Atrial fibrillation (AF) is a common clinical presentation of the short QT syndrome (SQTS). Despite its prevalence, the link between gene mutations underlying the SQTS and increased susceptibility to AF remains unclear. This study aimed to investigate the functional impact of the SQT1-related N588K gain-of-function mutation to human Ether-à-go-go-Related Gene (hERG) potassium channels on the electrical and mechanical activities of human atrial cells. Multiple contemporary human atrial action potential models (e.g. Colman et al. 2013) were coupled to the Rice et al. mechanics model (Rice et al. 2008). A Markov chain formulation of the rapid delayed rectifier current, IKr, (the α subunit of which is encoded by hERG) was implemented in both wild type (WT) and N588K conditions, based on whole-cell patch clamp recordings from CHO cells performed at 37°C (McPate et al., 2005). The effect of the mutation on action potential duration (APD), peak current density, intracellular calcium transient, and contractile force was evaluated both with and without inclusion of a stretch-activated current. Inclusion of the new formulation of IKr was validated by a complete block of this channel-current, reproducing the proportional APD prolongation observed under experimental IKr blocker (E-4031) conditions (Wettwer et al., 2004). The SQT1-related N588K mutation was found to increase peak IKr current density by ~2-fold, in agreement with experimental findings (McPate et al., 2009), which served to significantly accelerate atrial repolarisation, reduce the APD and stabilise re-entrant circuits in tissue. Secondary effects of the mutation resulted in a decreased calcium transient amplitude, consequently reducing the contractile force. This effect was reduced when stretch-activated channels were included in the model. Both the significant acceleration in atrial action potential repolarisation and the modest impairment in contractile function could have important implications for atrial electro-mechanical function and provide insight into the mechanisms underlying the relationship between SQT1 and AF.