The Short QT Syndrome (SQTS) is a recently identified genetic cardiac channelopathy. It is characterised by abnormally short QT intervals, an increased incidence of atrial and ventricular arrhythmias and an increased risk of sudden death (1). Currently, five distinct forms affecting different cardiac ion channels have been identified; KCNH2 (SQT1), KCNQ1 (SQT2), KCNH2 (SQT3), CACNA1C (SQT4) and CACNB2b (SQT5). However, due to the lack of phenotypically accurate animal models of the SQTS, the effects of SQTS on ventricular electro-mechanical dynamics have not been elucidated. The aim of this study was to investigate by computer modelling the functional consequences of the SQTS on ventricular electrical and mechanical behaviour. We developed an electromechanical model of the human ventricular myocyte by coupling a human ventricular myocyte model for electrical activity (2) with the Rice myofilament mechanical model (3). For SQT1, a Markov chain model was developed for simulating the experimentally-observed kinetic properties of the N588K-mutated hERG/IKr channel. SQT2 was modelled by modifying the IKs Markov chain model formulation of Silva and Rudy (4) to reproduce the experimentally-observed kinetic properties of the V307L-mutated IKs channel. For SQT3, we used our Hodgkin-Huxley model (5) to simulate the experimentally-observed kinetic properties of the D172N-mutant IKir2.1. The resulting electromechanical model was used to investigate the electromechanical consequences of SQT1, SQT2 and SQT3 at the single cell, 2D and 3D tissue levels. Our simulation data suggested that all three considered SQTS abbreviated the duration of action potentials (APs), which resulted in reduced amplitude of intracellular Ca2+ transient, leading to reduced contractile force by 20-80% for SQT1, SQT2 and SQT3. In conclusion, we have developed a human electromechanical model for ventricular myocytes and used it to investigate the functional consequences of the SQTS on ventricular contraction at single cell, 2D tissue and 3D organ levels. It has been shown that the SQT1-3 mutation compromises the binding of calcium to troponin leading to impaired interaction between actin and myosin and thereby less ventricular contractile force.