[Correlation between QT interval dispersion and ventricular arrhythmia in hypertension].

Objective: To evaluate the correlation between QT interval dispersion (QTd) and ventricular arrhythmias in hypertensive patients (pts) with or without left ventricular hypertrophy (LVH). A secondary aim was to investigate correlations of QTd with other markers of arrythmogenic propensity: ventricular late potentials (LP) and heart rate variability (HRV).
Methods: We retrospectively measured the QTd on the 12 standard surface ECG leads in 230 hypertensive pts (94F, 136M; 59.6 +/- 12.7 years old). A 24 hours ECG Holter recording was performed in 218 pts and ventricular arrhythmias were appreciated using the Lown classification. Left ventricular mass was determined by echocardiography (LVM-Devereux formula) and left ventricular mass index (LVMI) were determined in 202 subjects. LP (122 pts) and HRV (55 pts) were investigated.
Results: The QTd varied between 20 and 160 msec (57.8 +/- 32.7 msec). The distribution of pts classified using Lown criteria was: 29 pts (13.3%) class O; 106 pts (48.6%) class I; 8 pts (3.6%) class II; 13 pts (6%) class III; 29 pts (13.3%) class IVa; 33 pts (15.1%) class IVb; 116 pts (69.5%) had LVH determined by echocardiography. The QTd was strongly correlated with the Lown classes (p < 0.0001). The QTd was significantly broader in Lown classes III, IVa and IVb compared to classes O, I and II cumulated (p < 0.002); there was no difference concerning QTd between Lown classes III, IVa and IVb. The QTd was also correlated with the absolute number of premature ventricular depolarizations/24 hours (p = 0.02; r = 0.16). The 75 pts with an increased LVMI had significantly elevated QTd compared to pts without it (p < 0.0001). Qtd was correlated with LVMI (r = 0.37; p < 0.0001). There was no correlation between QTd and the existence of LP (which were correlated with the Lown classes; p < 0.03) and HRV parameters.
Conclusion: Elevated QT interval dispersion is associated with more severe ventricular arrhythmias in hypertensive subjects with LVH. The mechanism of an increased inhomogeneity of repolarisation is probably related to the anatomic modifications induced by LVH. No significant correlation between QTd, LP and HRV was observed.