The renin-angiotensin-aldosterone system (RAAS) is involved in the pathogenesis of Coronary Heart Disease and myocardial infarction. The crucial component of the RAAS is angiotensin II and its effects are carried out by angiotensin II receptors 1st type (AT1R). Aim of the study: determine the incidence of the mutant allele of the AT1R gene, estimate possible correlations between AT1R gene polymorphism and the extension of endothelial dysfunction in patients who have suffered MI in the age under 45. Materials and methods: 122 men suffering myocardial infarction under the age of 45 have been examined. In all patients we measured a relative increase of brachial artery diameter during the test with reactive hyperemia, the number of circulating endotheliocytes. Identification of A1166C polymorphism of the AT1R gene was carried out by means of polymerase chain reaction (PCR). Results: in patients with a history of myocardial infarction in the age under 45 we have found evidence of endothelial dysfunction: increased circulating endotheliocytes, decreased endothelium-mediated vasodilation. Among patients with a vasoconstrictive reaction the incidence of the C allele of the AT1R gene was higher than in patients exhibitng a vasodilative response during a test with reactive hyperemia (P<0.007). The incidence of the mutant allele of the AT1R gene was reliably lower in coronary patients with arterial hypertension than in those without hypertension.

Aim. To evaluate effects of long-term treatment with rilmenidine compared with atenolol on lipid and glucose metabolism and cardiovascular remodeling in hypertension. Material and methods. 37 patients with hypertension were randomized to rilmenidine 1-2 mg/day or atenolol 50-100 mg/day for 26 weeks. Standard oral glucose tolerance test with a parallel measurement of insulin and glucose levels was performed. The areas under the curve (AUC) for insulin and glucose were calculated. Plasma lipids, left ventricular mass index (LVMI) and intima-media thickness (IMT) were measured. Brachial artery diameter during reactive hyperemia was used to test endothelium-dependent vasodilatation (EDVD). Results. Blood pressure reduction was equally achieved in both treatment arms. The fasting glucose level increased in the atenolol group from 4.8±0.6 to 5.2±0.7 mmol/l (p

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.

AIM:To study myocardial remodeling (MR) in hypertensive patients with normal and excessive body mass, to analyse MR features depending on clinical and hemodynamic parameters.MATERIAL AND METHODS:Structural-functional conditions of the myocardium were studied with echocardiography, and determination of left ventricular remodeling (LVR) type was made in 734 untreated hypertensive patients aged 19-76 years.RESULTS:Patients with essential hypertension (EH) stage I had mostly excentric left ventricular hypertrophy (LVH). The number of patients with concentric LVH increases with age, disease severity. This type of LVH occurs more frequently in males than in females. In females, LVH severity depends, primarily, on the degree of obesity. If EH combines with obesity, structural alterations of the myocardium are more prominent than in isolated pathology. In android obesity, LVH is more frequent.CONCLUSION:In EH, structural alterations of the heart and a LVR variant are determined, besides arterial pressure, by such factors as age and gender, duration of EH, obesity, its degree and kind.

To examine the effects of eprosartan on the remodelling of the heart and large vessels, on endothelial dysfunction and autonomic circulatory regulation in patients with hypertensive disease, thirteen patients were included into the study: Doppler echocardiographic study and evaluation of left ventricular diastolic function were performed on a Vingmed CFM800 apparatus: the thickness of the carotid intima-media complex and the diameter of the brachial artery were determined on the same apparatus using a 7.5-MHz transducer in the reactive hyperemia test. Automatic balance was evaluated by the spectral assay of cardiac rhythm variations. The cardiopulmonary component of baroreflex was also tested. Blood pressure normalized in 3 patients following 24 weeks of therapy with eprosartan in a daily dose of 600 mg. Two patients were excluded due to therapeutic inefficiency. In the remaining patients, the antihypertensive effect was incomplete. The mass of the left myocardial myocardium decreased by 10.8%. there was an increase in brachial arterial dilatation in the reactive hyperemia test. The variations of cardiac rhythm were not significantly changed, the baroreflex tended to be decreased. Thus, long-term eprosartan therapy improves the structural and functional state of the heart and vessels and fails to affect the autonomic regulation of circulation.