The arrhythmic risk is increased in patients with heart failure (HF). In the failing left ventricle, this risk is related to a major electrophysiological remodelling. The failing right ventricle (RV) remodelling and the associated arrhythmic risk remain relatively unexplored. Here we have investigated the arrhythmic state of the failing RV of pulmonary hypertensive rats. Wistar rats were injected intraperitoneally with monocrotaline (60 mg/kg) to induce pulmonary hypertension and RV failure within 3-4 weeks (MCT) and compared to age-matched saline-injected animals (CON). Animals were killed by schedule 1 methods upon showing clinical symptoms of HF. Monophasic action potentials (MAPs) were recorded at the epicardial surface of isolated hearts paced at 5 Hz. A rapid-pacing protocol was used to estimate the arrhythmic risk and a S1-S2 protocol was used to construct standard action potential duration (APD) restitution curves. Failing hearts had a higher risk of developing sustained arrhythmias following rapid-pacing (probability was 0.14 in CON vs. 0.83 in MCT, Chi-square, P<0.05). We found a prolongation of MAP duration in the failing RV (MAP90, 39.9 ± 1.9 ms in CON vs. 80.7 ± 3.5 ms in MCT, t-test P<0.001). APD dispersion from right to left ventricle was also significantly increased (t-test, P<0.01). Standard restitution curves had steeper slopes in the failing RV (mean maximum slope was 0.18 ± 0.02 CON vs. 0.73 ± 0.28 MCT, t-test, P<0.001). Action potential prolongation – possibly linked to potassium channel downregulation -, increased APD dispersion and steep action potential duration restitution curves are typically associated with a pro-arrhythmic state. We conclude that the failing right ventricle of monocrotaline-injected rats undergo a profound electrophysiological remodelling responsible for the higher arrhythmic risk we observed.