Dilated cardiomyopathy patients had significantly higher beat-to-beat QT variance (60.4 vs 25.7 ms2, P<0.0001) and QT variability index (-0.43 vs -1.29, P<10^-12) compared to control subjects.
Case-Control (n=143)
Is beat-to-beat QT interval variability increased in patients with dilated cardiomyopathy compared to control subjects?
Patients with dilated cardiomyopathy exhibit significantly increased temporal lability in ventricular repolarization, as measured by beat-to-beat QT interval variability, which correlates with worsening functional class.
Absolute Event Rate: 60.4% vs 25.7%
p-value: p=<.0001
BACKGROUND: Dilated cardiomyopathy (DCM) is associated with a high incidence of malignant ventricular arrhythmias and sudden death. Abnormalities in repolarization of ventricular myocardium have been implicated in the development of these arrhythmias. Spatial heterogeneity in repolarization has been studied in DCM, but temporal fluctuations in repolarization in this setting have been largely ignored. We sought to test the hypothesis that beat-to-beat QT interval variability is increased in DCM patients compared with control subjects. METHODS AND RESULTS: Eighty-three patients with ischemic and nonischemic DCM and 60 control subjects served as the study population. Beat-to-beat QT interval variability was measured by automated analysis on the basis of 256-second records of the surface ECG. A QT variability index (QTVI) was calculated for each subject as the logarithm of the ratio of normalized QT variance to heart rate variance. The coherence between heart rate and QT interval fluctuations was determined by spectral analysis. In patients, ejection fractions were assessed by echocardiography or ventriculography, and spatial QT dispersion was determined from the standard 12-lead ECG. DCM patients had greater QT variance than control subjects (60.4+/-63.1 versus 25.7+/-24.8 ms2, P<.0001) despite reduced heart rate variance (6.7+/-7.8 versus 10.5+/-10.4 bpm2, P=.01). The QTVI was higher in DCM patients than in control subjects, with a high degree of significance (-0.43+/-0.71 versus -1.29+/-0.51, P<10-12). QTVI did not correlate with ejection fraction or spatial QT dispersion but did depend on New York Heart Association functional class. QTVI did not differ between DCM patients with ischemic and those with nonischemic origin. Coherence between heart rate and QT interval fluctuations at physiological frequencies was lower in DCM patients compared with control subjects (0.28+/-0.14 versus 0.39+/-0.18, P<.0001). CONCLUSIONS: DCM is associated with beat-to-beat fluctuations in QT interval that are larger than normal and uncoupled from variations in heart rate. QT interval variability increases with worsening functional class but is independent of ejection fraction. These data indicate that DCM leads to temporal lability in ventricular repolarization.
Berger et al. (Tue,) conducted a case-control in Dilated cardiomyopathy (n=143). Dilated cardiomyopathy vs. Control subjects was evaluated on QT variance (ms2) (p=<.0001). Dilated cardiomyopathy patients had significantly higher beat-to-beat QT variance (60.4 vs 25.7 ms2, P<0.0001) and QT variability index (-0.43 vs -1.29, P<10^-12) compared to control subjects.