СВЯЗЬ ОКИСЛИТЕЛЬНО-АНТИОКСИДАНТНЫХ ИЗМЕНЕНИЙ ЛИПОПРОТЕИНОВ НИЗКОЙ ПЛОТНОСТИ С ИШЕМИЧЕСКОЙ БОЛЕЗНЬЮ СЕРДЦА В ПОПУЛЯЦИИ МУЖЧИН НОВОСИБИРСКА

Aim. To investigate the association between potentially atherogenic oxidativeantioxidant modifications of low-density lipoproteins (LDL) and coronary heart disease (CHD) in a male population.  Material and methods. A population-based survey included 1024 male residents ofNovosibirskCity, aged 47–73 years. The participants underwent a questionnaire survey, a standard cardiologic survey, anthropometry, blood pressure measurement, and electrocardiography. “Definite CHD” (Functional Class II–IV stable effort angina) was registered in 223 men (21,8%), according to validated epidemiologic, clinical, and functional criteria. Blood biochemistry analyses focused on the levels of total cholesterol (TCH), triglycerides (TG), high-density lipoprotein cholesterol (HDL–CH), high-sensitivity C-reactive protein (hsCRP), glucose, baseline levels of lipid peroxidation (LPO) products and fat-soluble antioxidants (alpha-tocopherol, retinol, beta-carotene, and xanthines) in LDL, LDL oxidation resistance in vitro, and an concentration of autoantibodies to oxidised LDL (oxLDL).  Results. There were positive correlations and independent associations between the oxidative LDL modifications, in particular between reduced LDL oxidation resistance and CHD. On the other hand, there were negative correlations between the antioxidant LDL modifications (such as reduced alpha-tocopherol levels in LDL) and CHD. The prevalence of CHD was higher in participants with baseline levels of LPO products in LDL >0,8 nM MDA/mg LDL protein and with reduced LDL oxidation resistance (baseline levels >5,4 nM MDA/mg LDL protein vs. levels >13,2 nM MDA/mg LDL protein at later stages of LDL oxidation). However, the prevalence of CHD was lower in individuals with LDL levels of alpha-tocopherol >1,06 mg/mg LDL protein.  Conclusion. These findings agree with the previously obtained data on the key role of oxidative LDL modifications in the pathogenesis of atherosclerosis and CHD.