Motivation/problem solving statement: Vagus nerve stimulation (VNS) is being trialed clinically to treat patient with heart failure.1 In preclinical studies, our group has shown that VNS protects the heart against ventricular arrhythmias by increasing ventricular fibrillation threshold (VFT) and prolonging effective refractory period (ERP) in an isolated innervated rabbit heart preparation.2 This protection however, is accompanied by a large bradycardia, which would not be advisable in patients. To reduce unwanted excessive vagal-bradycardia, VNS at low levels (LLVS) has been tested to suppress atrial arrhythmias in humans.3 This study aims to evaluate LLVS effect on ventricular electrophysiology. Methods: The innervated isolated dual innervated heart preparation from adult male New Zealand White rabbits (n=11, 2.0-2.5 Kg) was harvested following pre-medication with medetomidine hydrochloride (0.2 mg/kg), ketamine (10 mg/kg), and butorphanol (0.05mg/kg) (sc) and, anesthetisia with propofol (5mg as required, i.v.). Animals were sacrificed by an overdose of pentobarbitone sodium (111 mg/kg, i.v.). Vagus nerve stimulation was performed at the cervical level with ERP and VFT measured using a single extrastimulus and burst pacing protocol respectively (30x30ms). ERP and VFT was measured at baseline (BL) and during unilateral LLVS using two methods 1) high voltage – low frequency [HVLF] at 1, 2, 3, and 5Hz, and 2) low voltage – high frequency [LVHF] at 10, 20, and 30Hz. Data are mean±SEM and analysed using 2-way ANOVA with Bonferroni post hoc test. *P<0.05, **P<0.01, ***P<0.001. Results: HVLF (5.5±0.9V; n=8) significantly decreased HR, prolonged ERP and increased VFT at 3 and 5Hz (Table 1). LVHF (1.5±0.4V; n=5) showed significant differences at 20Hz (Table 2). Conclusions: LLVSs displayed arrhythmogenic protection using both methods and shows potential to protect the heart against ventricular fibrillation and bradycardiac levels that should be safe in patients.