[The role of ADRB1 genes polymorphism in examined patients with chronic rheumatic heart disease]

The study purpose is to evaluate effect of ADRB1 gene polymorphism on echocardiography indices and endothelial function in patients with chronic rheumatic heart disease. The sampling consisted of 128 patients with chronic rheumatic heart disease. The echocardiography was performed on Philips Affinity 50 device and evaluation of endothelial function was implemented on "AngioScan01" device. The genetic typing was carried out according polymorphic markers Gly49Ser and Gly389Arg. The nucleotide replacement of glycine with serine resulted in increasing of left sections of heart both at Ser49Ser (left atrium 5.65±0.09 cm; LVED 5.61±0.27 cm; LVES 3.76±0.16 cm), and Gly49Ser (left atrium 5.65±0.09 cm; LVED 5.61±0.27 cm; LVES 3.76±0.16 cm), The similar situation occurred when glycine was replaced with arginine: for Arg389Arg homozygotes (left atrium 5.63±0.12 cm; LVED 5.97±0.20 cm; LVES 3.97±0.16 cm); and heterozygotes Gly389Arg (LVED 5.60±0.08 cm; LVES 3.78±0.07 cm). Homozygosity of Ser49Ser in endothelial function led to low values of index augmentation (5.83±0.80%) and indicators reflecting function of small resistive arteries were the worst (1.30±0.07). Arg389Arg homozygotes had the worst endothelial function in system of large arteries (-20.40±0.68 ms). highest severity of arterial stiffness (23.00±0.68%) as compared with Gly389Gly homozygotes (8.92±0.99% and 62.67±1.41 years). ADRB1 gene polymorphism in subjects with HRBS leads to dilatation of left heart. The effect on endothelial dysfunction is multidirectional: Ser49Ser homozygosity leads to minimal arterial stiffness and changes in small resistive arteries; homozygosity of Arg389Arg leads to maximum changes in large conducting arteries and the highest rates of vascular stiffness.