title: Chronic spinal cord stimulation modifies intrinsic cardiac synaptic efficacy in the suppression of atrial fibrillation.
abstract: We sought to determine whether spinal cord stimulation (SCS) therapy, when applied chronically to canines, imparts long-lasting cardio-protective effects on neurogenic atrial tachyarrhythmia induction and, if so, whether its effects can be attributable to i) changes in intrinsic cardiac (IC) neuronal transmembrane properties vs ii) modification of their interneuronal stochastic interactivity that initiates such pathology. Data derived from canines subjected to long-term SCS [(group 1: studied after 3-4 weeks SCS; n = 5) (group 2: studied after 5 weeks SCS; n = 11)] were compared to data derived from 10 control animals (including 4 sham SCS electrode implantations). During terminal studies conducted under anesthesia, chronotropic and inotropic responses to vagal nerve or stellate ganglion stimulation were similar in all 3 groups. Chronic SCS suppressed atrial tachyarrhythmia induction evoked by mediastinal nerve stimulation. When induced, arrhythmia durations were shortened (controls: median of 27 s; SCS 3-4 weeks: median of 16s; SCS 5 weeks: median of 7s). Phasic and accommodating right atrial neuronal somata displayed similar passive and active membrane properties in vitro, whether derived from sham or either chronic SCS group. Synaptic efficacy was differentially enhanced in accommodating (not phasic) IC neurons by chronic SCS. Taken together these data indicate that chronic SCS therapy modifies IC neuronal stochastic inter-connectivity in atrial fibrillation suppression by altering synaptic function without directly targeting the transmembrane properties of individual IC neuronal somata.
authors.affiliation: Department of Medicine, UCLA Health System, Los Angeles, CA, United States. Electronic address: jardell@mednet.ucla.edu.
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Ardell
authors.affiliation: Department of Pharmacology, Faculté de médecine, Université de Montréal and Centre de recherche, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada.
authors.forename: René
authors.initials: R
authors.lastname: Cardinal
authors.affiliation: Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States.
authors.forename: Eric
authors.initials: E
authors.lastname: Beaumont
authors.affiliation: Department of Pharmacology, Faculté de médecine, Université de Montréal and Centre de recherche, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada.
authors.forename: Michel
authors.initials: M
authors.lastname: Vermeulen
authors.affiliation: Department of Medical Neuroscience, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
authors.forename: Frank M
authors.initials: FM
authors.lastname: Smith
authors.affiliation: Department of Medicine, UCLA Health System, Los Angeles, CA, United States.
authors.forename: J
authors.initials: J
authors.lastname: Andrew Armour
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy*; D004285:Dogs; D004562:Electrocardiography; D058542:Implantable Neurostimulators; D008564:Membrane Potentials; D009474:Neurons / Q000502:physiology; D013116:Spinal Cord / Q000503:physiopathology; D062187:Spinal Cord Stimulation; D013233:Stellate Ganglion / Q000503:physiopathology; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology; D055536:Vagus Nerve Stimulation
keywords: Atrial tachyarrhythmia; Heart; Intrinsic cardiac neurons; Neuromodulation; Spinal cord stimulation