Objective. To study relation between carotid atherosclerosis and arterial hypertension, and possible benefits of surgery. Design and methods. 70 hypertensive patients operated on cerebral arteries were examined: 50 patients had stenosis of carotid arteries (CA) and 20 - cerebral arterial anomalies. Results. The patients with carotid atherosclerosis had higher blood pressure (BP) than patients with brachiocefalic arterial anomaly (103,6 ± 11,3 and 91,7 ± 6,6 mmHg, respectively; r = 0,00007). This difference has disappeared in postoperative period. Both systolic (from 145,1 ± 14,7 to 135,6 ± 12,3 mmHg; р = 0,02), and diastolic (from 83,3 ± 10,2 to 78,1 ± 9,7 mmHg; р = 0,02) blood pressure reduced after the surgery on CA. Conclusions. We conclude that there is an association between ВР level and carotid atherosclerosis. The reduction of BP was observed in postoperative period in patients with atherosclerosis of CA.

At present, the problem of concomitant diseases still remains very important for medical science as well as for medical practice. Arterial hypertension is one of the most actual global healthcare problems, holding the leading place among cardiovascular diseases. Acid-related diseases, including gastroesophageal reflux disease and duodenal ulcer are also widely-spread with the tendency of prevalence growth, and are having the leading place among gastrointestinal diseases. The combination of arterial hypertension and acid-related diseases is a new state of an organism regulation. Their synchronism is not accidental, as both diseases share links of the general etiology and pathogenesis. The daily arterial pressure profile and heart rhythm variability has a number of distinctive features when the diseases collide. The presence and progression of esophageal and duodenal mucous membranes inflammation in these patients promotes the certain arterial blood pressure profile formation. The data concerning the prevalence, common etiology and pathogenesis, features of hemodynamics and clinical manifestations in patients with arterial hypertension associated with peptic ulcer disease and gastroesophageal reflux disease are reviewed. Data of autonomic regulation features, 24-hour blood pressure profile and central hemodynamics condition in patients the combination with the mentioned diseases are also covered.

The intestinal microbiota is a marker of the organism state, capable of direct and indirect interacting. The main mechanisms underlying interactions are immunoregulation and energy metabolism. Metabolites, formed during the life of microbiota, realize their actions through these engagements. Some metabolites arouse negative effects on endothelial vessels, causing and maintaining a systemic inflammatory response, which stands behind major cardiac risk factors. Metabolites and molecules such as lipopolysaccharide or trimethylamine N-oxide initiate endothelial dysfunction, and thus trigger the processes of atherogenesis, insulin resistance and even increase blood pressure by activating inflammasomes and pro-inflammatory cytokines. Short-chain fatty acids including the main metabolites such as acetate, propionate and butyrate are antagonists of lipopolysaccharide and trimethylamine N-oxide. These substances are a source of energy for intestinal epithelial cells. They maintain homeostasis, stimulate the production of anti-inflammatory components and activating reparative processes. Another important factor influencing levels on blood pressure and systemic inflammation is intestinal barrier dysfunction, which is determined by the regulatory protein zonulin. Besides, there are proved receptor interactions, as well as qualitative and quantitative changes in the composition of the microbiota that can influence blood pressure and atherogenesis. Each cardiovascular disease is characterized by its own microbiological pattern and the predominance of specific metabolites. The article presents a review, summarizing experimental and clinical data on the role of microbiota in the development of atherosclerosis and cardiovascular diseases.

Purpose. The study of protein-producing and lipid-releasing ability of neutrophils and its clinical significance in patients with IHD.Materials and methods. 25 patients with arterial hypertension without clinical and ultrasound manifestations of atherosclerosis were examined; 47 patients with coronary artery disease with stable angina, as well as 19 patients with unstable primary angina. The comparison group — 33 healthy persons. In the serum, enzyme-linked immunosorbent assay was used to evaluate the concentration of C-reactive protein (CRP), lipoprotein a (LPa), VII coagulation factor VII (VIIf), defensins-alpha (1–3), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-alpha). Leukocytes, predominantly represented by neutrophils, which were further cultivated, were excreted from peripheral blood in the presence of dextrans; the levels of CRP, LPa, defensins-alpha (1–3), VIIf, and lipid-releasing ability of leukocytes (LRAL) were assessed according to the method of A. V. Tuev and V. Yu. Mishlanov. An angiographic study, duplex scanning arteries, and echocardiography were performed.Results. It has been established that in patients at the stage of preclinical atherosclerotic lesion, the ability of leukocytes to form protein-lipid complexes (PLC), marked by LRAL, practically does not differ from healthy individuals, but already at this stage of atherogenesis an increase in their ability to produce antimicrobial peptides — defensins-alpha (1–3). In patients with coronary artery disease with stable angina pectoris, an increase in leukocyte production of a wide range of proteins — defensins-alpha (1–3), VIIf, LPA and CRP in combination with signs of a systemic inflammatory reaction, marked by high concentrations of CRP, interleukin-6 and tumor necrosis factor alpha in serum, was noticed. At this stage of atherogenesis, the value of LRAL is significantly different from the values of healthy individuals. It is shown that the higher the LRAL value, the higher the functional class of chronic heart failure in these patients (R = 0.4; p = 0.02). In patients with coronary artery disease with primary unstable angina, the maximum LRAL value was detected, and in patients with ultrasound signs of plaque instability, high concentrations of CRP in neutrophilic supernatants were found. Correlation analysis revealed that, in patients with coronary artery disease, the average percentage of coronary artery stenosis, according to angiography, is directly related to the LRAL value (R = 0.7; p = 0.03) and the serum concentration of TNF-alpha (R = 0.5; p = 0.03), and the number of clinically significant stenoses — with the magnitude of LRAL (R = 0.4; p = 0.04) and the concentration in supernatants VIIf (R = 0.5; p = 0.04).Conclusion. The LRAL value, CRP and defensin-alpha content in leukocyte supernatants in IHD patients are interconnected with the severity and activity of atherosclerotic lesion of arteries, which is confirmed by the results of examination of patients at the stage of preclinical, clinically manifest stable and unstable atherosclerotic lesion.