The QT interval represents the duration of ventricular depolarization and subsequent repolarization, beginning at the initiation of the QRS complex and ending where the T wave returns to isoelectric baseline. Because of its inverse relationship to heart rate, the QT interval is routinely transformed (normalized) by means of various formulae into a heart rate independent “corrected” value known as the QTc interval. The QTc interval is intended to represent the QT interval at a standardized heart rate of 60 bpm. A delay in cardiac repolarization creates an electrophysiological environment that favors the development of cardiac arrhythmias, most clearly torsade de pointes, but possibly other ventricular arrhythmias as well.
While the degree of QT prolongation is recognized as an imperfect biomarker for proarrhythmic risk, there is a qualitative relationship between QT prolongation and the risk of TdP, especially for drugs that cause substantial prolongation of the QT/QTc interval.