Unlabelled: The aim of the study was to evaluate the QT dispersion and the severity of arrhythmias in hypertensive patients according to the asymmetry of the left ventricular hypertrophy. The study group consisted of 47 hypertensive patients. In 24 of them the left ventricular hypertrophy was symmetrical (group I) and in 23--asymmetrical (group II). For the evaluation of the left ventricular hypertrophy its thickness was analyzed in 13 segments. The ratio between the maximum and minimum thickness from any location was determined as the asymmetry index (AI). The value of this index 1,3 distinguished between patients with the symmetrical and asymmetrical left ventricular hypertrophy. 20 healthy subjects were examined as a control group (group III). All subjects underwent physical examination, the standard 12-lead electrocardiogram (ECG), twenty-four hour Holter recording and echocardiography. All the results for the QT dispersion (QTd, QTdc, QTdR) were highest in group II, lower in patients from group I and the lowest were observed in the control group. The differences in all parameters between group I and II were statistically significant: for QTd--V p < 0.01, QTdc--p < 0.05, QTdR--p < 0.05. The differences between groups II and III as well as I and III were statistically significant for all QT dispersion parameters: for QTd--p < 0.001 and p < 0.01 respectively, QTdc--p < 0.001, QTdR--p < 0.001 for both groups. We have observed a very distinct positive correlation between the asymmetry index and QTd, QTdc, QTdR (p < 0.001). These values correlated also, but less distinctly with the left ventricular mass index--LVMI (p < 0.05). The frequency and severity of ventricular ectopic beats did not differ significantly between group I and II. The results obtained indicate the lack of connection between the frequency of ventricular premature complexes and (1) all QT dispersion parameters, (2) LVMI, (3) AI. Supraventricular premature complexes occurred significantly more frequently in patients with the asymmetrical left ventricular hypertrophy compared to the group with the regular left ventricular hypertrophy (p < 0.05) and control group (p < 0.01).

Conclusions: The left ventricular hypertrophy in primary hypertension may increase the QT dispersion. It seems that asymmetry of the left ventricular hypertrophy reinforces this increase. The increased QT dispersion in primary hypertension does not influence significantly the occurrence of ventricular arrhythmias.

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