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dc.contributor.authorBatur, MK
dc.contributor.authorAcil, T
dc.contributor.authorOnalan, O
dc.contributor.authorYildirir, A
dc.contributor.authorOvunc, K
dc.contributor.authorKabakci, G
dc.contributor.authorOto, A
dc.contributor.authorOzkutlu, H
dc.contributor.authorNazli, N
dc.contributor.authorGursel, G
dc.contributor.authorKes, S
dc.date.accessioned2019-12-10T11:23:17Z
dc.date.available2019-12-10T11:23:17Z
dc.date.issued2000
dc.identifier.issn0160-9289
dc.identifier.urihttps://doi.org/10.1002/clc.4960230615
dc.identifier.urihttp://hdl.handle.net/11655/15554
dc.description.abstractBackground: It is well known that there is a close relation between sudden cardiac death and serious Ventricular tachyarrhythmias in patients with aortic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repolarization heterogeneity and has been proposed as an indicator for ventricular arrhythmias. Hypothesis: This study investigated the QTd and its relevance to the clinical and echocardiographic variables. Methods: In all, 51 patients (33 men, 18 women, mean age 56 +/- 12) with isolated AS and 51 age- and gender-matched healthy controls comprised the study group. Left ventricular mass index (LVMI) was calculated by the Devereux formula, and we used continuous-wave Doppler (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 LVMI (176 +/- 69 g/m(2) vs. 101 +/- 28 g/m(2), p < 0.001) in patients with AS were significantly different from those in the control group. The group of 21 patients had a significantly greater number of 24-h mean ventricular premature beats (VPB) and mean number of coupler VT episodes than did the control 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 dyspnea) 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 similar for all variables with uncorrected QTd values. Concluion: We found that ventricular repolarization heterogeneity was greater 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 with AS may be due to spatial ventricular repolarization abnormality.
dc.language.isoen
dc.publisherClinical Cardiology Publ Co
dc.relation.isversionof10.1002/clc.4960230615
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCardiovascular System & Cardiology
dc.titleIs Ventricular Repolarization Heterogeneity a Cause of Serious Ventricular Tachyarrhythmias in Aortic Valve Stenosis?
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalClinical Cardiology
dc.contributor.departmentKardiyoloji
dc.identifier.volume23
dc.identifier.issue6
dc.identifier.startpage449
dc.identifier.endpage452
dc.description.indexWoS


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