Previous experimental studies have revealed that heart failure (HF) is associated with ionic channel remodelling, which may be pro-arrhythmic. The aim of this study was to use biophysically detailed computer models of canine ventricular and Purkinje fibres to evaluate the functional impacts of HF-induced ionic channel remodellings on the transmural repolarisation heterogeneity within the ventricle wall and at the junction between ventricle and Purkinje Fibres (PVJ). The single cell models developed by Benson et al. (2008) for canine ventricular myocytes and by Aslanidi et al. (2010) for canine Purkinje fibre cells were used for this study. The two models were modified for simulating HF condition by incorporating extant experimental data on HF-induced remodellings on membrane ionic channels and intracellular Ca2+ handling. For ventricular cells, HF was simulated by increasing INaL by 30% as well as a 34% increase in its inactivation time (Maltsev et al. 2007), reducing INa by 32% (Maltsev et al. 2002), Ito1 by 43%(Li et al. 2002), IK1 by 41.1% (Li et al. 2002), IKs by 30% (Li et al. 2002), and INa/K by 42%. The steady-state activation curve of ICaL was shifted by -7.64 mV, resulted in a 13% reduction in its current density. For the calcium handling mechanisms, INaCa was increased by 20% in HF cells along with the down regulation of Iup by 87.5%, Ileak by 34.6% and Irel by 40%. These changes resulted in a ~60% reduction in peak [Cai2+]i, a ~24% increase in [Cai2+]i resting and a slow diastolic decay of [Cai2+]i which all matched to experimental observations (O’Rourke et al. 1999). For Purkinje fibre cell model, HF was simulated by reducing INa, IK1, Ito1, IKs, IKr, ICaL and ICaT by 30%, 33%, 30%, 10%, 8%, 14.5% and 13% respectively. With the resulting cell models, it was shown that the HF-induced ionic channel remodelling produced a remarkable APD prolongation in the ventricular cells as compared to the control condition. The APD prolongation was heterogeneous across the transmural wall, with a ~30%, ~60% and ~30% APD increase for endocardial, mid-cardial and epi-cardial cells respectively. However, the computed APD from the HF Purkinje cell model remained almost the same as compared to the control condition (CTR: 330.25 ms vs. HF: 328.95 ms). In conclusion, HF-induced ionic channel remodelling enhanced transmural APD dispersion within the ventricle wall, but not the APD difference at the junction between the Purkinje fibre and the ventricle wall.