Hearts susceptible to abnormal electrical rhythm (arrhythmia) show increased connective tissue (fibrosis) between muscle cells. Arrhythmia in the lower heart can lead to ventricular fibrillation and sudden cardiac death and in the upper heart to prevalent and debilitating atrial fibrillation. Mechanisms linking fibrosis and susceptibility to arrhythmia remain speculative. Proposed ideas will be tested using a combination of 3D electrical recordings and structural imaging with computer modelling, an approach pioneered by the Auckland Cardiac Electrophysiology Research Group. Significant value will be added through partnership with leading North American and European researchers. Outcomes will be communicated scientifically and translated clinically through web-based repositories, visualisation tools, and mark-up languages. Increased understanding of mechanistic links between fibrosis and arrhythmia will provide new targets for risk stratification based on fibrosis, and improve evaluation of therapies for countering ventricular fibrillation, sudden cardiac death, and the debilitations of atrial fibrillation.