In 1985, Mirvis1 reported on a significant spatial variation in QT intervals in normal individuals and patients with acute myocardial infarction. More recently, there has been an increasing interest in what has become known as QT dispersion, which is defined as the difference between the maximum and minimum QT interval of the 12 lead ECG.2 A number of publications has shown a relation between increased QT dispersion and death from a cardiac cause.3-5 Other studies have shown that QT dispersion can be reduced as a result of certain drug treatments.6 ,7 On the other hand, increased QT dispersion has been shown not to be associated with increased cardiac death in patients with idiopathic dilated cardiomyopathy.8 It has also been suggested that increased QT dispersion may be a marker of arrhythmia risk in patients with hypertrophic cardio- myopathy,9 long QT intervals,2 and sustained ventricular arrhythmias.10

All of these studies have involved relatively small numbers of patients and, with the exception of one report,3 sensitivity and specificity of criteria have not been considered. Even in this study,3 the receiver operator characteristic (ROC) curve assessing different cut off values for abnormal QT dispersion was essentially developed on the basis of a training set.

A major question arises—is a single measurement of QT dispersion of any clinical utility despite the fact that trends in QT dispersion can be linked with adverse outcome or improvement?

To know whether a single measurement is reliable enough to have any prognostic value requires an understanding of the accuracy of measuring QT dispersion. In this connection, the articles by Kors and van Herpen11 and Yi and colleagues12 in this issue are of relevance. They provide an interesting sequel to earlier studies on QT dispersion assessed by …