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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary fat intake is often regarded as a major determinant of coronary heart disease (CHD) rate and it has been deemed unnecessary to invoke racial or other factors to explain the differences in CHD rates among different ethnic groups. Despite a high prevalence of CHD risk factors such as hypertension, obesity, and smoking, CHD remains a rarity in westernized black Africans. Cord blood total cholesterol (TC), low density lipoprotein cholesterol (LDLC) and apolipoprotein B (apo B) levels were measured and found to be respectively 12.1%, 18.3% and 22.4% lower in black neonates when compared to white neonates. These differences were again studied in a group of young black African males and a comparable group of age-matched whites who had been exposed to the same environment and western diet for at least 2 years. Although the body mass indices and serum albumin concentrations in the adult males were not significantly different, serum levels of TC, LDLC and apo B were 10.7%, 18.7% and 39.7% lower in the blacks, respectively. Furthermore, high density lipoprotein cholesterol (HDLC) and Apolipoprotein AI were 20.2% and 9.5% higher, homocysteine 45.6% lower and coagulation factor VII 26.6% lower in the adult black Africans. It is concluded that blacks are biochemically less responsive to an atherogenic diet than whites and these differences are already present at birth.
Atherosclerosis 1991 Aug
PMID:Ethnic immunity to coronary heart disease? 179 43

We have explored earlier evidence that premature atherosclerosis in homocystinuria is triggered by homocysteine-induced loss of vascular endothelium. We used a reproducible sluicing assay to test in vitro detachment of human arterial endothelial cells. Cell detachment was induced by exposure of cultured endothelial cells to the sulphydryl-containing amino acids homocysteine and cysteine, whereas methionine, alanine, valine and isoleucine at comparable concentrations were ineffective. This cellular detachment was greatly diminished by growth of the endothelial cells on fibronectin coated- rather than plain tissue culture dishes. Considerably higher concentrations of homocysteine were required for in vitro effects than are associated with atherogenesis in homocystinuria, and despite the cysteine associated changes, cysteine itself is not known to be related to atherogenesis. These data suggested that in vitro detachment of cultured endothelial cells, induced by sulphydryl-containing amino acids, may have marginal relevance to mechanisms of atherogenesis in homocystinuria.
Atherosclerosis 1991 Nov
PMID:Human arterial endothelial cell detachment in vitro: its promotion by homocysteine and cysteine. 181 56

We have sought the very high levels of homocysteine-containing compounds in the plasma hydrolysates of myocardial infarct patients reported by Olszewski and Szostak (Atherosclerosis, 69 (1988) 109-113). We studied 6 adult males with recent myocardial infarcts and 6 healthy adult males. We found that after hydrolysis of their plasmas for 5 h in 4 mol/l HCl at 110 degrees C, the amino acid chromatographs contained several small peaks in addition to the expected substantial peaks of the protein-constituent amino acids. However, the small peaks which eluted at the same times as homocysteine, homocystine and the mixed disulphide of homocysteine and cysteine, were in each case shown not to represent these compounds. Furthermore no homocysteine thiolactone was found in the chromatographs. We found no significant differences in the size of the small peaks between the patients and the controls. Prolonged hydrolysis resulted in decreased size of all but one of the small peaks suggesting that they were hydrolytic intermediates in the breakdown of plasma proteins. Electrophoresis at pH 10.39 of the unhydrolysed plasmas showed that the proteins were not significantly more homocysteinylated in patients than in controls. Thus we have been unable to substantiate some key observations made by Olszewski and Szostak.
Atherosclerosis 1991 Feb
PMID:Failure to detect homocysteine in the acid-hydrolysed plasmas of recent myocardial infarct patients. 187 13

In order to study the connection between homocysteine and lipid metabolism in atherosclerosis, homocysteine was determined in lipoprotein fractions from men with hypercholesterolemia. All lipoprotein fractions contain a considerably higher level of homocysteine in hypercholesterolemia, compared to normolipemic men, varying from 2.2 to 7.2 times higher estimated per unit volume of serum used for lipoprotein isolation, and from 2.4 to 4.1 times higher, estimated per gram protein. The largest difference in homocysteine content, estimated per gram protein, is present in the LDL fraction, amounting to 4.1 times higher in the hypercholesterolemic than the normolipemic group. In contrast, cholesterol is not higher in hypercholesterolemic than normolipemic men in any lipoprotein fraction, estimated per gram protein, and cholesterol is higher in hypercholesterolemic men only in the LDL fraction, estimated per unit volume. In both LDL and VLDL fractions homocysteine is correlated with cholesterol (r = 0.78, P less than 0.001; r = 0.59, P less than 0.01, respectively) and with protein (r = 0.72, P less than 0.01; r = 0.78, P less than 0.001, respectively). The atherogenic index for homocysteine, LDLHCy/HDLHCy, is 3.5 times higher in the hypercholesterolemic than the normolipemic group. The atherogenic index for cholesterol, LDLChol/HDLChol, is 2.2 times higher in the hypercholesterolemic than the normolipidemic group. The results suggest that analysis of the homocysteine content of the serum and lipoprotein fractions may prove to be useful for assessing risk, prognosis and response to therapy in persons with atherosclerosis.
Atherosclerosis 1991 May
PMID:Homocysteine content of lipoproteins in hypercholesterolemia. 187 10

After acid hydrolysis, mean plasma homocysteine concentrations, measured as homocysteine disulphides, of about 1000 and 40 mumol/l have recently been reported in 26 survivors of myocardial infarction and 26 matched control subjects, respectively. This finding contrasts sharply with those more than 50 times lower total homocysteine concentrations found by other research groups in non-hydrolysed plasma from survivors of myocardial infarction. Using the same hydrolysis conditions, we could not detect any homocysteine disulphides in plasma hydrolysates from 9 survivors of myocardial infarction and 10 healthy subjects, who had mean total homocysteine concentrations in non-hydrolysed plasma of 16.9 +/- 6.5 and 15.8 +/- 10.3 mumol/l, respectively. The chromatograms contained several peaks, probably representing peptides, which disappeared with more complete hydrolysis and which might have been misinterpreted as homocysteine disulphides in the reported study. Only after reduction of disulphides and by using a sulphydryl-selective extraction procedure were we able to determine mean homocysteine concentrations in hydrolysed plasma to be 26.2 +/- 7.9 mumol/l in the survivors of myocardial infarction and 24.5 +/- 12.2 mumol/l in the healthy reference subjects. Thus, we could not confirm that survivors of myocardial infarction have homocysteine concentrations that are many times higher than found in healthy subjects.
Atherosclerosis 1991 Jun
PMID:Influence of hydrolysis on plasma homocysteine determination in healthy subjects and patients with myocardial infarction. 189 81

Elevated blood levels of homocysteine are associated with atherosclerosis and thrombotic disease. We previously reported that treatment of cultured endothelial cells with homocysteine increased endogenous factor V activity by activation of the cofactor. Because endothelial cell-associated factor Va would be regulated by the protein C mechanism, the ability of homocysteine-treated arterial and venous endothelial cells to activate protein C was investigated. Both arterial and venous endothelial cells activated protein C; 0.6 mmol/L homocysteine reduced endothelial cell protein C activation by 12%. Maximal inhibition (90%) of protein C activation occurred with 7.5 to 10 mmol/L homocysteine after 6 to 9 hours of incubation. Metabolism of homocysteine was not accelerated by cultured endothelial cells. Investigation of the mechanism(s) by which homocysteine reduced protein C activation indicated that the metabolite did not induce an inhibitor to activated protein C, but in low concentrations acted as a competitive inhibitor to thrombin. These data suggest that perturbation of the vascular endothelial cell protein C mechanism by homocysteine may contribute to the thrombotic tendency seen in patients with elevated blood levels of this metabolite.
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PMID:Homocysteine, an atherogenic stimulus, reduces protein C activation by arterial and venous endothelial cells. 215 69

Plasma homocyst(e)ine (that is, the sum of free and bound homocysteine and its oxidized forms, homocystine and homocysteine-cysteine mixed disulfide) levels were determined in 170 men (mean age +/- SD 50 +/- 7 years) with premature coronary artery disease diagnosed at coronary angiography and in 255 control subjects clinically free of coronary artery disease (mean age 49 +/- 6 years). Patients with coronary artery disease had a higher homocyst(e)ine level than control subjects (13.66 +/- 6.44 versus 10.93 +/- 4.92 nmol/ml, p less than 0.001). High density lipoprotein (HDL) cholesterol levels were lower (32 +/- 10 versus 46 +/- 13 mg/dl, p less than 0.001) and triglycerides levels were higher (193 +/- 103 versus 136 +/- 106 mg/dl, p less than 0.001) in the coronary disease group. Plasma total cholesterol and low density lipoprotein (LDL) cholesterol levels were not significantly different between patients with coronary disease and control subjects. The presence of hypertension, smoking or diabetes mellitus did not significantly alter homocyst(e)ine levels in the patient or the control group. Patients who were not taking a beta-adrenergic blocking drug (n = 70) had a nonsignificantly higher homocyst(e)ine level than did patients taking this class of drugs (n = 100) (14.67 +/- 8.92 versus 12.95 +/- 3.77 nmol/ml, p = 0.087). By design, none of the control subjects were taking a beta-blocker. No significant correlations were observed between homocyst(e)ine and age, serum cholesterol, LDL cholesterol, HDL cholesterol or triglyceride levels. It is concluded that an elevated plasma homocyst(e)ine level is an independent risk factor for the development of premature coronary atherosclerosis in men.
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PMID:Plasma homocyst(e)ine levels in men with premature coronary artery disease. 222 57

In order to study the relation of homocysteine and lipid metabolism to atherogenesis, rabbits were fed a synthetic atherogenic diet and treated with parenteral thioretinaco (N-homocysteine thiolactonyl retinamido cobalamin), thioretinamide (N-homocysteine thiolactonyl retinamide) or homocysteine thiolactone hydrochloride. All three substances were found to increase dietary atherogenesis. Thioretinaco and thioretinamide increase total homocysteine of serum, but there is no effect of parenteral homocysteine thiolactone hydrochloride on serum homocysteine. The synthetic diet with corn oil significantly lowers serum homocysteine, compared either to baseline chow diet or to the synthetic diet with butter. Atherogenesis is correlated with total homocysteine, total cholesterol and LDL + VLDL cholesterol, and serum homocysteine is correlated with total cholesterol, LDL + VLDL, and HDL cholesterol in the total sample. Both synthetic diets elevate serum cholesterol, triglycerides and LDL + VLDL, but not HDL, compared to baseline values. Thioretinamide causes significant elevation of cholesterol and LDL + VLDL, compared to controls. The results show that increased dietary saturated fat and cholesterol cause deposition of lipids within the arteriosclerotic plaques produced by homocysteine, converting fibrous to fibrolipid plaques. Facilitation of atherogenesis is attributed to the effect of homocysteine on artery wall, either from parenteral homocysteine or from the increased synthesis of homocysteine from methionine, produced by thioretinaco and thioretinamide.
Atherosclerosis 1990 Aug
PMID:Homocysteine and lipid metabolism in atherogenesis: effect of the homocysteine thiolactonyl derivatives, thioretinaco and thioretinamide. 224 97

A retrospective study examined 194 consecutive autopsies to determine the proportion of cases of atherosclerosis without elevated serum cholesterol, diabetes mellitus, or hypertension. The study cases were classified into four groups, according to the cause of death and the degree of atherosclerosis. Cases in Group 1, in which death resulted from complications of severe atherosclerosis, have a mean serum cholesterol of 186.7 +/- 41.8 mg/dL, and the cholesterol is less than 200 in 65% and less than 250 in 92% of cases. Cases in Group 2, with severe atherosclerosis dying of other diseases, have a mean serum cholesterol of 174.6 +/- 60.4 mg/dL, and the cholesterol is less than 200 in 79% of cases and less than 250 in 89% of cases. Cases in Groups 3 and 4, with moderate and minimal atherosclerosis, respectively, have mean serum cholesterol values of 172.3 +/- 54.8 and 143.5 +/- 47.8 mg/dL, and the cholesterol is less than 200 in 71% and 92% and less than 250 in 92% and 96% of cases, respectively. Serum cholesterol is significantly associated with severity of atherosclerosis in the total sample (P = 0.01). Three fourths of all cases (147/194) have neither diabetes nor hypertension, and in 74% of these cases (109/147) the cholesterol is less than 200 and in 92% (135/147) the cholesterol is less than 250. In 66% (80/122) of the cases with severe atherosclerosis, the disease developed without evidence of elevated serum cholesterol, diabetes, or hypertension. Blood homocysteine, which has been shown by other studies to be an independent risk factor for atherosclerosis, is recommended for assessing prognosis in these cases.
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PMID:Atherosclerosis, serum cholesterol and the homocysteine theory: a study of 194 consecutive autopsies. 232 63

Because of the importance of glycosaminoglycans and glycoproteins in the pathogenesis of atherosclerosis, the hexosamine concentrations of plasma were determined in 28 male survivors of acute myocardial infarction and in 50 healthy males aged 30-60 years. Glucosamine and galactosamine were determined by ion-exchange chromatography of hydrolyzed whole plasma and hydrolyzed deproteinized plasma. Considerably higher plasma levels of non-protein-bound hexosamine (500 nmol/ml) and lower levels of protein-bound hexosamines (3770 nmol/ml) were observed in the ischemic heart disease group, compared with the plasma levels of non-protein-bound hexosamine (320 nmol/ml) and protein-bound hexosamine (4260 nmol/ml) of the control group. This difference is due to changes in glucosamine concentration. The galactosamine concentration is similar in the two groups. The ratio of non-protein-bound to protein-bound hexosamines in patients is about twice as high as the ratio found in controls. The glucosamine/galactosamine ratio of protein-free plasma is significantly higher in patients (12.1) than in controls (8.3). These changes in plasma hexosamines correlate with increased plasma homocysteine, cholesterol, and triglycerides observed in the patient group. The findings show that characteristic quantitative and qualitative changes in plasma hexosamine levels accompany atherosclerosis. Determination of these substances may be helpful in diagnosis and management of patients with atherosclerosis.
Atherosclerosis 1990 May
PMID:Plasma glucosamine and galactosamine in ischemic heart disease. 236 Sep 22


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