Objective: the investigation of some modifiable and non-modifiable risk factors and poor explored as well of non-convectional diseases among men of working age.

Subjects and methods. Seven thousand thirty five men in age of 18 to 60 years were examined. History data included age, gender, nationality,
high blood pressure (BP) episodes, antihypertensive drugs taking in case of arterial hypertension, smoking. Instrumental examination included BP measurement when seated after 5 minutes of the rest with mean BP calculation. Total cholesterol and creatinine in blood, clearance of creatinine calculation by Cockcroft–Gault formula, microalbuminuria were assayed; depression level was estimated by Beck score. With purpose to analyze the risk factors structure all examined subjects were divided into three groups according to SCORE scale.

Results. Cholesterol level analysis revealed the increasing of parameter in 41.7 % of examined patients (n = 307). Microalbuminuria was revealed in 13.8 % (n = 102) of men, and 19.3 % of them (n = 80) had increased blood pressure. Some levels of depression were revealed in 42.5 % (n = 312), among them the arterial hypertension was observed in 62,5 % (n = 195). The group with low and moderate cardiovascular risk consisted of 594 persons (80.8 %). High cardiovascular risk was determined in 15.2 % men of working age (n = 112). Very high cardiovascular risk was revealed in 3.9 % (n = 29) of responders.

Conclusion. Increasing of traditional risk factors rate is associated with increasing of additional risk factors. Received data are widening the perception about risk factors structure in population. Particularly the question about renal filtration function role, depressive syndrome, trophologic insufficiency is raised. Consideration of those in prophylaxis system consideration requires a specific education of general practitioners.

Objective: to estimate the frequency and magnitude of acute kidney injury (AKI) in patients with acute decompensated chronic heart failure
(ADCHF) and to clarify the relationship of AKI to mortality.

Subjects and methods. One hundred and four patients (58 men and 46 women; mean age 65.3 ± 10.68 years) with ADCHF were examined.
AKI was diagnosed and classified by the KDIGO criteria.

Results. In terms of creatinine, AKI was diagnosed in 74 (71 %) patients (Stage I in 51 (49 %), Stage II in 20 (19 %), and Stage III in 3 (3 %)
patients. Five (5 %) patients died during hospitalization. All the dead patients had AKI. Multivariate regression analysis demonstrated that regardless of gender, age, chronic heart failure stage, the in-hospital mortality was associated with the level of creatinine (R = 0.29; β = 0.20;
p = 0.046). At the same time, in the patients with AKI Stages II-III the probability of in-hospital mortality was higher than that in the other patients (relative risk, 23.4; 95 % confidence interval 2.9–187.0; p = 0.003).

Conclusion. More than half of the patients with ADCHF have AKI according to the KRIGO criteria. The in-hospital mortality is much higher
amongst the patients with AKI Stages II-III.

Atherosclerotic lesion of lower extremity arteries frequently complicates the long-term course of hypertension and it is generally associated with coronary heart disease. Our study has attempted to evaluate the impact of combination antihypertensive therapy involving amlodipine, bisoprolol, and lisinopril on quality of life in this category of patients.

Objective: To show the efficiency of dyslipidemia control in patients with coronary heart disease (CHD) and diabetes mellitus (DM) in real outpatient clinical practice and the possibilities of its correction in the long-term use of simvastatin (simvastatin forte 40 mg) in one of the
Nizhny Novgorod polyclinics.

Subjects and methods. The efficiency of lipid profile control was analyzed in a sample from the entire dispensary group of patients with DM (n = 713). Patients at highest cardiovascular risk were selected from the dispensary group and included into a group of CHD and DM. There were a total of 461 (64.7 %) such patients. Forty-three patients were identified in this group, who were matched for baseline systolic and diastolic blood pressures, age, gender, and DM duration and were found to have significant hypercholesterolemia. Simvastatin forte 40 mg was
prescribed to these patients at their outpatient visit. During a year, the patient made 6 visits to his/her physician (5 visits at 6-werk intervals and the sixth visit by the end of the follow-up year). The dose of simvastatin was unchanged throughout the study.

Results.In the entire dispensary group, 64.7 % of the patients had a concurrence of CHD and DM. This group of patients was at high risk for dyslipidemia. In this group, 2.8 % had a total cholesterol (TC) level of ≤ 3.5 mmol/l; 4.7 % had a low-density lipoprotein cholesterol (LDL-C) level of < 1.8 mmol/l. The total lipid profile was analyzed in only 6.3% of the patients from the entire dispensary group. 28.6 % of the patients with type 1 DM and 21.3% of those with CHD and type 2 DM took statins. Fifty-two week therapy with simvastatin forte 40 mg showed its high efficiency in real practice in decreasing the levels of atherogenic lipids and lipoproteins: TC by 27.6 % (p < 0.001), LDL-C by 36.9 % (p < 0.001), and triglycerides by 34.3 % (p < 0.001) with antiatherogenic high-density lipoprotein cholesterol elevation by 15.2 % (p < 0,001). Simvastatin forte therapy was well tolerated: the mean values of liver enzymes and the activity of creatine phosphokinase remained within the normal range. After one-year simvastatin forte therapy, the blood concentration of glucose decreased by 10.5%.

Conclusion. Simvastatin forte (40 mg/day) demonstrated good hypolipidemic efficacy, tolerability, and high safety profile in patients with CHD and DM.

The paper considers the main causes of cardiac embolic events. It is emphasized that atrial fibrillation is a major risk factor for systemic embolism. Main approaches to assessing the risk of stroke/systemic embolisms and their prevention using the currently available anticoagulants are given.

The paper considers the current views of the prevalence, clinical picture, approaches to the diagnosis and treatment of one of the most common
neurological complications of diabetes mellitus – diabetic polyneuropathy, and both its somatic and autonomous manifestations. Neuropathy is
most common in diabetic patients and its clinical forms reflect the severe course of diabetes mellitus and serve as an unfavorable prognostic sign
that is associated with an approximately 5-fold increase in mortality. At the same time, the timely detection and adequate correction of the manifestations of neuropathy may substantially improve quality of life in the patients. The possibilities of pathogenetic therapy for diabetic polyneuropathy associated mainly with the use of benfotiamine and alpha-lipoic acid, as well as symptomatic therapy for its individual manifestations
are considered.

The paper considers the basic mechanisms for the occurrence of asthenic syndrome in chronic neurological diseases. It shows the significance of
this problem in nosological entities, such as stroke sequels, multiple sclerosis, and Parkinson’s disease. The main asthenia diagnostic scales are
described. Possible therapeutic strategies aimed at reducing the degree of asthenia in neurological patients are also presented.

Ischemic stroke (IS) is a severe disease associated with high mortality and persistent disability. Prior IS is related to the drastically increased risk of repeat IS. Antiplatelet therapy is an efficient way to prevent repeat IS. Acetylsalicylic acid, the administration of its enteric-coated formulation
can reduce the risk of gastric mucosal lesion, has a special efficacy. The possibilities of using other antiaggregants and indirect anticoagulants
are considered.

The paper discusses the problems of correct diagnosis and rational pharmacotherapy of depressive disorders in patients with cardiovascular
diseases frequently found by practical cardiologists and therapists.

Acute and chronic brain ischemia is accompanied by complex metabolic rearrangements in the neurons. The ability of the cells to survive is largely determined by the presence of energy substrates and oxygen, the synthesis of neurotransmitters, and some other factors. The increased
persistence of nerve tissue in ischemia and chances of recovering the impaired function can be achieved by the use of neuroprotective and neurotrophic agents. The efficiency of neurometabolic therapy is considered using Ceraxon and Actovegin as an example. It is emphasized that the
efficiency of their administration can be achieved by the mandatory concurrent use of a wide range of nondrug treatments.

Objective: to analyze the distribution of components of insulin resistance (IR) syndrome and to study the frequency of their combinations in relation to the genotypes and allelic variants of the angiotensin-converting enzyme (ACE) gene.

Subjects and methods. A group of clinically healthy patients (50 women and 42 men) with different genotypes of the ACE gene was examined.
The distribution of IR syndrome components and the frequency of their combinations were analyzed in relation to the genotypes and allelic
variants of the ACE gene.

Results. A group of D allele carriers compared to A allele ones showed a pronounced tendency for the frequency of IR to reduce due to the
higher proportion of patients with complete IR syndrome. This observation becomes statistically significant in the assessment of homozygous variants of the ACE gene. At the same time dyslipidemia and hypertension in the presence of IR significantly more frequently occurred in patients with the DD genotype than in those with genotype II.

Conclusion. There was a marked predominance of the manifestations of IR syndrome with a complete set of components in the DD genotypic
group, which confirms the significant strong association between ACE gene polymorphism and IR syndrome.

Objective: to study whether genotyping for single nucleotide polymorphisms (SNPs) rs10757278 and rs1333049 on the 9p21.3 locus may be applied to myocardial infarction (MI) risk stratification using the SCORE scale in young people (less than 45 years).

Subjects and methods. A group of patients with MI (n = 103) and a control group (n = 111) showed no statistically significant differences in
gender, age, hypertension, diabetes mellitus, hypercholesterolemia, overweight and obesity, abdominal obesity, and smoking history. The phenolchloroform method was employed to extract genomic DNA from venous blood. Genetic tests were carried out using real-time polymerase
chain reaction systems (TagMan and AB 7900HT).

Results. There was a statistically significant association of rs1333049 and rs 10757278 with the development of MI. The odds ratio for the latter was 2.53 (95 % confidence interval (CI) 1.31-4.89) in carriers of the risk allele C of rs1333049 and 2.11 (95 % CI 1.11–4.01) in those with the risk allele G of rs10757278. The statistical significance also remained with consideration for the family history of MI. Multiple logistic regression analysis established that the presence of the C allele of rs1333049 in the genotype was of great predictive value as compared with the high/very high risk of fatal and nonfatal events according to the SCORE scale.

Conclusion. SNPs 1333049 and rs10757278 on the 9p21.3 locus are the predictors of MI in young people, which are independent of both traditional risk factors and family history. Having regard to the pattern of an association, it will suffice to genotype one of them, namely rs 1333049, in our population

Mitochondria are not only the major producers of adenosine triphosphate, but also an endogenous source of reactive oxygen species. Mitochondrial
dysfunction plays a key role in the trigger and progression of atherosclerotic lesion. Impaired function in the mitochondria due to their elevated level of oxidized oxygen species, the accumulation of mitochondrial DNA damages, and the exhaustion of respiratory chains induces dysfunction and apoptosis in the endothelial cells; activation of matrix metalloproteinases; growth of vascular smooth muscle cells and their migration into the intima; expression of adhesion molecules, and oxidation of low-density lipoproteins. Mitochondrial dysfunction may be an important unifying mechanism that accounts for the atherogenic effect of major cardiovascular risk factors. Small clinical pilot studies have shown an association of different mitochondrial genome mutations with atherosclerotic lesion in the artery. Taking into account the available data on the possible role of mitochondria in atherogenesis, novel drugs are now being designed to affect mitochondrial function.