Cardiac sodium channel Nav1.5 and drug-induced long QT syndrome

摘要

Genetic factors and acquired pathologies, such as cardiac ischemia and heart failure, may lead to an increase in the late sodium current carried by the cardiac sodium channel Nav1.5. As a result, cardiac action potential repolarization is delayed, which in turn reduces the cardiac repolarization reserve of afflicted patients. This repolarization alteration may cause polymorphic ventricular arrhythmias called Torsades de pointes. This review summarizes the genetic and molecular mechanisms explaining why such patients are more susceptible to drug-induced long QT syndrome when taking QT-prolonging drugs.