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Aim. To investigate the relationship between the osmotic fragility of erythrocytes and the course of acute myocardial infarction (MI).Methods. An analysis of the osmotic fragility of erythrocytes was conducted using beta-blocker-based osmotic fragility test in sixty-two patients within the first 6 hours after onset of MI symptoms.Results. The results revealed that the patients with increased erythrocyte osmotic fragility experienced more complications after acute MI, such as left ventricular failure and cardiac arrhythmias (ventricular extrasystoles and ventricular tachycardia) (p = 0.026). Moreover, these patients exhibited greater myocardial injury - the concentration of biomarkers of myocardial necrosis, such as creatine phosphokinase, creatine phosphokinase MB and Troponin I was increased - p = 0.009, p = 0.032 and p = 0.001, respectively. In addition to that, the patients with high osmotic fragility had a larger number of hypokinetic and akinetic segments, high impaired myocardial contractility index, and low ejection fraction. The impaired myocardial contractility index was significantly higher in patients with increased erythrocyte osmotic fragility (1.5 (1.22; 1.75) vs 1.12 (1.0; 1.56), U = 157.5, p = 0.032).Conclusion. Increased erythrocyte osmotic fragility in patients was associated with greater myocardial injury, manifesting through the higher concentration of biomarkers of myocardial necrosis in blood, as well as higher number of hypokinetic segments.

Objective: To study the association of beta-adrenergic reactivity index of erythrocyte membranes with polymorphisms of the beta-1-adrenergic receptor gene ADRB1 (Ser49Gly and Arg389Gly).Material and methods: the study included 62 patients with myocardial infarction (MI) — 49 men (median age of 58.0 (47.5; 64.5) years) and 13 women (median age of 76.0 (61.5; 81.0) years). All patients underwent analysis of beta-adrenoreactivity of erythrocyte membranes using the BETA-ARM AGAT reagent kit within the first 6 hours from the onset of MI. The patients were divided into 2 groups depending on the value of the beta-adrenergic reactivity index (β-ARM). The first group (n = 11) included patients with a normal P-ARM level (from 2 to 20 conventional units). The second group (n = 51) consisted of patients with increased values of β-ARM (more than 20 standard units). Genetic analysis for the determination of ADRB1 gene polymorphisms (Ser49Gly and Arg389Gly) was carried out by isolating DNA from peripheral blood leukocytes (Wizard Genomic DNA Purification Kit) with PCR amplification and further electrophoretic detection. Statistical processing of the obtained data was carried out using Statistica 10 software and the demo version of IBM SPSS Statistics 20.0.Results: patients with elevated β-APM values were characterized by higher levels of myocardial necrosis markers in the blood (CPK, CPK-MB, and troponin I) in acute myocardial infarction than for patients of the first group (p = 0.009, p = 0.032 and p = 0.001, respectively). In addition, the second group of patients was characterized by a more frequent development of acute left ventricular failure (33.3%, p = 0.026), as well as a history of arterial hypertension before the development of index MI (90.2%, p = 0.044). With regard to the Arg389Gly polymorphism, significant differences were found among patients with normal and increased P-APM values in the acute period of MI. Thus, the second group of patients consisted mainly of carriers of the 1165CC genotype of the ADRB1 gene (n = 29, 56.9%, p = 0.043). The carriage of the 1165G allele was much more often observed among patients of the first group (81.8%; OR = 5.93; CI 1.16-30.25; p = 0.043).Conclusion: an association of the 1165CC genotype of the Arg389Gly polymorphism of the ADRB1 gene with increased β-APM values in acute MI was established. The detected associations may indicate a possible genetic predisposition to SAS hyperactivation, and also indicate the need for further study of polymorphisms and the level of expression of the ADRB1 gene in patients with high individual values of β-APM established in the acute period of MI.

Aim. To identify the associations between beta-adrenergic reactivity of erythrocytes and the progression of heart failure (HF) in patients after myocardial infarction (MI).Material and methods. The study included 50 patients with HF and history of MI 6 months ago. To determine the level of sympathoadrenal system activity, we analyzed beta-adrenergic reactivity by changing the osmotic resistance of erythrocytes by use of adrenoceptor blocking agent.Results. The frequency of HF progression after index MI was 26% (n=13). All patients were divided into 2 groups depending on the presence/absence of HF progression in the postinfarction period. When determining beta-adrenergic reactivity, it was found that patients with HF progression compared with patients without it had the higher level of beta-adrenergic reactivity of membrane (β-ARM) of erythrocytes: 58,8 (50,9; 78,0) CU and 46,8 (38,0; 66,3) CU, p=0,025). A ROC analysis made it possible to establish the β-ARM level ≥49,53 CU a cut-off point, which can be considered as a marker of HF progression in patients after MI (sensitivity 92,3%, specificity 62,2%). This level of β-ARM is associated with a more than five-fold increase of HF progression risk in patients after MI (OR 5,48; 95% CI 1,28-23,37; p=0,024).Conclusion. In patients with HF and MI history, there is a decrease in the adrenergic reactivity of erythrocyte cell membrane, which is reflected by an increase of β-ARM above normal range of 20 CU. At the same time, β-ARM in patients with HF progression compared with patients without it is significantly increased. Established cut-off point of β-ARM (≥49,53 CU) allows predicting the HF progression with high sensitivity and specificity.

Objective. To identify associations of beta-adrenoreactivity with stage of chronic heart failure (CHF) in patient with previousmyocardial infarction (MI).Material and Methods. A total of 50 patients with CHF underwent an analysis of adrenoreactivity based on the changes in red blood cellosmoresistance in the presence of adrenergic blocker to determine the activity of the sympathoadrenal system a year after MI.Results. Higher levels of beta-adrenoreactivity (β-ARM) were characteristic of patients with CHF of higher gradations: 61.8(47.5;74.8) с.u. in patients with stage IIA CHF versus 48.7 (39;65.2) с.u. in patients with stage I CHF, p=0.037.Conclusion. These results may suggest the diagnostic value of the indicator of adrenoreactivity and its possible use as a newbiomarker for assessing the severity of CHF in patients with previous myocardial infarction.

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This study was funded by (subject of fundamental scientific research on a state assignment № АААА-А17-117052310073-6 от 23.05.2017 Introduction. Growth differentiation factor-15 (GDF-15) is a biomarker associated with inflammatory processes in the pathogenesis of chronic heart failure (CHF) which expresses in cardiomyocytes under pathological conditions. The relationship between the level of GDF-15 and type 2 diabetes mellitus (T2DM) has also been proven. It is necessary to study GDF-15 in patients with CHF and T2DM. Aim To investigate the association between serum GDF-15 levels in patients with CHF of ischemic etiology and the concentration of the main leukocyte fractions depending on presence or absence of T2DM. Material and methods. The study included 42 patients. The patients were divided into 2 groups. The first group consisted of patients with CHF and T2DM (n = 14). The second group consisted of patients with CHF without T2DM (n = 28). Determination of GDF-15 concentration was carried out by enzyme-linked immunosorbent assay (BioVendor, Czech Republic). The absolute concentration of lymphocytes, neutrophils, as well as the ratio of neutrophils to lymphocytes in the blood were analyzed. Statistical analysis was performed using the Statistica software (v.10.0). The data were described as a median and interquartile range, the Mann-Whitney test was used to compare them. The correlation analysis was tested using the Spearman"s correlation coefficient. Results and discussion. The average level of the GDF-15 in the study groups was comparable: 2389 (2104; 3375) pg/ml and 2309 (2047; 3014) pg/ml in the first and second groups, respectively (p = 0.6). In the general cohort of CHF patients, the GDF-15 concentration was not correlate with the lymphocytes concentration (r = -0.001, p = 0.95), neutrophils (r = -0.14, p = 0.4) and the ratio of neutrophils to lymphocytes (r = -0.12, p = 0.25). At the same time, in the group of patients with T2DM, a significant negative correlation was revealed between the concentration of GDF-15 in the serum and the concentration of neutrophils (r = -0.6, p = 0.022). While both other analyzed parameters did not demonstrate significant correlations with GDF-15 (p > 0.05). In the group of CHF patients without T2DM, no correlations were found between GDF-15 and the studied parameters, including neutrophils (r = 0.02, p = 0.3). Along with this the median of the neutrophils concentration did not vary among groups (3.5 (2.3; 5.3) vs 3.2 (2.7; 4.1) * 109 / l; p = 0.8). Conclusion The concentration of the inflammatory marker GDF-15 in the blood of patients with CHF in combination with T2DM correlates with the concentration of neutrophils. In the absence of T2DM, no significant correlations were found between GDF-15 and the main leukocyte fractions. The results obtained indicate the possible prospect of using the GDF-15 biomarker in a cohort of patients with CHF in combination with T2DM.

Aim To analyze associations between levels of the inflammatory marker, growth differentiation factor 15 (GDF-15), and echocardiographic indexes in CHF patients with mid-range and preserved left ventricular ejection fraction (LV EF) depending on the history of myocardial infarction (MI).Material and methods This study included 34 CHF patients with preserved and mid-range LV EF after MI (group 1, n=19) and without a history of MI (group 2, n=15). Serum concentration of GDF-15 was measured with enzyme immunoassay (BioVendor, Czech Republic). Statistical analysis was performed with STATISTICA 10.0.Results Patients of the study groups were age-matched [62 (58;67) and 64 (60;70) years, p=0.2] but differed in the gender; group 1 consisted of men only (100 %) whereas in group 2, the proportion of men was 53.3 % (p=0.001). Median concentration of GDF-15 was 2385 (2274; 2632.5) and 1997 (1534;2691) pg/ml in groups 1 and 2, respectively (p=0.09). Patients without MI showed a moderate negative correlation between LV EF and GDF-15 concentration (r= – 0.51, p=0.050) and a pronounced correlation between GDF-15 and LV stroke volume (r= –0.722, p=0.002). For patients after MI, a correlation between the level of GDF-15 and the degree of systolic dysfunction was not found (р>0.05).Conclusion Blood concentration of the inflammatory marker, GDF-15, correlates with LV EF and stroke volume in CHF patients with preserved or mid-range LV EF and without a history of MI while no such correlations were observed for patients with a history of MI.

The purpose of this study was to investigate the angiotensin-converting enzyme (ACE) gene associations with the clinical picture of the most frequent complications of acute myocardial infarction (MI). The study included 190 patients who underwent one or more MI included in the WHO Register of Acute Myocardial Infarction. All the patients underwent genetic research for the identification of allelic variants of the ACE gene (polymorphism I/D). It was found that the DD genotype of the ACE gene is associated with a more frequent occurrence of acute left ventricular aneurysm (ALVA) (OR = 2.46, 95% CI 1.08–5.63, p = 0.037, χ2 = 4.73). In the group of patients with acute left ventricular failure (ALVF), the picture looked different: the genotype II of the ACE gene was more frequent (OR = 2.86, 95% CI 1.35–6.08, p = 0.007, χ2 = 7.81). Patients in the group without ALVF were carriers of the allele D more often (77.1%) (p = 0.007, χ2 = 7.81). Discovered genetic associations favor the consideration of the ACE gene as a genetic predictor of the development of ALVA in the acute period of MI. Further study of this gene in combination with other genetic markers of MI, as well as analysis of distribution of the genotypes of the ACE gene among deceased patients who underwent MI, will allow us to understand the genetic mechanisms of the development of other complications of MI, in particular, ALVF. All this will ensure the development of new highly effective personalized approaches to the prevention and treatment of complications of acute MI and the improvement of immediate and remote prognosis of patients.

Aim. To evaluate long term outcomes of acute myocardial infarction (MI), based on the populational registry. Material and methods. In the study, the survived post-MI patients were included, in the year 2007 registered in database of MI (n=439). Prospective observation was done during 5 years after index event. In the case of fatal outcome the protocols were analyzed, of pathology studies and summaries of forensic autopsies; relatives were interviewed and the witnesses of clinical cases. For statistics, the software “Statistiсa” V.10 was applied. Results. Mortality among patients included into the study, was 11% in one year post MI, and 35% at 5 years. In overall structure of the causes of fatal outcomes there were cases of second MI — 37%. Chronic coronary heart disease was found as a cause of death in 21%, and in 2% there was fatal stroke; in 5% pulmonary embolism, and in 5% sudden cardiac death. In 17% causes of death were not related to cardiovascular pathology. Conclusion. Patients after MI do demonstrate high level of mortality in 5 year outcomes. Leading causes of fatal outcomes during first 2 years are recurrent acute coronary events, acute strokes, thromboembolism.

Aim. To identify predictors of major adverse cardiovascular events (MACE) in patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI).Material and methods. This prospective single-center study included 225 patients with stable CAD requiring drug-eluting stent implantation. The average follow-up period for patients was 14,5 (6;23) months. Levels of glycated hemoglobin (HbA1c), insulin, tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), interleukin-10 (IL-10), endothelin-1 (ET-1) and the serum lipid profile were evaluated. Insulin resistance was assessed by the HOMA-IR index. The patients were divided into 2 groups: group 1 (n=98) — patients with MACE, group 2 (n=127) — patients without MACE over the follow-up period.Results. During the follow-up period, MACE were recorded in 43,5% of patients, of which: fatal outcome in 3 (3,1%) patients, acute coronary syndrome (ACS) — 14 (14,3%), decompensated heart failure (HF) — 8 (8,2%), non-fatal myocardial infarc tion (MI) — 4 (4,1%), stroke — 3 (3,1%), in-stent restenosis — 18 (18,4%), target vessel revascularization due to progression of atherosclerosis — 25 (25,4%), lifethreatening arrhythmias — 18 (18,4%), implantation of a cardiac resynchronization therapy defibrillator — 5 (5%). To determine critical levels for quantitative predictors, ROC curves were created with threshold values that increase the likelihood of MACE.Conclusion. As a result of the study, we found that the waist-to-hip ratio >1,0495, the HOMA-IR index >3,13 and the endothelin-1 >0,75 mmol/L are independent predictors of unfavorable prognosis in patients with CAD after PCI.