ABSTRACT
Drugs that alter ventricular repolarization (generally characterized as drugs that prolong the QT interval) have been associated with malignant ventricular arrhythmias (especially the distinctive polymorphic ventricular tachycardia called torsades de pointes, TdP) and death [4-8]. Many of the drugs now known to alter ventricular repolarization were developed as antiarrhythmics (e.g., dofetelide, sotalol), but others (e.g., cisapride, terfenadine) were developed without the expectation of any effect upon electrically excitable membranes. This has lead to the International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use (ICH) promulgating ICH S7A [9] with speci˜c guidance for evaluation of such electrophysiologic function.
