Abstract

Abstract Introduction Growing interest has emerged around cardiac autonomic nervous system driven by ablation approaches for the treatment of neurally-mediated syncope (NMS). Ganglionated-plexi (GPs) located in the epicardial fat pads are the main target of ablative therapies, but little is known about the finest method to track their location from the endocardium. Most current techniques rely on empirical research of signal fragmentation and/or vagal response at anatomical landmarks. A poor accuracy in targeting GPs may lead to the risk of incomplete or over-extensive ablation. Purpose We analyzed the atrial electrograms (EGMs) in healty subjects and their response to atropine to describe physiological fragmentation and the relationship with vagal output. Methods Study partecipants were selected from young patients without structural heart desease who underwent electrophysiological study (EPS) for standard indications. High-density mapping of right atrium was performed before and after administration of 2 mg atropine at the end of the planned procedure. Offline analyses were performed comparing the two maps of each patient focusing on the fragmentation of the atrial EGMs. Results The study cohort comprised 10 patients (mean age of 39±11 years, 6 males). The indication for EPS was: supraventricular tachycardia (SVT) ablation in 9 patients, syncope in 1 patient. High density three-dimensional electro-anatomic maps (EAM) were all obtained with a multipolar catheter during sinus rhythm (number of points: 8794±937 in basal maps and 9007±1296 after atropine, p=0,87). The response to atropine was documented by an increase in heart rate (mean increase 59 ± 19% of basal cycle length). All basal maps showed a similar pattern of fragmentation in the posterior-septal wall reflecting the anatomical distribution of right GPs. In particular, three main stations were identified in the supero-, mid- and infero-posterior regions. Fragmentation of EGMs was found to progress from the edge to the core of each area. After administration of atropine, a reduction in fractionated area was observed in all patients. Filtering the maps according to a cut-off of fragmentation ≥ 6 peaks allowed identification of the nucleus with the highest degree of variation after atropine injection (mean basal area = 0,89 ± 0,81 cm2 ; mean atropine area = 0,44 ± 0,56 cm2 p<0,001). Conclusion Fragmentation of atrial electrograms is a dynamic property related to vagal output. High density mapping with a high pass filter of 6 peaks allows to identify the smallest vagal sensitive area in the anatomical stations of the GPs.

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