Is QT dispersion a reliable index of heterogeneity of ventricular repolarization and a pro-arrhythmic marker?

This letter has been prompted by a study on QT dispersion (QTd) in patients with arrhythmogenic right ventricular dysplasia, published in the European Heart Journal. In this study QTd was found to be increased in individuals with right ventricular dysplasia, but the magnitude of QTd was not related to the incidence of sustained ventricular arrhythmia or sudden death. In addition, QTd was not influenced by sotalol. Although QTd has been used for several years as an index of heterogeneity of ventricular repolarization (thought to be associated with an increased pro-arrhythmic potential), it has not been found to be a useful parameter in every-day clinical cardiology. Part of the problem is that values of QTd in various study groups overlap and, consequently, it is impossible to reliably interpret an absolute value of QTD in an individual patient, unless the magnitude of QTd is very large. Even more importantly, the true pathophysiological meaning of QTd is not known. Recent basic studies have shaken our traditional understanding of the pathophysiological basis of QTd and called the methodology used in question. In the study by Zabel et al., a correlation between QTd and the dispersion of epicardial action potential durations was found. These results, however, do not necessarily imply that myocardial action potentials map onto discrete areas on the body surface and are reflected as QTd. In fact, in the very same paper a correlation was also found between dispersion of action potentials and the average T peak to T end interval (TpTe). The latter has been recently suggested to represent transmural dispersion of repolarization, resulting from differences in action potentials in the epicardium, endocardium and M cells. There-