Patients with congenital LQTS most commonly have mutations to the Kv11.1 and Kv7.1 potassium channel proteins, responsible for the rapid (IKR) and slow (IKS) delayed potassium rectifier currents, respectively.8 These altered IKR and IKS currents can lead to excessive local extracellular potassium levels and ultimately repolarization abnormalities.12 Should these gradients worsen, the patient is at risk for entering torsades de pointes. This evidence concerns the gene KCNQ1 and familial long QT syndrome.