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Low-Level Vagosympathetic Nerve Stimulation Inhibits Atrial Fibrillation Inducibility: Direct Evidence by Neural Recordings from Intrinsic Cardiac Ganglia


  • Supported in part by a grant from the College of Medicine Alumni Association of the University of Oklahoma (SSP) and from the Helen and Wil Webster Arrhythmia Research Fund (BJS).

  • Dr. Scherlag reports participation on a research grant supported by St. Jude Medical and serving as a consultant to Atricure, Inc. and Symphony Medical. Dr. Po reports participation on a research grant supported by College of Medicine Alumni, University of Oklahoma; serving as a consultant to Atricure, Inc.; and honoraria from St. Jude Medical and Johnson & Johnson. Other authors: No disclosures.

Address for correspondence: Sunny S. Po, M.D., Ph.D., Heart Rhythm Institute, 1200 Everett Drive (6E103), Oklahoma City, OK 73104, USA. Fax: 405-272-7455; E-mail:


Intrinsic Cardiac Ganglia Activity Inhibited by Low-Level Vagal Stimulation. Introduction: 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 ICANS, as evidenced by (1) LL-VNS suppression of the ability of the ARGP stimulation to slow the sinus rate, (2) the frequency and amplitude of the neural activity recorded from the ARGP or SLGP was markedly suppressed by LL-VNS, and (3) the spatial gradient of the ERP and WOV from the PV-atrial junction toward the atrial appendage was eliminated by LL-VNS.

Conclusions: LL-VNS suppressed AF inducibility by inhibiting the neural activity of major GP within the ICANS. (J Cardiovasc Electrophysiol, Vol. 22, pp. 455-463)