Aim. To evaluate the effectiveness of combined antihypertensive chronopharmacotherapy and estimate the daily blood pressure profle (BP) parameters, such as: stiffness of the vascular wall and central aortic pressure in patients with arterial hypertension (AH) who underwent transient ischemic atack (TIA) or ischemic stroke (IS).

Materials and methods. 235 patients with hypertension who underwent acute cerebrovascular accident were examined. Tere were 116 patients with TIA and 119 with IS. All patients were randomized in 4 groups according to regimen of antihypertensive drugs combination. Te 1st group (n = 59) included patients with AH, who underwent TIA and received indapamide retard 1.5 mg and valsartan 160 mg in the morning regiment of drug therapy. Te 2nd group (n = 57) included patients with AH, who underwent TIA and received indapamide retard 1.5 mg in the morning and valsartan 80 mg twice a day (morning and evening). Te 3rd group (n = 47) included patients with AH, who underwent IS and received indapamide retard 1.5 mg and valsartan at a dose of 160 mg in the morning. Te 4th group (n = 56) included patients with AH, who underwent IS and received indapamide retard 1.5 mg in the morning and valsartan 80 mg twice a day (morning and evening). Ambulatory blood pressure monitoring (ABPM), central aortic pressure (CAP) measurement and vessel wall stiffness values were evaluated before treatment and afer 12 months of therapy.

Results. Before the start of combined antihypertensive chronopharmacotherapy, most of the parameters for ABPM, vessel wall stiffness values and CAP in groups 1 and 2, 3 and 4 were comparable. Achievement of the target level of BP afer 8 weeks of treatment, was signifcantly more ofen in groups with a double sartan therapy (group 2 and group 4) in compare with its single time application only in the morning hours (group 1 and group 3) (p<0.05). Statistically signifcant positive dynamics of the main values of the daily profle of blood pressure, stiffness of the vascular wall and central aortic pressure (p <0,05) were registered in all groups. However, more pronounced decline of main parameters of ABPM, stiffness of the vascular wall and central aortic pressure values were noted in group with double use sartan therapy in compare with single time sartan therapy in the morning time. (p <0.05). Signifcant positive dynamics of the main values of the ABPM, stiffness of the vascular wall and CAP were registered in patients who underwent IS and received double application sartan therapy (4th group) in compare with patients with TIA (2nd group) (p = 0.02).

Conclusion. Double use sartan therapy, combined with a thiazide diuretics in patients, who underwent IS or TIA more ofen promotes to get target values of blood pressure, improve the main values of the ABPM, stiffness of the vascular wall and CAP in compare with single time sartan therapy in the morning time

Aim. To perform a repeated epidemiological study of a representative sample in the European part of the Russian Federation in 2017 and to compare the dynamics of arterial hypertension (AH) prevalence with the effectiveness of blood pressure (BP) control in the population compared to 1998, 2002, and 2007.

Materials and methods. A representative sample of the European part of the Russian Federation was created in 2002 and re-examined in 2007 and 2017. In 1998, a pilot project was performed for examining a representative sample for the Nizhniy Novgorod region.

Results. During 19 years of follow-up, the AH prevalence increased from 35.5 to 43.3%. Te awareness and treatment coverage reached 76.9 and 79.3%, respectively, in 2017. Achievement of the target BP with a single measurement also increased among patients receiving antihypertensive medication from 14.3 to 34.9%. For the treatment of AH, medium-acting antihypertensive drugs are used, ofen at suboptimal doses.

Conclusion. Epidemiological indices of awareness, treatment coverage, and number of effectively managed patients with AH have improved. However, the AH prevalence has increased by 7.8% for 19 years, which indicates inefciency of the primary prevention of this disease.

Cardiovascular toxicity is one of the important problems of clinical oncology. Atherosclerosis progression was demonstrated in patients with cancer and chemotherapy.

Te aim – to evaluate the vascular wall characteristics and to determine the predictors of AS of brachiocephalic arteries progression during anticancer therapy in patients with breast cancer.

Methods. Te study involved 43 patients with newly diagnosed breast cancer (BC) (II–III stage) with overexpression of HER2; median age 50 (40;57) years. All patients underwent neoadjuvant drug therapy with antracyclines, taxanes and trastuzumab followed by surgery, radiation and hormone therapy according to the indications. Before anticancer therapy the general clinical examination was conducted and lipid profle, plasma lipoprotein (a) [Lp(a)] level, titres of autoantibodies IgM and IgG to lipoproteins and their oxidized derivatives were estimated. Te vascular wall stiffness (pulse wave velocity on the carotid-femoral (PWVcf) and shoulder-ankle (PWVsa) segments, the central pressure, carotid intima-media thickness (CIMT) and the degree of stenosis of the brachiocephalic arteries) were determined at baseline and at each stage of anticancer therapy. Te atherosclerosis progression was determined if the new stenosis (≥15%) or increase of preexisting stenosis (≥5%) were revealed; CIMT increase ≥ 0.1 mm. Te parameters of cellular immunity (peripheral blood lymphocyte phenotyping via direct immunofluorescence and flow cytometry), lipid spectrum parameters, serum concentration of Lp (a), autoantibodies IgM and IgG against lipoproteins and their oxidized derivatives, as well as PWVсf and PWVsa were assessed in 17 BC patients before the onset of neoadjuvant therapy and in 20 healthy women.

Results. BC patients and healthy women were comparable in traditional cardiovascular risk factors but differed in PWVsa and PWVcf levels (p<0.05). In BC patients the activation of T-cell immunity with the stimulation of both subpopulations with pro-inflammatory and regulatory properties was observed (p<0.05). Te direct correlations between the content of activated T-lymphocytes (T-act), T-helpers (T) 1 and PWVsa (p<0.05), as well as T-act, T1 and T2 and PWVcf (p<0.05) were revealed in the general group. Te decrease of systolic blood pressure (SBP), central SBP (SBPc), central diastolic blood pressure (DBPc), PWVcf and PWVsa levels accompanied with a temporary heart rate increase were observed during anticancer therapy; SBP, SBPc, PWVcf levels restored by the end of the follow-up period. Te CIMT increase was detected in 22 (51%), and the atherosclerosis progression in 26 (60%) BC patients during anticancer therapy. Lp (a) level above 12.8 mg/dl was associated with CIMT increase (p<0.05). Age > 48 years and radiation therapy were risk factors for CIMT increase and atherosclerosis progression (p<0.05), respectively.

Conclusions. Te vascular stiffness is increased in BC patients, which is associated with the activation of effector subpopulations of T-lymphocytes and the elevation of circulating level of both pro-atherogenic and anti-atherogenic T-cells. Te level of Lp (a) above 12.8 mg/dl is associated with atherosclerosis progression, which requires further research. Age and radiation therapy are the risk factors for atherosclerosis progression during anticancer therapy.

Purpose: to study prognostic value of various biomarkers and their combinations in patients who survived decompensation of chronic heart failure.

Materials and methods. Patients (n=159) who were hospitalized with diagnosis of heart failure (HF) decompensation were included in a prospective single-center study. Examination on admission and the day of hospital discharge, included measurement of concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hsTnT), copeptin, soluble suppression of tumorigenicity 2 (sST2), kopetin, neutrophil gelatinase-associated lipocalin (NGAL), and galectin-3. Te combined primary endpoint comprised cardiovascular (CV) death, frst hospitalization because of HF heart failure decompensation, episodes of HF deterioration which required additional i/v diuretics, and CV death with successful resuscitation.

Results. During one-year follow-up 56 pts (35.2%) reached the combined primary endpoint. Tere were 78 (49.1%) cardiovascular events. During hospitalization, patients with the decompensation of heart failure experienced a decrease of sST2, NT-proBNP, galectin-3, kopetin, hsTnT and an insignifcant increase of NGAL. ROC analysis identifed signifcant relation between concentrations of NT-proBNP, sST2, copeptin and, to a lesser degree, hsTnT, determined at hospital discharge, and risk of combined primary endpoint during 1-year follow-up: area under the curve (AUC) was 0.733 [95% CI 0.645–0.820], p<0.0001, 0.772 [95% CI 0.688–0.856], p<0.0001, 0.735 [95% CI 0.640–0.830], p<0.0001, and 0.659 [95% CI 0.553–0.764], p=0.005, respectively. Patients who during hospitalization did not achieve cut-off values of NT-proBNP ≤1696 rg/ml, sST2≤37.8 hg/ml, copeptin≤28.31 rmol/L and hsTnT≤28.37 rg/ml, had higher risk of reaching adverse events during 1 year; OR and 95% CI were 2.96 [1.61, 5.42] p<0.0001, 4.31 [2.34, 7.93] p<0.0001, 3.06 [1.59, 5.89] and 2.19 [2.12, 4.27]), respectively. According to Cox regression analysis, risk of the combined primary end point was the highest in patients with 3 or more elevated markers (OR = 6.6 [3.584, 12.158], p<0.0001), average in patients with 2 elevated markers (OR = 1.123 [0.51, 2.48]), p=0.7), and the lowest in patients with no markers increase or increase of only one marker (OR = 0.11 [0.049, 0.241], p<0.0001). In the Kaplan-Mayer survival analysis all three groups were statistically different. In order to identify the most prognostically strong model, a reclassifcation analysis was performed. According to this analysis, the combination of sST2 and NT-proBNP concentrations determined at hospital discharge, exceeded one NT-proBNP (reclassifcation = –8.1%). At the same time, predictive value of only sST2 just insignifcantly less than value of sST2 and NT-proBNP combination (reclassifcation = –1.9%).

Conclusion. Patients with three and more elevated markers at hospital discharge have high risk of adverse events. Te biggest prognostic value has combination of sST2 and NT-proBNP concentrations. In order to determine the long-term prognosis of a patient with HF decompensation, it is sufcient to measure concentrations of sST2 and NT-proBNP at hospital discharge. Alternatively, it is possible to limit to sST2 only, which is just insignifcantly inferior to the sST2 and NT-proBNP combination. Patients with concentrations of sST2 ≥37.8 hg/ml and NT-proBNP ≥1696 rg/ml at hospital discharge have maximal 1year risk of death due to recurrent HF decompensation.

Te increase in the prevalence of arterial hypertension (AH) in populations, ineffective treatment, the need for risk stratifcation, prevention, early diagnosis and successful treatment, actualize genomic studies to develop a personalized therapeutic approach to AH. Te review investigates the possible genetically determined mechanisms of the development of hypertension and endothelial dysfunction caused by polymorphism of the genes of endothelial nitric oxide synthase (eNOS) and enzymes of phases I and II of the xenobiotics detoxifcation system. Te probable interaction of both systems under the influence of harmful environmental factors, including tobacco smoking, and in the gestational period is discussed. It is proposed to study AH candidate genes in the xenobiotics detoxifcation system, the carriage of different variants of which can determine the sensitivity or resistance to antihypertensive pharmacotherapy, which can be useful for developing of the personalized tactics of managing patients with AH.

Tis review presents data on prevalence, control, and effectiveness of treatment of hypertension in male and female. Te features of protective action and manifestations of undesirable effects of antihypertensive therapy in male and female, as well as situations influencing the choice of a drug depending on sex are discussed.

Goal of research. Study the role of thrombosis risk factors and polymorphisms in genes in young age patients with acute coronary syndrome (ACS).

Materials and methods. Te study included 299 patients of age 25 to 44 years old with ACS were treated from 2012 to 2017 at the department of myocardial infarction 1st KGBUZ Altay regional cardiological clinic. Te middle age of patients with ACS was 40.3 ± 0.2 years. Te control group included of 53 apparently healthy volunteers aged from 25 to 44 years old, the average age those patients was 39.94 ± 0.79 years. Also, those patients hadn’t any comorbid conditions. Te control group hadn’t any datas of ischemic heart disease by the results of exercise tolerance tests. All patients had standard clinical, anamnestic, biochemical tests, lipid profle, fasting plasma glucose, electrocardiogram, echocardiography and coronaroangiography, also they were determined growth and weight with body-weight index. 116 patients from the ACS group and 53 patients fromthe control group had screening of polymerase chain reaction for determine polymorphism of the FII genes G20210-A, FV G1691-A, and MTHFR C677-T.

Results. We identifed the most signifcant sets of risk factors associated with ACS in young age patients based on our multifactorial statistical analysis with binary logistic regression. Tis combination of risk factors was: increased levels of low-density lipoproteins, decreased levels of high-density lipoproteins, smoking, existence of MTHFR homozygous polymorphism, heredity in combination with smoking, FV homozygote, MTHFR homozygote, smoking with MTHFR-homozygote.

Conclusion. Te ability predicting the risk of developing cardiovascular disease in young people based on traditional risk factors, partly modifable, as well as the researching of "new" risk factors, opens up new opportunities for developing a clinical approach of treating young patients with high risk of ACS.