Excitation conducted through the Purkinje fibres (PF) to the ventricles determines synchronized timing and sequencing of ventricular contraction. However, marked differences in action potential (AP) morphology and duration between the PF and ventricular cells may lead to abnormalities in excitation conduction through the Purkinje-ventricular junction (PVJ). The aim of this study is to develop a novel electrophysiologically detailed model for the canine PF cell, and link it to the existing 3D computer model of the canine ventricular wedge in order to explore excitation conduction through the PVJ into the ventricles under physiological and pathological conditions. The 3D wedge model has been developed earlier [1] to incorporate detailed geometry and fibre orientation of the canine left ventricular free wall and transmural AP heterogeneity between epicardial (epi), midmyocardial (M) and endocardial (endo) ventricular cells. The canine endo cell AP model [1] was modified to incorporate detailed voltage-clamp experimental data on characteristics of all major ion channels in the canine PF cells [2]. The model was validated by its ability to reproduce AP restitution properties similar to various experimental measurements for the canine PF cells. Finally, the single Purkinje cell model was incorporated into a fibre entering the 3D ventricular wedge model, with intercellular electrical coupling conductances chosen to produce AP propagation velocities of about 1.5 m/s and 0.5 m/s for the PF and the ventricular tissues, respectively [3]. Simulations of the resultant model produced physiologically realistic transmural action potential duration (APD) dispersion patterns, as well as a conduction time delay of about 5 ms at the PVJ reported in experiments [3]. The removal of voltage-dependent inactivation of the delayed rectified current, I_Kr, was used to simulate pathological short QT syndrome (SQTS) associated with a gain-in-function of I_Kr channel due to HERG N588K mutation [4]. Such ‘mutant’ I_Kr resulted in heterogeneous APD shortening among epi, M, endo and PF cells, which augmented the transmural APD dispersion at the PVJ and shortened the QT interval in pseudo-ECG by about 70 ms. This provides causative link between HERG N588K mutation to SQTS. In summary, the constructed detailed 3D model provides a powerful computational tool for non-invasive studies of electrical phenomena within and around the heterogeneous PVJ. Shortening of the QT interval under the defected I_Kr inactivation conditions substantiates a link between SQTS and the HERG N588K mutation.