Open AccessRelation of ventricular repolarization to cardiac cycle length in normal subjects, hypertrophic cardiomyopathy, and patients with myocardial infarction
Author(s) -
Savelieva Irina,
Yap Yee Guan,
Yi Gang,
Guo Xiao Hua,
Hnatkova Katerina,
John Camm A.,
Malik Marek
Publication year - 1999
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960221011
Subject(s) - medicine , cardiology , qt interval , myocardial infarction , repolarization , hypertrophic cardiomyopathy , heart failure , electrocardiography , heart rate , heart disease , blood pressure , electrophysiology
Background : Prolonged QT interval and QT dispersion have been reported to reflect an increased inhomogeneity of ventricular repolarization, which is believed to be responsible for the development of arrhythmic events in patients with long QT syndrome, coronary heart disease, and myocardial infarction, congestive heart failure, and hypertrophic cardiomyopathy (HC). Hypothesis : This study was undertaken to determine whether an abnormal QT/RR dynamicity may reflect autonomic imbalance and may contribute to arrhythmogenesis in patients with heart disease. Methods : The relation between QT, QT peak (QT p ), T peak ‐T end (T p T c ) intervals and cardiac cycle length was 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 compared with normals (p <0.001 for QT and QT p ; p <0.04 for T p T c ); in survivors of MI, this was true for the maximum QT and QT p intervals (p <0.05). A strong linear correlation between QT, QT p , and RR intervals was observed 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). T p T c interval only showed a weak correlation with heart rate in normals (r = 0.24, p <0.05) and was rate‐independent 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 T p T e R/RR lines between groups (0.0110, 0.0076, 0.0163, respectively). T p T e /QT p ratio was similar in normals and in patients with MI and HC (0.30 ± 0.03, 0.31 ± 0.07, 0.30 ± 0.04, respectively), in the absence of any correlation between QT p and T p T e intervals, suggesting disproportional prolongation of both components of QT interval. Conclusion : Compared with normals, a progressive increase in QT and QT p intervals at slower heart rates in patients with MI and HC may indicate an enhanced variability of the early ventricular repolarization and may be one of the mechanisms of arrhythmogenesis.