Aberrations in intracellular calcium (Ca2+) handling, in diseases such as heart failure (HF), increase vulnerability to lethal arrhythmias and resultant sudden cardiac death. The underlying mechanisms for these processes are difficult to explore experimentally, but recent data from our laboratory sug-gests that reduced inward rectifier current (IK1) expression in failing rat myo-cytes increases pro-arrhythmic spontaneous Ca2+ release. However, existing computational models of rat cardiac electrophysiology are unable to capture the complex underlying phenomena, so we have been unable to computation-ally explore the hypothesis that this results from increased sarcoplasmic re-ticulum (SR) loading in the presence of a destabilised membrane. A new computational model was therefore developed by combining a re-cent rat ventricular electrophysiology model with a novel model of stochastic spatio-temporal Ca2+ handling dynamics developed in our laboratory. The newly-developed model was used to dissect and quantify the electrophysio-logical changes associated with remodelling of IK1 and Ca2+ homeostasis in HF. A similar reduction in IK1 to that observed experimentally resulted in a 57% increase in action potential duration (APD) in simulations, from 58.1 to 91.4 ms. This prolonged APD allowed greater SR loading, leading to raised [Ca2+]SR and more frequent spontaneous release events. These events, in turn, triggered forward-mode sodium-calcium exchange, resulting in triggered action potentials. Resting membrane potential was also depolarised in HF myocytes by 3.3 mV. The newly-developed model has reproduced experimental results from the laboratory and provided insight into the underlying mechanisms of spontane-ous Ca2+ release in HF. Thus, it provides a powerful research tool that can be used to explore how HF-induced sub-cellular remodelling may result in ar-rhythmias at the tissue and organ levels.