We have recently established that LDL of most patients with coronary atherosclerosis differ from the LDL of most healthy subjects by the ability to cause primary atherosclerotic changes, i.e. the accumulation of intracellular cholesterol in the cells of smooth muscle origin cultured from unaffected intima of human aorta. We assumed that patients LDL is modified lipoprotein differing from native LDL by chemical composition. It has been established in the present study that patients LDL has a substantially lower content of sialic acid as compared with the LDL of healthy subjects. Desialylation of native LDL of healthy subjects with neuraminidase makes them atherogenic, therefore, capable of causing the accumulation of intracellular cholesterol similarly to patients LDL.