Assessment of repolarization heterogeneity for prediction of mortality in cardiovascular disease: peak to the end of the T wave interval and nondipolar repolarization components

Abstract

Background In the canine wedge preparation, the interval from the peak to the end of the T wave (TpTe) reflects transwedge heterogeneities. Increase of ventricular dispersion of action potential durations has been repeatedly shown to be arrhythmogenic; thus, prolonged TpTe intervals were assumed to reflect increased risk. However, despite attempted extrapolation to clinical electrocardiograms, the appropriateness of this assumption has not been investigated in a large population. In another animal model, nondipolar components of the descending T-wave limb (TWRd) have been shown to correlate with TpTe interval. Although total T-wave nondipolar components (TWRt), believed to reflect heterogeneities during total repolarization, were shown associated with worse outcome of cardiac patients, this has not been investigated for TWRd. Methods and Results Male cardiovascular patients (n = 813) had digital 12-lead electrocardiograms recorded between 1984 and 1991 and were followed until 2000. Using commercial and previously validated technology, QT intervals, TpTe intervals, TWRd, and TWRt were calculated, heart rate corrected, and compared between survivors and nonsurvivors. Their predictive power was also compared with established markers of mortality risk. In contrast to former reports, TpTe c intervals were significantly shorter in nonsurvivors (98.76 ± 20.63 milliseconds vs 103.14 ± 20.87 milliseconds, P = .016) and not predictive of outcome. Although TWRd c was significantly higher in nonsurvivors (0.007% ± 0.02% vs 0.005% ± 0.08%, P = .03), it was also not predictive of outcome. Only increased TWRt c, increased heart rate, and increased age were predictive of death. Conclusions The findings challenge the concept that prolongation of TpTe corresponds to higher risk of death from any cause in every population. Further investigations are needed to confirm that clinically measured TpTe reflects transmural repolarization heterogeneity in all clinical populations and indeed is a useful risk marker.