Early afterdepolarizations, U waves, and torsades de pointes.

Torsades de pointes (TdP) is defined as a polymorphic ventricular tachycardia (VT) with a twisting QRS morphology associated with a prolonged QT interval and/or increased U wave amplitude in the ECG.1,2 Patients with acquired or congenital long-QT syndrome (LQTS) can develop TdP that results in sudden cardiac death. Fifty or more drugs, both typical antiarrhythmic agents such as quinidine as well as other classes of drugs such as some antibiotics, affect membrane ionic currents, prolong the duration of the QT interval in the ECG, and have been associated with the acquired LQTS.3 Similarly, inherited genetic defects in the cardiac membrane ion channels can cause congenital LQTS. Some patients with apparent acquired LQTS may actually have mild congenital forms and remain asymptomatic until exposed to one of the drugs noted above.4 Congenital LQTS can be divided into multiple subtypes depending on the affected membrane ionic currents (eg, LQT1, LQT2, and LQT3 for alterations in IKs, IKr, and the inactivation process of INa ). Due to the possible fatal outcome and involvement of many drugs, it is important to understand the mechanism of TdP, predict its occurrence, and manage it clinically.