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

The von Willebrand factor (VWF) is a link in the platelet-vessel wall interaction which plays an essential role in the response of the vessel wall to an atherosclerosis-including aggression. However, can von Willebrand's disease really prevent the development of atherosclerosis? The authors report 3 cases of young men aged 36, 40 and 51 years with atherogenic risk factors and von Willebrand's disease (two mild and one severe form). The three patients developed both atherosclerotic lesions and thrombosis. This would suggest that VWF deficiency does not protect humans from atherosclerosis.
Arch Mal Coeur Vaiss 1989 Nov
PMID:[von Willebrand's disease and coronary atherosclerosis. Apropos of 3 cases]. 251 40

Two of the many mediators synthesized by vascular endothelial cells (EC), are involved in maintaining the surface of the normal, healthy endothelium in a non-thrombogenic state. The first is prostacyclin, a product of arachidonic acid metabolism, discovered in 1976. This labile prostanoid, with a half life of approximately 3 minutes, relaxes vascular smooth muscle and inhibits the aggregation of blood platelets. Prostacyclin and its analogues are currently being tested in the clinic for cardiovascular diseases such as primary pulmonary hypertension. A number of drugs including defibrotide, nafazatrom, ronicol and cicletanine may exert their therapeutic effects by releasing prostacyclin from the EC. The second mediator discussed is endothelium-derived relaxing factor (EDRF), discovered in 1980, which also relaxes smooth muscle and inhibits the aggregation and adhesion of platelets. Substances which stimulate release of EDRF include acetylcholine, bradykinin and ADP. EDRF is even more labile than prostacyclin with a half life counted in seconds. It has recently been identified as nitric oxide formed from L-arginine by an unknown mechanism. Prostacyclin and EDRF are released together following stimulation of endothelial receptors and synergize to inhibit platelet aggregation. It is suggested that these mediators form the endothelial defence mechanism against blood-borne cells and chemicals and that breakdown of this barrier results in diseases such as hypertension and atherosclerosis. The peptide, endothelin is the third mediator under discussion. Characterised and synthesised in 1988, it is the most potent vasoconstrictor so far discovered. Three isomers of endothelin have been identified. Paradoxically, endothelin strongly releases both prostacyclin and EDRF thus modulating its own vasoconstrictor actions.
Arch Mal Coeur Vaiss 1989 Nov
PMID:Vasoactive mediators derived from the endothelium. 251 50

A series of 134 patients with left main coronary stenosis was followed up for an average of 18 months. The majority of patients presented with unstable angina and per-critical ECG changes. Coronary angiography showed that left main coronary stenosis is rarely an isolated entity but generally associated with diffuse coronary atherosclerosis. Left ventricular function is usually normal. Treatment is surgical whenever the coronary lesions, left ventricular function and general condition of the patient allow it. The medium-term surgical results are excellent on clinical symptoms and quality of life at the price of low perioperative mortality and morbidity.
Arch Mal Coeur Vaiss 1989 Dec
PMID:[Clinical, angiographic aspects and 18-month follow-up of 134 cases of left coronary trunk stenosis]. 251 28

Monocytes and endothelial cell interactions play a key role in the development of vascular lesion, inflammation and atherosclerosis. Leukocyte adhesion is mediated through specific molecules CD11/CD18 complexes on the leukocyte side and the ELAM (Leukocyte Adhesion Molecule) ICAM (Intercellular Adhesion Molecule) on the endothelium cell surface. Several monocyte products damage endothelial cells such as free radicals, oxygen peroxides, proteases, hydrolases, lipases... Various monokines alter endothelial cell function and proliferation. Interleukin 1, gamma interferon, alpha tumor necrosis factor increase ELAM, further more they induce the synthesis of procoagulant activity by endothelial cells. Monocyte derived growth factor stimulates endothelial cells proliferation while transforming growth factors, beta (TGF beta) and TNF alpha inhibit endothelial cell growth. Lipid products of monocyte origins such as leukotrienes induce an activation of endothelial cells which results in a production of prostacyclin. Monocytes may also participate in the coagulation process by producing thromboplastin and coagulation factors and facilitating the tenase (activation of factor X) complex formation. On the other hand, monocyte also synthesize tissue plasminogen activator and inhibitor. The numerous factor produced by monocytes may affect in different ways the endothelial cell behavior.
J Mal Vasc 1989
PMID:[Monocyte-endothelium relations]. 265 10

Phagocytes (P), i.e. neutrophils, monocytes and macrophages, may be involved as well as reactive oxygen species (ROS) in the initiation and development of atherosclerosis. Evidences for this assumption are the following; P and ROS are both able to damage endothelial cells whose dysfunction is crucial in the etiology of atherosclerosis. ROS generated by endothelial cells, smooth muscle cells or mainly blood cells such as neutrophils but also monocytes platelets and erythrocytes, peroxide directly endothelial cell membranes. Damage to cell membranes can be induced by P that adhere to, and release on endothelial cells large amounts of proteolytic and lipolytic enzymes. ROS can also induce formation in the blood of lipoperoxides which are often included in LDL (low density lipoproteins). These modified LDL are cytotoxic, possess phospholipase A2 activity and are recognized by the LDL scavenger receptor which is on the monocyte-macrophage membrane. The modified LDL are also immunogenic inducing formation of autoantibodies directed against them and normal LDL. Modified LDL and LDL immune complexes can be ingested by monocytes leading to foam cells and ROS. The damaged endothelial cells have an increased permeability to macromolecules, synthetize chemotactic factors, decrease their prostacyclin production and favour the adherence of neutrophils and monocytes to their surface. All these factors could increase ROS production and lipid peroxidation amplifying intra and extra-cellular accumulation of lipoperoxides in vascular walls. The ability of ROS and P to damage endothelial cells, to induce lipid peroxidation and thus to be involved in atherosclerosis relies on in vitro experimental results.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mal Vasc 1989
PMID:[Oxygen, phagocytic cells and atheroma]. 265 11

Inflammation is the reaction of a vascularized living tissue to local injury. Acute and chronic inflammation result from complex interactions between leukocytes, mesenchymal cells and various components of plasma. The aim of inflammation is reparation, but persisting chronic inflammation is a source of disease. Atherosclerosis can be viewed as an impairment of the normal relationships between blood and arterial wall. As proposed by pathologists of the last century, inflammation may provide a physiopathologic frame for atherosclerosis. Human atherosclerotic lesions at any step of their evolution, as well as the pathogenic models that have been developed to explain atherogenesis, share many features of an inflammatory reaction of arterial intima: increased penetration of plasma components, proliferation of smooth muscle cells, infiltration by monocytes/macrophages and by lymphocytes, building up of a sclerotic extracellular matrix and of a rich neovascularization. The inflammatory model neither contradicts nor jeopardizes the established knowledge on the roles of lipids and thrombosis in atherosclerosis. Rather, introducing the numerous cellular and molecular mediators of inflammation into the pathogenesis of atherosclerosis widens our field of investigations, and may open new avenues for prevention and treatment. There remains the major question of identifying the cause(s) which initiate(s) and perpetuate(s) arterial inflammation that lead to complicated atherosclerosis with ischemic manifestations.
J Mal Vasc 1989
PMID:[Inflammation and atherosclerosis]. 265 13

Pentoxifylline has been used for several years in various types of peripheral and cerebrovascular diseases because of its hemorheological properties: pentoxifylline improves the red cell deformability, decreases platelet and red cell aggregation, decreases fibrinogen and plasma viscosity. Its new properties on the leukocyte function can lead to new therapeutical ways. Adherence and peroxidative free radicals production are induced by inflammatory cytokines (IL1, TNF) and can induce vascular tissue damages and development of atherosclerosis. Pentoxifylline has no effect on the normal leukocyte function. However, in all inflammatory diseases, Pentoxifylline acts on the activated neutrophil function: Pentoxifylline decreases adherence to endothelial cells or other surfaces, the superoxide and lysozyme release, and increases chemotaxis. In some animal models of shock and infection, pentoxifylline decreases cellular and tissue damages, mediated by activated neutrophils. Furthermore, in inhibiting neutrophil adhesion to cultured endothelium cells, pentoxifylline, modulates leukocyte-endothelium and leukocyte-platelets interactions which are important factors in the development of inflammation and thrombosis. Pentoxifylline increases the leukocytes mediated activation of fibrinolytic pathways and could play an important role in the prevention of thrombosis. In addition to its well-known effects on chronic vascular diseases, pentoxifylline is also effective in some acute injuries in animal models. This can lead to new research fields allowing a better understanding of atheromatous processes.
J Mal Vasc 1989
PMID:[New aspects of the pharmacology of pentoxifylline]. 265 14

Results of treatment of a personal series of 12 patients developing a thrombus in branches of prostheses after aorto-iliac surgery are presented. A therapeutic procedure used over the last two years consists of initial local and regional thrombolysis to remove the acute obstruction, followed by surgery at the level chosen, and if necessary to correct a faulty technique or progression of the atherosclerosis. Good results were obtained even for thrombosis originating after the conventional 8-10 day postoperative period, insofar as the thrombus that develops in a graft may differ from one forming in an artery. This aspect requires further studies, which will also provide greater clarification of the etiopathogenicity.
J Mal Vasc 1986
PMID:[Role of local and regional thrombolysis in late thromboses of the branches of prostheses]. 294 10

This article is a short update of the role played by dietary polyunsaturated fatty acids in atherosclerosis and thrombosis, with special reference to the interactions between the platelets and endothelium. The n-3 family of fatty acids, especially eicosapentaenoic (20:5n-3) and docosahexaenoic acids (22:6n-3), seem to be beneficial in the prevention of these diseases.
Arch Mal Coeur Vaiss 1985 Dec
PMID:[Polyunsaturated fatty acids, atherosclerosis and thrombosis]. 301 Aug 92

Ultrasonic investigations of the peripheral vessels (continuous Doppler with spectral analysis, echotomography) were performed to evaluate atherosclerosis of the main arteries (abdominal aorta, cervical arteries, lower limb arteries) in 50 coronary patients and 40 control subjects. In the main, our results support those of previously published series (epidemiological and autopsy studies): Atherosclerosis of the main arterial vessels is significantly more common (p less than 0.01) in coronary patients than in control subjects: carotid lesions: 70% (including 10% with severe stenosis) compared to 32% (no severe stenosis); aortic lesions: 50% (including 20% with severe stenosis) compared to 17.5% (7.5% severe stenosis); lower limb arteries: 58% (including 16% severe stenosis) compared to 12.5% (no severe stenosis). The difference of incidences of associations of atherosclerosed vessels between the two groups was significant (p less than 0.01): no peripheral vascular disease was detected in 57.5% of controls compared to only 12% of coronary patients; more than one territory diseased in 15% of controls compared to 58% of coronary patients. The severity of these lesions correlated with the presence of the three major cardiovascular risk factors which were studied (hypertension, smoking, hypercholesterolaemia) and was significantly higher (p less than 0.01) in coronary patients (38% had more than one major risk factor and only 10% had none) than in controls (47% had no risk factors and 6% had more than one). In addition, the preferential sites of atherosclerosis were also confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Ultrasonic detection of arteriosclerosis of the main arterial trunks in the coronary patient]. 309 28


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