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.
232 [21, 22]. Intracellular uric acid activates NADPH oxidase, which leads to the production of superoxide radicals, neutralization of nitric oxide (NO), and, consequently, to vasoconstriction [23, 24]. Comparing our results with classical studies (for example, INTERHEART), one can confidently recommend identifying the phenotype of "comorbid patient with high non-HDL-C and metabolic imbalance" [25]. Traditional prognostic scales (SCORE2) may underestimate the danger for such patients, as they do not take into account the impact of Lp(a) and remnant cholesterol [26, 27]. Accordingly, the diagnostic search must necessarily include an extended lipid profile and detailed metabolic screening. Conclusions 1. A specific and extremely unfavorable "metabolic-inflammatory" profile is formed in patients with a combined course of hypertensive disease and atherosclerosis. It is characterized by a synergistic increase in the HOMA-IR index (2.1 times higher than the control) and the level of uric acid (by 26%), which is a sign of deep maladaptation of the body's systems. 2. Lipoprotein (a) acts as a powerful and independent risk factor. Its peak concentrations (65.95±5.20 mg/dL) are associated with isolated atherosclerosis. At the same time, in patients with comorbidity, its increase (48.31±2.91 mg/dL) under conditions of hemodynamic load creates ideal conditions for accelerated vascular damage. 3. Non-HDL cholesterol confirmed its role as the most sensitive and universal marker of atherogenicity, which reliably exceeded the norm in all studied groups. It accumulates the entire spectrum of atherogenic lipids, particularly triglyceride-enriched remnant particles, which support intimal inflammation against the background of reduced insulin sensitivity. 4. In the group of patients with comorbid pathology, a direct correlation between carbohydrate metabolism imbalance and hyperuricemia was recorded. This dictates the necessity to consider uric acid as an independent therapeutic target and to include uricosuric drugs in comprehensive treatment regimens for patients with a combination of AH and AS.
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