The aim – the determination of the mechanisms of acute coronary syndrome development and role of acquired immune response. We enrolled 15 patients with ACS hospitalized within 6 hours after appearance of clinical symptoms. Fifteen patients with stable angina pectoris formed the control group. The specific clinical feature of the ACS was the sharp increase of systemic inflammation and CRP blood content in average by 3.7 times more than in patients of the control group. This inflammation reflected acquired immune response, with circulating immune complexes increase by 2.5 times more than in patients with stable angina. The development of the immune reaction was combined with increase of modified lipoproteins blood content: modified LDL – by 2.6 times, VLDL – 4.5 times more than in control group. More increased content of cholesterol (CH) (by 2 times) and TG (by 2.5 times) in circulating immune complexes in patients with ACS indicated autoimmune character of the reaction. There reactions were accompanied by significant moderate changes of blood lipoprotein spectrum: the increase of CH LDL content in patient with ACS by 25 % more and CH VLDL – by 27 % more than in control patients. Much more pronounced were lipoprotein functional changes, reflected by appearance of LDL small dense particles and decrease of HDL protective properties as a result of diminishing their apo-A-1 content. In conclusion, atherogenic and immunogenic blood lipoprotein modification followed by development of autoimmune response is one of the main mechanism of atherogenic plaque destabilization with subsequent development of ACS.