Research Article, Int J Cardiovasc Res Vol: 5 Issue: 3
QT Dispersion: Can it predict the Extent of Stable Coronary Artery Disease?
Neama Elmelegy, Ahmed Masoud*, Heba Mansour and Khaled Elrabbat |
Department of Cardiology, Faculty of Medicine, Benha University, Egypt |
Corresponding author : Ahmed Masoud Department of Cardiology, Faculty of Medicine, Benha University, Egypt Tel: +20 122 8622 373 E-mail: ahmedmasoud89723@yahoo.com |
Received: March 10, 2016 Accepted: May 05, 2016 Published: May 12, 2016 |
Citation: Elmelegy N, Masoud A, Mansour H, Elrabbat K (2016) QT Dispersion: Can it predict the Extent of Stable Coronary Artery Disease?. Int J Cardiovasc Res 5:3. doi:10.4172/2324-8602.1000269 |
Abstract
QT Dispersion: Can it predict the Extent of Stable Coronary Artery Disease?
Background: QT dispersion was found to increase during episodes of myocardial ischemia or infarction. A substantial body of evidence now supports the notion that prolongation of ventricular repolarization as measured by the QT interval is related to the underlying ischemia in patients with coronary artery disease. Objectives: To explore a possible relationship between QT dispersion and the extent of coronary artery disease.
Methods: This study enrolled 120 cases admitted for elective coronary angiography. The cases were divided, according to the number of the affected coronary vessels, into four groups [normal, single vessel disease (SVD), double vessel disease (DVD) and three vessel disease (TVD)] with 30 patients in each group. The QT interval was measured by the manual technique and we recorded the maximal and minimal QT intervals, QT dispersion (QTD) and corrected QT dispersion (QTcD) for each patient individually.
Results: QTD was found to increase significantly with the increasing number of stenosed coronary vessels (33.3 ± 6, 49.6 ± 6, 79.2 ± 8 and 119.8 ± 12 msec for the normal, SVD, DVD and TVD groups respectively, p=0.001). In this study, QTcD also showed a significant difference between the groups with different number of affected coronary vessels (35.9 ± 6, 53.7 ± 7, 86.9 ± 8 and 131 ± 10 msec for the normal, SVD, DVD and TVD respectively, p=0.001). Moreover, the sensitivity of QTD in detection of CAD increased with the increase in number of diseased coronary vessels (53.3%, 86.7% and 93.3% for SVD, DVD and TVD respectively).
Conclusion: We concluded that QTD and QTcD are prolonged in patients with stable CAD. Furthermore, we established a strong correlation between QTD and QTcD with the number of stenosed coronary vessels at rest. So, we assumed that QTD and QTcD can be used to predict the extent of stable CAD and the number of diseased coronary vessels.