Antiarrhythmic effects of vagal nerve stimulation after cardiac sympathetic denervation in the setting of chronic myocardial infarction

Naoko Yamaguchi; Kentaro Yamakawa; Pradeep S Rajendran; Tatsuo Takamiya; Marmar Vaseghi

doi:10.1016/j.hrthm.2018.03.012

Antiarrhythmic effects of vagal nerve stimulation after cardiac sympathetic denervation in the setting of chronic myocardial infarction

Heart Rhythm. 2018 Aug;15(8):1214-1222. doi: 10.1016/j.hrthm.2018.03.012. Epub 2018 Mar 9.

Authors

Naoko Yamaguchi¹, Kentaro Yamakawa², Pradeep S Rajendran¹, Tatsuo Takamiya², Marmar Vaseghi³

Affiliations

¹ Division of Cardiology, David Geffen School of Medicine at University of California, Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, California; Neurocardiology Research Center of Excellence, UCLA, Los Angeles, California.
² Neurocardiology Research Center of Excellence, UCLA, Los Angeles, California.
³ Division of Cardiology, David Geffen School of Medicine at University of California, Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, California; Neurocardiology Research Center of Excellence, UCLA, Los Angeles, California. Electronic address: mvaseghi@mednet.ucla.edu.

Abstract

Background: Neuraxial modulation with cardiac sympathetic denervation (CSD) can potentially reduce burden of ventricular tachyarrhythmia (VT). However, despite catheter ablation and CSD, VT can recur in patients with cardiomyopathy and the role of vagal nerve stimulation (VNS) in this setting is unclear.

Objective: The purpose of this study was to evaluate the electrophysiological effects of VNS after CSD in normal and infarcted hearts.

Methods: In 10 normal and 6 infarcted pigs, electrophysiological and hemodynamic parameters were evaluated before and during intermittent VNS pre-CSD (bilateral stellectomy and T2-T4 thoracic ganglia removal) as well as post-CSD. The effect of VNS during isoproterenol was also assessed pre- and post-CSD. Multielectrode ventricular activation recovery interval (ARI) recordings, a surrogate of action potential duration, were obtained. VT inducibility was tested during isoproterenol infusion after CSD with and without VNS.

Results: VNS increased the global ARI by 4% ± 4% pre-CSD and by 5% ± 6% post-CSD, with enhanced effects observed during isoproterenol infusion (10% ± 8% pre-CSD and 12% ± 9% post-CSD) in normal animals. In infarcted animals pre-CSD, VNS increased ARI by 6% ± 7% before and by 13% ± 8% during isoproterenol infusion. Post-CSD, VNS increased ARI by 6% ± 5% before and by 11% ± 7% during isoproterenol infusion. VT was inducible in all infarcted animals post-CSD during isoproterenol infusion; this inducibility was reduced by 67% with VNS (P = .01). In all animals, the hemodynamic effects of VNS remained after CSD.

Conclusion: After CSD, the beneficial electrophysiological effects of VNS remain. Furthermore, VNS can reduce VT inducibility beyond CSD in the setting of circulating catecholamines, suggesting a role for additional parasympathetic modulation in the treatment of ventricular arrhythmias.

Keywords: Autonomic modulation; Stellectomy; Sympathetic; Vagal nerve stimulation; Ventricular arrhythmias.

Publication types

Research Support, N.I.H., Extramural

MeSH terms

Animals
Chronic Disease
Disease Models, Animal
Heart Rate / physiology*
Heart Ventricles / physiopathology*
Myocardial Infarction / complications*
Swine
Sympathectomy / methods*
Tachycardia, Ventricular / etiology
Tachycardia, Ventricular / physiopathology
Tachycardia, Ventricular / therapy*
Vagus Nerve Stimulation / methods*

Grants and funding

DP2 HL132356/HL/NHLBI NIH HHS/United States