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QT interval on the surface electrocardiogram reflects the time for repolarization of myocardium. Prolongation of rate-corrected QT interval, QTc is strongly associated with sudden cardiac death. Recent studies using novel techniques on beat-to-beat QT interval variability have shown that an increase in QT interval variability is associated with increased sympathetic activity and is a predictor of sudden cardiac death. We studied QT variability in patients with congestive cardiac failure, as it is associated with an increase in cardiac sympathetic activity and also sudden death.We compared beat-to-beat heart rate and QT interval data in 2 3 patients with congestive cardiac failure and 19 age-matched normal controls. The electrocardiographic data were acquired in lead II configuration at a sampling rate of 1000 Hz. Heart rate variability was found to be significantly lower while QT variability measures were significantly higher in patients compared to controls. QTvi (a common log ratio of QT variability normalized for mean QT interval squared divided by heart rate variability normalized for mean heart rate squared) was also significantly higher in patients compared to controls. Clinical improvement in some of these patients is associated with a decrease in QTvi, due mainly to an increase in cardiac vagal function.Our results suggest a decrease in cardiac vagal and an increase in cardiac sympathetic functions in patients with congestive cardiac failure. QTvi may prove to be a useful surrogate end point to evaluate treatment effect in these patients.

Background: Congestive cardiac failure is associated with increased sympathetic activity and impaired baroreflex function. We sought to test the hypothesis that these patients also have blunted response of beat-to-beat QT interval variability during orthostatic challenge. Methods: We compared beat-to-beat heart rate and QT interval data in 17 patients with congestive cardiac failure and 17 age-matched normal controls in supine normal breathing, supine controlled breathing, and standing controlled breathing conditions. The ECG data were acquired in lead II configuration at a sampling rate of 1000 Hz. Results: Supine controlled breathing was associated with an increase in spectral HF power (0.15–0.5 Hz) of HR and QT interval time series compared to spontaneous breathing condition only in controls. While there were significant changes in HR, HR LF power, HR LF/HF ratios, and QT variability measures in standing posture in controls, there were no such changes in patients. Conclusions: This impairment of postural changes of HR variability is most likely due to an impaired baroreceptor function in patients with congestive heart failure. The etiology of this is likely due to an increased cardiac sympathetic and a decreased vagal function. However, the relationship of postural changes in beat-to-beat QT interval variability and baroreflex need further investigation.