Citalopram has been reported to have cardiac adverse effects. Although citalopram is known to be a racemic compound comprised of S-citalopram (escitalopram) and R-citalopram, it is still unclear which enantiomer is responsible for cardiac adverse effects induced by citalopram. In the present study, we investigated whether citalopram, escitalopram and R-citalopram had an electrophysiological effect on Nav1.5 voltage-gated sodium channel (VGSC) current and how their electrophysiological properties affected Nav1.5 VGSC. When whole-cell patch clamp was performed for analysis, the IC₅₀ of citalopram, escitalopram and R-citalopram were 89.2, 58.6 and 174.0 µM, respectively. In addition, treatment with 100 μM citalopram and escitalopram changed the voltage-dependence of activation and induced a negative shift of the voltage of half-maximal activation compared to 100 μM R-citalopram. In contrast, treatment with 100 μM citalopram and escitalopram changed the voltage-dependence of inactivation, and the voltage at half-maximal inactivation slightly shifted toward negative potential. These results suggest that the adverse cardiac effect produced be citalopram might result from modification of the electrophysiological properties of Nav1.5 VGSCs, and escitalopram might contribute more to this adverse effect than R-citalopram.