The relation of QT dispersion and localized QT difference to coronary pathology in a population with unstable coronary artery disease
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Milos Kesek1, Anders Englund, Tomas Jernberg
1Department of Cardiology, Norrland University Hospital, 90185 Umea, Sweden. milos.kesek@zeta.telenordia.se
Insights
QT dispersion (QTd), a marker of heart repolarization, is elevated in patients with unstable coronary artery disease. However, this increase is not linked to the location or severity of coronary artery blockages.
Area of Science:
- Cardiology
- Electrophysiology
- Ischemic Heart Disease
Background:
- QT dispersion (QTd) is a prognostic indicator in various patient groups.
- QTd elevation is observed in conditions involving ischemia, potentially reflecting repolarization inhomogeneity.
- The underlying mechanism of QTd increase during ischemia requires further elucidation.
Purpose of the Study:
- To investigate the relationship between QT dispersion and angiographic measures in patients with unstable coronary artery disease.
- To explore potential local mechanisms contributing to QT dispersion during ischemia.
Main Methods:
- Utilized data from 276 patients in the FRISC II trial.
- Measured mean QT dispersion (QTdMean) over 27 hours post-admission.
- Assessed maximal difference in QT between adjacent ECG leads (QTdiffMean) and correlated with angiographic scores in 174 patients.
Main Results:
- QTdMean was significantly higher (55 ms) compared to unselected chest pain patients (40 ms).
- QTdiffMean showed a strong correlation with QTdMean.
- No significant differences in QTdMean were found based on angiographical scores or coronary pathology localization.
Conclusions:
- QT dispersion in ischemic conditions appears to be influenced by factors independent of coronary artery localization and severity.
- The mechanism driving increased QTd in ischemia may not be directly related to local coronary pathology.
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.
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