Is ventricular repolarization heterogeneity a cause of serious ventriculartachyarrhythmias in aortic valve stenosis?

Citation
Mk. Batur et al., Is ventricular repolarization heterogeneity a cause of serious ventriculartachyarrhythmias in aortic valve stenosis?, CLIN CARD, 23(6), 2000, pp. 449-452
Citations number
24
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
CLINICAL CARDIOLOGY
ISSN journal
01609289 → ACNP
Volume
23
Issue
6
Year of publication
2000
Pages
449 - 452
Database
ISI
SICI code
0160-9289(200006)23:6<449:IVRHAC>2.0.ZU;2-W
Abstract
Background: It is well known that there is a close relation between sudden cardiac death and serious Ventricular tachyarrhythmias in patients with aor tic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repol arization heterogeneity and has been proposed as an indicator for ventricul ar arrhythmias. Hypothesis: This study investigated the QTd and its relevance to the clinic al and echocardiographic variables. Methods: In all, 51 patients (33 men, 1 8 women, mean age 56 +/- 12) with isolated AS and 51 age- and gender-matche d healthy controls comprised the study group. Left ventricular mass index ( LVMI) was calculated by the Devereux formula, and we used continuous-wave D oppler (n = 15) and cardiac catheterization (n = 36) for the determination of the maximum aortic valve pressure gradient (PG). Results: Corrected QTd (QTcd) (89 +/- 39 vs. 49 +/- 15 ms, p < 0.001) and L VMI (176 +/- 69 g/m(2) vs. 101 +/- 28 g/m(2), p < 0.001) in patients with A S were significantly different from those in the control group. The group o f 21 patients had a significantly greater number of 24-h mean ventricular p remature beats (VPB) and mean number of coupler VT episodes than did the co ntrol group (p < 0.05). QTcd also correlated significantly well with LVMI ( r = 0.58, p < 0.001), PG (r = 0.41, p = 0.003), and number of 24-h VPB (r = 0.56, p = 0.008). With respect to symptoms (e.g., angina, syncope, and dys pnea) patients without symptoms (n = 19) displayed less QTcd (71 +/- 31 vs. 100 +/- 39 ms, p = 0.007) and less LVMI (144 +/- 80 g/m(2) vs. 195 +/- 57 g/m(2), p = 0.01) than patients with symptoms. Statistical analysis was sim ilar for all variables with uncorrected QTd values. Concluion: We found that ventricular repolarization heterogeneity was great er in patients with AS than in controls. Our findings also showed that QTd in the patient group correlates well with LVMI, severity of AS, and PG. The present results suggest that serious ventricular arrhythmias in patients w ith AS may be due to spatial ventricular repolarization abnormality.