Clinical conditions associated with sudden cardiac death due to arrhythmia are frequently accompanied by abnormalities of mechanical loading and wall stretch. These arrhythmias may result from several mechanisms including secondary depolarisations during or following the action potential or from a combination of conduction slowing and action potential shortening. Mechanical perturbations have been shown to reproduce these electrophysiological effects experimentally. However the effect of mechanical intervention is complex depending on the timing and intensity of the stimulus and the interplay between effects mediated via stretch activated channels and calcium cycling. Studies in patients during cardiac catheterisation or cardiac surgery using monophasic action potentials have shown alteration in the time course and shape of action potential repolarisation in response to changes in ventricular loading. Although stretch in experimental preparations has been shown to be arrhythmogenic, particularly in pathological conditions, the role of mechanically induced electrophysiological changes in important clinical ventricular arrhythmias remains to be established.