Relation of ventricular repolarization to cardiac cycle length in normal subjects, hypertrophic cardiomyopathy, and patients with myocardial infarction

Background: Prolonged QT interval and QT dispersion have been reported to r eflect an increased inhomogeneity of ventricular repolarization, which is b elieved to be responsible for the development of arrhythmic events in patie nts with long QT syndrome, coronary heart disease, and myocardial infarctio n, congestive heart failure, and hypertrophic cardiomyopathy (HC). Hypothesis: This study was undertaken to determine whether an abnormal QT/R R dynamicity may reflect autonomic imbalance and may contribute to arrhythm ogenesis in patients with heart disease. Methods: The relation between QT, QT(peak) (QT(p)), T-peak-T-end (TpTe) intervals and cardiac cycle length wa s assessed in 70 normal subjects, 37 patients with HC, and 48 survivors of myocardial infarction (MI). A set of 10 consecutive electrocardiograms was evaluated automatically in each subject using QT Guard software (Marquette Medical Systems, Milwaukee, Wisc.). Results: In patients with HC, all intervals were significantly prolonged co mpared with normals (p < 0.001 for QT and QT(p); p < 0.04 for TpTe); in sur vivors of MI, this was true for the maximum QT and QT(p) intervals (p < 0.0 5). A strong linear correlation between QT, QT(p), and RR intervals was obs erved in normals and in patients with MI and HC (r = 0.65-0.59, 0.82-0.77, 0.79-0.74, respectively, p < 0.0001). TpTe interval only showed a weak corr elation with heart rate in normals (r = 0.24, p < 0.05) and was rate-indepe ndent in both patient groups (p = NS). Compared with normals, the slopes of QT/RR and QT(p)/RR regression lines were significantly steeper in patients with MI and HC (0.0990-0.0883, 0.1597- 0.1551, 0.1653-0.1486, respectively ). Regression lines were neither parallel nor identical between normals and patients (T> 1.96, Z> 3.07). There was no difference in steepness for TpTe R/RR lines between groups (0.0110, 0.0076, 0.0163, respectively). TpTe/QT(p ) ratio was similar in normals and in patients with MI and HC (0.30 +/- 0.0 3, 0.31 +/- 0.07, 0.30 + 0.04, respectively), in the absence of any correla tion between QT(p) and TpTe intervals, suggesting disproportional prolongat ion of both components of QT interval. Conclusion: Compared with normals, a progressive increase in QT and QT(p) i ntervals at slower heart rates in patients with MI and HC may indicate an e nhanced variability of the early ventricular repolarization and may be one of the mechanisms of arrhythmogenesis.