Vagus Nerve Stimulation in Early Stage of Acute Myocardial Infarction Prevent Ventricular Arrhythmias and Cardiac Remodeling

These genes, including 55 up-regulated genes and 151 down-regulated genes, showed more protective expressions under level left vagus nerve stimulation.Conclusions: This study suggests that LLVNS was delivered without altering heart rate, contributing to reduced incidences of ventricular arrhythmias and improved left ventricular function

Shuang Zhao; Yan Dai; Xiaohui Ning; Min Tang; Yunzi Zhao; Zeyi Li; Shu Zhang


Scholarcy highlights

  • Acute myocardial infarction is a major cause of morbidity and mortality worldwide and continues to pose significant therapeutics challenges
  • In the vagus nerve stimulation+MI group, the stimulators were turned on for 120 min after left anterior descending coronary artery occlusion with the following stimulus parameters, which were described as optimal dosing by a previous study : the output amplitude was set at the stimulation threshold of minus 1 volt and did not cause a heart rate change; the pulse width was 0.5 ms; and the frequency was programmed at 10 Hz with continuous recurring cycles of 12 s on and 60 s off
  • level left vagus nerve stimulation did not show any significant effects on the HR at 1 h after the VNS device implantation and before sacrifice
  • The main findings of the present canine experimental study are as follows: LLVNS applied at 2 h after MI significantly reduced ventricular arrhythmias with improved left ventricular function but without HR changes; LLVNS caused 206 cardiac differentially expressed genes, and the effects of LLVNS were likely associated with cardiac neuronal sprouting suppression and decreased inflammation reaction, which could be explained by the patterns of gene expressions
  • LLVNS significantly prevented the incidence of VAs, which was consistent with published findings of VNS during myocardial ischemia in animal models
  • The present study demonstrates that LLVNS applied for 2 h after MI significantly reduces the incidence of VAs without HR changes and improves the left ventricular function over a 3-week follow-up period
  • The potential mechanisms included suppressing cardiac neuronal sprouting, inhibiting excessive sympathetic nerve sprouting and subduing pro-inflammatory responses by regulating gene expressions from a canine experimental study

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