Key result
Low-voltage, high-frequency VNS raises VF threshold ~82% alongside increased nitric oxide and minimal heart rate changes.
Why the study?
The precise mechanisms by which vagus nerve stimulation reduces susceptibility to ventricular fibrillation, and the stimulation parameters needed clinically, were not well understood.
Does vagus nerve stimulation at varying parameters alter ventricular electrophysiology and nitric oxide release in an isolated innervated rabbit heart model?
Does vagus nerve stimulation at varying parameters alter ventricular electrophysiology and nitric oxide release in an isolated innervated rabbit heart model?
Absolute Event Rate: 5.1% vs 2.8%
p-value: p=<0.05
Vagus nerve stimulation exerts cardioprotective anti-fibrillatory effects independent of heart rate reduction, likely mediated by nitric oxide release and specific neural fiber recruitment.
May support NO-mediated anti-fibrillatory VNS effects in animal models; leaves open translation to human arrhythmia prevention.
Background: Abnormal autonomic activity including impaired parasympathetic control is a known hallmark of heart failure (HF). Vagus nerve stimulation (VNS) has been shown to reduce the susceptibility of the heart to ventricular fibrillation, however the precise underlying mechanisms are not well understood and the detailed stimulation parameters needed to improve patient outcomes clinically are currently inconclusive. Objective: To investigate NO release and cardiac electrophysiological effects of electrical stimulation of the vagus nerve at varying parameters using the isolated innervated rabbit heart preparation. Methods: The right cervical vagus nerve was electrically stimulated in the innervated isolated rabbit heart preparation ( n = 30). Heart rate (HR), effective refractory period (ERP), ventricular fibrillation threshold (VFT) and electrical restitution were measured as well as NO release from the left ventricle. Results: High voltage with low frequency VNS resulted in the most significant reduction in HR (by −20.6 ± 3.3%, −25.7 ± 3.0% and −30.5 ± 3.0% at 0.1, 1 and 2 ms pulse widths, with minimal increase in NO release. Low voltage and high frequency VNS significantly altered NO release in the left ventricle, whilst significantly flattening the slope of restitution and significantly increasing VFT. HR changes however using low voltage, high frequency VNS were minimal at 20Hz (to 138.5 ± 7.7 bpm (−7.3 ± 2.0%) at 1 ms pulse width and 141.1 ± 6.6 bpm (−4.4 ± 1.1%) at 2 ms pulse width). Conclusion: The protective effects of the VNS are independent of HR reductions demonstrating the likelihood of such effects being as a result of the modulation of more than one molecular pathway. Altering the parameters of VNS impacts neural fibre recruitment in the ventricle; influencing changes in ventricular electrophysiology, the protective effect of VNS against VF and the release of NO from the left ventricle.
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Allen et al. (2022) studied Normal cardiac electrophysiology (animal model) (n=30). Vagus nerve stimulation (VNS) vs. Baseline (no stimulation) was evaluated on Ventricular fibrillation threshold (VFT) during low voltage VNS at 5 Hz (0.1 ms pulse width) (p=<0.05). Low voltage, high frequency vagus nerve stimulation significantly increased ventricular fibrillation threshold from 2.8 mA to 5.1 mA and increased nitric oxide release with minimal heart rate changes.
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