BACKGROUND: QT dispersion (QTd) contains prognostic information in several patient groups. The variable increases in several conditions with ischemia. Originally, it was thought to reflect the local repolarization inhomogeneity. Even though this explanation has been questioned lately, it continues to be put forward. In order to elucidate a possible local mechanism, we investigated the relation between QT dispersion, an ECG parameter reflecting the local dispersion, and angiographical measures in a population with unstable coronary artery disease. METHODS: The 276 patients were recruited from the FRISC II trial. As the QTd parameter we used the mean value of automatically measured QTd during 27 hours after admission (QTdMean). As a local repolarization measure we used the maximal difference in QT between two adjacent ECG leads (QTdiffMean). The computations were performed on all available ECG leads and on a restricted set without the V1-V2 combination. Previously published angiographic scoring tools were adapted for rating and localizing the coronary pathology by two approaches and applied on 174 patients undergoing angiography. RESULTS: QTdMean was significantly higher than that reported in previous material with unselected chest pain patients (55 vs 40 ms). QTdiffMean correlated strongly with QTdMean. No differences in QTdMean were detected between patients with different angiographical scores. No relation could be shown between the region with dominating coronary pathology as expressed by the scoring tools and the localization of QTdiffMean. CONCLUSIONS: QTd in ischemia seems to be increased by a mechanism unrelated to localization and severity of coronary disease.
BACKGROUND: QT dispersion (QTd) contains prognostic information in several patient groups. The variable increases in several conditions with ischemia. Originally, it was thought to reflect the local repolarization inhomogeneity. Even though this explanation has been questioned lately, it continues to be put forward. In order to elucidate a possible local mechanism, we investigated the relation between QT dispersion, an ECG parameter reflecting the local dispersion, and angiographical measures in a population with unstable coronary artery disease. METHODS: The 276 patients were recruited from the FRISC II trial. As the QTd parameter we used the mean value of automatically measured QTd during 27 hours after admission (QTdMean). As a local repolarization measure we used the maximal difference in QT between two adjacent ECG leads (QTdiffMean). The computations were performed on all available ECG leads and on a restricted set without the V1-V2 combination. Previously published angiographic scoring tools were adapted for rating and localizing the coronary pathology by two approaches and applied on 174 patients undergoing angiography. RESULTS: QTdMean was significantly higher than that reported in previous material with unselected chest painpatients (55 vs 40 ms). QTdiffMean correlated strongly with QTdMean. No differences in QTdMean were detected between patients with different angiographical scores. No relation could be shown between the region with dominating coronary pathology as expressed by the scoring tools and the localization of QTdiffMean. CONCLUSIONS: QTd in ischemia seems to be increased by a mechanism unrelated to localization and severity of coronary disease.
Authors: P Dilaveris; G Andrikopuolos; G Metaxas; D Richter; C Avgeropoulou; A Androulakis; E Gialafos; A Michaelides; P Toutouzas; J Gialafos Journal: J Electrocardiol Date: 1999-07 Impact factor: 1.438