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The spatial QRS-T angle as a marker of ventricular repolarisation in hypertension
P Dilaveris,
E Gialafos,
A Pantazis,
A Synetos,
F Triposkiadis, & J Gialafos
The State Department of Cardiology, Hippokration Hospital, Athens, Greece
Correspondence to: Dr Polychronis Dilaveris, 22 Miltiadou Street, GR-15561 Holargos, Athens, Greece. E-mail: hrodil@yahoo.com
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Ventricular repolarisation abnormalities are important in arrhythmia provocation. The dispersion of repolarisation duration is not the only aspect of repolarisation heterogeneity. Spatial vectorcardiographic descriptors constitute a novel approach to quantify ventricular repolarisation. To test the ability of vectorcardiographic descriptors to discriminate between hypertensives with high or low blood pressure (BP), 110 treated hypertensives (mean age 63.6 ± 12.1 years) were classified in the high (systolic BP  160 mm Hg or diastolic BP 95 mm Hg) (n = 67), or the low (systolic BP < 160 mm Hg and diastolic BP <95 mm Hg) (n = 43) BP group. The maximum QT, JT, and T peak-T end intervals and the QT, JT, and T peak-T end dispersion were calculated from a digitally recorded 12-lead electrocardiogram (ECG). X, Y, and Z leads were reconstructed from the 12-lead ECG. The amplitude of the maximum spatial T vector (spatial T amplitude), the angle between the maximum spatial QRS and T vectors (spatial QRS-T angle) and the frontal plane QRS-T angle were calculated. The spatial QRS-T angle was higher in patients with high compared to those with low BP (P = 0.025). All conventional ECG markers of the dispersion of ventricular repolarisation duration failed to demonstrate significant differences between hypertensives with high or low BP. In conclusion, the spatial QRS-T angle was significantly increased in those treated hypertensive patients who showed repeatedly high BP values. Hence, we may suggest that the angle between the directions of ventricular depolarisation and repolarisation is a sensitive marker of the repolarisation alterations in systemic hypertension. Journal of Human Hypertension (2001) 15, 63-70 |
