КЛИНИКО-ГЕНЕТИЧЕСКИЕ АСПЕКТЫ РЕГРЕССА ГИПЕРТРОФИИ МИОКАРДА ЛЕВОГО ЖЕЛУДОЧКА. РЕЗУЛЬТАТЫ ПРОСПЕКТИВНОГО ИССЛЕДОВАНИЯ В ГОРНОЙ ШОРИИ

Abstract

Abstract. Introduction. Left ventricular hypertrophy is an independent predictor of adverse outcomes in patients with arterial hypertension. Aim. To evaluate clinical and genetic factors, as well as the effectiveness of antihypertensive drugs classes in terms of regression of left ventricular hypertrophy in the indigenous population of Mountain Shoria within 5-year prospective observations. Material and methods. The study was based on the results of a 5-year observation of the indigenous population of Mountain Shoria. The study included 901 people aged 18 and over. At the one-stage stage (from 2013 to 2017), an anamnesis and complaints were collected, a clinical examination by a cardiologist, anthropometry, a biochemical blood test was performed, and genetic testing of polymorphisms of arterial hypertension candidate genes (ACE (I/D, rs 4340), AGT (c.803T>C, rs699), AGTR1 (А1166С, rs5186), ADRB1 (с.145A>G, Ser49Gly, rs1801252), ADRA2B (I/D, rs28365031), MTHFR (С677Т, rs1801133), eNOS (VNTR 4b/4a)), performed electrocardiography, echocardiography. The prospective stage included 263 patients with hypertension without previous antihypertensive therapy. Blood pressure figures were monitored and corrected annually, and left ventricular hypertrophy dynamics was assessed 5 years after inclusion in the study. Statistical processing of the results of the study was carried out using the program "Statistica 10.0". Results and discussion. In the Shors cohort, left ventricular hypertrophy regression was associated with a lower degree of arterial hypertension (odds ratio 1.39) and with the achievement of target blood pressure levels (odds ratio 1.71), as well as with the addition of a diuretic, indapamide retard, to renin-angiotensin-aldosterone system blockers (odds ratio 2.65). In the present study, an association was found between carriage of the D/D genotype of the ACE gene (odds ratio 0.43) and 4a/4a of the eNOS gene (odds ratio 0.35) with negative dynamics in relation to myocardial mass of the left ventricle. With respect to genotype I/I of the ADRA2B gene (odds ratio 2.00) and 4b/4b of the eNOS gene (odds ratio 2.93), an associative relationship with regression of left ventricular hypertrophy was demonstrated. Conclusion. The results obtained once again prove the promise of using genetic approaches for the early diagnosis of left ventricular hypertrophy.