Dynamics of plasma lipoprotein content in patients with peripheral and coronary atherosclerosis under the influence of hemosorption

According to modern concepts, atherosclerosis of the coronary arteries and its clinical manifestation - coronary artery disease (CHD) — are caused by three main factors: dyslipoproteidemia. violation of the blood clot-forming system and vascular wall permeability. In terms of timely detection and treatment of this disease, the greatest attention is paid to dyslipoproteidemia. It is known that in the blood plasma of most patients with coronary heart disease, along with a possible increase in the concentration of low- and very low-density lipoproteins (LI), VLDL), there is a decrease in the concentration of high-density LI (LIBI). At the same time, in population studies, an increased frequency of cases of coronary heart disease was noted among persons with these disorders in the plasma LI system. Similar changes were found in patients with peripheral obliterating atherosclerosis, which, in all likelihood, have some common pathogenetic links with coronary atherosclerosis [8J. This correlation of biochemical and clinical data is mainly due to the ability of LDL and VLDL (that is, WHETHER containing a specific apoprotein B) to give cholesterol to cell membranes both through endocytosis and by a non-receptor mechanism during contact interaction with the cell [11]. At the same time, HDL, which has recently been called "anti-atherogenic", is not only able to accept cholesterol from cell membranes, transporting it to the liver, but also to inhibit the capture of endothelial cells of the LINI, inhibit cell proliferation and synthesis of aortic glycosaminoglycans [5]. These specific properties of individual classes of LP necessitate the search for ways to target the plasma LP system in order to reduce the concentration of apo-B-containing LP and increase the level of HDL. At the same time, with a number of dietary and drug effects that reduce the concentration of cholesterol in plasma (and, consequently, the level of LDL - its main transport form), for example, with a diet with polyunsaturated fatty acids or taking a number of drugs, in particular probucol [12], the concentration of anti—atherogenic HDL also decreases, which undoubtedly reduces the therapeutic effectiveness of these effects.