Key result
Carriage of the mutant allele T of the endothelial NO-synthase gene was associated with endothelial dysfunction, but not with daily blood pressure profile or large artery remodeling.
Why the study?
Is endothelial NO-synthase gene polymorphism associated with large vessel remodeling and endothelial dysfunction in hypertensive patients with left ventricular hypertrophy?
Observational (n=51)
Is endothelial NO-synthase gene polymorphism associated with large vessel remodeling and endothelial dysfunction in hypertensive patients with left ventricular hypertrophy?
In hypertensive patients with left ventricular hypertrophy, the mutant T allele of the endothelial NO-synthase gene is associated with endothelial dysfunction but not with large artery remodeling or blood pressure profile.
T allele carriage may prompt endothelial monitoring in LVH hypertension; leaves open any role in remodeling or BP profile.
Remodeling of large arteries and endothelial dysfunction, as left ventricular hypertrophy, is associated with the development of severe cardiovascular events and worse prognosis in patients with hypertensive disease. The impact of genetic determinants on the development of such lesions to target organs in this group of patients was the subject of wide speculation. We determined the genotype of endothelial NO-synthase (the polymorphisms 4a/4b and Glu298Asp) in 51 patients (28 males and 23 females; mean age |48,0±6,3 years) with hypertensive disease and left ventricular hypertrophy; the profile of blood pressure (BP) was assessed by its 24-hour monitoring data; the thickness of an intima-media complex was measured during ultrasound study. Endothelial function was determined by the increase in the diameter of the brachial artery during a reactive hyperemia test. The remodeling of large arteries in the examinees was found to be associated with both the average BP levels and age. There was no relationship of the gene polymorphism of endothelial NO-synthase to the daily BP profile and the remodeling of the large arteries alike. Endothelial dysfunction in t lie examinees was associated with the carriage of the mutant allele T of the gene of endothelial NO-synthase.
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Yakovleva et al. (2005) conducted an observational in Hypertensive disease and left ventricular hypertrophy (n=51). Endothelial NO-synthase gene polymorphisms (4a/4b and Glu298Asp) vs. Non-carriers / other genotypes was evaluated on Endothelial dysfunction and remodeling of large arteries. Carriage of the mutant allele T of the endothelial NO-synthase gene was associated with endothelial dysfunction, but not with daily blood pressure profile or large artery remodeling.
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