Cardiac arrhythmias are among cardiovascular diseases with high morbidity and mortality rates worldwide, associated with impaired cardiac ion channel function and abnormal conduction of electrophysiological signals in cardiomyocytes. The cardiac sodium channel NaV1.5 plays a crucial role in the initiation and propagation of action potentials in cardiomyocytes. Abnormal expression and regulation of NaV1.5 due to gene mutations constitute a significant biological basis for the occurrence of arrhythmias. This article summarizes the structure and function of NaV1.5, as well as its relationship with cardiac arrhythmias, with the aim of providing a theoretical basis for future research and development of cardiovascular drugs, their clinical applications, and drug-induced cardiotoxicity.