QT changes associated with intracranial hemorrhage.
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Electrocardiography↗
Biomedical subjects
A G Kacharava
Publications and source records attributed to A G Kacharava.
Autoantibodies against low-density lipoprotein and atherogenic potential of blood.
Blood serum of ischaemic heart disease patients possesses an atherogenic potential which manifests itself in the accumulation of cholesterol in cultured smooth muscle cells of human aorta and in mouse peritoneal macrophages. Recently it was found that serum atherogenicity is associated with the presence in the blood of modified (desialylated) low-density lipoprotein (LDL) and of autoantibodies against LDL (anti-LDL). In the blood, anti-LDL and LDL form circulating immune complexes (CIC). Blood serum atherogenic potential is directly related to the content of LDL cholesterol or apolipoprotein B in CIC. The present study elucidates the effect of LDL and anti-LDL concentrations on the atherogenic properties of blood serum. After the addition of exogenic LDL, in certain atherogenic sera a significant increase in CIC cholesterol as well as the increase of serum atherogenic potential revealed in cell culture were registered. In these sera free anti-LDL capable of binding to exogenous LDL were detected. In other atherogenic sera and in all non-atherogenic sera, the LDL increase failed to be accompanied by any changes in the CIC cholesterol. In these sera no free anti-LDL were detected. The addition of exogenous anti-LDL into non-atherogenic sera was accompanied by 2.5-fold increase in CIC cholesterol and by the appearance of atherogenic properties in these sera. Affinity chromatography was used to remove anti-LDL from atherogenic sera. This removal was accompanied by 2.5- to 3-fold decrease in the CIC cholesterol up to the level characteristic of non-atherogenic serum of healthy donors. The removal of anti-LDL led to disappearance of serum atherogenic properties. From these data we assume that the CIC LDL level and, consequently, serum atherogenic potential is to a considerable degree determined by anti-LDL concentration in the serum.
Adult↗
[Effects of lovastatin therapy on the level of low density lipoproteins and atherogenic potential of serum in patients with ischemic heart disease and hypercholesterolemia].
The serum atherogenic potential in patients with coronary heart disease (CHD) concurrent with hypercholesterolemia (LDL cholesterol more than 200 mg/dl), which is able to cause accumulation of intracellular cholesterol in cultured cells has been recently shown to be directly related to the level of total cholesterol and LDL cholesterol. The study was undertaken to examine how a lovastatin-induced decrease in LDL levels affects serum atherogenicity in patients with CHD and hypercholesterolemia. It was shown that the therapy of 22 patients with CHD and hypercholesterolemia led to a reduction in total and LDL cholesterol levels on an average by 24% and 32%, respectively. There were 3- and 1.5-2-fold decreases in circulatory immune complexes and the atherogenic potential, respectively. The findings suggest that the significant reduction in serum LDL cholesterol levels in patients with CHD concurrent with hypercholesterolemia who take hypolipidemic therapy is followed by a decrease in the atherogenic potential.
Animals↗
[Relations between the levels of lipoprotein-containing immune complexes and lipids in the blood of patients with ischemic heart disease].
The sera from most patients with coronary heart disease concurrent with angiographically documented coronary atherosclerosis were found to contain apolipoprotein B (Apo B), neither apolipoprotein E (Apo E) nor apolipoprotein AI (Apo AI) in the circulating immune complexes precipitated by polyethylene glycol-6000 (PEG). Low density lipoproteins are the major components of cholesterol-containing immune complexes precipitated by PEG. A correlation was established between the serum levels of total cholesterol (r = 0,74; p less than 0.01), and low density lipoprotein (LDL) cholesterol (r = 0.77; p less than 0.01) in patients with coronary heart disease and cholesterol in LDL-containing No relationship was found in healthy individuals. The in vitro increase in LDL levels in most patients with coronary heart disease concurrent with coronary atherosclerosis was not followed by an elevation in LDL-containing immune complexes.
Antigen-Antibody Complex↗
Low density lipoprotein-containing circulating immune complexes and coronary atherosclerosis.
Blood serum of most patients with coronary heart disease (CHD) caused a 2- to 5-fold increase in the lipid content of smooth muscle cells cultured from unaffected human aortic intima, i.e., possessed an atherogenic potential manifested in culture. Treatment of the CHD patients' serum with 2.5% polyethylene glycol 6000 removed the circulating immune complexes. The serum subjected to this treatment lost its atherogenic properties, i.e., failed to increase the content of lipids in cultured cells. Incubation of smooth muscle cells derived from human aortic intima with circulating immune complexes isolated from an atherogenic patient's serum caused a 1.5- to 3-fold rise in the intracellular cholesterol. Circulating immune complexes contained apolipoprotein B (apo B), but not apolipoproteins A1 and E. The apo B content strongly correlated with the total cholesterol content. The cholesterol/apo B ratio of the complexes was characteristic of low density lipoproteins (LDL), but not of very low density lipoproteins or intermediate density lipoproteins. The composition of the main lipid classes in these complexes was similar to that in LDL. Blood sera of most (90%) CHD patients was characterized by a high cholesterol and apolipoprotein B content in circulating immune complexes. The ability of these sera to induce lipid accumulation in cultured cells directly correlated with the cholesterol and apolipoprotein B level of circulating immune complexes (r = 0.91). These findings suggest that the atherogenic potential of CHD patients' blood serum is due to LDL-containing immune complexes.
Adult↗
Correlation between cholesterol content in circulating immune complexes and atherogenic properties of CHD patients' serum manifested in cell culture.
Blood serum of most patients with coronary heart disease (CHD) caused a 2-5-fold increase in the total cholesterol content of smooth muscle cells cultured from unaffected human aortic intima, i.e. possessed an atherogenic potential manifested in culture. Removal of immunoglobulins G and M from an atherogenic serum brought about a fall in its atherogenic potential. The serum deficient in immunoglobulins A retained its ability to induce the cholesterol accumulation in cells. Treatment of the CHD patients' serum with 2.5% polyethylene glycol 6000 removed the circulating immune complexes. The serum subjected to this treatment lost its atherogenicity, i.e. failed to increase the cholesterol content in cultured cells. Incubation of smooth muscle cells derived from human aortic intima with circulating immune complexes isolated from an atherogenic patients' serum caused a 1.5-3-fold rise in the intracellular cholesterol. Blood sera of most (89%) CHD patients was characterized by a high cholesterol content in circulating immune complexes. More than 75% of healthy subjects and patients without stenosis of coronary arteries had low level of cholesterol in immune complexes. Blood sera atherogenicity manifested in culture directly correlated with the cholesterol level of circulating immune complexes (r = 0.90). These findings suggest that the atherogenicity of CHD patients blood serum is due to cholesterol-containing immune complexes.
Adult↗
[Desialylated low density lipoproteins--atherogenic lipoproteins occurring in blood of patients with coronary atherosclerosis].
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.
Adult↗
[Low density lipoproteins isolated from the blood of patients with ischemic heart disease induce accumulation of lipids in human aortic intima cells].
Very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL) were isolated from the blood of healthy subjects and CHD patients. LDL from the blood of healthy individuals did not raise the intracellular lipid values within 24 h of cultivation. During intracellular lipid values within 24 h of cultivation. During the same incubation period. LDL obtained from the blood of CHD patients caused a 2- to 5-fold rise in cholesterol esters as well as a 1.5- to 3-fold rise in free cholesterol and triglycerides, while the intracellular phospholipid levels remained unchanged. In one of the three cases, the ability to raise the intracellular level of cholesterol esters was demonstrated by VLDL (500 micrograms/ml) derived from CHD patients blood. HDL did not affect the lipid levels in smooth muscle cells cultured from unaffected intima. The obtained data suggests that circulating LDL and, possibly, VLDL in the blood of CHD patients are capable of inducing the accumulation of fat in vascular wall cells.
Adult↗
[Cholesterol-containing circulating immune complexes--a component of the blood serum in patients with ischemic heart disease that determines its atherogenic properties].
In most patients with coronary heart disease (CHD) and angiographically documented stenosed 1-3 coronary arteries, serum contained cholesterol (C) in the circulating immune complexes (CIC), cholesterol levels in these complexes being directly related to serum atherogenicity, i.e. to their ability to cause a 2-5-fold accumulation of lipids in cultured smooth muscle cells (SMC) of the uninvolved human aortic intima (r = 0.91). Removal of IgG and IgM from the patients' sera led to a 75 and 37% decrease, respectively, in their atherogenic properties displayed in cultured SMC. Much more decrease in the atherogenic potential of the sera was seen in 2.5% polyethylene glycol-induced precipitation of CIC. At the same time, incubation of human aortic intimal SMC with CIC isolated from the atherogenic sera from CHD patients caused a 1.5-3-fold increase in intracellular C levels. It was suggested that CIC cholesterol was a determinant of atherogenicity of the sera from patients with coronary atherosclerosis.
Antigen-Antibody Complex↗
[Atherogenic properties of sera from patients with ischemic heart disease demonstrated in vitro].
The sera of coronary patients with angiographically-documented stenosis of 1 to 3 coronary arteries caused a two-to-fivefold accumulation of intracellular cholesterol in intact human aortic intimal cell culture. This property, qualified as "atherogenic", was exhibited by the sera of 90% of the coronary patients examined (97 males and females, aged 29 to 55 years). Only 20% of normal subjects revealed atherogenic properties in cell cultures. The capacity of the sera to accumulate intracellular cholesterol was unrelated to the levels of total cholesterol, high density lipoprotein cholesterol, apo-B or apo-AI, taken separately, but showed a weak correlation to the apo-B/apo-AI ratio. The sera of coronary patients caused lipid accumulation in human aortic medial smooth-muscle cells and blood mononuclear cells, in human and mouse peritoneal macrophages, but never in human aortic or umbilical vein endothelial cells, nor human embryo fibroblasts.
Adult↗