Abstract

Background— The vein of Marshall (VOM) is an attractive target during ablation of atrial fibrillation because of its autonomic innervation, its location anterior to the left pulmonary veins, and its drainage in the coronary sinus. Methods and Results— We studied 17 dogs. A coronary sinus venogram showed a VOM in 13, which was successfully cannulated with an angioplasty wire and balloon. In 5 dogs, electroanatomical maps of the left atrium were performed at baseline and after ethanol infusion in the VOM, which demonstrated a new crescent-shaped scar, extending from the annular left atrium toward the posterior wall and left pulmonary veins. In 4 other dogs, effective refractory periods (ERP) were measured at 3 sites in the left atrium, before and after high-frequency bilateral vagal stimulation. The ERP decreased from 113.6�35.0 to 82.2�25.4 ms ( P <0.05) after vagal stimulation. After VOM ethanol infusion, vagally-mediated ERP decrease was eliminated (from 108.6�24.1 to 96.4�16.9 ms, P =NS). The abolition of vagal effects was limited to sites near the VOM (ERP, 104�14 versus 98.6�12.2 ms postvagal stimulation; P =NS), as opposed to sites remote to VOM (ERP, 107.2�14.9 versus 78.6�14.7 ms postvagal stimulation; P <0.05). To test feasibility in humans, 6 patients undergoing pulmonary vein antral isolation had successful VOM cannulation and ethanol infusion; left atrial voltage maps demonstrated new scar involving the inferoposterior left atrial wall extending toward the left pulmonary veins. Conclusions— Ethanol infusion in the VOM achieves significant left atrial tissue ablation, abolishes local vagal responses, and is feasible in humans.

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