Background and objectives: Altered sodium channel expression and function can cause sudden death. A knock-in mouse model with increased late sodium current, mimicking long QT syndrome 3 (δ-KPQ-SCN5A), was used to study effects of ageing on ventricle-ventricle conduction. Methods: Electrophysiology-Hearts were removed from δ-KPQ-SCN5A (dKPQ) and their wildtype (WT) littermates under terminal anaesthesia with urethane (2mg/kg), and immediately perfused on a modified upright Langendorff apparatus, where monophasic action potentials were recorded using custom-made Ag-AgCl electrodes. Interventricular activation times were measured during right ventricular pacing at 100ms fixed-rate cycle length, in three age groups (very young: 2-5 months, young: 6-9 months, and old: 18-24 months). Histology- 4μm-thick sections of paraffin-embedded hearts were stained with picrosirius red/haematoxylin. Collagen deposition was quantified using NIS Elements imaging software (Nikon) and Image J (National Institutes of Health, USA). Fibrosis was expressed as % of connective tissue relative to the total tissue inside the region of interest. Results: In old WT mice (18-24 months) there was no significant increase in activation time, compared with very young mice (2-5 months, 11±1, n=11 vs. 13±1, n=8). Conduction times were consistently longer in dKPQ mice in older mice (very young: 11±1, n= 11 vs. 13±1, n=8; young: 10±1, n= 7 vs. 16±1, n=7*; old: 13±1, n= 8 vs. 17±1, n=9*). Consistent with the subtle conduction defect, there was subtle ventricular fibrosis in old dKPQ hearts and upregulation of several genes involved in fibrosis and structural remodelling, compared with old WT hearts. Conclusion: A selective increase of the late sodium current may adversely affect ventricular conduction and this may be linked with ventricular fibrosis. All values are expressed as mean±SEM, *p<0.05.