Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indian and black patients admitted to King Edward VIII and R. K. Khan Hospitals with a diagnosis of cardiac infarction and diabetes mellitus were studied. The mean serum cholesterol levels were higher in the indian group. This preliminary study suggests a negative correlation between leucocyte ascorbic acid and serum cholesterol levels in Indians, especially in patients with infarction. This, however, does not preclude an effect of latent ascorbic acid deficiency on the vessel wall. The possible relevance of the findings to the development of atherosclerosis is discussed.
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PMID:Ascorbic acid and cholesterol levels in patients with diabetes mellitus and coronary artery disease. 378 79

We have reported that pigs with severe homozygous von Willebrand disease (vWd) are resistant to spontaneous and high fat, high cholesterol, diet-induced atherosclerosis. In this study we report the quantitation of aortic atherosclerotic plaques in three groups of pigs fed with a high fat, high cholesterol (2%) diet from age 3 to 9 months. Nine normal pigs (normal factor VIII antigen, VIII R:AG, and ristocetin co-factor, VIII:RWF) had a mean of 21% atherosclerotic involvement of the distal aortic surface and a 4.5% mean involvement of the entire aorta. Five homozygous vWd pigs (undetected VIII R:AG and VIII:RWF) had a mean of 4.2% atherosclerotic involvement of the distal aortic surface and 1.2% involvement of the entire aorta (p less than 0.01, rank sum test). Five heterozygous vWd pigs (approximately 35% VIII R:AG and VIII:RWF) had a mean of 25% atherosclerotic involvement of the distal aortic surface and 6% involvement of the entire aorta; the results were not significantly different from those in the normal pigs. We concluded that resistance to atherosclerosis is not found in animals with moderate reduction of VIII R:AG and VIII:RWF. This may have implications for humans, since in human vWd both factors are almost always present.
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PMID:Aortic atherosclerosis in pigs with heterozygous von Willebrand disease. Comparison with homozygous von Willebrand and normal pigs. 387 19

Von Willebrand pigs have all the manifestations of the severe human disease. The role of Willebrand antigen (VIII R:AG) and ristocetin cofactor (VIII: RWF) was assessed in these pigs by (1) transfusion and (2) "in vitro" bleeding time assay. The skin bleeding time became normal when the level of transfused Willebrand factor (VIII R:AG/RWF) was raised in the plasma above 30 U/dl. After single or repeated transfusions, skin capillary endothelium and platelets were still distinguished from normal by VIII R:AG deficiency. When incisions in excised porcine skin ("in vitro" bleeding time) were perfused with blood and plasma fractions, haemostasis occurred when plasmatic Willebrand factor exceeded 30 U/dl whether the skin or platelets came from normal or from von Willebrand pigs. The platelet plug occluding the skin incision contained VIII R:AG by immunofluorescence. Willebrand factor appears to coat surfaces and to serve as a platelet attachment protein. These bleeder pigs are resistant to atherosclerosis. If platelets are involved in early atherosclerotic lesions, the role of Willebrand factor in platelet - blood vessel interaction may be important.
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PMID:The role of Willebrand factor in platelet - blood vessel interaction, including a discussion of resistance to atherosclerosis in pigs with von Willebrand's disease. 611 90

In order to investigate the relationship between the in vivo platelet activation in diabetes mellitus and the endothelial damage connected with the diabetic micro- and/or macroangiopathy, plasma levels of beta-thromboglobulin (B-TG) and of factor VIII-related antigen (VIII R:Ag) were studied (1) in juvenile-onset (Type I) diabetics without clinical signs of angiopathy (age under 12 years) and (2) in mostly maturity-onset (Type II) diabetics with and without overt angiopathy (age between 14 and 60 years). Normal controls and nondiabetics with atherosclerosis were also studied. Plasma levels of both proteins were found to be elevated in all the groups of diabetic and atherosclerotic patients in comparison with the controls. Highest levels were found in adult diabetics with angiopathy and in atherosclerotics even without diabetes, but values of the diabetic children were also elevated. The data suggest a causal relationship between the vascular damage and the enhanced platelet reactivity in which the former may play the primary role.
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PMID:Plasma levels of beta-thromboglobulin and factor VIII-related antigen in diabetic children and adults. 618 37

Primary cultures of confluent human endothelial cells (ECM) were grown in media containing the major lipoproteins (LP) and lipoprotein deficient serum (LDS). The release of 6-keto-PGF1 alpha, von Willebrand factor (VIII RAg) and apolipoproteins (apo) A-I and A-II were investigated by radioimmunoassay. The cell-associated VIII RAg, apo A-I and apo A-II were also confirmed by fluorescein antibodies, and the synthesis of the apolipoproteins was examined by incorporation of [3H]leucine. Apo A-I and apo A-II were located and synthesized in ECM, yet only apo A-I was released into the medium. Very low density (VLDL) and low density lipoproteins (LDL) in concentrations of 50-600 micrograms/ml stimulated release of apo A-I. Stimulation of ECM for 5 min with thrombin (T) or arachidonic acid (A) did not induce apo A-I release. VIII RAg was always released into the media from ECM. The release was not affected by the lipoproteins. VIII RAg was also localized on the cell surface (VIII RAgC) and approximately 80% was released by trypsin. LDL stimulated the occurrence of factor VIII RAg on the cell surface. 6-Keto PGF1 alpha was always released into the medium and the production was stimulated by T and AA. The main lipoproteins (50-600 micrograms/ml) and apo A-I and A-II did not affect the release of 6-keto-PGF1 alpha. This study shows that endothelial cells synthesize and release proteins important for thrombogenesis and atherosclerosis. The release of apolipoproteins A-I was stimulated by VLDL and LDL, and the concentration of cell-related factor VIII RAg was stimulated by LDL.
Atherosclerosis 1984 Mar
PMID:The effect of lipoproteins on the synthesis of prostacyclin, von Willebrand factor and apolipoproteins A-I and A-II in cultured human endothelial cells. 642 92

The effects of exercise (EX) and guanethidine (G) or its combination on plasma cholesterol and incidence and severity of aortic atherosclerosis of atherogenic-fed (AD) cockerels were studied. Eighty-five 16-week-old Hyline cockerels were subdivided as follows: I. Plain mash (PM); II. PM + EX; III. PM + G; IV. PM + EX + G; V. AD only; VI. AD + EX; VII. AD + G; and VIII. AD + EX + G. Birds ran approximately 500 yards for 20 minutes twice daily for twelve consecutive weeks. G (2.5 mg) was administered per os daily. The atherogenic diet consisted of 2% cholesterol + 5% cottonseed oil added to mash. At the end of 12 weeks the following results were obtained: 1) EX or G or its combination had no effect on plasma cholesterol of birds on PM. All AD-fed groups showed marked hypercholesterolemia as compared to their initial values. The AD + EX group had significantly lower plasma cholesterol level when compared to AD controls or AD + G group; 2) no gross aortic atherosclerosis was observed in cockerels on PM. The group on AD only had the most severe gross aortic atherosclerosis while the AD birds treated with G or EX + G had slightly lower aortic atheromatosis. This was in contrast to AD + EX group which showed a significant decrease in aortic atherogenesis. These results indicate that EX reduces plasma cholesterol and aortic atherosclerosis of AD birds while these effects of EX were negated by G.
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PMID:Effect of exercise and guanethidine on plasma cholesterol and aortic atherosclerosis of atherogenic-fed cockerels. 667 79

When compared to the values obtained in healthy normal-weight, normolipemic controls, the plasma level of ristocetin-cofactor (VIII:R-cof.) was found to be much higher in patients with acute myocardial infarction and in postoperative conditions (4--5 days after a major surgical intervention). A lesser increase of VIII:R-cof. was noted in atherosclerotic patients without acute occlusive accidents and no significant changes of this plasma factor could be observed in hyperlipemic subjects without obvious clinical atherosclerosis. Serial studies emphasized a tendency towards normalization of plasma VIII:R-cof. as the acute phenomena of a myocardial infarction subsided. The above mentioned data suggest that the high levels of VIII:R-cof. recorded in myocardial infarction are mainly caused by a systemic acute phase reaction and to a lesser extent by endothelial damage. Delayed clearance of VIII:R-cof. subsequent to a hepatic dysfunction or to a modified pattern of protein metabolism during the above mentioned acute phase reaction might also contribute to the high level of this plasma factor.
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PMID:Increased ristocetin-cofactor in acute myocardial infarction: a component of the acute phase reaction. 677 72

In order to investigate the factor VIII complex trend in atherosclerosis, 96 patients suffering from atherosclerosis, divided in 6 groups (angina pectoris, previous myocardial infarction, transient ischemic attacks, previous cerebral thrombosis, diabetes without symptoms of vascular injury and diabetes with vascular complications), were studied and compared to a control group of normal subjects. Plasma levels of Factor VII Coagulant (VIII C), Factor VIII-Related von Willebrand Factor (VIII-RWF) and Factor VIII-related Antigen (VIII ARg) were measured in all subjects. A significant rise of VIII RAg was noticed in all groups of patients as compared to the control group: this increase appears to be related to the severity of vascular injury. A significant rise of VIII RWF, parallel to the VIII RAg increase, was also noticed in all groups. Besides, all groups of patients showed a significant and uniform increase of VIII C. The average ratio of VIII RAg/VIII C was raised in all groups, except diabetics without complications; but the increase was statistically significant only in those patients with a heavier vascular injury which is related to the marked rise of VIII RAg in such clinical situations. The findings of this study are discussed in relation to the literature data. The significance of the determination of VIII RAg/VIII C ratio and of the VIII RAg assay as methods for monitoring the severity of the vascular injury in atherosclerosis are also discussed.
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PMID:[The factor VIII complex in atherosclerosis]. 681 35

The study includes 119 patients with minor ischemic cerebrovascular lesions before the age of 55 during 1976-78. Atherosclerotic signs were found in 65% at aortocranial angiography and/or exercise test (ST depression). Abnormalities in hemostasis (defective fibrinolytic response in 50%, high Factor VIII activity in 45% of those investigated, and high Factor VIII related antigen (VIII R:Ag) in 20%) could not be explained by accumulation of atherosclerotic risk factors as most often no significant independent correlations were found at stepwise multiple regression. Significant correlations with aortocranial atherosclerosis was found for age, VIII R:Ag and blood pressure reaction at exercise test. Only E-SR showed significant correlation to ST depression at exercise test. These results indicate different determinants and risk indicators for atherosclerosis with different locations. An early evaluation of the longitudinal study (mean 42 months' follow up) showed that 16 patients had suffered new occlusive vascular incidents. The malign prognostic subgroup (cerebral or myocardial infarction or death; n = 10) showed significantly higher levels of VIII R:Ag (p less than 0.005) and triglycerides (p less than 0.05) than the benign group (new TIA, n = 6). This indicates that VIII R:Ag may be a useful marker for development of atherosclerosis and predictor for the outcome of ICD.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. V. A multivariate evaluation of risk indicators and predictors. Early results of a longitudinal study. 681 52

The composition and structure of adaptive intimal thickening and of atherosclerotic lesions that can develop in human coronary arteries is described. Adaptive thickening occurs in defined locations from birth and represents a self-limited response of the intima to hemodynamic forces present within specific locations. Adaptive thickening does not indicate or presage an atherosclerotic lesion. However, some of the identical intima locations (progression-prone locations) accumulate more lipoprotein in persons exposed to risk factors of atherosclerosis and are first to develop advanced lesions if such lesions develop at all. Atherosclerotic disease can be resolved into eight (I-VIII) lesion types, each characteristic by its cells, matrix, architecture, or other specific features. The numerals I-VI represent the usual sequence in which lesions develop and progress from the initial accumulations of lipoproteins and macrophages to atheroma and fibroatheroma stages which are susceptible to thrombotic deposits and ischemic clinical episodes. The numerals VII and VIII represent morphological variants that may follow or precede Type VI. Types I-IV are the lesions most frequent in the first four decades of life. Type III is a lesion we identified in adolescents and young adults as morphologically intermediate between the small lesions of children (I and II) and the potentially symptom-producing Type IV lesion. Identification of Type III provides evidence that small lesions of children can develop into clinical ones. Because we know the age at which Type III lesions are present in our population, we also known the age when progression to advanced lesions generally begins and when preventive measures should already be in place.
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PMID:Changes in components and structure of atherosclerotic lesions developing from childhood to middle age in coronary arteries. 794 71


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