Alteration of the QT variability index in end-stage liver disease / 대한마취과학회지

BACKGROUND: A prolonged QT interval can lead to malignant ventricular arrhythmias and sudden cardiac death, and has frequently been found in end-stage liver disease (ESLD). However, myocardial repolarization lability has not yet been fully investigated. We evaluated the QT variability index (QTVI), a marker of temporal inhomogeneity in ventricular repolarization and an abnormality associated with re-entrant malignant ventricular arrhythmias. We determined whether QTVI is affected by the head-up tilt test in ESLD. METHODS: We assessed 36 ESLD patients and 12 control subjects without overt heart disease before and after the 70-degree head-up tilt test. The electrocardiography signal (lead II) was recorded on a computer with an analog-to-digital converter. The RR interval (RRI) and QT interval were measured after recording 5 min of the digitized electrocardiography. Then, the QT intervals were corrected with Bazett's formula (QTc). QTVI was calculated through the following formula: QTVI = log10 [(QTv/QTm2)/(RRIv/RRIm2)], QTv/RRIv: variance of QTI/RRI, QTm/RRIm: mean of QT interval/RRI. RESULTS: Cirrhotic patients exhibited an elevated QTVI. In particular, Child class C patients had a significantly increased QTVI compared to Child class A patients and the control subjects in the supine position. However, the head-up tilt test did not cause a significant difference in QTVI in relation to the severity of ESLD. CONCLUSIONS: Myocardial repolarization lability was significantly altered in end-stage liver disease. Our data suggest that the severity of ESLD is associated with the degree of the alteration in the QT variability index.

Ventricular Inhomogeneity and Beat-to-beat QT Interval Variability after Surgical Repair of Tetralogy of Fallot

PURPOSE: The object of this study is to determine whether QT interval variability in patients with postoperative tetralogy of Fallot increases. METHODS: We enrolled 41 patients who had total correction of tetralogy of Fallot, and 31 healthy controls. They were 6-12 years old. Patients were divided into 2 groups : arrhythmia-positive patients(n=10) who had ventricular premature contractions more than 30/hour or who had couplets, and arrhythmia-negative patients(n=31). We selected the 10-minute arrhythmia-free portion of 24-hour ambulatory ECG recorded during sleep(1-3AM). We selected the 2nd beat of recordings for a template, then found the QT interval for each beat. The method was that T-wave shape best matches template T-wave under the time-stretch model. The mean heart rate and variance and mean QT interval and variance were computed and then a QT variability index(QTVI)-which represents the log ratio between QT interval variability and heart rate variability-was derived. RESULTS: Postoperative tetralogy of Fallot patients with/without ventricular arrhythmia showed significantly increased QTVI compared with the control(-0.481+/-0.310/-0.661+/-0.376 vs -1.200+/-0.380, P<0.0001). There was a trend that QTVI in patients with ventricular arrhythmia increased more than in patients without ventricular arrhythmia, but there were no statistical significances. CONCLUSION: QT interval variability increased in repaired tetralogy of Fallot patients with/without ventricular arrhythmia compared with the control. And this finding indicates that inhomogeneity of temporal ventricular repolarization exists in repaired tetralogy of Fallot patients.