|My research programme focuses on characterizing the properties of the heart that provide the ‘substrate’ for arrhythmias. The central hypothesis is that the determinants of arrhythmic risk, including atrial and ventricular fibrillation, lie within the heart itself, and that much of this risk is genetic. The core activities of the group are therefore concerned with linking genetic alterations determining fibrillation syndromes to arrhythmogenic phenotypes through the use of GM mouse and human iPS cell-derived models. I have a strong group of collaborators facilitating these aspects of the programme. My clinical research involves electrophysiological phenotyping and is firmly based on the laboratory models. A large, wide ranging referral base allows the efficient delivery of this translational limb of the programme. I have also developed links with industry based on translational (‘cell-to-bedside’) principles that provide novel and even ‘disruptive’ approaches (drugs and devices) for patient management largely based on the insights obtained through the pre-clinical programmes.