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The concepts of atherosclerosis as afatly acids pathology, deficiency syndrome in cells ofpolyene fatty acids were expounded in 1990. The spirits cholesterol and glycerin play integrated physical chemical function in fatly acids' metabolism in transforming polar fatty acids into such non-polar form as ethers cholesterol and triglycerides. The amount of fatty acids transferred by lipoproteins to triglycerides significantly exceeds amount of fatty acids as ethers cholesterol. The triglycerides dominate in cells and ethers cholesterol outside cells. The hypertriglyceridemia is a disorder of transformation in blood of phylogenetically late insulin-dependent palmitic and oleinic lipoproteins of very low density and receptor apoE/B-100-endocytosis by cells of non-ligand lipoproteins of very low density. The hypertriglyceridemia is a disorder of support of cells with energy substrates, problem of cell "energetics", formalton of adenosine triphosphate. It is proposed to evaluate prognostic value of spirits cholesterol in blood plasma only in case of physiological level of triglycerides. The spirits cholesterol never exceeds content of triglycerides however high would be content of spirits cholesterol in blood plasma under family hypercholesterolemia. The increasing of concentration of triglycerides always results in increasing of content of spirits cholesterol and especially spirits cholesterol-lipoprotein of low density. If level of triglycerides and spirits cholesterol is increased normalization of content of triglycerides using diet is to be implemented To evaluate content of spirits cholesterol in blood plasma is rational only under physiological level of triglycerides. Quite often, after decreasing of content of triglycerides content of spirits cholesterol spontaneously decreases by itself. It is supposed that functions of phylogenetic early resident macrophages of intima and late monocytes-macrophages differs. The functional characteristics of second ones under surplus induction by substrate (non-ligand lipoproteins) forms atheromatosis. The increasing of content of apoC-III in blood plasma--test of accumulation of blood of a physiologicpal mitic lipoproteins of low density, compensatory activation of lipolysis of triglycerides in lipoproteins of low density, but not blockade of biological function of trophology, biological reaction of exotrophy.

According to phylogenetic theory of general pathology, the function of low density lipoproteins (LDL) and hydrolysis of triglycerides (TG) in them under the effect of hepatic glycerol hydrolase apoC-III (HGH) developed at much earlier stages of phylogenesis than functioning of insulin-dependent phylogenetically late very low density lipoproteins (VLDL). For millions ofyears, lipolysis and HGH+apoC-III have activated transfer of polyenic fatty acids (FA) in the form of cholesteryl polyesters (CLE) from high density lipoproteins (HDL) to linoleic and linolenic LDL under the effect of cholesteryl ester transfer protein. It is reasonable to suggest that hepatocytes physiologically secrete oleic and palmitic VLDL and linoleic and linolenic LDL. Cells uptake ligand oleic and palmitic VLVL by apoE/B-100 receptor-mediated endocytosis. Physiologically, VLDL are not converted to LDL. If hepatocytes secrete palmitic VLDL in greater amounts than oleic VLDL upon slow hydrolysis ofpalmitic TG and under the effect of postheparinic lipoprotein lipase+apoC-II, only some proportion of palmitic TG is uptaken by cells as VLDL, and the rest is converted in ligand-free palmitic LDL These LDL increase plasma contents of TG and LDL-cholesterol and form small dense palmitic LDL. Expression of HGH+apoC-III synthesis compensates TG hydrolysis in nonphysiological palmitic LDL. In vivo, apoC-III is neither physiological no pathological inhibitor of lipolysis. Increase in plasma apoC-III content is an indicator of accumulation of non-physiological palmitic LDL and atherosclerosis-atheromatosis risk factor ApoE content ofpalmitic LDL increases together with apoC-III, i.e., apoE in ligand VLDL is not internalized via apoE/B-100 endocytosis. An increase in apoC-III and apoE contents are reliable in vivo tests for the rise inpalmitic FA, palmitic TG and excessive secretion of palmitic VLDL by hepatocytes. ApoC-III and apoE contents in LDL are additional tests to evaluate the efficiency of atherosclerosis prevention when physiological function of trophology and biological reaction of exotrophy are normalized.

The relationship of the values of serum apolipoproteins and uric acid (UA) was studied in healthy individuals and patients with cardiovascular diseases. It was shown that the development of coronary heart disease (CHD) was attended by the inversion of a correlation between the values of serum apo-CIII and apo-E and UA whereas in patients with CHD these relationships were also significant, but they were negative. It was ascertained that in patients with hypertensive disease there was no significant correlation between the serum levels of apo-CIII, apo-E, and UA.

Aim: To investigate correlations between the levels of uric acid and apo-E in patients with normo- and hyperlipidemia., Material and Methods: Serum lipids, apolipoprotein spectrum and uric acid levels were measured with Chronolab (Switzerland) kits in 78 patients: 58 with normolipidemia and 25 patients with hyperlipidemia of type IIa and IIb., Results: Significantly higher levels of apo-E were registered in patients with hyperlipidemia than in patients with normolipidemia, but there were no differences by content of uric acid. A comparative correlation analysis detected a significant correlation between uric acid levels and apo-E in both groups but in normolipidemic patients the correlation was positive while in hyperlipidemic patients it was negative., Conclusion: Hyperlipidemia provokes inversion of correlation between the levels of uric acid, apo-E and apo-C3. A rise of apo-C3 may serve an adaptive mechanism of inhibition of apo-E induced hyperlipidemia.