ST-segment elevation myocardial infarction (STEMI) is an acute life-threatening condition that requires urgent, complex, well-coordinated treatment, aimed primarily at the earliest possible reperfusion. The adverse effect of delay to reperfusion on the prognosis of in-hospital mortality in patients with STEMI was demonstrated with both thrombolysis and PPCI in the 1996–2004 studies. More recent data are inconsistent regarding the association of adverse hospital outcomes with time to PPCI. The purpose was to examine the time from the onset of pain in ST-segment elevation myocardial infarction to primary percutaneous coronary intervention in association with the hospitalization outcome. Material and methods. For the study, we selected 177 records of patients with a fatal outcome and 380 records of patients discharged with a favorable outcome of myocardial infarction with ST-segment elevation from Kazan Emergency Care Center for patients with acute coronary syndrome. The study included 349 men and 208 women from 32 to 96 years old; the median age was 67 (58–76) years. Results. The time from the onset of pain syndrome (PS) to the primary medical contact (PMC) in patients with a lethal and favorable outcome did not differ significantly and amounted to 180 (75–540) and 168 (88–450) minutes, respectively (p = 0.639). From the moment of PMC to the registration of the first ECG in patients with a fatal outcome, 26 (19–36) minutes passed, and in patients with a favorable outcome, 25 (17–40) minutes (p = 0.747). From the registration of the first ECG to hospitalization in patients with a fatal outcome, 42 (35–60) minutes passed, in patients with a favorable outcome 48 (40–60) minutes (p = 0.041). The time from hospitalization to primary PCI was 60 (45–104) minutes in patients with a fatal outcome and 60 (45–91) minutes in patients with a favorable outcome (p = 0.981). Conclusion. In patients with STEMI, the time from the pain onset to the first medical contact, from the first medical contact to the first electrocardiogram, from the first electrocardiogram to the hospital door and from the hospital door to balloon inflation during PPCI does not differ significantly in patients with a favorable and fatal outcome.

Diabetes mellitus is widespread in developed countries and plays an important role in the pathogenesis of coronary artery atherosclerosis leading to coronary heart disease. There are many markers of genetic polymorphism that determine the predisposition to type 2 diabetes mellitus, and their list is growing. The purpose of the study was to research the effect of genetic factors characteristic for patients with acute coronary syndrome with and without diabetes mellitus on the severity of coronary artery disease among polymorphic variants of the rs699947 VEGF-A gene, rs9349379 of the PHACTR1 gene, rs3825807 of the ADAMTS7 gene, rs2891168 of the CDKN2B gene, rs3184504 of the gene SH2B3, and rs1746048 of the CXCL12 gene. Material and methods. The study included 238 patients hospitalized in the Cardiology Department of Municipal Clinical Hospital No. 7 of Kazan with acute coronary syndrome (mean age was 62.6±11.1 years), including 158 (66.4%) men and 80 (33.6%) women. In 44 (18.5%) patients with diabetes mellitus, on average, the Gensini scale value was 12 points higher, which characterizes a more severe coronary artery disease; they also had a higher frequency of occurrence of the AA rs699947 genotype of the VEGF gene (OR 2.8; 95 % CI: 1.415–5.711) and CT genotype rs3825807 of the ADAMTS7 gene (OR 2.5; 95% CI: 1.207–4.622). However, the analysis of polymorphic variants rs699947 of the VEGF gene and rs3825807 of the ADAMTS7 gene in patients with acute coronary syndrome associated with diabetes mellitus in a linear regression model did not reveal their significant effect on the severity of coronary artery lesions assessed by the Gensini scale.

The purpose was to examine atherosclerotic changes in the anatomy of coronary arteries in patients with early acute coronary syndrome among carriers of different genotypes: rs3825807 of the ADAMTS7 gene and rs699947 of the VEGF-A gene.The study included 116 patients, 69 (59%) men and 47 (41%) women with the first manifestation of acute coronary syndrome (ACS) before 55 years and 65 years respectively. Coronary angiography revealed at least one stenosis ≥ 40% in all patients during in-house treatment. The genotype of rs3825807 ADAMTS7 gene and rs699947 VEGF-A gene was determined by PCR in all patients. The prevalence of CC genotype rs699947 VEGF-A gene in patients with left circumflex artery stenosis was less than in patients without such a lesion (0.26 versus 0.46, p = 0,03; OR = 0,419; 95% CI: 0,187–0,941). The prevalence of TT genotype rs3825807 ADAMTS7 gene in patients with early manifestation of ACS with stenosis of the posterior basal branch and posterior interventricular branch of the right coronary artery was significantly higher (0,78 versus 0,35, p = 0,027) than in patients without these lesions (OR = 6,36; 95% CI: 1,27–32,59). Thus, with the development of acute coronary syndrome in men up to 55 years old, in women up to 65 years old, the carriage of the Аallele rs699947 VEGF-A gene is associated with lesions of left circumflex artery, and the carriage of TT genotype rs3825807 ADAMTS7 gene is associated with lesions of the posterior interventricular branch and the posterior basal branch of the right coronary artery.

Abstract Introduction According to the GRACE registry the largest amount of deaths occurs in the first year after ST elevation myocardial infarction (STEMI). Purpose To investigate the incidence of Major Adverse Cardiovascular Events (MACE), which include cardiovascular death, nonfatal myocardial infarction, nonfatal stroke one year after STEMI and Wall Motion Index Score (WMSI) in patients with different genotypes A/G of rs2891116 polymorphism in CDKN2B gene. Materials and methods A total of 141 patients, diagnosed with STEMI based on the Third Universal Definition of Myocardial Infarction (ESC, 2013) were included in the study, composed of 52 females and 89 males. The study group mean age was 63.8±11.8 years. Informed consent was obtained. During hospitalization echocardiography was performed and a blood sample was taken for genetic testing. Over the one-year period MACE were recorded. 17 patients were lost to follow up. Data was analysed using Kaplan-Meier estimator; to compare differences between groups log-rank test was applied; continuous data analysis was performed by Mann-Whitney test. The measured genotype frequencies fit the Hardy-Weinberg equilibrium (p>0.05). Results Kaplan-Meier survival analysis revealed that in patients with AA genotype the proportion of individuals who experienced MACE over the one year period after STEMI was higher in comparison with AG genotype carriers (log rank p=0.022). Participants with GG genotype did not show significant differences compared to other genotypes carriers (Picture 1). WMSI value in patients with AA genotype was higher (Me = 1.25; Q(0.25) = 1.13; Q(0.75) = 1.56) than in AG genotype carriers (Me = 1.13; Q(0.25) = 1.13; Q(0.75) = 1.25; p=0.037). In participants with GG genotype compared to AA and AG the WMSI value was not significantly different (Me = 1.19; Q(0.25) = 1.13; Q(0.75) = 1.32). Picture 1 Conclusions Genotype AA in CDKN2B gene rs2891168 in patients after STEMI is associated with higher probability of the development of MACE over the one year period after the index event, compared to AG genotype carriers. Participants with AA genotype exhibited a higher WMSI value after STEMI compared to patients with AG genotype.

The aim of the study was to analyze clinical features of patients with premature acute coronary syndrome (ACS) in relation to family history of cardiovascular disease (CVD) and familial hypercholesterolemia (FH).MATERIALS AND METHODS:Of 2832 patients included in ORACUL 1 and ORACUL 2 multicenter observational trials 512 pts who developed premature ACS (≤55 years for men, ≤60 years for women) and had known family history and LDL level were selected for this study. Of these patients 297 had positive family history (51 with FH, 246 no FH), 215 had negative family history.RESULTS:Among patients with positive family history there were more women (31 vs 20.9 %), while among patients with negative family history there were more men (79.1 vs 69 %). The fact of regular alcohol consumption was significantly more frequently observed among patients with positive family history but without FH, compared to patients with positive family history with FH (69.6 vs 47.1 %). Women with positive family history smoked more frequently than females with negative family history (51.1 vs 31.1 %). Among patients with negative family history compared with patients with positive family history there were more people who at admission had hyperglycemia exceeding 11.1 mmol / l (10.3 vs 4.4 %). Multiple vessel disease and coronary calcinosis were present in 73.2 and 24.7 %, respectively, of patients with positive family history, and in 56.9 and 9.8 %, respectively, of those with negative family history. Among patients with positive family history multivessel disease was more frequent in the subgroup with FH, while coronary calcinosis was more frequent in the subgroup without FH.CONCLUSION:Thus, premature development of ACS might be associated not only with genetic factors but also with family history ("inheritance") of adverse habits. Herewith coronary calcinosis is more prevalent in patients with FH.

The aim of the study was to analyze clinical features of patients with premature acute coronary syndrome (ACS) in relation to family history of cardiovascular disease (CVD) and familial hypercholesterolemia (FH). Materials and methods. Of 2832 patients included in ORACUL 1 and ORACUL 2 multicenter observational trials 512 pts who developed premature ACS years for men, <= 60 years for women) and had known family history and LDL level were selected for this study. Of these patients 297 had positive family history (51 with FH, 246 no FH), 215 had negative family history. Results. Among patients with positive family history there were more women (31 vs 20.9%), while among patients with negative family history there were more men (79.1 vs 69%). The fact of regular alcohol consumption was significantly more frequently observed among patients with positive family history but without FH, compared to patients with positive family history with FH (69.6 vs 47.1%). Women with positive family history smoked more frequently than females with negative family history (51.1 vs 31.1%). Among patients with negative family history compared with patients with positive family history there were more people who at admission had hyperglycemia exceeding 11.1 mmo1/1 (10.3 vs 4.4%). Multiple vessel disease and coronary calcinosis were present in 73.2 and 24.7%, respectively, of patients with positive family history, and in 56.9 and 9.8%, respectively, of those with negative family history. Among patients with positive family history multivessel disease was more frequent in the subgroup with FH, while coronary calcinosis was more frequent in the subgroup without FH. Conclusion. Thus, premature development of ACS might be associated not only with genetic factors but also with family history ("inheritance") of adverse habits. Herewith coronary calcinosis is more prevalent in patients with FH.