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The presented literature review allows us to understand and supplement the existing ideas about the pathogenesis of coronary calcification and aortic valve calcification at the stage of formation of these changes. To study in detail the participation of the most studied immunocompetent cells of innate immunity, such as macrophages, dendritic and mast cells, neutrophils, natural killers in calcification of arteries and aortic valve, their functional role in the progression of this process. The review also presents gaps and missing data present in the study of these cell populations, the replenishment of which will contribute to the development of targeted therapy for the calcification process.The search for literature sources was conducted in the following databases: Scopus, web of Science, MedLine, The Cochrane Library, RSCI, Springer, Science Direct — taking into account the year of publication (no more than 10 years), language of publication (English/Russian), availability of full-text publications and access to them.

Aim. To assess the relationship between the prevalence of visceral obesity (VO) and the severity of coronary calcification (CC) in patients with verified coronary artery disease (CAD). Materials and methods. 125 patients with CAD were examined. Assessment of the morphometric characteristics of visceral adipose tissue (VAT) and CC was perform using multislice computed tomography (MSCT). The calcium index (CI) of the coronary arteries (CA) was determine by the Agatston method. Statistical analysis was perform using Statistica 10.0. Results. VO was detect in 82 (65.6%) patients with CAD. In the presence of VO, higher CC values were observed in the projection of the envelope (p=0.00014), right coronary (p=0.00002) arteries, total CI (p=0.0003), and the prevalence of massive CC. Correlation analysis showed the relationship between the area of VAT and the CC of all the studied localizations. According to the ROC analysis, VO is a significant predictor of massive CC (area under the ROC curve AUC 0.72, 95% CI 0.560.89), in contrast to body mass index BMI (AUC 0.56, 95% CI 0.310.82). Conclusion. The index of the ratio of VAT to subcutaneous adipose tissue (VAT/SAT), but not BMI, had a direct correlation with CC. Morphology of VAT may be a significant diagnostic sign of massive CC in patients with CAD, as a factor affecting treatment and prognosis.

Aim: To assess predictors of progression of coronary artery calcification (CAC) in men with stable coronary heart disease (CHD) after coronary artery bypass graft surgery (CABG) based on longterm (5 years) follow-up. Materials and methods. The prospective study included 111 men who were hospitalized for planned CABG using cardiopulmonary bypass. All patients in the preoperative period underwent the following procedures: color duplex scanning (CDS) of the brachiocephalic arteries (BCA), multi-slice computed tomography (MSCT) coronary angiography to assess the degree of CAC using the Agatson method (calculation of the coronary artery calcium score – CAC) and estimation of femoral neck bone mineral density with the T-score calculation. The vital status of patients was ascertained after 3-5 years of follow-up after CABG, CDS of the BCA and MSCT-coronary angiography were repeated. To identify the most significant clinical and anamnestic risk factors and form a model of predictors of CAC progression, patients were divided into two groups depending on the high increase in CAC score (an increase in the score of more than 100 Agatston units (AU). Results. 16 (14.4 %) out of 111 patients failed to establish contact for the next stage of the study. In 4 (3.6%) cases death was registered (3 – fatal myocardial infarction, 1 – fatal stroke). The CAC progression was assessed in 91 patients (81.9 %). Patients who showed signs of CAC progression comprised a group of 60 (65.9 %) patients; without CAC progression – 31 (34.1 %) patients. The “end points” in the groups were comparable and were detected in 18 cases (19.7 %): recurrent angina in 16 patients (p = 0.368), non-fatal myocardial infarction in 1 (p = 0.162) and 1 emergency stenting (р = 0,162) of the coronary artery that was not subjected to CABG. The five-year risk model for CAC progression included an initial decrease in femoral neck bone mineral density and nonadherence to statins for 5 years after CABG (p = 0.001). Conclusions. 65.9 % of men with stable CHD showed the signs of CAC progression for 5 years after CABG, according to MSCT. The main predictors were: nonadherence to statins after CABG and initial low femoral neck bone mineral density.

Aim. To assess the relationship of various clinical and biological markers of bone metabolism with the progression of coronary artery calcification (CAC) in patients with stable coronary artery disease (CAD) within 5 years after coronary artery bypass grafting (CABG).Material and methods. This single-center prospective observational study included 111 men with CAD who were hospitalized for elective CABG. In the preoperative period, all patients underwent duplex ultrasound of extracranial arteries (ECA) and multislice computed tomography (MSCT) to assess CAC severity using the Agatston score, as well as densitometry with determination of bone mineral density in the femoral neck, lumbar spine and T-score for them, In all participants, the following bone metabolism biomarkers were studied: calcium, phosphorus, calcitonin, osteopontin, osteocalcin, osteoprotegerin (OPG), alkaline phosphatase, parathyroid hormone. Five years after CABG, ECA duplex ultrasound, MSCT coronary angiography and bone metabolism tests were repeated. Depending on CAC progression (>100 Agatston units (AU)), patients were divided into two groups to identify significant biomarkers and clinical risk factors associated with CAC progression.Results. For 5 years after CABG, contact with 16 (14,4%) patients was not possible; however, their vital status was assessed (they were alive). Death was recorded in 4 (3,6%) cases (3 — due to myocardial infarction, 1 — due to stroke). In 18 (19,7%) cases, non-fatal endpoints were revealed: angina recurrence after CABG — 16 patients, myocardial infarction — 1 patient, emergency stenting for unstable angina — 1 patient. There were no differences in the incidence of events between the groups with and without CAC progression. According to MSCT 5 years after CABG (n=91 (81,9%)), CAC progression was detected in 60 (65,9%) patients. Multivariate analysis allowed to create a model for predicting the risk of CAC progression, which included following parameters: cathepsin K