QT interval and drug therapy

The QT interval is measured from the beginning of the QRS complex to the end of the T wave on a surface electrocardiogram and represents the period from onset of depolarisation to completion of repolarisation of the ventricular myocardium.1 The interval varies greatly and is affected by age, sex, sympathetic tone, and diurnal pattern.2 Because it increases as heart rate falls, measurements of QT interval are usually corrected for heart rate (QTc). Several methods have been used (box 1) but, as the relation between QT interval and heart rate varies between individuals, guidelines recommend use of linear regression functions such as the Framingham rather than the Bazett or Fridericia method.4 #### Box 1: Formulae used to correct the QT interval for heart rate3 Measurement of the QT interval is not straightforward and is associated with considerable intraindividual and interindividual variability. There is currently no agreed consensus on how to measure the QT interval in patients with broad complex ventricular conduction abnormalities or paced ventricular rhythm, and measurement in patients with atrial fibrillation requires special consideration. The QT interval also differs between electrocardiograph (ECG) leads, and it is unclear whether normal values—historically derived from single lead measurements—relate directly to those obtained from multi-lead ECG recordings. In addition, details of algorithms used in semi-automated ECG machines are not always readily available. QTc intervals of 450 ms and 460 ms are generally accepted as the upper limits of normal for adult men and women, respectively.4 Although QT prolongation is associated with torsades de pointes (TdP) and sudden cardiac death,5 it is an imperfect predictor. Many patients with prolonged QT never experience TdP, whereas many who experience TdP have a normal QT before the episode. Similarly, some drugs (eg amiodarone) can markedly prolong QT but …