blocked by hexamethonium, injected into the fat pad. The ESCV after the hexa-methonium injection did not result in complete disappearance of the PPI. Thus, right PV RFCA markedly damaged the vagal innervation of the SA node, whereas left PV RFCA produced little damage. The major type of damage was partial postganglionic fiber damage. An alternate vagal pathway external to the fat pads is proposed.