Background Clinical observations have shown that the complex fractionated atrial electrogram （CFAE） associates with ganglionated plexus activity in the cardiac autonomic nervous system. This study aimed to investigate the impact of CFAE ablation on vagal modulation to atria and vulnerability to develop atrial fibrillation （AF）. Methods Ten adult mongrel dogs were involved. Cervical sympathovagal trunks were decentralized and sympathetic effects were blocked. CFAE was color tagged on the atrial 3-dimensional image and ablated during AF induced by S1S2 programmed stimulation plus sympathovagal trunk stimulation. Atrial effective refractory period （ERP） and vulnerability window （VW） of AF were measured on baseline and at vagal stimulation at 4 atrium sites. Serial tissue sections from ablative and control specimens received hematoxylin and eosin staining for microscopic examination. Results Most CFAE areas were localized at the right superior pulmonary quadrant, distal coronary sinus （CS~） quadrant, and proximal coronary sinus （CSp） quadrant （21.74%, separately）. Sinus rhythm cycle length （SCL） shortening did not decrease significantly after ablation at the sites, including right atrial appendage, left atrial appendage, CSd, and CSp （P 〉0.05）. ERP shortening during vagal stimulation significantly decreased after ablation （P 〈0.01）; the VW to vagal stimulation significantly decreased after ablation （P 〈0.05）. The architecture of individual ganglia altered after ablation. Conclusions CFAE has an autonomic basis in dogs. The decreased SCL and ERP shortening to vagal stimulation after CFAE ablation demonstrate that CFAE ablation attenuates vagal modulation to the atria, thereby suppressing AF mediated by enhanced vagal activity. CFAE ablation could suppress AF mediated by enhanced vagal activity.
Objective Mechanisms of pulmonary vein isolation(PVI)for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling(AER)was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period(ERP),vulnerability window(VW)of atrial fibrillation,and sinus rhythm cycle length(SCL)were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage(RAA),left atrial appendage(LAA),distal coronary sinus(CSd)and proximal coronary sinus(CSp).Results(1)Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A(P<0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI(P<0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI(P<0.05).(2)Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A(P<0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B(P<0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.
Yingxue DongShulong ZhangLianjun GaoHongwei ZhaoDonghui YangYunlong XiaYanzong Yang
