Proceedings of the International scientific and practical conference ― Cambridge Science and Education Conference‖ (February 23-25, 2026) / Publisher website: www.naukainfo.com. – Cambridge, United Kingdom, 2026. - 289 p.

231 consistent with the conclusions of the Multinational Cardiovascular Risk Consortium (2019), where the strongest correlation of CVD risk specifically with this parameter was proven [11]. In our sample, the non-HDL-C level was elevated regardless of the type of disease. The pathophysiological basis of this phenomenon lies in the fact that non-HDL- C accumulates the cholesterol of all apoB-containing lipoproteins, including very low-density lipoproteins (VLDL) and their remnants. With hyperinsulinemia (evidenced by the high HOMA-IR in the 1st group), the function of lipoprotein lipase decreases, which causes the accumulation of triglyceride-rich remnants in the blood plasma [12, 13]. It is critically important that these particles freely penetrate the vascular intima, are absorbed by macrophages, and provoke the rapid formation of foam cells, accelerating the progression of AS [14]. The impact of Lp(a) deserves special attention. We recorded its highest indicators in isolated AS (65.95±5.20 mg/dL), which proves its role as an independent driver of atherogenesis. However, in AH patients with concomitant AS, the level of Lp(a) was also significantly elevated (48.31±2.91 mg/dL), which corresponds to the position of the European Atherosclerosis Society Consensus (2022) [15]. The toxic effect of Lp(a) on blood vessels is carried out through proatherogenic (due to oxidized phospholipids) and prothrombotic mechanisms [16, 17]. Probably, a synergistic mechanism works in patients of the 1st group: high blood pressure and blood turbulence mechanically damage the endothelium, facilitating the infiltration of Lp(a) molecules into the vascular wall. Therefore, plaques grow rapidly even at somewhat lower concentrations of Lp(a) compared to isolated AS [18]. In addition, we noted a clear parallelism between hyperuricemia and insulin resistance, which peaks precisely in comorbidity (uric acid 351.56±5.42 µmol/L). The synchronous growth of these two indicators indicates their deep molecular connection. As the results of the URRAH study demonstrate, uric acid functions not only as a metabolite but also as an active mediator of vascular inflammation [19, 20]. A high insulin level stimulates the reabsorption of urates and sodium in the kidneys (thanks to the URAT1 transporter), leading to the accumulation of uric acid in AH