2010 SSP Low-Level Vagosympathetic Nerve Stimulation.pdf

2010 SSP Low-Level Vagosympathetic Nerve Stimulation.pdf

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2010 SSP Low-Level Vagosympathetic Nerve Stimulation

455 Low-Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia LILEI YU, M.D.? BENJAMIN J. SCHERLAG, Ph.D.,? SHUYAN LI, M.D.,? XIA SHENG,? ZHIBING LU, M.D.,? HIROSHI NAKAGAWA, M.D., Ph.D.,? YING ZHANG, Ph.D.,? WARREN M. JACKMAN, M.D.,? RALPH LAZZARA, M.D.,? HONG JIANG, M.D.,? and SUNNY S. PO, M.D., Ph.D. From the ?Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan, PR China; ?Department of Medicine and Heart Rhythm Institute, Oklahoma City, Oklahoma, USA; and ?School of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA Intrinsic Cardiac Ganglia Activity Inhibited by Low-Level Vagal Stimulation. Introduc- tion: We hypothesized that low-level vagosympathetic stimulation (LL-VNS) can suppress atrial fibrillation (AF) by inhibiting the activity of the intrinsic cardiac autonomic nervous system (ICANS). Methods and Results: Wire electrodes inserted into both vagosympathetic trunks allowed LL-VNS at 10% or 50% below the voltage required to slow the sinus rate or atrioventricular conduction. Multielectrode catheters were attached to atria, atrial appendages and all pulmonary veins. Electrical stimulation at the anterior right and superior left ganglionated plexi (ARGP, SLGP) was used to simulate a hyperactive state of the ICANS. Effective refractory period (ERP) and window of vulnerability (WOV) for AF were determined at baseline and during ARGP+SLGP stimulation in the presence or absence of LL-VNS. Neural activity was recorded from the ARGP or SLGP. ARGP+SLGP stimulation induced shortening of ERP, increase of ERP dispersion and increase of AF inducibility (WOV), all of which were suppressed by LL-VNS (10% or 50% below threshold) at all tested sites. Sham LL-VNS failed to induce these changes. The effects of LL-VNS were mediated by inhibition of the IC

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