Introduction Patients with pulmonary arterial hypertension (PAH) have a high incidence of arrhythmias including AV node dysfunction. We investigated the mechanisms of AV node dysfunction in PAH using an animal model. Hypothesis We hypothesized that PAH in monocrotaline (MCT) treated rats would result in impairment of AV nodal function as evidenced by changes in Wenckebach cycle length, AV effective refractory period (AVERP) and AV functional refractory period (AVFRP). Methods An intraperitoneal injection of MCT (60mg/kg) was given to 200g Wistar rats. The rats were monitored daily and the MCT treated rats were sacrificed if they showed clinical deterioration, or on day 28. Control rats were injected with an equal volume of saline and were sacrificed within 24 hours of the paired MCT treated rats. An ECG was recorded and Echocardiography was performed to record pulmonary artery acceleration time (PAAT), pulmonary artery deceleration (PAD), right ventricle (RV) chamber size and wall thickness immediately prior to sacrifice. The heart was excised and mounted on a Langendorff perfusion column. Baseline ECGs were recorded then the right atrium was stimulated using an S1-S1 protocol to determine Wenckebach cycle length, and an S1-S2 protocol to determine AVERP and AVFRP. Results Echocardiography demonstrated PAH and RV hypertrophy in the MCT treated rats with a decrease in PAAT and an increase in PAD and RV wall thickness. The MCT treated rats had a reduction in AV node function with an increase in AVERP; demonstrating reduced safety of conduction across the AV node, and an increase in AVFRP, demonstrating reduction in the maximum speed of conduction through the AV node (Table 1). Conclusions These data suggest that remodelling takes place within the AV node in response to PAH, which may account for conduction disturbances.