Aim.To investigate on the relation of lipoproteide(a) (Lpa), subfractions of atherogenic lipoproteides and titers of specific autoantibodies (autoAb) with the presence and severity of carotid arteries (CA) lesion in statin-naïve patients with severe hypercholesterolemia.Materialandmethods.To the study, 133 statin-naïve patients included, age 18 to 75 y.o., with absent clinical signs of coronary heart disease, and with first time diagnosed severe hypercholesterolemia (total cholesterol >7,5 mM/L and/or low density lipoproteides cholesterol >4,9 mM/L) with ultrasound duplex scan data of CA. All patients underwent measurement of Lpa concentration, lipid profile, subfractional content of apoB-100-containing lipoproteides and autoAb titer against them.Results.According to the data from duplex CA scan, patients were selected to 2 groups: control group (n=76) with no CA atherosclerosis; main group — patients with CA stenosis >20% (n=57). The participants of main group were older than controls, with no other clinical or lipid profile differences. Titre of autoAb IgM specific for Lpa and its oxidized modifications was significantly lower in CA atherosclerosis comparing to controls. The grade of CA stenosis in severe hypercholesterolemia patients positively correlated with age (r=0,24, p=0,005) and negatively — with autoAb IgM to apoB100-containing lipoproteides (r=-0,28 and r=-0,26, p<0,005). Also, a correlation found for CA stenosis grade with subfractions of intermediate density lipoproteides of moderate size (r=0,21, p=0,032). AutoAb titre against Lpa was an independent predictor of CA lesion severity regardless the age and traditional risk factors by the data from multifactorial regression. By ROCanalysis with the highest diagnostic value (square under AUC =0,68) the level of autoAb IgM to Lpa lower than 0,083 lab. units, with sensitivity 40% and specificity 88% is related to the lesion of common CA.Conclusion.In patients with severe hypercholesterolemia Lpa is an autoantigen, and IgM autoantibodies to Lpa play antiatherogenic role.