Acute transmural ischaemia often shortens ventricular repolarization and increases repolarization dispersion, leading to life threatening ventricular arrhythmias in animal models and human subjects. Experimental studies and clinical observations have shown that acute subendocardial ischaemia rarely causes serious ventricular arrhythmia. We hypothesized that the different arrhythmia outcomes between transmural and subendocardial ischaemia are largely due to the homogenous prolongation in ventricular repolarization after acute subendocardial ischaemia. Further experimental studies on a subendocardial model are required to assess the changes in ventricular repolarization and its spatial dispersion, and to investigate the role of these changes in the pathogenesis of ventricular arrhythmias. These studies will facilitate our understanding on the mechanisms of life-threatening ventricular arrhythmias during acute myocardial ischaemia.