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      QT Interval Dispersion as a New Marker of Restenosis after Percutaneous Transluminal Coronary Angioplasty of Isolated Single-Vessel Coronary Artery Stenosis


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          Background: There are no reliable non-invasive markers of restenosis after percutaneous transluminal coronary angioplasty (PTCA). The aim of our study was to measure changes in QT interval dispersion after PTCA and to determine whether restenosis subsequently affects QT interval dispersion. Methods and Results: Fifty-six consecutive patients – 41 men and 15 women (mean age: 56.2 ±8.3 years) – with isolated stenosis of the left anterior descending artery who underwent successful PTCA were studied. A symptom-limited treadmill exercise test was performed within 7 days after PTCA and then again before repeated angiography. Repeated coronary angiography revealed restenosis in 15 patients (26.8%) and no signs of significant stenosis in 41 patients (73.2%). QT interval dispersion in the group of patients with restenosis measured before exercise increased from baseline 34 ± 7 to 49 ± 15 ms after 6 months (p < 0.01) and QT interval dispersion measured immediately after exercise increased from baseline 38 ± 4 to 68 ± 21 ms after 6 months (p < 0.001). In contrast, patients without restenosis showed no significant changes in QT interval dispersion measured before (baseline: 34 ± 9 ms; after 6 months 33 ± 12 ms; p = NS) and immediately after exercise (baseline: 34 ± 12 ms; after 6 months: 33 ± 10; p = NS). When QT interval dispersion ≧60 ms (measured 6 months after PTCA procedure) was considered as a potential marker of restenosis, this indicator had very high sensitivity and specificity when measured immediately after exercise (80 and 95% respectively). Conclusions: QT interval dispersion significantly increases in the group of patients with documented restenosis and may be a simple, non-invasive marker of restenosis. However, further studies are needed to confirm this observation.

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          Most cited references 22

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          QT dispersion: an indication of arrhythmia risk in patients with long QT intervals.

          Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.
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            Dispersion of QT interval in patients with and without susceptibility to ventricular tachyarrhythmias after previous myocardial infarction.

            The aim of this study was to estimate the value of QT dispersion measurement from the standard 12-lead electrocardiogram (ECG) in identifying patients susceptible to reentrant ventricular tachyarrhythmias after a previous myocardial infarction. Variability in QT interval duration on the different leads of the 12-lead ECG has been proposed as an indicator of risk for ventricular arrhythmias in different clinical settings, but the value of QT dispersion measurement in identifying patients at risk for reentrant ventricular tachyarrhythmias after myocardial infarction is not known. The QT interval duration, QT dispersion and clinical and angiographic variables were compared between 30 healthy subjects; 40 patients with a previous myocardial infarction but no history of arrhythmic events or inducible ventricular tachycardia during programmed electrical stimulation; and 30 postinfarction patients with a history of cardiac arrest (n = 12) or sustained ventricular tachycardia (n = 18) and inducible, sustained monomorphic ventricular tachycardia by electrical stimulation. Dispersion of the corrected QT interval (QTc) differed significantly between the study groups and was significantly increased in patients with susceptibility to ventricular tachyarrhythmias ([mean +/- SD] 104 +/- 41 ms) compared with that in both healthy subjects (38 +/- 14 ms, p < 0.001) and postinfarction patients with no susceptibility to arrhythmias (65 +/- 31 ms, p < 0.001). Maximal QT interval duration was also prolonged in the group with arrhythmias compared with that in the other groups (p < 0.001). Multivariate analysis, including clinical and angiographic variables, QT dispersion and maximal QT interval, showed that QT dispersion was the independent factor that most effectively identified the patient groups with and without susceptibility to ventricular tachyarrhythmias (p < 0.001). Increased QT dispersion is related to susceptibility to reentrant ventricular tachyarrhythmias, independent of degree of left ventricular dysfunction or clinical characteristics of the patient, suggesting that the simple, noninvasive measurement of this interval from a standard 12-lead ECG makes a significant contribution to identifying patients at risk for life-threatening arrhythmias after a previous myocardial infarction.
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              QT interval dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?

              To assess QT interval dispersion on the surface electrocardiogram in patients with sustained ventricular arrhythmias. A retrospective and prospective blinded controlled study of patients referred for investigation of ventricular arrhythmias at a tertiary cardiac centre. 89 consecutive patients with sustained ventricular arrhythmias due to chronic ischaemic heart disease, cardiomyopathy, or ventricular tachycardia (VT) in a normal heart. 32 patients did not meet the inclusion criteria; therefore 57 patients were compared with a control group of 40 patients with myocardial disease but no history of arrhythmias and 12 normal controls with no myocardial disease. Standard 12 lead electrocardiograms were enlarged, the QT intervals for each lead measured, and QT dispersion calculated. There was a significantly greater mean QT dispersion (77 ms) in patients with sustained ventricular arrhythmias compared with the control group (38 ms, p < 0.01). This held for all groups; after myocardial infarction VT (82 (22) ms v control 38 (10) ms; p < 0.01), dilated cardiomyopathy VT (76 (18) ms v control 40 (11) ms, p < 0.01), and normal heart VT (65 (7) ms v control 32 (8), p < 0.05). There was also a greater QT dispersion in patients with impaired left ventricular function and VT, with a correlation between left ventricular function and QT dispersion in patients with VT (r = 0.56, p < 0.01). QT interval dispersion may be a further non-invasive marker of susceptibility to ventricular arrhythmias.

                Author and article information

                S. Karger AG
                August 2006
                16 August 2006
                : 106
                : 2
                : 89-97
                aChair and 1st Department of Cardiology, and bDepartment of Clinical Pharmacology, Poznan University of Medical Sciences, Poznan´, Poland
                92637 Cardiology 2006;106:89–97
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 6, References: 31, Pages: 9
                Original Research


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