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Evaluation of catheter ablation of periatrial ganglionic plexi in patients with atrial fibrillation
Authors:Danik Stephan  Neuzil Petr  d'Avila Andre  Malchano Zachary J  Kralovec Stepan  Ruskin Jeremy N  Reddy Vivek Y
Institution:Cardiac Arrhythmia Service, Massachusetts General Hospital-Harvard Medical School, Boston, Massachusetts, USA. sdanik@partners.org
Abstract:Recent data suggests that the cardiac autonomic nervous system has an important role in the initiation and maintenance of atrial fibrillation (AF). This study investigated (1) the feasibility of identifying and targeting these autonomic ganglia using endocardial radiofrequency stimulation and ablation, respectively; (2) the efficacy of endocardial ablation to completely eliminate the vagal response elicited from epicardial stimulation; and (3) the effect of autonomic ablation on the acute inducibility of AF. The study included 18 patients referred for catheter ablation of suspected vagal-mediated AF. The endocardial left atrial surface was stimulated at high frequency (20 to 50 Hz) to elicit a vagal response. In selected patients (n = 5), pericardial access was obtained using a subxyphoid puncture to permit epicardial stimulation. Catheter ablation of the putative autonomic ganglionic sites was performed from the left atrial endocardium using irrigated radiofrequency energy. After ablation of all identifiable autonomic ganglia, high-frequency pacing was repeated to induce AF. In all patients, stimulation at certain endocardial sites elicited a vagal response. Endocardial ablation abrogated this vagal responsiveness. Furthermore, for sites accessible from the pericardium, the vagal response elicited using epicardial stimulation was also eliminated. Despite successful ablation of these ganglia, AF was still inducible in 17 of 18 patients. In conclusion, successful ablation of autonomic ganglia from an endocardial approach can be reliably achieved using an irrigated catheter. In addition, ablation of these structures in patients with vagal-mediated AF is insufficient to prevent its acute reinduction with high-frequency atrial stimulation.
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