Ventricular failure is associated with remodelling of ion channels and intracellular Ca²⁺ dynamics. A model (Preibe & Beuckelmann, 1998) for normal and failing (remodelled I_K1, I_NaCa, I_NaK, Ca²⁺-ATPase of the SR) heart cells was incorporated into a partial differential equation (PDE) tissue model to determine how the remodelling associated with heart failure can alter propagation patterns. We use the simple Euler method to integrate the PDE with a time step of 0.02 ms and a space step of 0.2 mm with a diffusion constant, D = 0.154 mm²/ms. Dynamic action potential duration (APD) restitution was obtained by pre-pacing the cell models 40 times to obtain the final diastolic interval (DI) and APD. Conduction velocity (CV) restitution was obtained by pacing the 1D spatial models for 5 s at a frequency of 1 Hz. CV of a 6th premature propagating wave was measured. Vulnerable window (VW) (Biktashev et al. 1998) in 1D was measured. The dynamic restitution curve for the failing case has a region of negative slope at high stimulation rate (small period) while is positive in the control case. The maximal magnitude of the slopes of both curves is < 1 and both the normal and failing models show alternans. At fast pacing rates electrical alternans were observed for a basic cycle length (BCL) of < 392 ms in control cell, and for BCL of < 665 ms in the failing cell. The CV for a solitary wave in the failing case is marginally greater than in the non-failing case (7%). The CV restitution is shifted upward in failing tissue. The measured vulnerable window (VW) for the tissue to re-entry is 5 ms for the control and 7 ms for the failing case. Heart failure increased vulnerability of the tissue to re-entry by 40% and shifted the timing of the window significantly. In conclusion, heart failure induced remodelling ion channel kinetics and intracellular Ca²⁺ handling has a significant impact on the rate dependent electrical action potential and conduction properties of excitation waves. It also increases vulnerability of the tissue to arrhythmogenesis.