The generation and propagation of the cardiac impulse is dependent upon the function of the cardiac isoform of the voltage gated, Na⁺ channel, encoded by the SCN5A gene. Haploinsufficiencies in this gene have been associated with cardiac disorders that include the Brugada (BrS) and Lev-Lenegre syndromes. Recent studies suggest that the SCN5A mutation is not directly causal to a Brugada Syndrome (BrS) like ECG pattern, suggesting further background complexity for the condition. Such a finding is consistent with the possibility that BrS-like electrocardiographic (ECG) patterns may vary with both age and sex. In the present study we validate our model through patch-clamp studies in single cells. We then investigate for interacting effects of age and sex on ECG features of Scn5a^+/­ mice used to model BrS. Action potential measured by patch-clamp showed reduced rate of rise of action potential in Scn5a^+/­ mice confirming loss of voltage-gated sodium channel function. In in-vivo ECG we observed that: (1) Sinoatrial function: RR intervals in old male Scn5a^+/­ hearts were greater than old female Scn5a^+/­. (2) Atrial function: P-wave durations were indistinguishable between fully separated groups. (3) Atrioventricular function: Scn5a^+/­ mutation prolonged PR intervals only in older males compared to Scn5a^+/­older females. PR intervals were in general longer in young female compared to young male regardless of genotype. However, age dependent prolongation of PR interval was observed in older male Scn5a^+/­ mice but not in older male and female WT and older female Scn5a^+/­. (4) Ventricular activity: T-wave durations were greater in old male Scn5a^+/­ compared to old male WT. QRS durations and QTc intervals were indistinguishable between fully separated groups. We demonstrate for the first time interacting effects of age and sex on the Scn5a^+/­ phenotype resulting in alterations particularly in pacemaker and atrioventricular conduction greatest in ageing males. This establishes that a complex interplay of age and sex on cardiac electrophysiological changes may have a profound effect on the pathophysiology of conditions related to Scn5a mutations.