With a purpose to study the state of platelet haemostasis and vasoactive prostanoids system 78 patients with ischemic heart disease aged 28 to 59 years were examined. Among them there were 22 patients with "isolated" hypo-alpha-cholesterolemia and 14 patients who had hypo-alpha-cholesterolemia combined with hypertriglyceridemia (HTG). The data obtained show that hypo-alpha-cholesterolemia is accompanied by platelet disorders aggravation and characterized by activated platelet percentage growth. There is a reverse relationship between alpha-cholesterol plasma level and activated platelet percentage (r = -0.52). There is a direct relationship between high-density lipoprotein cholesterol plasma level and concentration of stable prostacyclin metabolite (6-keto-PGF1 alpha) in plasma (r = 0.64). Hypo-alpha-cholesterolemia in combination with HTG is characterized by more significant disorders in prostacyclin-thromboxane system consisting in an increase of plasma thromboxane system consisting in an increase of plasma thromboxane A2 concentration (p < 0.001) and a decrease of 6-keto-PGF1 alpha plasma level (p < 0.05). An inverse apolipoprotein A-1 plasma level (r = -0.48) has been revealed in the group of patients who had hypo-alpha-cholesterolemia combined with HTG.
The paper presents a clinical and genealogical characterization of 50 probands suffering from coronary heart disease concurrent with various lipid metabolic disturbances and 211 first-degree relatives whose data have been obtained from the probands' histories while making up their pedigrees. The prevalence of atherosclerosis among the first-degree relatives has been demonstrated to be related to the nature of lipid metabolic disturbances in a proband. Some dyslipoproteinemias in the proband have been characterized by early onset of coronary heart disease, stroke, and their grave course in close relatives.
The review is devoted to hypercholesterolemia which is one of the leading risk factors for IHD. By its origin it can be primary and secondary. Three major mechanisms of primary hypercholesterolemia in humans are discussed. They are: low activity of LDL receptors, reduced affinity of LAL for receptors and overproduction of lipoproteins containing apo B. Depending on mechanism nonidentical molecular defects leading to cholesterol imbalance in cells or in circulating lipoproteins are occurred. The understanding of the nature and mechanisms of hypercholesterolemia development is of great clinical value, because having determined molecular defect and using drugs combinations the majority of patients are a success to have their lipids normal. Only in the case of homozygous familial hypercholesterolemia medicamentous treatment becomes secondary and the principal therapeutic methods are plasmapheresis or selective LDL apheresis. Gene therapy as a method of homozygous familial hypercholesterolemia correction is in forthcoming future.
