Sodium-glucose transporter 2 inhibitors have been identified as pleiotropic pharmacological agents with demonstrated efficacy in a wide range of pathologies. Given the strong association between arrhythmias and significant comorbidities, exploring the potential antiarrhythmic effects of sodium-glucose transporter 2 inhibitors represents a critical therapeutic opportunity, particularly considering the limited efficacy and adverse profile of current antiarrhythmic drugs. The antiarrhythmic mechanisms of sodium-glucose transporter 2 inhibitors operate through direct cardiac ion channel modulation. Along with the ion channel effects, sodium-glucose transporter 2 inhibitors improve gap junction coupling by modulating connexin-43, lower sympathetic tone, maximize mitochondrial function, and induce metabolic reprogramming through adenosine monophosphate-activated protein kinase/sirtuin 1 activation and autophagy enhancement. Translating these encouraging mechanisms into focused antiarrhythmic strategies still requires establishing clear cause-and-effect links between sodium-glucose transporter 2 inhibitor therapy and arrhythmia prevention. Nevertheless, the current evidence regarding these effects remains inconsistent, underscoring the necessity for further research to elucidate the underlying mechanisms and resolve existing controversies.