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.
229 zone). To assess the state of carbohydrate metabolism, the level of glycated hemoglobin (HbA1c) was determined, and the insulin resistance index HOMA-IR was calculated using the formula: (glucose × insulin) / 22.5. Statistical processing of data arrays was performed using modern biostatistical methods. The test for normality of distribution was carried out visually and using the Shapiro-Wilk test. With a normal distribution, ANOVA analysis of variance with Tukey's post-hoc test was applied, and with a non-normal distribution, the Kruskal- Wallis test was used. When significant differences were detected, pairwise comparisons were additionally performed using the Mann-Whitney test with Bonferroni correction. Data with a normal distribution are presented as M ± SD, and with a non-normal distribution as Me [IQR] (in the table as M±m). Differences were considered reliable at p < 0.05. Results of the study and their discussion Evaluation of the indicators in the four identified groups allowed tracing clear regularities. The deepest metabolic disturbances were recorded in patients of the main group (AH + AS), while healthy volunteers from the control group demonstrated baseline (lowest) values. This confirms the thesis that the comorbid course of the two pathologies causes a synergistic effect, which significantly aggravates the patient's condition. The level of lipoprotein (a) demonstrated the greatest contrast between the subgroups. In particular, in patients with isolated atherosclerosis (Group 3), its concentration was 65.95 ± 5.20 mg/dL. This is almost 1.7 times higher than the value of the control group (24.36 ± 2.88 mg/dL; p=0.0002). In patients with comorbidity (Group 1), Lp(a) was also significantly elevated — 48.31 ± 2.91 mg/dL (which is 98% higher than the control, p=0.0012). Interestingly, in individuals with isolated hypertension (Group 2), this indicator was reduced by 49% (12.53 ± 0.63 mg/dL; p=0.0002). These facts convincingly prove the independent role of Lp(a) in the development of specifically atherosclerotic changes. The non-HDL-C indicator turned out to be reliably higher than normal in all clinical groups. In the 3rd group, it reached 4.77 ± 0.11 mmol/L (exceeding the control by 29%, p=0.0006). In the 1st group, it equaled 4.66 ± 0.07 mmol/L (+26%;
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