Electrophysiological basis of QT dispersion measurements

Abstract

Dispersion of ventricular repolarization is a now widely used term describing nonhomogeneous recovery of excitability or heterogeneity of ventricular repolarization. It is usually expressed as the difference or the range of various repolarization measurements obtained from a heart. Experimentally, an increased dispersion of ventricular repolarization was found to be tightly associated with increased propensity for ventricular arrhythmias, and, therefore, is considered an important arrhythmogenic mechanism. Noninvasively, this arrhythmogenic substrate was approached using multilead body surface potential mapping, but also QT interval dispersion (QTd) and similar electrocardiogram (ECG) variables from the 12-lead surface ECG. Standard QTd from the ECG correlates significantly with dispersion of repolarization measured from the myocardium. A causal relationship is, however, still unclear, and there are 2 main hypotheses to explain the electrophysiological basis of QTd. The local hypothesis explaining QTd with spatial differences in action potential duration mirrored in the various QT intervals competes with the global hypothesis explaining the variation in surface ECG measurements with different projections of a common T-wave vector. Notwithstanding the final explanation for QTd, and particularly for technical reasons, new markers like advanced T-wave loop variables may best reflect the abnormal repolarization substrate on the surface ECG.