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Objective. To study the dose-dependent effect of simvastatin on the change of content of individual fatty acids (FA) profile of blood serum and their complexes with secondary prevention of chronic coronary heart disease (CHD) in groups of men and women.Materials and methods. Gas-liquid chromatography-mass spectrometry was used to establish the absolute and relative levels of FA in serum of 155 CHD patients before and after treatment by simvastatin in doses of 40 mg (89 people) and 80 mg (36 people).Results. The statin lowered the content of the FA proportionally by reducing the unsaturated (UFA), mainly polyunsaturated (PUFA) FA, and saturated (SFA) FA. The level of monounsaturated fatty acids (MUFA) decreased in women at a dose of 40 mg. The statin increased endogenous formation of ω6 PUFA, ω9 MUFA, and SFA even (except 80 mg), in group of women (40 mg) – ω3 PUFA, and in men (80 mg) – ω7 MUFA. In women after receiving simvastatin 80 mg, the ratio ω3/ω6 PUFA has been shifted to ω6 PUFA, but in men after receiving simvastatin 40 mg in the direction of ω3 PUFA. Only the dose of 80 mg shifted the ratio of C20:5/C20:4 in the direction of ω3 PUFA. In group of women after receiving simvastatin 40 mg was observed a shift to β-oxidation of C18:1(9), and in men at the dose of 80 mg in the direction of its synthesis. In all cases, increased antioxidant protection of PUFA, but less strong it was at the dose of 40 mg. At the same time the formation of MUFA prevailed over the synthesis of SFA. Absolute content of FA - substrates of energy decreased. In all cases, was noticed the decrease of content of FA this very long chain (C22-26), stronger in women.Conclusion. Simvastatin controlling the quantitative composition of the pool of circulating lipoproteins, FA and cholesterol, is ambiguous, depending on dose, affect the metabolism of fatty acids, changing their quantitative and qualitative composition and performing biological functions.

Aim. To assess genetic issues in the ischemic stroke development in AF and to invent an analytical programmed complex for genetic risk estimation of stroke development in a patient with AF.Material and methods. Totally 43 patients studied with AF and stroke in anamnesis, 78 — with AF and no stroke. Controls consisted of 188 persons without cardiovascular pathology. The participants underwent ECG, EchoCG, Holter ECG-monitoring, exercise test, TELAS, thyroid gland hormones analysis. For confirmation of the ischemic nature of stroke in participating probands we performed computed tomography of the brain. All participants also underwent molecular genetic testing.Results. According to the odds ratio, allele A polymorphism -455G>A of gene FGB increases the risk of ischemic stroke development in atrial fibrillation 1,7 times comparing to those patients without the allele; genotypes with the rare T allele in homoand heterozygous state of polymorphism 807С>Т of gene GPI? increases 2,5 times the risk of stroke in AF; presence of allele C polymorphism -5Т>С of gene GPI?? increases 1,9 times the risk of stroke comparing to its absence; presence of the rare genotypes allele C in homoand heterozygous state -5Т>С of gene GPI?? increases 2,3 times stroke risk; allele A of the polymorphism 10976G>A gene FVII decreases the risk of stroke 2,6 times. According to the results, there was a “Clinical-genetic riskometer of the ischemic stroke in AF” developed. Using this informational-analytic complex it is possible to estimate genetic risk of the stroke.Conclusion. Therefore, the study has shown that homozygous genotype AA of the rare polymorphism 455G>A gene FGB, heterozygous genotype СТ and homozygous genotype ТТ of the rare polymorphism allele 807С>Т gene GPI?, heterozygous genotype TC and homozygous genotype CC by the rare allele polymorphism -5Т>С gene GPI?? are defined as genetic predictors of ischemic stroke development in atrial fibrillation. Allele А of polymorphism 10976G>A gene FVII is protective against ischemic stroke in patients with AF. Knowing the parameters of genetic assessment in AF, it is possible to calculate genetic risk of ischemic stroke development in AF via invented by us a “Clinical-Genetic riskometer of ischemic stroke in AF”.

Aim. To reveal genetic predictors of the ischemic stroke in patients with AF. Material and methods. Totally 121 patient studied with AF and 155 their relatives of I-III grade of relation. First group consisted of 43 probands with AF and stroke anamesis and 54 their relatives, the second group – 78 probands with AF without stroke and 101 their relative. Control group consists of 188 subjects. The patients underwent ECG, EchoCG, Holter ECG-monitoring, VEM, TELAS, molecular-genetic investigation.Results. Genotype AA of polymorphism -455 G>A of gene FGB statistically significantly predominated in subjects with AF and stroke comparing to those with AF without stroke (20,94% vs 6,4%; p=0,036). Risk relation shows that the chance of stroke development with AA homozygous genotype at rare allele is 3,9 times higher than in its absence. Overall the genotypes CT and TT by the rare allele 807C>T gene ITGA2 statistically significantly predominated in the patients with AF and stroke comparing to controls (76,7% vs 56,9%, p=0,026). The chance of stroke development while carrying CT and TT by the rare allele is 2,5 times higher than in their absence. Genotypes TC and CC by the rare polymorphism 5 T>C gene GPIBA statistically more significantly were found in patients with AF and credibly increasesthe chance for stroke 2,3 times. Allele A of polymorphism 10796 G>A gene F7 statistically more significant rarer found in patients with AF and stroke comparing to controls (6,98% vs 16,22%; p=0,043). Chance of stroke in absence of allele A is 2,6 times higher, than in its presence.Conclusion. The study revealed that homozygous genotype AA by the rare polymorphism -455G>A gene FBG, heterozygous CT and homozygous TT by the rare allele 807C>T gene ITGA2, heterozygous TC anf homozygous CC by the rare – 5 T>C gene GPIAB are set as genetic predictors for ischemic stroke development in AF. Allele A of the polymorphism 10976 G>A gene F7 show protective effect in the ischemic stroke development in AF. Genetic risk estimation might improve the primary ischemic stroke prevention in AF.

The accumulation of triacylglycerol in peripheral tissues is one of mechanisms of insulin resistance. This paper presents the investigation of the influence of aerobic and anaerobic physical exercises on triacylglycerol level in skeletal muscles and on insulin resistance in dietary-induced obese rats. It is estimated that a high-energy (HE) diet causes the accumulation of triacylglycerols in skeletal muscles that leads to high resistance to insulin. Aerobic and anaerobic physical exercises reduce the level of triacylglycerols in skeletal muscles and raise sensitivity to insulin in obese rats. Physical exercises raise the level of triacylglycerols in skeletal muscles in standard-diet rats that probably is the adaptation to high energy expenditure, but does not lead to high insulin resistance.

The research of unsaturated and saturated of fatty acids (UFAand SFA) in the erythrocytes in men and women with chronic ischemic heart disease was done by the method of a gas-liquid chromatography-mass spectrometry before and after simvastatin intake. Increase in the ratio of ω3 / ω6 FA at the expence of reducing of the rate of ω6 UFAwas revealed in men after treatment for 2 months which is the condition for the changing of type of synthesized eicosanoids. The decrease in the total content of ω6 and ω9 UFAled to the fall in the amount of the UFAin both sexes, despite of the heightened rate of amount of ω7 UFAin women. The treatment led to the increasing of saturated FA amount (SFA) and it led to the decrease of unsaturation index FA on the back of the reduction of nonsaturated fatty acids level (NFA). The results confirm the presence of lipid-lowering effect of Simvastatin, but there is a need for therapy, taking into account of the normalization of the exchange FA in patients with chronic coronary ischemic heart disease.

The intake of Simvastatin in a dosage of 40 mg daily within two months in patients with ischemia heart disease has caused increase in the general percentage of ω6 fat acids (FA) at a constant level of ω3 FA, that was not accompanied by change of a ratio ω3/ω6 FA. Despite of progressing increase in total concentration of ω7 FA (at women) and increase of a level ω9 FA (at men) during simvastatin treatment at women and at men led to decrease in the total percentage of nonsaturated fat acids concerning corresponding parameters at healthy donors. The Simvastatin treatment was accompanied by increase in blood plasma in patients with ischemia heart disease (and first of all at women) percentage of the separate saturated fat acids, and also their total level. The index of nonsaturation of fat acids of blood plasma is decreased.

In men and women suffering from stable angina pectoris of 1-2 functional classes and aged from 35 to 69 years old, decrease of C 23:0 and increase of C 18:1(11) fatty acids was observed regardless of sex, the content of the rest fatty acids changed depending on patients sex. Correlation was found that metabolism of fatty acids in this pathology group depends on patients sex: men in the control group showed decrease in the sum of omega-3 fatty acids as well as in the omega-3/omega-6 fatty acid ratio, while women showed decrease of omega-6 fatty acids at the constant sum of omega-3 fatty acids. Regardless of sex, the presence of this pathology is accompanied with decrease in correlations between fatty acids, as the number of correlations between saturated fatty acids increases and the number of correlations between not saturated and saturated fatty aсids decreases. Change in correlations between not saturated fatty acids depends on sex. In the number of patients having supernormal fatty acid contents, no pronounced differences were found between men and women.

Aim. To assess the associations between the polymorphism of the glycoprotein integrin alpha (I