Russian Heart Failure Journal 2008year Interleukin 1β and interleukin-1 receptor antagonist gene polymorphisms in patients with chronic heart failure


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2008/

Interleukin 1β and interleukin-1 receptor antagonist gene polymorphisms in patients with chronic heart failure

Mayanskaya S.D., Yakovleva N.F., Yakovlev A.V., Filipenko M.L., Voronina E.N., Berezikova E.N., Shilov S.N., Zakharova T.I., Mayer S.V.

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Urgency. IHD and AH are the most common causes for development of CHF. Despite substantial progress in the treatment of these conditions, prediction in CHF remains extremely serious, which continuously warrants their timely prevention and early detection. Aim. To study effects of IL-1β and IL-1Pa gene polymorphic variants on endothelial function and risk for development and severity of CHF in patients with IHD and AH. Materials and methods. 165 patients with CHF (121 men and 44 women; mean age 56.7 ± 5.3 years) were evaluated. Vasomotor endothelial function was evaluated using the ultrasound method in the reactive hyperemia and trinitroglycerol tests. Genotypes were identified using RFLP analysis of PCR products. Control group included 114 patients (54 men and 60 women; mean age 53.2±4.9 years). Results. It was shown that C allele of the IL-1β gene C+3953T polymorphic locus was associated with a risk for development, severity and unfavorable course of CHF in patients with IHD and AH whereas T allele of the IL-1β gene C+3953T polymorphic locus alleviated the risk for development of this pathology and was associated with a favorable course of CHF. However these associations were not found in female patients. In addition patients with homozygous C allele of the IL-1β gene C+3953T polymorphic locus had much more pronounced disorders of vasomotor endothelial function and LV systolic function than patients with allele 3953Т. The study did not reveal any associations between IL-1Pa gene polymorphic variants (VNTR intron 2) and risk for development and severity of CHF or endothelial dysfunction in patients with IHD and AH.
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