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

The concept that lipoprotein(a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis.
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PMID:Hypothesis: lipoprotein(a) is a surrogate for ascorbate. 214 82

Authors determined the plasma levels of total cholesterol, HDL-cholesterol, apoprotein B-100 (apo B-100), apoprotein A-I (apo A-I) and lipoprotein(a) in 202 (139 female and 63 male) randomized blood donors. The phenotypes of lipoprotein(a) were detected by SDS-polyacrylamide gelelectrophoresis and Western blotting. The average plasma total cholesterol concentration of this Hungarian population was 5.7 +/- 1.1 mmol/l. The other lipoprotein parameters were HDL-cholesterol: 1.36 +/- 0.04 mmol/l; and the apoprotein B-100 concentration: 70 +/- 17.4 mg/dl. In these parameters no difference between males and females could be found. The average plasma apoprotein A-I in females was 156.3 +/- 23.6 mg/dl and in males 143.8 +/- 26.8 mg/dl and the difference was statistically significant (p less than 0.01). The average lipoprotein(a) concentration of this population was 10.5 +/- 13.5 mg/dl and there was no significant difference between males and females (9.0 +/- 10.7 and 13.9 +/- 17.7 mg/dl, respectively). The distribution of plasma Lp(a) was highly skewed in the direction of low concentration values. In females a moderate bimodial distribution could be demonstrated. Documented by several authors lipoprotein(a) level higher than 30 mg/dl serves as an independent risk factor for atherosclerosis. In this population only 9.4% of subjects had lipoprotein(a) concentrations over this limit (5.9% female and 3.5% male). The relative alle frequency of different phenotypes showed the following distribution: B 0.007, S1 0.015, S2 0.154, S3 0.231, S4 0.230 and null 0.362. In this population the F phenotype could not be detected.
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PMID:[Plasma concentration of lipoprotein(a) and distribution of its subtypes in the healthy population of Hungary]. 214 42

The plasma concentration of lipoprotein (a) (Lp(a] varies widely in humans, and elevated concentrations of this lipoprotein are correlated with progression of atherosclerosis. Structural studies of Lp(a) have revealed that it is a low density lipoprotein (LDL)-like particle containing a unique glycoprotein, apo(a), which shares extensive homology with plasminogen. The apo(a) portion of Lp(a) binds to the carboxy-terminal heparin-binding domain of fibronectin. Incubation of Lp(a) or isolated apo(a) with fibronectin results in proteolytic cleavage of fibronectin which is, as visualized by gel electrophoresis and immunoblotting, distinct from that caused by plasmin or kallikrein. The proteolytic activity of apo(a) is of serine proteinase-type and displays specificity for arginine rather than lysine bonds. The molecular mechanism(s) underlying the association between Lp(a) and atherosclerosis remains an enigma.
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PMID:Interaction of lipoprotein(a) with fibronectin and its potential role in atherogenesis. 214 25

Lipoprotein (Lp)(a) represents a quantitative genetic trait. Elevated Lp(a) levels (greater than 25-30 mg/dl) have been linked epidemiologically to cardiovascular disease. A high Lp(a) level seems to be an additional independent risk factor for the accelerated progression of atherosclerosis, although the exact mechanism involved is not yet known. Individuals with familial hypercholesterolaemia (FH) have also been shown to have elevated Lp(a) levels, but again the reason for this is unclear. A preliminary investigation of serum Lp(a) levels in 30 apparently healthy individuals, 38 FH patients and 34 individuals with coronary artery disease (CAD) was conducted. Lp(a) levels were distributed over a wide range, varying from barely detectable to above 84.0 mg/dl. A greater incidence of elevated Lp(a) levels (greater than 30 mg/dl) was found in both the FH group (71%) and the CAD group (41%) compared with 'normal' individuals (30%). Analysis of the circulating Lp(a) level may be useful in determining an individual's long-term risk for cardiovascular disease.
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PMID:Serum lipoprotein (a) levels in 'normal' individuals, those with familial hypercholesterolaemia, and those with coronary artery disease. 214 99

W examined the short-term effects of a high-complex carbohydrate, low fat diet on the plasmin-dependent fibrinolytic pathway. A population of 27 adult American Caucasians exposed to the diet for 3 weeks showed highly significant reductions in the levels of plasminogen (P = 0.0001), tissue plasminogen activator (tPA) (P = 0.0001) and plasminogen activator inhibitor (tPAI) (P = 0.0017). Fibrinogen levels also decreased, but the changes did not reach statistical significance (P = 0.07). In contrast, the levels of the Lpa(a) lipoprotein, a potential inhibitor of fibrinolysis, remained remarkably constant despite a marked decrease in the levels of apolipoprotein B, a major constituent of Lp(a). Correlations between the levels of tPA, tPAI and plasma triglyceride were observed among the individuals both before and after the dietary challenge. Although the mechanisms responsible for the effects are unknown, the dramatic responsiveness of the thrombolytic pathway to dietary challenge is likely to be of importance in understanding the etiology of coronary artery disease and other vascular disorders.
Atherosclerosis 1990 Sep
PMID:Dietary regulation of fibrinolytic factors. 214 72

Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein. Lp(a) has been found in the plasma of humans and other primates, but until now only in a few other species. The mechanism by which it exerts its atherogenicity is still poorly understood. We observed that Lp(a) has been found in the plasma of several species unable to synthesize ascorbate and not in other species. We have now detected apoprotein(a) in the plasma of the guinea pig. We induced atherosclerosis in this animal by dietary ascorbate depletion and, using SDS/PAGE and subsequent immunoblotting, we identified Lp(a) as accumulating in the atherosclerotic plaque. Most importantly, adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall. We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis.
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PMID:Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. 214 14

The extracellular lipid that accumulates in fibrous atherosclerotic lesions appears to be derived directly from plasma low density lipoprotein (LDL). One factor that may influence the lipid deposition is immobilization of part of the LDL in lesions, and an immobilized fraction can be released by incubation with the fibrinolytic enzyme, plasmin, suggesting that it is associated with fibrin. The lipoprotein variant Lp(a) is associated with increased risk of arterial disease, and its characteristic apoprotein, apo(a), is structurally related to plasminogen, suggesting that it might bind to the plasminogen binding sites on fibrin. In this study we have compared blood Lp(a) and the soluble and plasmin-releasable Lp(a) in 45 samples of normal intima and different types of lesion. Levels of soluble and plasmin-releasable Lp(a) were dependent on both blood level and type of tissue sample. Although the amount of soluble LDL was 5-20 times higher than Lp(a) in intima, the amounts released by plasmin were similar, and Lp(a) appears to account for most of the apo B-containing lipoprotein that is immobilized in lesions.
Atherosclerosis 1990 Oct
PMID:Factors influencing the accumulation in fibrous plaques of lipid derived from low density lipoprotein. II. Preferential immobilization of lipoprotein (a) (Lp(a)). 214 68

The effect of low dose (600 mg/day) alpha-tocopheryl nicotinate on serum lipoprotein(a) (Lp(a] concentration was studied in 28 hyperlipidaemic patients. Serum lipids, lipoproteins and apolipoproteins, except for Lp(a), tended to increase after treatment. In particular, the changes in HDL-cholesterol and apo C-II levels were statistically significant. On the other hand, serum Lp(a) levels in all patients decreased significantly after 2 months of treatment. Furthermore, no difference between before and after treatment was observed in the group with initial Lp(a) levels less than 18 mg/dl, whereas Lp(a) concentrations decreased significantly after treatment in the group with levels greater than or equal to 18 mg/dl. The effects of probucol and alpha-tocopheryl nicotinate on serum Lp(a), total cholesterol and HDL-cholesterol were entirely different. Possible mechanisms of alpha-tocopheryl nicotinate on serum Lp(a) and lipoprotein metabolism are discussed.
Atherosclerosis 1990 Oct
PMID:Reduction of serum lipoprotein(a) levels in hyperlipidaemic patients with alpha-tocopheryl nicotinate. 214 70

The serum lipoprotein Lp(a) concentration was measured in 1065 individuals in order to assess whether there was a relation between the type of dyslipidemia and the level of Lp(a). Males and females, aged between 2 and 83 years old, were included in the study. Quantification was performed by an immunonephelometric technique. The whole population was divided into normolipidemic (NL), type IIa without xanthoma (type IIa), type IIa with xanthoma (FH), type IIb and type IV phenotypes. Lp(a) level was arbitrarily divided into 5 subclasses in each group of dyslipidemia and in the normolipidemic group. In addition each group was divided according to sex and whether or not they were under treatment. We observed a significant difference between the median Lp(a) level of the normolipidemic group (NL) and of the dyslipidemic group as a whole. Median Lp(a) levels in the 4 dyslipidemic groups did not differ significantly. Sex, age and treatment did not influence the distribution of Lp(a) values distribution. Only weak correlations (Spearman's rank test) were observed between Lp(a) and other lipid parameters (total cholesterol, LDL, apo B, HDL, triglycerides): the highest correlation (r' = 0.15) was between Lp(a) and apo B. We conclude that Lp(a) level is not influenced by the type of dyslipidemia, sex or hypolipidemic drugs.
Atherosclerosis 1990 Nov
PMID:Lp(a) levels in different types of dyslipidemia in the French population. 214 72

Plasma lipids and apolipoproteins were quantified in two kindreds of hypobetalipoproteinemia. All affected members were asymptomatic but showed a decrease of 75% in apolipoprotein B and of 69% in LDL-cholesterol. There were no major changes in apo A-I and A-II but all affected family members had reduced levels of apo C-II (by 58%) and C-III (by 59%) without significant decrease in apo C-I and no specific decrease of apo C-III1. Apolipoprotein E is decreased in SDS-PAGE. The plasma level and phenotype of Lp(a) are not affected by HBL, suggesting that a catabolic rather than a synthetic mechanism is responsible for the disease. As shown by density gradient ultracentrifugation, HDL2 particles that contain essentially apolipoprotein A-I, cholesterol and phospholipids represent in affected subjects the major part of HDL. Due to the net reduction of apolipoprotein B-containing particles (VLDL and LDL) as acceptors of lipids in HBL, there is an accumulation of large particles rich in cholesteryl esters.
Atherosclerosis 1990 Aug
PMID:Plasma lipids, lipoproteins and apolipoproteins in two kindreds of hypobetalipoproteinemia. 224 96


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