Non-invasive Vagus Nerve Stimulation in Patients Undergoing Electrophysiological Study

Background The acute electrophysiologic effects of low-level tragus stimulation (LLTS) on sinoatrial and atrioventricular nodal function as well as the potential therapeutic role for managing arrhythmias remain incompletely characterized. Objective To evaluate the acute effects of LLTS on electrophysiologic parameters in patients undergoing clinically indicated EPS. Methods Patients undergoing clinically indicated EPS were prospectively enrolled. LLTS was delivered using a non-invasive tragus stimulation device, with stimulation intensity titrated to an individualized comfort threshold. Electrophysiologic parameters, including corrected sinus node recovery time (CSNRT), Wenckebach cycle length (WCL), and effective refractory periods, were measured at baseline and during stimulation using a within-subject design. Heart rate variability (HRV) was assessed as an exploratory measure of autonomic modulation. Paired analyses were performed to evaluate changes in electrophysiologic and autonomic parameters. Results Ten patients (50% female; median age 47.5 years [IQR 29.3–52.8]) were included. LLTS was associated with significant shortening of CSNRT (−135 ms, p=0.022) and VA WCL (−24 ms, p=0.002), indicating enhanced nodal electrophysiologic responsiveness during stimulation. No significant changes were observed in atrial, atrioventricular nodal, or ventricular effective refractory periods, or induced supraventricular tachycardia cycle length. HRV analysis in seven patients demonstrated non-significant trends toward reduced parasympathetic indices during stimulation and relative increases following stimulation cessation, consistent with dynamic and reversible autonomic modulation. Conclusions LLTS was associated with paradoxical shortening of CSNRT and atrioventricular nodal conduction parameters during EPS, highlighting complex and state-dependent autonomic effects. These findings suggest that LLTS influences cardiac autonomic regulation through mechanisms distinct from direct parasympathetic activation.