Spatial heterogeneity of cardiac tissue causes cells to repolarize at different rates, leading to a dispersion of repolarization time and even arrhythmia phenomena. In this study, we investigate the role of heterogeneities of cardiac tissue due to M cells in the initiation and maintenance of re-entrant waves by using the biophysically-detailed ten Tusscher et al. human ventricular model of electrophysiology. This model has been extended to include short QT syndrome (SQTS) variant 1, 2, 3, and is studied in both one dimensional model, corresponding to a strand traversing the ventricular wall, and two dimensional model, representing a transmural slice. M cells exhibit a prolonged action potential duration and the resulting dispersion of repolarization is exacerbated in patients with SQTS. Using this computer modelm, we focus on possible mechanisms for the generation of re-entrant arrhythmias. We study whether or not island distribution of M cells (with their slow repolarization) can function as wave blocks for premature stimuli under SQTS conditions. We find that the inclusion of an island distribution of M cells can initiate and maintain re-entrant waves under SQTS consitions compared to the control condition.