| Objective The superior vena cava (SVC) isolation1 is effective for some patients with atrial fibrillation (AF). However, little was known about the impact of SVC isolation on parasympathetic nerve. This study hypo thesized that SVC isolation could resulted in the vagal innervation to atrial due to the SVC very close to the fat pad of vagal.Methods 9 adult mongrel dogs under general anesthesia were involved in this study. Bilateral cervical sympathovagal trunks were decentralized. Metoprolol was given to block sympathetic effects. Multipolar catheters were placed into right atrial(RA), coronary sinus(CS) and right ventricle (RV) through right internal jugular vein and left femoral vein respectively. SVC isolation was performed guided by mapping catheter (Lasso) placed at junction of SVC and right atrial through right femoral vein. Complete atrioventricular block was achieved by His bundle ablation and RV pacing was applied through RV catheter. Atrial effective refractory period (ERP), vulnerability window(VW)of atrial fibrillation, and sinus cycle length( SCL) were measured at RA, distal end of CS(CSd) and proximal end of CS(CSp) at baseline (without vagal stimulation) and vagal stimulation before and after SVC isolation.Results SCL decreased significantly during vagal stimuli before SVC isolation(142.67±15.42 VS 65.78±28.49beat per minute,p<0.001)while SCL remained unchanged during vagal stimuli after SVC isolation(134.89±19.19 vs 114.33±31.41 beat per minute, p>0.05), which indicated that SVC isolation eliminated vagal modulation to sinus node. ERP at baseline increased significantly before SVC isolation compared with that during vagal stimulation (101.11±27.59 vs 51.11±18.33ms at RA, p<0.001; 98.89±14.53 vs 56.67±22.36ms at CSd, p<0.001; 101.11±12.69 vs 48.89±25.22ms at CSd, p<0.001). While ERP remained unchanged during vagal stimulation after SVC isolation compared with that at baseline (94.44±16.67 vs 94.4±16.70ms at RA, p<0.001; 96.7±18.00 vs 89±15ms at CSd, p<0.05; 98.9±20.3 vs 93.3±18.7ms at CSp, p<0.05), it indicated that SVC isolation attenuated vagal tone. The shortening of ERP after SCV isolation decreased significantly compared with that before isolation (50±19.36 vs 0±10ms at RA, p<0.001; 42±22.8 vs 7.78±13.94ms at CSd, p<0.001; 47.78±26.8 vs 6.68±10 ms at CSd, p<0.001). Atrial fibrillation was very difficult induced at baseline before and after SVC isolation (VW close to 0), while VW of atrial fibrillation to vagal stimuli significantly decreased after SVC isolation(21.11±20.88 vs 6.67±11.18 ms at RA; 16.66±23.97 vs 8.89±14.52ms at CSd; 22.22±18.55 vs 2.22±6.67ms at CSp, p <0.05).Conclusions The decreased ERP shortening to vagal stimuli after SVC isolation indicates that SVC isolation may result in the damage of the epicardia fat pad, thereby attennate the vagal innervation to atrial. The decreased VW to atrial fibrillation by SVC isolation indicates that attenuated vagal tone may contribute to the suppression of atrial fibrillation. |