Pathophysiology of the cardiac late Na current and its potential as a drug target

► INaL can disrupt cellular repolarization and increase propensity to ventricular arrhythmia. ► Although small compared to peak Na+ current, INaL increases Na+ loading in cardiac cells. ► Multiple cardiac pathological conditions share phenotypic manifestation of INaL upregulation. ► Specific pharmacological inhibition of INa is desired.