QT Prolongation

Certain drugs have the ability to delay cardiac repolarization, an effect that is manifested on the surface electrocardiogram (ECG) as prolongation of the QT interval. The QT interval represents the duration of ventricular depolarization and subsequent repolarization, beginning at the initiation of the Q wave of the QRS complex and ending where the T wave returns to isoelectric baseline. QT interval prolongation creates an electrophysiological environment that favours the development of cardiac arrhythmias, most clearly torsade de pointes, but possibly other ventricular arrhythmias as well. Torsade de pointes (TDPTdP) is a polymorphic ventricular tachyarrhythmia that appears on the ECG as continuous twisting of the vector of the QRS complex around the isoelectric baseline in association with a prolonged QT interval. A feature of TDPTdP is pronounced prolongation of the QT interval in the sinus beats preceding the arrhythmia. TDPTdP can degenerate into life-threatening cardiac rhythms, such as ventricular fibrillation, which can result in sudden death.