Chronic median nerve modulation reduces ventricular arrhythmia and improves ventricular function in a postmyocardial infarction rabbit model

Cardiovasc Ther. 2018 Aug;36(4):e12437. doi: 10.1111/1755-5922.12437. Epub 2018 Jun 28.

Abstract

Aim: Median nerve stimulation (MNS) is a novel neuromodulation approach for treatment of ventricular arrhythmia, but little is known about its chronic effects. The aim of this study was to investigate the effects of chronic MNS on ventricular arrhythmia and ventricular dysfunction postmyocardial infarction (MI).

Method: Two weeks after MI, 12 rabbits were randomly divided into control and MNS groups, and chronic MNS was performed in MNS group for 2 weeks. Ventricular function and arrhythmias; sympathetic innervation and activity; and interleukin-1 β (IL-1 β) and norepinephrine (NE) levels were analyzed.

Results: Both the total number of premature ventricular complex and episodes of ventricular tachycardia were lower in MNS group than in control group (20 560 ± 10 314 beats vs 70 079 ± 37 184 beats, P = .021, and 115 ± 63 episodes vs 307 ± 164 episodes, P = .034, respectively). Compared with control group, MNS decreased the cardiac sympathetic nerve density and level of circulating NE in MNS group (1798.42 ± 644.07 μm2 /mm2 vs 1003.79 ± 453.00 μm2 /mm2, P = .041, and 20.86 ± 4.54 pg/mL vs 11.07 ± 1.43 pg/mL, P = .002, respectively). MNS also improved the left ventricular ejection fraction (59.07 ± 1.91% vs 49.77 ± 3.47%, P = .003) and inhibited the level of IL-1 β in serum (69.19 ± 4.71 pg/mL vs 85.93 ± 12.80 pg/mL, P = .013).

Conclusion: Chronic MNS appears to protect against ventricular arrhythmia and improves ventricular function post-MI, which may be mediated by suppressing cardiac sympathetic activity and anti-inflammatory effects.

Keywords: chronic electrical stimulation; median nerve; myocardial infarction; sympathetic nervous system; ventricular arrhythmia; ventricular function.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Electric Stimulation Therapy / methods*
  • Heart / innervation*
  • Interleukin-1beta / blood
  • Median Nerve*
  • Myocardial Infarction / blood
  • Myocardial Infarction / complications
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy*
  • Norepinephrine / blood
  • Rabbits
  • Stroke Volume*
  • Tachycardia, Ventricular / blood
  • Tachycardia, Ventricular / etiology
  • Tachycardia, Ventricular / physiopathology
  • Tachycardia, Ventricular / prevention & control*
  • Time Factors
  • Ventricular Function, Left*
  • Ventricular Premature Complexes / blood
  • Ventricular Premature Complexes / etiology
  • Ventricular Premature Complexes / physiopathology
  • Ventricular Premature Complexes / prevention & control*

Substances

  • Interleukin-1beta
  • Norepinephrine