Key result
Right upper pulmonary vein isolation in dogs attenuated vagal innervation and significantly decreased the vulnerability window of atrial fibrillation to vagal stimulation at the right atrium (40 vs 0 ms, P<0.001).
Why the study?
Does right upper pulmonary vein isolation attenuate vagal innervation and reduce vulnerability to atrial fibrillation in a canine model?
Does right upper pulmonary vein isolation attenuate vagal innervation and reduce vulnerability to atrial fibrillation in a canine model?
Right upper pulmonary vein isolation attenuates atrial vagal innervation and decreases vulnerability to atrial fibrillation in a canine model, likely due to damage to epicardial fat pads.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open translation of vagal attenuation by pulmonary vein isolation to human AF.
BACKGROUND: Based on the hypothesis that pulmonary vein isolation could result in the damage of the epicardial fat pads, this study aimed to investigated the impact of right upper pulmonary vein (RUPV) isolation on vagal innervation to atria. METHODS: Bilateral cervical sympathovagal trunks were decentralized in 6 dogs. Metoprolol was given to block sympathetic effects. Multipolar catheters were placed into the right atrium (RA) and coronary sinus (CS). RUPV isolation was performed via transseptal procedure. Atrial effective refractory period (ERP), vulnerability window (VW) of atrial fibrillation (AF), and sinus rhythm cycle length (SCL) were measured at RA and distal coronary sinus (CSd) at baseline and vagal stimulation before and after RUPV isolation. Serial sections of underlying tissues before and after ablation were stained with haematoxylin and eosin. RESULTS: SCL decreased significantly during vagal stimulation before RUPV isolation (197 +/- 21 vs 13 +/- 32 beats per minute, P < 0.001), but remained unchanged after RUPV isolation (162 +/- 29 vs 140 +/- 39 beats per minute, P > 0.05). ERP increased significantly before RUPV isolation compared with that during vagal stimulation [(85.00 +/- 24.29) ms vs (21.67 +/- 9.83) ms at RA, P < 0.001; (90.00 +/- 15.49) ms vs (33.33 +/- 25.03) ms at CSd P < 0.005], but ERP at baseline hardly changed after RUPV isolation compared with that during vagal stimulation [(103.33 +/- 22.50) vs (95.00 +/- 16.43) ms at RA, P = 0.09; (98.33 +/- 24.83) vs (75.00 +/- 29.50) ms at CSd, P = 0.009]. The ERP shortening during vagal stimulation after RUPV isolation decreased significantly [(63.33 +/- 22.51) ms vs (8.33 +/- 9.83) ms at RA, P < 0.005; (56.67 +/- 20.66) ms vs (23.33 +/- 13.66) ms at CSd, P < 0.05]. AF was rarely induced at baseline before and after RUPV isolation (VW close to 0), while VW of AF to vagal stimulation significantly decreased after RUPV isolation [(40.00 +/- 10.95) vs 0 ms at RA, P < 0.001; (45.00 +/- 32.09) vs (15.00 +/- 23.45) ms at CS, P < 0.05]. The architecture of individual ganglia was significantly altered after ablation. CONCLUSIONS: The less ERP shortening to vagal stimulation and altered architecture of individual ganglia after right upper pulmonary vein isolation indicate that isolation may result in damage of the epicardial fat pads, thereby attenuating the vagal innervation to atria. The decreased vulnerability window of atrial fibrillation indicates that vagal denervation may contribute to its suppression.
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Liu et al. (2006) studied Atrial fibrillation vulnerability (n=6). Right upper pulmonary vein (RUPV) isolation vs. Baseline (before RUPV isolation) was evaluated on Vulnerability window (VW) of atrial fibrillation to vagal stimulation at the right atrium (p=<0.001). Right upper pulmonary vein isolation in dogs attenuated vagal innervation and significantly decreased the vulnerability window of atrial fibrillation to vagal stimulation at the right atrium (40 vs 0 ms, P<0.001).
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