Abstract
Aims: To evaluate whether low level left vagus nerve stimulation (LLVNS) in early stage of myocardial infarction (MI) could effectively prevent ventricular arrhythmias (VAs) and protect cardiac function, and explore the underlying mechanisms.Methods and Results: After undergoing implantable cardioverter defibrillators (ICD) and left cervical vagal stimulators implantation and MI creation, 16 dogs were randomly divided into three groups: the MI (n = 6), MI+LLVNS (n = 5), and sham operation (n = 5) groups. LLVNS was performed for 3 weeks. VAs, the left ventricular function, the density of the nerve fibers in the infarction area and gene expression profiles were analyzed. Compared with the MI group, dogs in the MI+LLVNS group had a lower VAs incidence (p < 0.05) and better left ventricular function. LLVNS significantly inhibited excessive sympathetic nerve sprouting with the evidences of decreased density of TH, GAP43 and NF positive nerves (p < 0.05). The gene expression profiling found a total of 206 genes differentially expressed between MI+LLVNS and MI dogs, mainly involved in cardiac tissue remodeling, cardiac neural remodeling, immune response and apoptosis. These genes, including 55 up-regulated genes and 151 down-regulated genes, showed more protective expressions under LLVNS.Conclusions: This study suggests that LLVNS was delivered without altering heart rate, contributing to reduced incidences of VAs and improved left ventricular function. 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.
Highlights
Acute myocardial infarction (MI) is a major cause of morbidity and mortality worldwide and continues to pose significant therapeutics challenges [1]
Level Left Vagus Nerve Stimulation (LLVNS) did not show any significant effects on the heart rate (HR) at 1 h after the vagus nerve stimulation (VNS) device implantation and before sacrifice
The main findings of the present canine experimental study are as follows: [1] LLVNS applied at 2 h after MI significantly reduced ventricular arrhythmias (VAs) with improved left ventricular function but without HR changes; [2] LLVNS caused 206 cardiac differentially expressed genes (DEGs), 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
Summary
Acute myocardial infarction (MI) is a major cause of morbidity and mortality worldwide and continues to pose significant therapeutics challenges [1]. Timely myocardial reperfusion is the most effective therapeutic to reverse myocardial damage, the abrupt restoration of blood flow to ischemic tissue can induce ventricular arrhythmias (VAs) [2]. Vagus Nerve Stimulation have been proven to be an effective treatment to terminate VAs. no trials have shown benefits on long-term mortality due to ICD implantation after MI [4]. Left vagus nerve stimulation (VNS) is a safe and effective treatment for neurological disorders [5]. VNS treatment before or during ischemia has been shown an antiarrhythmic effect and protect against cardiac remodeling in animal models [6,7,8,9]. Two large clinical trials failed to demonstrate that VNS could improve cardiac function or reduce mortality [10, 11]. All the published trails focused on refractory HF rather than the onset of HF
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