Cardiometabolic Effects of Empagliflozin in Patients Undergoing Elective Percu-taneous Coronary Intervention for Type 2 Diabetes Mellitus.

Aim      To evaluate cardiometabolic effects of empagliflozin in patients with ischemic heart disease and type 2 diabetes mellitus (DM) following elective percutaneous coronary intervention (PCI).Materials and methods Patients meeting the inclusion/non-inclusion criteria were randomized into two groups of equal number using simple randomization with successively assigned numbers. Group 1 included 37 patients (18 men and 19 women) who gave their consent for the treatment with empagliflozin 10 mg/day in addition to their previous hypoglycemic therapy. The drug administration started one month prior to the elective PCI and continued for the next 11 months (treatment duration, 12 months). Group 2 (comparison group) consisted of age- and DM duration-matched patients (37 patients; 18 men and 19 women) who continued on their hypoglycemic therapy previously prescribed by endocrinologists during the entire study period. Before the study, 36.11 % patients of the empagliflozin group and 27.03 % of the comparison group had unsatisfactory glycemic control as shown by the level of glycated hemoglobin (HbA1c).Results At 6 and 12 months of the study, fasting glycemia and HbA1c were significantly lower in the empagliflozin treatment group. The groups were comparable by the incidence of adverse outcomes: 8 (22.24 %) patients in the empagliflozin group and 10 (27.04 %) patients in the comparison group (р=0.787). The 12-month empagliflozin treatment reduced total cholesterol (C) by 5.56 % (p<0.05), low density lipoprotein (LDL) C by 3.67 % (p<0.05), visceral adipose tissue area (VATA) by 5.83 % (p<0.05), and subcutaneous adipose tissue area (SATA) by 3.54 % (p<0.05).Conclusion      The empagliflozin treatment for 30 days prior to and after elective PCI can enhance the effectiveness of myocardial revascularization due to the demonstrated beneficial cardiometabolic effects.

The relationship of the epicardial fat and adipo-fibrokines in myocardial infarction.

Analysis of the relationship between the epicardial fat with adipokine and system ST2/IL-33 in-hospital period, and also with the extent of fibrosis of the atrial myocardium through the year after myocardial infarction in patients with visceral obesity. Examined 88 patients with myocardial infarction (MI). Visceral obesity (VO) is established by computed tomography. In fact the presence VO the patients divided into two groups. Determined the concentration of leptin, adiponectin, stimulating growth factor (ST-2) and interlekin-33 (IL-33) in serum on 1st, 12-day in-hospital period and 1 year after MI. Thickness epicardial adipose tissue (EAT) and the percentage of cardiovirus of the myocardium was measured by the method MRI, respectively, on the 12th day of hospitalization and a year after MI. The control group consisted of 30 people. Statistical analysis of data was performed using nonparametric tests. Patients with MI is associated with an increase in the thickness of EAT, imbalance of adipokines with increased leptin, decreased adiponectin in early in-hospital period and development of cardiovirus. Higher values of IL-33 and ЅT2 in the early in-hospital period MI patients with no accompanied by a lower prevalence of cardiovirus in the post-hospital period. The thickness of epicardial fat is directly dependent on the prevalence of myocardial fibrosis, the concentrations of IL-33 and in inverse proportion to the concentration of ЅT2. The degree of cardiovirus is in inverse proportion to the concentration of IL-33 and directly dependent on the concentration of ST2. The increase in EAT closely linked to the development of fibrosis of the atrial myocardium after year. The thickness of EAT more patients MI, which is most pronounced imbalance of adipokines. The metabolic activity of EAT correlated with increased IL-33 and ST2 decrease.

[Effect of empagliflosin on renal filtration in patients with coronary heart disease undergoing percutaneous coronary intervention].

Aim To evaluate the effect of empagliflozin on glycemia and renal filtration function in patients with stable ischemic heart disease (IHD) and type 2 diabetes mellitus (DM2) who underwent a percutaneous coronary intervention (PCI).Materials and methods This study included 40 patients with stable IHD and DM2 (age, 63 (58; 65) years; DM2 duration, 7 (4; 15) years) who had indications for an elective PCI. At baseline in the total sample, the level of glycated hemoglobin was 7.2 (6.5; 8.3)%; 48.7 % failed to achieve glycemic goals. A decrease in glomerular filtration rate (GFR) to below 60 ml/min/1.73 m2 was observed in 10.3 % of patients. All patients were divided into two group by simple randomization with successively assigned numbers. The main group consisted of 20 patients who received empagliflozin 10 mg/day in addition to their previous hypoglycemic therapy irrespective of their baseline glycemic control. Patients of the comparison group (n=20) continued on their previous hypoglycemic therapy as prescribed by their endocrinologist. The follow-up duration was 6 months. Statistical analysis was performed with the Statistica 10.0 software.Results The empagliflozin treatment improved the glycemic control; in the comparison group, no significant changes in glycemic control were observed. In both groups, GFR significantly decreased during the follow-up period; median decreases in GFR were -6.0 (-16.0; 4.0) and -8.4 (-26.5; 2.5) ml/min / 1.73 m2 in the main and comparison groups, respectively (p = 0.646). No significant changes in 24-h proteinuria were observed for patients taking empagliflozin. In the control group, the 24-h urinary protein excretion significantly progressed (p=0.011) during the follow-up period.Conclusion In patients with DM2 and stable IHD who underwent a PCI, addition of empagliflozin 10 mg/day to their current hypoglycemic therapy was associated with a significant improvement of glycemic control. The decrease in GFR during the empagliflozin treatment did not significantly differ from the value for patient receiving the other hypoglycemic therapy.

[Dynamics of Parameters of Transmitral Blood Flow and Markers of Myocardial Fibrosis in Patients with Myocardial Infarction].

Aim      To study possible correlations between echocardiography (EchoCG) indexes and markers of myocardial fibrosis, procollagen I C-terminal propeptide (PICP) and procollagen III N-terminal propeptide (PIIINP) during one year following ST-segment elevation myocardial infarction (STEMI).Material and methods  120 patients with STEMI were evaluated. EchoCG was used to assess dimensions and volumes of heart chambers, left ventricular (LV) systolic function, mean pulmonary arterial pressure (mPAP), and indexes of LV diastolic function (Em, early diastolic lateral mitral annular velocity; e', peak early diastolic septal mitral annular velocity; E / e', ratio of peak early diastolic transmitral inflow velocity and mitral annular velocity  -, Е / А, ratio of peak early and late transmitral inflow velocities; DT, deceleration time of LV early diastolic filling). EchoCG indexes and serum concentrations of PICP and PIIINP were determined at 1 (point 1) and 12 (point 2) days of disease and one year after STEMI (point 3). The sample was divided into two groups: group 1 (n=86; 71.7 %) included patients with a LV ejection fraction (EF) ≥50 % and group 2 (n=34; 28.3 %) consisted of patients with LV EF ≤49 %.Results At one year, the number of patients with signs of diastolic dysfunction increased by 10% in group 1 whereas myocardial systolic dysfunction worsened in both groups. LV EF decreased in 15 (17.4%) patients of group 1 and in 4 (11.8%) patients of group 2. Concentrations of PIIINP were correlated with Em, E / e', mPAP, PICP, e', and LV EF.Conclusion      Direct correlations between PIIINP concentrations and Em, E / e', and mPAP were found in the group with LV EF ≥50 %. In the group with LV EF <50 %, correlations were observed between PICP concentrations, LV EF, and e'. Also, in this group, the increase in PIIINP was statistically more significant. These results indicate continuing formation of myocardial fibrosis in a year following MI, which may underlie progression of chronic heart failure.

[Adiponectin gene expression in local fat depots in patients with coronary heart disease depending on the degree of coronary lesion].

AIM: To determine the dependence of adiponectin gene expression by subcutaneous, epicardial and perivascular adipocytes on the degree of coronary lesion in coronary heart disease. MATERIALS AND METHODS: 84 patients with coronary artery disease were examined. Of these, 39 people showed a moderate degree of atherosclerotic lesion of the coronary bed (less than or equal to 22 points) on the SYNTAX Score scale, 20 severe (2231 points), and 25 extremely severe (more than 32 points). Upon admission to the hospital, all patients underwent an echocardiographic study (Echocardiography, Acuson, Germany) with the calculation of the ejection fraction (EF) of the left ventricle (LV) to assess its systolic function. During a planned surgical intervention (coronary bypass surgery, CABG), adipocytes of subcutaneous, epicardial (EAT) and perivascular adipose tissue (PVAT) were taken. Adiponectin gene expression was evaluated by polymerase chain reaction (real-time PCR) using TaqMan probes. Statistical analysis was performed using Statistica 9.0. RESULTS: The maximum level of adiponectin expression was detected in adipocytes of PVAT, and the minimum EAT. With an increase in the degree of atherosclerotic lesion of the coronary bed, the expression of the adiponectin gene in adipocytes of local depots significantly decreases r=-0.82; p=0.023. Moreover, the low level of gene expression in EAT correlated with a decrease in LV EF by r=0.73; p=0.03. In adipocytes of subcutaneous and especially PVAT, gene expression was the highest in patients with a moderate degree of coronary lesion. CONCLUSIONS: Low adiponectin gene expression in EAT is associated with an increase in the degree of atherosclerotic lesion of the coronary bed and a decrease in LV EF.

[Expression of gene and content of adiponectin in fatty tissue in patients with ischemic heart disease]. / Ékspressiia gena i soderzhanie adiponektina v zhirovoi tkani u patsientov s ishemicheskoi bolezn'iu serdtsa.

The purpose of the study was to investigate the features of expression and adiponectin content in the adipocyte culture of subcutaneous, epicardial, and perivascular adipose tissue and the effect of various doses of rosuvastatin on these processes. 29 patients with coronary artery disease were examined. Adipocytes were isolated from the samples of SAT, EAT and PVAT which were taken during coronary artery bypass surgery, followed by cultivation in the presence of rosuvastatin and evaluation of gene expression and adiponectin concentration. Adipocytes SAT, EAT and PVAT differed in the level of adiponectin secretion and expression of its gene. On day 1 of cultivation the expression of the adiponectin gene in the EAT was 2.3 times lower than in the PVAT. On day 2 of cultivation the expression of the adiponectin gene was reduced both in the EAT and the PVAT as compared to the SAT. When rosuvastatin was added at a concentration of 1 mmol/L, adiponectin gene expression in PVAT was higher than when rosuvastatin was added at a concentration of 5 mmol/L, in the adipocyte culture of SAT effect was opposite. Thus, the adipocytes of EZhT and, to a greater extent, PAS, can be a therapeutic target for statins in the case of the pathological activation of adipose tissue.

The marker of adverse prognosis 1.5-anhydroglucitol in patients with coronary heart disease in the long-term period after planned myocardial revascularization.

AIM: Determination of the prognostic value of 1.5-anhydroglucitol (1.5-AG) for the development of cardiovascular events in patients with coronary heart disease (CHD) within a year after a planned percutaneous coronary intervention (PCI). MATERIALS AND METHODS: A prospective study was conducted in Federal State Budgetary Institution Research Institute for Complex Issues of Cardiovascular Disease among 149 patients admitted to planned PCI in the period from 2016 to 2017. Criteria for inclusion in the study: age up to 70 years, angina I-IV functional classes or post-infarction cardiosclerosis, the presence of indications for planned PCI. -Exclusion criteria from the study: previous myocardial revascularization; prosthetic heart valves; decompensation of chronic heart failure, anemia of any degree; acute coronary syndrome in index hospitalization; exacerbation of somatic diseases. The results of the research were processed by Statistica Windows 6.0. RESULTS: During the year after planned PCI, 39 (26.14%) cardiovascular events were registered in patients with CHD, of whom more than half of the cases (51.28%) were associated with the presence of indications for PCI of de novo. Lower levels of 1.5-AG were observed in the group of patients with cardiovascular events (p=0.000). When patients were divided according to median of the studied marker patients with a concentration of 1.5-AG less 20.96 µg/ml (before PCI) were more likely to have PCI after restenosis of the stent, compared with patients whose median concentration of this marker was higher (p=0.028). The logistic regression method revealed a significant direct relationship reflecting the prognostic value of lower concentration of 1.5-AG in relation to the development of cardiovascular events in patients regardless of the presence of carbohydrate metabolism disorders [OR 0.25 (0.10-0.62)]. CONCLUSION: According to the results of the study, the prognostic value of the concentration of 1.5-AG less 20.96 µg/ml was established in relation to the development of cardiovascular events in patients with CHD during the year after a planned PCI, regardless of the presence of carbohydrate metabolism disorders.

[Polyvascular disease in patients with myocardial infarction and chronic kidney disease].

AIM: To study polyvascular disease in patients with myocardial infarction (MI) and chronic kidney disease (CKD). MATERIALS AND METHODS: A total of 954 patients older than 18 years old with ST-segment elevation MI (STEMI) up to 24 hours of pain onset were included in the study. Clinical and demographic data were collected for all patients, including physical examination, 16-lead electrocardiogram recording, echocardiography, laboratory assessment with the measurements of cardiospecific enzymes and serum creatinine. Glomerular filtration rate (GFR) was estimated according to the CKD-EPI equation. Of them, 771 (81%) underwent coronary angiography, duplex scanning of the brachiocephalic (BCA) and lower extremity arteries (LEA). Patients with stage 1-4 CKD diagnosed according to the criteria provided by the Russian Society of Nephrologists were allocated into a separate group (n=281; 36.5%). CKD stages were determined with the level of GFR. Patients with stage 5 CKD were excluded from the study. Renal dysfunction was defined as the presence of an estimated GFR less than 60 ml/min/1.73 m2. RESULTS AND DISCUSSION: The results of the study indicate a high prevalence of PolyVD in patients with CKD. Every second patient had LEA stenosis (p.

[The association of biological markers with echocardiographic indices in patients with myocardial infarction with ST segment elevation and preserved left ventricular ejection fraction].

AIM: To compare dynamics of biological marker concentrations with echocardiographic data in patients with ST elevation myocardial infarction (STEMI) and preserved LV function during the hospitalization period. MATERIALS AND METHODS: The study successively included 100 patients with diagnosis of STEMI and LV ejection fraction.

Influence of visceral obesity on the secretion of adipokines with epicardial adipocytes in patients with coronary heart disease.

AIM: To study adipokine-cytokine profile of epicardial adipocytes (EAT) and subcutaneous adipose tissue (SAT) in conjunction with the area of visceral adipose tissue (VAT), biochemical and clinical characteristics of patients with coronary heart disease. MATERIALS AND METHODS: Examined 84 patients (70 men and 14 women) with coronary artery disease. In fact the presence of visceral obesity (VO) the patients were divided into two groups. Patients VO the sampling of adipocytes of EAT and SAT, with subsequent cultivation and evaluation of adipokine and provospalitelna activity. Carried out the determination of carbohydrate and lipid metabolism, adipokine and pro-inflammatory status in the blood serum. RESULTS: It was found that adipokine-cytokine profile of adipocytes of EAT and SAT differ. Adipocytes art of the disease on the background characterized by an increase IL-1, TNF-α, leptin-adiponectin relationships and a decrease in the content of protective factors: adiponectin and anti-inflammatory cytokine IL-10. While the SAT adipocytes was characterized by a decrease in the concentration of soluble receptor for leptin and the more pronounced leptinresistance, and the increase in proinflammatory cytokines was offset by the increase in the concentration of IL-10. The presence associated with multi-vessel coronary bed lesion, multifocal atherosclerosis, insulin resistance, atherogenic dyslipidemia, an imbalance of adipokines and markers of inflammation. So the value of the square VAT determined higher concentrations of leptin, TNF-α in adipocytes and serum, lipid and carbohydrate metabolism and a lower content of soluble receptor for leptin. CONCLUSION: Thus, the disease on the background of the status of the adipocytes of EAT characterized as a "metabolic inflammation", and may indicate the direct involvement of adipocytes in the pathogenesis of coronary artery disease, due to the formation of adipokine imbalance and the activation of proinflammatory reactions.

Adipokine and Cytokine Profiles of Epicardial and Subcutaneous Adipose Tissue in Patients with Coronary Heart Disease.

The content of adipokines, pro- and anti-inflammatory cytokines were studied in adipocytes isolated from epicardial and subcutaneous adipose tissue of 24 coronary heart disease patients. The content of leptin and soluble leptin receptor in adipocytes of epicardial adipose tissue was higher by 28.6 and 56.9% and the level of adiponectin was lower by 33% than in adipocytes of the subcutaneous fat. In culture of epicardial adipocytes, the levels of proinflammatory cytokines TNF-α and IL-1 were higher. Subcutaneous adipose tissue adipocytes were characterized by higher levels of anti-inflammatory cytokines IL-10 and FGF-ß. In epicardial adipocytes of coronary heart disease patients, the concentrations of leptin, TNF-α, and IL-1 were higher, while the levels of defense regulatory molecules (adiponectin, IL-10, and FGF-ß) were lower than in subcutaneous adipocytes.

[Myocardial fibrosis: Current aspects of the problem]. / Fibroz miokarda: sovremennye aspekty problemy.

Fibrosis is one of the main components in the progression of most cardiovascular diseases, including coronary heart disease, by causing structural changes in the myocardium and vascular wall. The quantitative and qualitative characteristics of fibrosis of the myocardium are responsible for decreasing its elastic properties, developing diastolic dysfunction, impairing myocardial contractility, developing systolic dysfunction and cardiac arrhythmias, and worsening coronary blood flow in patients with heart failure of different etiologies. The important aspect of studying fibrosis is not only its interpretation as a model of the typical pathological process, but also its consideration as a systemic lesion of various organs and tissues. At the same time, the identification of myocardial fibrosis biomarkers that are available for their determination in circulating blood is of particular interest. Since there was evidence for the role of fibrosis in developing dysfunction of various organs and ensuring the systematicity of most diseases, especially at their development stages, the process of fibrosis came to be regarded as a promising therapeutic target. It is relevant to further investigate myocardial fibrosis, which is aimed at increasing the efficiency of its diagnosis and predicting its course and pathogenetically sound therapy.

[The role of chronic kidney disease in assessing the risk of the poor course of hospital ST-segment elevation myocardial infarction].

AIM: To evaluate the prognostic impact of chronic kidney disease (CKD) during hospital stay in patients with ST-segment elevation myocardial infarction (STEMI) and to specify factors showing a negative impact of CKD. SUBJECTS AND METHODS: 954 patients with STEMI were examined. The diagnosis of CKD was verified in 338 (35.4%). In all the patients, glomerular filtration rate (GFR) was calculated using the CKD-EPI formula with regard to serum creatinine levels on admission and before discharge (on days 10--12). In the patients who had undergone X-ray contrast intervention, serum creatinine levels were additionally determined on days 2--3 of this procedure in order to identify contrast-induced nephropathy (CIN). Cardiovascular events were assessed in the hospital period. RESULTS: Endovascular interventions into the coronary vessels were made much more rarely in the patients with CHD; but CIN cases were twice more commonly recorded. Nonfatal cardiovascular events were 1.5 times more frequently observed in the CKD patients in the hospital period. The odds of fatal outcomes in both the total sample of STEMI patients and in those with CKD increased by 3.5 and 3.1 times, respectively, in the over 60 age group and by 7.9 and 5.8 times in the presence of Killip Classes II--IV clinically relevant acute heart failure (AHF). In the total sample, the independent predictors for a fatal outcome were a decreased admission GFR less than 60 ml/min/1.73 m(2), CIN, and Killip II--IV AHF. The hospital nonfatal complications were also associated with a decreased admission GFR less than 60 ml/min/1.73 m(2). CONCLUSION: The independent predictor of a poor hospital period of STEMI, including fatal outcomes, was a decreased admission GFR less than 60 ml/min/1.73 m(2); the presence of CKD was of no independent value.

[Diagnostic value of the stimulating growth factor ST2 during hospitalization for myocardial infarction]. / Diagnosticheskoe znachenie stimuliruyushchego faktora rosta ST2 v gospital'nom periode infarkta miokarda.

AIM: To determine the concentration of the stimulating growth factor ST2 and its relationship to the clinical course of myocardial infarction (MI) over time during hospitalization. MATERIALS AND METHODS: Eighty-eight MI patients whose mean age was 59±8.36 years were examined. On days 1 and 12 of MI, the serum levels of ST2 and N-terminal pro-brain natriuretic peptide (NT-proBNP) were determined by ELISA. A control group consisted of 30 people. RESULTS: On day 1 of hospitalization for MI, the concentrations of ST2 and NT-proBNP were higher 2.4 and 4.5 times, respectively, than those in the controls; by day 12, there was a statistically significant decrease in the level of ST2 while that of NT-proBNP was unchanged. During hospitalization, the investigators recorded MI complications, according to which the patients were divided into favorable and unfavorable MI groups. On day 1 of hospitalization, the level of ST2 in the patients with unfavorable MI was twice higher than in those with favorable MI and 3.7 times higher than in the control group. On day 12, both favorable and unfavorable MI groups showed a reduction in the level of the marker. On day 1 of MI, the concentration of NT-proBNP in the patients with a poor prognosis was 6.8 times greater than in the controls and 1.8 times more than in the patients with a good prognosis. On day 12, NT-proBNP levels remained elevated in both groups. Logistic regression analysis revealed that the determination of ST2 in combination with NT-proBNP increased their diagnostic significance (odds ratio, 1.92; 95% CI, 1.7-3.2; area under characteristic curve, 0.89; p=0.004). CONCLUSION: The level of ST2 was a more sensitive indicator of hospitalization for MI than that of NT-proBNP. The combined use of ST2 and NT-proBNP was found to have a high diagnostic sensitivity and specificity.

[Renal function estimation formulas in predicting long-term cardiovascular outcomes in patients with myocardial infarction concurrent with diabetes mellitus]. / Formuly otsenki funktsii pochek pri prognozirovanii otdalennykh serdechno-sosudistykh iskhodov u bol'nykh infarktom miokarda v sochetanii s sakharnym diabetom.

AIM: To comparatively assess formulas for estimating glomerular filtration rate (GFR) in the prediction of poor outcomes in patients with type 2 diabetes mellitus (DM) within one year after myocardial infarction (MI). MATERIALS AND METHODS: The investigators examined 89 patients with ST-segment elevation myocardial infarction (STEMI) within 24 hours after the onset of clinical symptoms of the disease. All the patients underwent standard laboratory and instrumental tests. GFR was calculated using the Modified of Diet in Renal Diseases (MDRD) formulas in terms of serum creatinine levels, the Hoek equation: GFR [ml/min/1.73 m2] = (80.35/cystatin C [mg/l]) - 4.3 (CKD-EPI), as well as from cystatin C levels, and the creatinine clearance rate was determined using the Cockcroft and Gault formula (ml/min). During a year after STEMI, the investigators recorded cardiovascular events (CVEs), such as death, recurrent MI, progressive angina pectoris, emergency coronary revascularization, and decompensated chronic heart failure (CHF). The examinees were divided into two groups: 1) 70 (78.6%) patients with MI and no DM; 2) 19 (21.3%) patients with MI and DM. RESULTS: Comparative analysis revealed a tendency towards a difference in the detection rate of GFR <60 ml/min/1.73 m2 calculated using the Hoek formula from cystatin C levels: 42.1% in Group 2 and 21.4% in Group 1 (р=0.067). There were no great differences in the GFR estimated using other formulas. Logistic regression analysis was carried out to determine the most sensitive formula for estimating GFR to assess the risk of CVEs in the patients within a year after MI concurrent with and without type 2 DM. A univariate analysis showed that GFR calculations using the CKD-EPI (odds ratio (OR), 13.5; p=0.046) and MDRD (OR, 6.5; р=0.040) formulas and creatinine clearance estimation (OR, 2.4; p=0.025) were most sensitive in selecting MI patients without DM and with poor outcomes. This analysis revealed that GFR estimates using the Hoek formula from cystatin C levels (OR, 6.15; p=0.018) were most sensitive for patients with MI concurrent with type 2 DM. In both models, multivariate analysis included none of the analyzed indicators. CONCLUSION: To estimate cardiovascular risk in the long-term post-infarction period, the CKD-EPI formula in the patients without type 2 DM and the Hoek formula from cystatin C levels were noted to be of the greatest prognostic value in patients with DM.

[The Study of Associations of Polymorphisms of Candidate Gene of Cardiovascular Diseases With Reduction of Glomerular Filtration Rate in Patients With ST Segment Elevation Myocardial Infarction].

AIM: to study associations of polymorphic genetic variants of inflammatory response, endothelial function, lipid metabolism, and blood coagulation with impaired renal function in patients with ST elevation myocardial infarction (STEMI). MATERIAL AND METHODS: We enrolled in the study 171 patients admitted to the Kemerovo Cardiology Dispensary within 24 hours after onset of STEMI. All patients underwent genotype identification of 25 polymorphic variants of 18 major candidate genes for cardiovascular disease. Genotyping was performed with DNA chip SINKAR-1 (Institute of Medical Genetics and LLC "Genomic Diagnosis"). Glomerular filtration rate (GFR) was estimated using serum creatinine level measured at admission. RESULTS: Comparison of allelic and genotype frequencies of the studied polymorphisms revealed that angiotensin-converting enzyme (ACE) gene rs4291 was associated with decreased GFR: odds ratio (OR) for carriers of rare TT genotype was 2.31 [1.01-5.25], =0.043. Analysis of genotype combinations of ACE rs4343 polymorphism and hepatic lipase gene (LIPC) rs1800588 showed that AA genotype of rs4343 polymorphism in combination with CC genotype of rs1800588 polymorphism was associated with lowest risk of renal dysfunction, whereas GG and AG genotypes of ACE rs4343 in combination with TT and CT genotypes of LIPC rs1800588.

[Relationship Between Blood Serum Galectin and Renal Dysfunction in ST Elevation Myocardial Infarction].

AIM: to assess value for inhospital and 1 year prognosis of unfavorable course of ST-elevation myocardial infarction (STEMI) of blood serum galectin and markers of renal dysfunction (RD). MATERIAL AND METHODS: Standard laboratory and instrumental examination, calculation of glomerular filtration rate using MDRD formula and by cystatin C level, determination of galectin in blood serum were carried out in 128 patients with STEMI. According to GFR by cystatin C level on day 12 of STEMI patients were divided into 2 groups - with normal renal function (GFR more or equal 60 ml/min/1.73 m2, n=47) and with RD (GFR <60 ml/min/1.73 2, n=81). RESULTS AND CONCLUSION: In patients with STEMI presence of RD (lowering of GFR by cystatin C, by blood serum creatinine <60 ml/min/1.73 2, creatinine clearance <60 ml/min), and elevation of galectin concentration >17.8 hg/ml on day 12 of STEMI were independent predictors of unfavorable 1 year prognosis. Elevation of galectin level directly correlated with presence of early postinfarction angina.

[Clinical and Prognostic Value of Serum Neutrophil Gelatinase-Associated Lipocalin in Patients With ST-Segment Elevation Myocardial Infarction].

PURPOSE: to study clinical and prognostic significance of serum neutrophil gelatinase-associated lipocalin (s-NGAL) in patients with ST-segment elevation myocardial infarction (STEMI). MATERIAL AND METHODS: Patients with STEMI (n=85) of less than 24 hours duration admitted to the Kemerovo Cardiology Dispensary were included in the study. s-NGAL levels (ng/ml) were measured on day 1 and 12 of hospital stay by ELISA using commercial kit. Reinfarction rate and mortality were assessed over 3-year follow-up. RESULTS: Median s-NGAL levels on day1 and 12 were 1.33 (0.36-1.90) and 1.63 (1.25-2.61) ng/ml, that corresponded to a 3.32- and 4.07-fold increase, respectively, compared to reference values. Between days 1 and 12 s-NGAL levels increased by 22.55 % (p=0.0009). Higher values of serum NGAL on day 12 of MI were associated with presence of renal structural lesions, three-vessel coronary artery disease and anterior MI. Patients who underwent percutaneous coronary intervention (PCI) demonstrated only a negligible increase of s-NGAL level by day 12 while in those not subjected to PCI 3-fold increase was observed. Patients with s-NGAL levels >2.6 ng/ml compared with other patients had higher mortality (9.52 vs 31.83%; odds ratio 4.42 [1.30-15.16], p=0.012). CONCLUSION: High values of serum NGAL in STEMI patients were associated with severe clinical status. s-NGAL level above 2.6 ng/ml on day 12 of hospital stay was associated with 4- fold increase of all-cause mortality during 3-year follow-up.

[The possibility of application of stimulant growth factor (ST2) for verifying postinfarction remodeling of myocardium.]

PURPOSE OF STUDY: To detect level ST2 in blood serum of patients with myocardium infarction in dynamics of hospital period and their relationship with remodeling of myocardium. MATERIALS AND METHODS: The study sampling included 87 patients (65 males and 22 females) with myocardium infarction and the ST-segment elevation and average age of 59 years. All patients were allocated in two groups: with adaptive alternative of remodeling of myocardium (67 patients) and deadaptive alternative (20 patients). The control group consisted of 30 individuals. At the first and twelfth days after myocardium infarction in blood serum content of ST2 and NT-proBNP were detected using immune-enzyme technique with application of test-systems produced by Critical Diagnostics (USA) and Biomedica (Slovakia) correspondingly. The data statistical analysis was processed using non-parametric criteria. THE RESULTS: He content of ST2 and NT-proBNP at the first day of myocardium infarction increased in 2.4 and 4.5 times correspondingly as compared with control group. The patients with deadaptive remodeling were characterized by in 1.5 times higher content of ST2 at the first day than in group of adaptive remodeling and in 5.3 times higher that in control group. In the end of hospital period (twelfth day) in both groups decreasing of level of ST2 was observed. The concentration of NT-proBNP at the first day was increased in 1.8 times in patients of both groups and decreased at twelfth day. At that there were no differences between both groups. The high level of ST2 at the first day increases the risk of development of deadaptive remodeling in 4.5 times, NT-proBNP only in 2.3 times. CONCLUSION: The high level of stimulant growth factor ST2 at the first day of myocardium infarction was associated with deadaptive alternative of post-infarction remodeling that permits using ST2 as prognostic marker with high sensitivity and specificity.

[Impact of chronic obstructive pulmonary disease on one-year prognosis in patients with ST-segment elevation myocardial infarction].

AIM: To assess the role of chronic obstructive pulmonary disease (COPD) in the development of unfavorable outcomes of long-term (one-year) prognosis of ST-elevation myocardial infarction (STEMI). SUBJECTS AND METHODS: A total of 529 patients diagnosed with STEMI and no age limits were examined. Group 1 included 65 (12.3%) patients with previously diagnosed COPD; Group 2 consisted of 464 (87.7%) patients without COPD. One-year prognosis was studied in 384 (81.5%) patients. The investigators evaluated the following endpoints: evolving recurrent myocardial infarction (MI), progressive angina pectoris, decompensated chronic heart failure (CHF), repeat percutaneous coronary interventions, stroke, and death. RESULTS: The prevalence of COPD was 12.3% in the patients with STEM]. Unfavorable one-year prognosis was significantly more often registered in the comorbidity group regardless of age, gender, and smoking status. COPD increased the risk of combined endpoints by 1.9 times within a year after MI and that of decompensated CHD by 2.6 times during a year after STEM. CONCLUSION: COPD may be an independent risk factor for unfavorable outcomes during a year after MI.