ABSTRACT
As indicated by Tsong and Zhang (2008), delay in cardiac repolarization creates an electrophysiological environment that may set off cardiac arrhythmias, particularly a polymorphic ventricular tachycardia. This condition can degenerate into ventricular Œbrillation, leading to sudden cardiac death. The QT interval represents the duration of ventricular depolarization and subsequent repolarization and is typically measured on a 12-lead surface electrocardiogram (ECG) from the beginning of the QRS complex to the end of the T wave (see Figure 18.1). The RR interval, which is the distance between two consecutive R waves, is the inverse of the heart rate. In pharmaceutical research and development, drug-induced prolongation of the QT interval has been used as an indicator of possible cardiac safety problems. The QT interval is often used to indirectly assess the delay in cardiac repolarization, which can predispose to the development of lifethreatening cardiac arrhythmias such as torsade depointes (Moss, 1993). The QTc interval is referred to as the QT interval corrected by heart rate. In clinical practice, it is recognized that the prolongation of the QT/QTc interval is related to the increased risk of cardiotoxicity, such as a lifethreatening arrhythmia (Temple, 2003). Thus, it is suggested that a careful evaluation of potential QT/QTc prolongation be assessed for potential drug-induced cardiotoxicity.
