Purpose: Ivabradine is a novel bradycardic drug used in clinical practice. It acts on the sinoatrial node by blocking the If channel responsible for the pacemaker potential1. Our aim was to investigate the electrophysiological effects of Ivabradine in the guinea pig ventricle. Method: Hearts were isolated from adult male Dunkin Hartley guinea pigs (N=6, 0.42-0.52kg) and perfused in constant flow Langendorff mode with Tyrode solution at 20ml/min (37°C, pH 7.4). Left Ventricular Pressure (LVP) was recorded with a pressure transducer connected to a fluid filled balloon in the LV. Contact Monophasic Action Potential (MAP) electrode recorded apical and basal LV MAP duration at 90% decay (MAPD90) during constant pacing (CP, 200ms CL). Effective Refractory Period (ERP) was obtained using a single extra-stimulus protocol (S1 200ms CL). Restitution curves were plotted using MAPD90 vs. the preceding diastolic interval. Ventricular Fibrillation Threshold (VFT) was measured as the minimum current required to induce sustained (>10s) VF with burst pacing (30x30ms). Measurements were taken at baseline (BL) and during 0.1uM – 0.5uM Ivabradine (with constant pacing at BL and 0.2uM). Data is shown as mean±SEM with one-way ANOVA and Bonferroni post-hoc test or Paired T-Test. P<0.05 was taken as significant. Results: Ivabradine reduced HR and LVP but prolonging ERP and VFT significantly (see Table 1). During constant pacing, apical and basal MAPD90 were significantly prolonged with 0.2uM Ivabradine. Ivabradine had significant effects on both the apical and basal MAPD90 restitution curves shifting them up and to the left with a trend towards steeper maximum slopes at high concentrations (see Figure 1). Conclusion: 0.2uM Ivabradine significantly affects ventricular electrophysiology in the isolated guinea pig heart despite current literature suggesting If channels to be absent in guinea pig ventricles. The mechanisms underlying these ventricular electrophysiological effects merit further investigation.