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.

228 is recognized as an independent predictor of oxidative stress and endothelial dysfunction [4, 5, 6]. However, in modern scientific literature, there is still a lack of in-depth analysis of the relationships between these novel markers specifically in patients with comorbid conditions. This creates barriers to the development of individualized programs for secondary prevention and rehabilitation. Objective of the work. To improve approaches to cardiovascular risk stratification by studying the role of lipoprotein (a) (Lp(a)), non-high-density lipoprotein cholesterol (non-HDL-C), and insulin resistance indices in patients with a combined course of AH and AS. Material and methods During the study, a comprehensive clinical and laboratory examination of a cohort of 100 patients (men and women) in the age range from 45 to 70 years was carried out. The diagnosis of AH and AS was based on the current recommendations of the European Society of Cardiology (ESC) and valid national protocols [7, 8]. The presence of atherosclerotic changes was confirmed using carotid artery Doppler ultrasonography: the key criterion was a change in the intima-media thickness complex with visualization of atherosclerotic plaques [8]. The study design involved distributing the participants into four groups:  Group I (AH+AS, main, n=35): patients with a combined course of stage II-III AH and atherosclerosis (confirmed by Doppler).  Group II (AH without AS, comparison, n=22): patients with isolated hypertensive disease without signs of AS.  Group III (AS without AH, comparison, n=22): individuals with detected atherosclerotic lesions of the carotid arteries who do not have a history of AH.  Group IV (control, n=21): practically healthy individuals of the corresponding age. The laboratory complex included the analysis of the lipid profile by the enzymatic method. The non-HDL-C value was calculated using the formula: Total cholesterol (TC) minus HDL-C. The concentration of Lp(a) was measured by the immunoturbidimetric method (values >50 mg/dL were assigned to the high-risk