Актуальность Ишемическая болезнь сердца (ИБС) занимает лидирующую позицию среди причин смертности во всем мире. Сохраняется необходимость поиска новых эпигенетических маркеров, определяющих риск и прогноз ИБС. Цель Оценить уровень экспрессии микроРНК-21 в крови и в миокарде правого предсердия у больных ИБС, перенесших коронарное шунтирование (КШ). Материал и методы В исследование включено 98 больных ИБС, перенесших КШ, и 40 пациентов без ИБС (группа сравнения) сопоставимого возраста, перенесших операцию по поводу клапанных пороков сердца. Уровни экспрессии микроРНК-21 в крови и в миокарде предсердий оценивали с помощью полимеразной цепной реакции в реальном времени. Уровень глюкозы в крови определяли энзиматическим глюкозооксидативным методом, показатели липидного спектра сыворотки крови определяли ферментативным методом на биохимическом анализаторе «ARCHITECT 8000 C» (Россия, группа компаний “Ниармедик”). Оценку уровня инсулина сыворотки крови проводили методом иммуноферментного анализа (DRG, США). Для оценки степени резистентности к инсулину использовали малую модель гомеостаза (Homeostasis Model Assesment – HOMA) с определением показателя НОМА-ИР. Результаты Уровень экспрессии микроРНК-21 в кардиомиоцитах выше, чем в крови как у больных ИБС, так и в группе сравнения. У больных ИБС уровень экспрессии микроРНК-21 в крови, а также в миокарде выше, чем у пациентов группы сравнения. Установлено, что уровень экспрессии микроРНК-21 в крови более 3,61 УЕЭ ассоциируется с увеличением риска ИБС в 2,7 раза. Уровень экспрессии микроРНК-21 в крови ниже у больных ИБС с ИМТ≥30 кг/м2, чем при нормальной и избыточной массе тела. Аналогичные закономерности выявлены при оценке уровня экспрессии микроРНК-21 в миокарде у больных ИБС и в группе сравнения. Заключение У больных ИБС уровень экспрессии микроРНК-21 в крови и в миокарде выше, чем в группе сравнения. Уровень экспрессии микроРНК-21 в крови более 3,61 УЕЭ ассоциируется с увеличением риска ИБС в 2,7 раза.

Aim. To determine the distribution of genotypes and the allele frequency of rs2290201 and rs16909192 variants of the fatty acid binding protein 4 gene (FABP4), to compare the concentration of fatty acid binding protein 4 (FABP4) in blood serum, lipid metabolism and glucose metabolism in patients with coronary artery disease (CAD), who underwent coronary artery bypass grafting (CABG), and persons without CAD who have different genotypes of the studied gene variants. Design. A single-stage, randomized case-control study. Materials and methods. The main study group included 105 patients with CAD who had undergone CABG; the comparison group consisted of 171 people without clinical signs of CAD of comparable age (p > 0.05). All patients were measured in height, body weight, waist circumference, and body mass index was calculated. Identification of variants rs2290201 and rs16909192 of the FABP4 gene was carried out by polymerase chain reaction followed by restriction analysis. The concentration of FABP4 in blood serum was determined by enzyme immunoassay (Biovendor, Germany). The level of glucose in blood plasma was determined by the enzymatic glucose oxidative method, serum lipid spectrum parameters (total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL), non-HDL cholesterol (non-HDL), low-density lipoprotein cholesterol (LDL)) were determined by the enzymatic method on the biochemical analyzer ARCHITECT 8000 C (Russia, Niarmedic Group of companies). Serum insulin levels were assessed by enzyme immunoassay (DRG, USA). To determine the degree of insulin resistance, a small homeostasis model (HOMA) was used with the determination of the HOMA-IR index. Results. The distribution of genotypes and the occurrence of alleles of the FABP4 gene (rs2290201, rs16909192 variants) in patients with CAD who underwent CABG and in the comparison group were established. It was shown that carriage of the A allele (rs2290201 variant) of the FABP4 gene is associated with a 2.07-fold increase in the risk of CAD (odds ratio (OR) = 2.07; 95% confidence interval (CI): 1.44–3.002, p < 0.05), and the C allele (rs16909192 variant) — 1.92 times (OR = 1.92; 95% CI: 1.28–2.88, p < 0.05). Men with CAD who are carriers of the G allele (rs2290201 variant) of the FABP4 gene have a 2.44-fold increased risk of developing abdominal obesity (AO) (OR = 2.44; 95% CI: 1.2–5.0, p < 0.05). The concentration of FABP4 in serum in patients with CAD after CABG and in the comparison group did not differ (75.83 (63.44; 107.75) ng/ml and 80.22 (62.14; 141.71) ng/ml, respectively; p > 0.05). In patients with CAD who have undergone CABG, carriers of various genotypes of the FABP4 gene (variants rs2290201 and rs16909192), concentrations of FABP4, TC, LDL cholesterol, HDL cholesterol, non-HDL cholesterol, TG, glucose, insulin in blood serum, and the HOMA-IR index did not differ (p > 0.05). Conclusion. For the first time, the distribution of genotypes and the occurrence of alleles of the FABP4 gene (rs2290201 and rs16909192 variants) in patients with CAD after CABG and in the comparison group were established. It has been determined that the presence of the A allele (rs2290201 variant) and the C allele (rs16909192 variant) of the FABP4 gene is associated with an increased risk of CAD, and in men with CAD, carriage of the G allele (rs2290201 variant) of the FABP4 gene increases the risk of AO. No differences in the concentration of FABP4 in the blood were found in patients with CAD who underwent CABG and in comparison group. In patients with CAD after CABG, carriers of different genotypes of the FABP4 gene (variant rs2290201 and rs16909192), the concentration of FABP4 in the blood, glucose metabolism, and lipid metabolism did not differ. Keywords: coronary artery disease, coronary artery bypass grafting, fatty acid binding protein 4 (FABP4), fatty acid binding protein 4 gene (FABP4), rs2290201, rs16909192.

Aim. The purpose of the review is to summarize the results of studies on the relationship between the level of omentin-1 and coronary artery disease (CAD). Key points. Adipose tissue is currently considered as an endocrine organ synthesizing biologically active factors known as adipocytokines, which may be involved in the pathogenesis of obesity-related metabolic and cardiovascular diseases, in particular, CAD. Omentin-1 is an adipocytokine that is predominantly secreted by visceral adipose tissue and plays an important role in the development of chronic inflammatory diseases, including CAD. Two isoforms of omentin are known: omentin-1 and omentin-2. Omentin-1 is the main circulating form of omentin. Its blood level in healthy people, according to different authors, varies from 1.61 to 815.3 ng/ml. A number of studies have found that the concentration of omentin-1 in the blood of women is higher than that of men, which may be due to sexual dimorphism of adipose tissue. The results of the studies indicate that the levels of omentin-1 circulating in the blood are associated with various metabolic risk factors. The review describes the main molecular mechanisms that determine these effects of omentin-1. A decrease in serum omentin-1 levels can be considered as an independent predictor of CAD and correlates with the severity and prognosis of this disease. A number of studies have established an association between the carriage of various variants of the omentin-1 (ITLN1) gene, CAD and obesity. The article analyzes the available data on the role of the level of omentin-1 in CAD, determined not only in the blood, but also in subcutaneous and visceral adipose tissue. The possible prospects for the use of various molecules capable of increasing the level of omentin-1 in the blood are analyzed. Conclusion. A decrease in the level of omentin-1 may be an independent predictor of CAD and is associated with the severity and progression of the disease. It is likely that omentin-1 can act as an alternative diagnostic tool to ensure optimal management of patients with CAD. Studies of the effect of omentin-1 on the prognosis in patients with various forms of CAD are largely ambiguous and therefore further, more comprehensive studies are needed. Keywords: coronary artery disease, acute coronary syndrome, omentin-1, adipokines, subcutaneous and visceral adipose tissue, omentin-1 gene (ITLN1).

Aim. To identify the most significant factors contributing to the development of abdominal obesity (AO) in young and middle-aged residents of St. Petersburg. Design. A single-stage study conducted according to the “case — control” type. Materials and methods. We examined 966 employees of various institutions of the city of St. Petersburg who underwent a dispensary examination in 2008–2009. Of these, 503 patients (366 women and 137 men) with AO were included in the study, whose diagnosis was established according to anthropometric studies (measurements of waist circumference, WC). The comparison group consisted of 50 people (38 women and 12 men) without AO, comparable in age and gender with patients with AO. Results. 82.7% of people aged 30 to 39 years were obese, 91.3% of patients aged 40–49 years and 97.9% of participants aged 50–55 years, the prevalence of obesity increased with age (p < 0.01). Patients with AO were significantly more likely than participants in the comparison group to eat easily digestible carbohydrates (268 (53.3%) and 12 (24%), respectively, p < 0.001) and fats (248 (49.3%) and 11 (22%), respectively, p < 0.001). Among patients with AO, those who ate 1–2 times a day or, conversely, 6 or more times a day had body weight (p < 0.001) and body mass index (BMI) (p < 0.01) significantly higher than those examined who ate 4 times a day. When comparing BMI and WC in AO patients with different birth weights, it was found that AO patients whose birth weight was more than 4 kg had higher BMI and WC values. 482 (95.8 %) patients with abdominal obesity (AO) had low physical activity — less than 210 minutes weekly; 21 (4.2 %) patients with AO — at least 210 minutes weekly (р < 0.001). Almost all the examined patients without AO had higher education 49 (98%), while among patients with AO — only 297 (59%), p < 0.001. The analysis of the income level structure revealed that the income level of individuals with AO is slightly lower than in the group without AO. Conclusion. The prevalence of AO among residents of St. Petersburg aged 30–55 years is 52.1%. We have created a model based on the calculation of the logistic regression equation to assess the risk of AO development. The most significant parameters influencing its formation are highlighted: the level of education, age, type of nutrition, number of meals per day, birth weight, gender, income level, physical activity. Keywords: abdominal obesity, risk factors for the development of abdominal obesity, body mass index, waist circumference.

Актуальность. Адипонектин (АН) - протективный адипоцитокин, продуцируемый жировой тканью и циркулирующий в крови в виде различных изомеров. При абдоминальном ожирении (АО) сниженная концентрация АН ассоциируется с развитием метаболи- ческого синдрома (МС), его отдельных компонентов и различных сердечно-сосудистых заболеваний. АН кодируется геном ADIPOQ . Показано, что генетические варианты ADIPOQ ассоциированы с изменением концентрации АН сыворотки крови.Цель исследования. Выявить ассоциации полиморфных вариантов T(+45)G rs2441766 и С(-11377)G rs 266729 гена ADIPOQ с кон- центрацией АН сыворотки крови, АО и МС у женщин.Результаты. Обследованы 302 женщины с АО в возрасте от 30 до 55 лет. Группу сравнения составила 161 практически здоровая женщина без АО. У 185 обследованных с АО был диагностирован МС в соответствии с критериями Международной федерации диа- бета (IDF, 2005). Частоты генотипов и аллелей вариантов T(+45)G и С(-11377)G гена ADIPOQ у женщин с АО и без АО не различались (р>0,05). Среди женщин с АО и МС реже встречались носители аллеля G варианта T(+45)G гена ADIPOQ , чем среди женщин с АО без МС (р<0,05). Частоты генотипов и аллелей варианта С(-11377)G гена ADIPOQ у женщин с АО и МС и у пациенток с АО без МС не разли- чались (р>0,05). У женщин с АО - носителей аллеля G варианта T(+45)G гена ADIPOQ концентрация высокомолекулярного АН (ВМАН) была выше, чем у носителей генотипа TТ этого гена. При анализе частот гаплотипов вариантов T(+45)G и С(-11377)G гена ADIPOQ в обследованных группах достоверных различий не выявлено (р>0,05). Концентрации общего АН в сыворотке крови у женщин с АО и МС - носителей различных генотипов и гаплотипов вариантов T(+45)G и С(-11377)G гена ADIPOQ не различались (р>0,05). Концен- трация ВМАН у женщин с АО - носителей гаплотипа TGC(X) (Х - аллель С или G варианта С(-11377)G ) была выше, чем у женщин с АО - носителей других гаплотипов гена ADIPOQ (р<0,05).Выводы. Носительство аллеля G варианта T(+45)G гена ADIPOQ является протективным в отношении МС у женщин с АО. У женщин с АО - носителей аллеля G концентрация ВМАН выше, чем у женщин с АО - носителей TT генотипа варианта T(+45)G гена ADIPOQ . Background. Adiponectin (AN) - a protective adipocytokine, produced by fat tissue and circulating in the form of various isomers in the blood. With obesity, a decreased level of AN is associated with the development of metabolic syndrome (MS) and various cardiovascular diseases. Regulation of its level can be caused by genetic factors, including single nucleotide polymorphism T(+45)G and C(-11377)G of the ADIPOQ gene. Allelic variants of the ADIPOQ gene was associated with AN concentrarion in blood.Objective. To identify the association of genetic variants of ADIPOQ with adiponectin level, AO and MS in women.Results. A total of 302 women with abdominal obesity (AO) aged 30-55 years were examined. The comparison group consisted of 161 practically healthy women without AO. 185 patients with AO had MS according to the criteria of the International Diabetes Federation (IDF, 2005). The frequencies of genotypes and alleles of variants T (+45) G and C (-11377) G of the ADIPOQ gene among women with and without AO did not differ (p> 0,05). Among women with AO and MS, carriers of G allele variant T (+45) G of the ADIPOQ gene were less common than among women with AO without MS (р<0,05). The frequencies of genotypes and alleles of variant C (-11377) G of the ADIPOQ gene did not differ in women with AO and MS and in patients with AO without MS (p> 0.05). In women with AO - carriers of the G allele variant T (+45) G of the ADIPOQ gene, the concentration of high molecular weight AN (HMWA) was higher than that of the TT carriers of the genotype of this gene The haplotypes of the T (+45) G and C (-11377) G variants of the ADIPOQ gene did not differ in the studied groups (p> 0,05). The con- centration of total AN in the serum of women with AO and MS - carriers of different genotypes and haplotypes of variants T (+45) G and C (-11377) G of the ADIPOQ gene did not differ (p> 0,05). The concentration of HMWA in women with AO - carriers of the TGC(X) haplotype (X - allele C or G variant C (-11377) G) was higher than in women with AO - carriers of other haplotypes of the ADIPOQ gene (p <0,05). Coclusions. G allele of the T(+45)G variant the ADIPOQ gene is protective against MS in women with AO. In women with AO - carriers of the G allele, the concentration of HMWA is higher than in women with AO - carriers of the TT genotype of variant T(+45)G of the ADIPOQ gene.

Background. Omentin-1 (QM-1) — one of the most important anti-inflammatory adipocytokines produced by adipose tissue. It is known that its concentration is reduced in obese patients. However, the role of OM-\ in the pathogenesis of coronary heart disease (CHD), including acute coronary syndrome (ACS), is not fully determined. T he objective of the study — to assess the level of OM-1 in blood serum of patients with ACS without ST-segment elevation (ACSWEST) who underwent percutaneous coronary intervention (PCI) and patients with stable CHD. Design and methods. Examined 104 patients with ACSWEST undergoing PCI. Comparison groups consisted of 38 patients without CHD according negative results of stress-echocardiography or coronary angiography, as well as 80 patients with stable CHD. All patients were evaluated anthropometric indicators: height, weight, waist circumference (WC), body mass index (BMI). Serum concentrations of OM-I were determined by enzyme immunoassay (DRG,USA), serum lipid profile was determined by enzymatic method. Results. In patients with ACSWEST who underwent PCI, the concentration of OM-I in the blood is lower than in those examined without atherosclerotic lesions of the coronary arteries [7.53 (5.00-10.55) ng/ml and 12.56 (7.84-15.34) ng/ml, respectively; p 0.05). In patients with ACSWEST, the concentration of OM-1 blood with multivascular lesions of the coronary arteries is lower than with 1-2 vascular lesions [7.30 (3.91- 8.17) ng/ml and 9.44 (6.54-9.93) ng/ml, respectively; p < 0.001. Similar patterns were established in patients with a stable CHD (p < 0.001). The concentration of OM-1 inthe blood in women with ACSWEST, with stable CHD and in those examined without CHD was higher than in men of the corresponding groups (p < 0.001). In patients with ACSWEST and with a stable CHD with overweight and obesity (WHO, 1999), the concentration of OM-1 inblood serum is lower than in patients with CHD and normal BMI (p < 0.001). In patients with ACSWEST and AO, the level of OM-1 inthe blood is lower than in patients with ACSWEST without AO, both in men and women (p < 0.001). When conducting a regression analysis, it was found that the concentration of OM-1 inthe blood of patients with ACSWEST is determined by BMI (b = -0.30, beta = -0.23, p = 0.002) and patient gender (b = 2.21, beta = 0.16, p = 0.029); in patients with a stable CHD — BMI (b = -0.38, beta = -0.27, p = 0.029). Conclusion. For patients with CHD, both with ACSWEST and with stable CHD, a low level of OM-1 in the blood is characteristic. The lowest OM-1 values were found in patients with multivascular coronary artery disease and obesity. The gender characteristics of the concentration of OM-1 in serum were established: the concentration of OM-1 in serum in women is higher than in men. A decrease in the concentration of OM-1 in the blood in patients with ACSWEST and with stable CHD is associated with BMI, the patient’s gender, and the severity of coronary atherosclerosis.

Background. Omentin-1 (QM-1) — one of the most important anti-inflammatory adipocytokines produced by adipose tissue. It is known that its concentration is reduced in obese patients. However, the role of OM-\ in the pathogenesis of coronary heart disease (CHD), including acute coronary syndrome (ACS), is not fully determined.The objective of the study — to assess the level of OM-1 in blood serum of patients with ACS without ST-segment elevation (ACSWEST) who underwent percutaneous coronary intervention (PCI) and patients with stable CHD.Design and methods. Examined 104 patients with ACSWEST undergoing PCI. Comparison groups consisted of 38 patients without CHD according negative results of stress-echocardiography or coronary angiography, as well as 80 patients with stable CHD. All patients were evaluated anthropometric indicators: height, weight, waist circumference (WC), body mass index (BMI). Serum concentrations of OM-I were determined by enzyme immunoassay (DRG,USA), serum lipid profile was determined by enzymatic method.Results. In patients with ACSWEST who underwent PCI, the concentration of OM-I in the blood is lower than in those examined without atherosclerotic lesions of the coronary arteries [7.53 (5.00-10.55) ng/ml and 12.56 (7.84-15.34) ng/ml, respectively; p < 0.001). The concentration of OM-1 in the blood in patients with ACSWEST and a stable CHD did not differ (p > 0.05). In patients with ACSWEST, the concentration of OM-1 blood with multivascular lesions of the coronary arteries is lower than with 1-2 vascular lesions [7.30 (3.91- 8.17) ng/ml and 9.44 (6.54-9.93) ng/ml, respectively; p < 0.001. Similar patterns were established in patients with a stable CHD (p < 0.001).The concentration of OM-1 inthe blood in women with ACSWEST, with stable CHD and in those examined without CHD was higher than in men of the corresponding groups (p < 0.001).In patients with ACSWEST and with a stable CHD with overweight and obesity (WHO, 1999), the concentration of OM-1 inblood serum is lower than in patients with CHD and normal BMI (p < 0.001). In patients with ACSWEST and AO, the level of OM-1 inthe blood is lower than in patients with ACSWEST without AO, both in men and women (p < 0.001). When conducting a regression analysis, it was found that the concentration of OM-1 inthe blood of patients with ACSWEST is determined by BMI (b = -0.30, beta = -0.23, p = 0.002) and patient gender (b = 2.21, beta = 0.16, p = 0.029); in patients with a stable CHD — BMI (b = -0.38, beta = -0.27, p = 0.029).Conclusion. For patients with CHD, both with ACSWEST and with stable CHD, a low level of OM-1 in the blood is characteristic. The lowest OM-1 values were found in patients with multivascular coronary artery disease and obesity. The gender characteristics of the concentration of OM-1 in serum were established: the concentration of OM-1 in serum in women is higher than in men. A decrease in the concentration of OM-1 in the blood in patients with ACSWEST and with stable CHD is associated with BMI, the patient’s gender, and the severity of coronary atherosclerosis.

Objective. To assess the expression of the leptin gene (LEP) in the epicardial (EAT) and subcutaneous (SAT) adipose tissue in coronary artery disease (CAD) patients. Methods . 107 people were examined: 87 with CAD (57 men, 30 women), 20 without CAD (10 men, 10 women). Biopsy of EAT, SAT, coronary angiography, heart computed tomography, blood leptin levels were estimate, mRNA expression of the LEP gene evaluated by PCR. Results. In CAD patients with multivessel coronary artery lesion, the level of blood leptin is the highest. The expression of the LEP gene in EAT is higher in men than in women, in men with CAD higher than in non-coronary artery disease patients, and with a multivascular coronary lesion higher than in a 1–2 vascular lesion. Expression of the LEP gene in EAT in women with CAD is higher than with no CAD, and does not depend on the severity of coronary atherosclerosis. In SAT, LEP gene expression in men with CAD is higher than without CAD; women with CAD are lower than without CAD. Expression of the LEP gene in SAT is higher in men with a multivascular lesion than in 1–2 vascular lesion, and lower in women with a multivascular damage. Conclusions . The expression of the leptin gene in women is higher in SAT, and in men in EAT. Expression of the leptin gene in EAT with CAD is higher than without CAD. The expression of the leptin gene in SAT in men with CAD, especially with multivessel lesions, is higher than without coronary artery disease.

Coronary artery disease (CAD) is a multifactorial disorder. Previously have been identified genes whose polymorphic variants are associated with an increased risk of CAD. Genetic control of the development of CAD at the post-transcriptional level is carried out using step-wise and multicomponent regulation of gene expression with the participation of specific molecules called micro-ribonucleic acids (miRNAs). Currently, many authors consider these molecules, in particular miRNA-27a, as potential sensitive diagnostic markers for acute coronary syndrome (ACS).Aim. To assess the level of miRNA-27a expression in the serum of patients underwent percutaneous coronary intervention (PCI) after non-ST elevation ACS.Material and methods. Forty patients with non-ST elevation ACS who underwent coronary artery stenting were examined. The comparison groups consisted of 80 patients with a stable CAD who underwent coronary artery bypass surgery, and 20 patients without clinical signs of CAD operated due to valvular disorders without atherosclerotic lesions. All patients underwent coronary angiography. The expression level of miRNA-27a was determined in serum by real-time polymerase chain reaction.Results. In patients with non-ST elevation ACS, who underwent PCI, the expression level of miRNA-27a in serum was higher than in patients without atherosclerotic lesions (6,99±1,69 and 3,05±0,89, respectively; p<0,05). Moreover, patients with multivessel coronary lesions (3 or more arteries) had a higher level of miRNA-27a expression in serum than patients with a single or dual vascular lesion (8,00±2,19 and 5,87±2,64, respectively; p<0,05). In patients with non-ST elevation ACS and patients with a stable CAD, the expression level of miRNA-27a was not significantly different (6,99±1,69 and 8,57±3,90, respectively; p>0,05).Conclusion. High levels of miRNA-27a expression can be considered as a marker of coronary lesion severity in patients with CAD, but not as a marker for ACS.

Objective.To assess the expression of the leptin gene (LEP) in the epicardial (EAT) and subcutaneous (SAT) adipose tissue in coronary artery disease (CAD) patients.Methods. 107 people were examined: 87 with CAD (57 men, 30 women), 20 without CAD (10 men, 10 women). Biopsy of EAT, SAT, coronary angiography, heart computed tomography, blood leptin levels were estimate, mRNA expression of the LEP gene evaluated by PCR.Results.In CAD patients with multivessel coronary artery lesion, the level of blood leptin is the highest. The expression of the LEP gene in EAT is higher in men than in women, in men with CAD higher than in non-coronary artery disease patients, and with a multivascular coronary lesion higher than in a 1–2 vascular lesion. Expression of the LEP gene in EAT in women with CAD is higher than with no CAD, and does not depend on the severity of coronary atherosclerosis. In SAT, LEP gene expression in men with CAD is higher than without CAD; women with CAD are lower than without CAD. Expression of the LEP gene in SAT is higher in men with a multivascular lesion than in 1–2 vascular lesion, and lower in women with a multivascular damage.Conclusions. The expression of the leptin gene in women is higher in SAT, and in men in EAT. Expression of the leptin gene in EAT with CAD is higher than without CAD. The expression of the leptin gene in SAT in men with CAD, especially with multivessel lesions, is higher than without coronary artery disease.

Objective: to investigate influence of different forms of adiponectin on carotid intima-media thickness (CIMT) in women with abdominal obesity (AO) in St-Petersburg. It has been recognized before that AO is associated with cardiovascular diseases, including atherosclerosis, but mechanism of this association remains unclear. AO leads to imbalance of adipokines, in particularly decrease of adiponectin, which may lead to atherosclerotic lesion of carotid arteries. Materials and methods. We investigated 81 women with AO (IDF criteria, 2005) and 21 women with normal waist circumference. CIMT was evaluated by an ultrasound scanner. Results. Among patients with AO 54.9% had CIMT >0.9 mm and 38.5% had atherosclerotic plaques in common carotid arteries. The total adiponectin level (TA) was lower in women with CIMT> 0.9 mm, than in women with normal CIMT (23.20 [2.55; 40.65] and 18.09 [1.60; 38.92] mu g/ml, respectively; p<0.05). Level of high molecular weight adiponectin (HMWA) was lower in women with CIMT >0.9 mm, than in women with normal CIMT (2.21 [0.50; 6.85] and 2.88 [1.29; 15.45] mu g/ml, respectively; p<0.01). Level of HMWA but not of TA was more in women with CIMT >0.9 mm, than in women with CIMT >0.9 mm and atherosclerotic plaques in carotid arteries (3.09 [1.34; 6.85] and1.82 [0.50; 2.94] mcg/ml, respectively; p<0.05). According to logistic regression analysis CIMT >0.9 mm depended on waist circumference, diastolic blood pressure and level of C-reactive protein (CRP), while presence of atherosclerotic plaques was associated with levels of HMWA and CRP. Conclusions. Factors that make the greatest contribution at early stages of atherosclerosis development in carotid arteries in women with AO can be increased waist circumference, high diastolic blood pressure, and high level of CRP. At later stages of atherosclerosis development lowered HMWA level can contribute to the formation of atherosclerotic plaques.

Objective . Evaluate leptin gene expression in epicardial adipose tissue in males with coronary heart disease (CHD). Design and methods. We enrolled 106 males: 57 males with CHD aged 61,3 ± 1,1 years old and 49 males without CHD aged 57,3 ± 1,3 years old (p > 0,05). Epicardial adipose tissue (EAT) specimens were obtained in 65 males (57 males with CHD and 8 males with valvular heart disease without CHD) undergoing cardiac surgery. Serum leptin was measured by immune enzyme assay (IEA). Leptin mRNA (messenger ribonucleic acid) level in EAT was assessed by real-time polymerase chain reaction. All patients underwent coronaroangiography and echocardiography. Results. Leptin mRNA level in EAT was significantly higher in males with CHD and atherosclerosis of main coronary arteries. Patients with multivessel (3 and more coronary arteries) atherosclerotic lesions showed higher leptin mRNA level in EAT than in subjects with lesions of 1–2 coronary artery and in patients without CHD: 2,84 ± 0,04 (RU), 1,91 ± 0,03 RU and 1,41 ± 0,02 RU, respectively (р < 0,05). Conclusions . Paracrine activity of epicardial adipose tissue plays a role in the pathogenesis of coronary atherosclerotic lesions in males

Objective. The activity of renin-angiotensin-aldosterone system (RAAS) is increased in patients with ab-dominal obesity (AO). However, till present time it is unclear whether RAAS activation or hypertension (HTN) found in 50 % patients is the primary disorder.Design and methods. We have studied plasma renin activity (PRA), plasma aldosterone concentration (PAC), their ratio PAC/PRA in patients with AO and related HTN and in subjects without AO.Results. PRA was higher in patients with AO versus people without obesity (2,5 ± 0,2 and 1,7 ± 0,7 ng/ml/hr, p = 0,013), there was a tendency to the reduction of the ratio PAC/PRA in obese patients (14,6 ± 0,9 and 19,7 ± 3,3, p = 0,08). In the subgroup of patients with AO and HTN the PRA was higher, and the ratio PAC/PRA was lower than in obese patients without HTN (PRA: 3,3 ± 0,4 and 1,7±0,2 ng/ml/hr, p = 0,005; PAC/PRA: 11,4 ± 1,1 and 17,4 ± 1,4, p < 0,0001). PRA and systolic blood pressure positively correlated. In patients with morbid obesity (3 degree according to the WHO classiication) obesity may play a signiicant role in the increase of RAAS activity, especially in the absence of concomitant HTN. The ratio PAC/PRA in over weight patients with AO was higher than in patients with AO and body mass index ? 30,0 kg/m (17,2 ± 1,7 and 12,5 ± 1,0 kg/m, p = 0,04). PRA was higher only in patients with AO and co-existing hypertension (3,4 ± 0,7 and 1,1 ± 0,2 ng/ml/hr, p = 0,04).Conclusions. RAAS activity is increased in patients with AO, also due to the co-existing HTN. However, in the absence of elevated blood pressure obesity per se may play a signiicant role in RAAS hyperactivity.