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

The central role of the thrombocytes in the initial atherogenesis and the secondary formation of the thrombus on sclerotically changed walls of the vessels is the basis of all experiments to perform a primary or secondary prevention of the atherosclerosis with thrombocyte aggregation inhibitors. Of the numerous thrombocyte-inhibiting substances acetyl salicylic acid, dipyridamol and sulfinpyrazone proved most suitable for clinical purposes. Apparantly for methodical reasons experiments of a primary prevention of the atherosclerosis with aggregation inhibitors have hitherto not be performed. On the other hand, in numerous quantitatively very different studies on patients with manifest cerebral, coronary and peripheral arteriosclerosis the influencibility of the course of the disease was tested by thrombocyte inhibitors. Since correct prospective studies are connected with enormous organisational expenditure and must extend for a longer period many extensive examinations have not yet finished. In the present survey the hitherto existing reports from literature are critically summarized, taking into particular consideration the per ipheral angioorganopathies and first informations on an own study concerning the prophylaxis of the diabetic angiopathy with Micristin are given. The present state of knowledge allows the conclusion that the well founded theoretical concept is apparantly confirmed by practice. However, the successes observed could be statistically ascertained only in individual cases, so that at present a final estimation of the prophylactic value of these preparations is not yet possible.
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PMID:[Inhibitors of platelet aggregation in the therapy of arteriosclerosis obliterans]. 48 16

Thromboxane A2 (TxA2) is the main arachidonic acid metabolite in human platelets and exhibits two major activities; stimulation of platelet function, including secretion of platelet-derived storage products, e.g., 5-HT, PDGF, and vasoconstriction. Platelet hyperreactivity is typical for advanced stages of atherosclerosis and is paralleled by elevated circulating thromboxane levels. This is the target for TX-antagonistic compounds. Three classes of selective compounds are available: inhibitors of thromboxane synthase, antagonists of thromboxane receptors, and mixed-type agents. Positive experimental data with all of these compounds are available. However, clinical experience is limited and, in general, not convincing. This review discusses possible reasons for that and suggests that, in particular, the use of combined-type agents as antithrombotics may be superior to acetyl-salicylic acid in several forms of ischemic cardiovascular diseases.
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PMID:[Thromboxane A2 and prevention of cardiovascular diseases]. 129 Feb 97

Patients leaving the hospital after a myocardial infarction are given a prescription containing several drugs. The purpose of this paper is to determine which of these drugs have a proven value and for which types of patients. Antithrombotic agents (be it acetyl-salicylic acid or antivitamin K drugs) have been shown to be efficient after a myocardial infarction. Beta-blockers are certainly useful, notably in cases with severe necrosis. Conversely, the usefulness of calcium antagonists for secondary prevention has not been demonstrated and indeed, it seems probable that the drugs of this class might be harmful in patients who had severe infarction. There is little divergence concerning the necessity to control the risk factors for coronary atherosclerosis after a myocardial infarction. The evidence is strong concerning giving up smoking; it is intuitive as regards controlling arterial hypertension and more controversial as regards the need for lowering blood cholesterol levels. The systematic prescription of antiarrhythmic agents after myocardial is certainly noxious. Finally, prospects are now opened by the prevention of left ventricular remodelling under treatment with angiotensin-converting enzyme inhibitors.
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PMID:[Which medical treatment after myocardial infarction?]. 136 53

Experimental atherosclerosis was induced in a rabbit model by intimal damage of the infrarenal aorta followed by two months cholesterol feeding. The influence of four different antiplatelet drug regimens on acute platelet and fibrin deposition after transluminal angioplasty of the atherosclerotic abdominal aorta was then evaluated. The study group consisted of 32 New Zealand rabbits: 7 controls, 7 treated with prostacyclin (10 mg/kg/min i.v.), 5 treated with low-dose acetylsalicylic acid (2 mg/kg i.v.), 7 treated with acetyl-salicylic acid (5 mg/kg i.v.) and dipyridamole (2 mg/kg i.v.), and 6 treated with low molecular dextran (5 ml/kg). By 2 hours after angioplasty, there was a significant increase of the deposition of platelets (P less than 0.001) as well as fibrin (P less than 0.01) when comparing dilated to non-dilated segments in the control animals. There was no significant difference in the amount of platelets and fibrin deposition among the control and drug treated groups. Thus, in this animal model there appears to be no immediate benefit in using antiplatelet drugs during transluminal angioplasty. Although, this study did not address the potential long-term effects of antiplatelet drug therapy, future evaluation of the clinical benefits of these drugs in conjunction with transluminal angioplasty seems warranted.
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PMID:Effect of platelet inhibitors on platelet and fibrin deposition following transluminal angioplasty of the atherosclerotic rabbit aorta. 169 Nov 11

Platelets play an important role in the pathogenesis of early thrombus formation and might even be involved in initiating the process of artherosclerosis. Various platelet adhesiveness test methods are discussed. Results of an in vitro test in about 600 patients with various diseases are given. The effect from anti-platelet drugs like dipyridamole and acetyl salicylic acid in preventing increase of platelet adhesiveness due to a biologic stressor are compared with those obtained with isoxsuprine. Platelets play an important role in the pathogenesis of early thrombus formation. Platelets might also be involved in initiating the process of atherosclerosis. Therefore, it is understandable that various test methods to measure platelet behavior has been developed.
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PMID:Platelet adhesiveness: methodology for testing in humans. 722 34

The high density lipoprotein HDL) response of 14 hyperlipidemic subjects to four hypolipidemic agents was studied through serial measurement of HDL cholesterol and apolipoproteins A-I and A-II before and during 3 months each (separated by 2 months off drug) of clofibrate (2 g/day, n = 14), colestipol (20 g/day, n = 12), para-amino salicylic acid--ascorbate (PAS-C, 6--8 g/day, n = 14) taken in random sequence and oxandrolone (7.5 mg/day, n = 11) as the final drug. The maximal effect of each drug appeared by the first monthly evaluation, and A-1, A-II and HDL cholesterol levels returned to pretreatment levels by one month after discontinuation of each agent. With clofibrate, HDL cholesterol increased by 16 +/- 20% from baseline (mean +/- SD) (P less than 0.05), A-I by 11 +/- 13% (P less than 0.05) and A-II by 39 +/- 17% (P less than 0.01). During oxandrolone HDL cholesterol declined by 36 +/- 20% from baseline (P less than 0.01), A-I by 21 +/- 13% (P less than 0.01), and A-II by 16 +/- 11% (P less than 0.025). Neither PAS-C nor colestipol exerted major effects on HDL, or any of the variables although both were associated with a slight rise in the A-I/A-II ratio (11 +/- 15% and 12 +/- 12%, respectively).
Atherosclerosis 1980 Mar
PMID:High density lipoproteins during hypolipidemic therapy. A comparative study of four drugs. 736 96

Twelve patients with varying degrees of peripheral atherosclerotic disease were given an antiaggregatory drug, ticlopidine [5-(6-chlorobenzyl)-4,5,6,7-tetrahydrothieno-(3,2-C)-pyridine HCl] in a single blind trial for one or four months and the effects on platelet aggregation, blood coagulation, marcro- and micro-circulation and walking distance were studied. Two patients were excluded; one because of nausea attributable to the drug, one because of lack of co-operation. No statistically significant changes in circulation parameters or walking distance were noted. No changes were observed in APT-time, thrombine- and Reptilase-clotting time, platelet counts, concentrations of fibrinogen and fibrinopeptide A in plasma or serum antithrombin activity. The mean concentration of fibrinopeptide A was slightly increased in all patients. ADP-induced aggregation was inhibited in all patients. Aggregation induced by arachidonic acid was partially inhibited but not abolished in all patients. Prostaglandin G2-induced aggregation was not altered by ticlopidine but collagen-induced aggregation was inhibited. Ticlopidine, in contrast to acetyl-salicylic acid, inhibits the primary aggregation but also seems to interfere with the release action. Treatment of larger patient groups for longer periods are necessary to determine the clinical usefulness of ticlopidine.
Atherosclerosis 1980 Aug
PMID:Antiaggregatory, physiological and clinical effects of ticlopidine in subjects with peripheral atherosclerosis. 741 66

Garlic has been reported to provide protection against hypercholesterolemic atherosclerosis and ischemia-reperfusion-induced arrhythmias and infarction. Oxygen free radicals (OFRs) have been implicated as causative factors in these diseases and antioxidants have been shown to be effective against these conditions. The effectiveness of garlic in these disease states could be due to its ability to scavenge OFRs. However, the OFR-scavenging activity of garlic is not known. Also it is not known if its activity is affected by cooking. We therefore investigated, using high pressure liquid chromatography, the ability of garlic extract (heated or unheated) to scavenge exogenously generated hydroxyl radical (.OH). .OH was generated by photolysis of H2O2 (1.2-10 mumoles/ml) with ultraviolet (UV) light and was trapped with salicylic acid (500 nmoles/ml). H2O2 produced .OH in a concentration-dependent manner as estimated by .OH adduct products 2,3-dihydroxybenzoic acid (DHBA) and 2,5-DHBA. Garlic extract (5-100 microliters/ml) produced an inhibition (30-100%) of 2,3-DHBA and 2,5-DHBA generated by photolysis of H2O2 (5.00 pmoles/ml) in a concentration-dependent manner. Its activity is reduced by 10% approximately when heated to 100 degrees C for 20, 40 or 60 min. The extent of reduction in activity was similar for the three heating periods. Garlic extract prevented the .OH-induced formation of malondialdehyde in the rabbit liver homogenate in a concentration-dependent manner. It alone did not affect the MDA levels in the absence of .OH. These results indicate that garlic extract is a powerful scavenger of .OH and that heating reduces its activity slightly.
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PMID:Evaluation of hydroxyl radical-scavenging property of garlic. 871 17

Iron overload, with its associated toxic effects, has serious health consequences and results in damage to the liver, heart and other organs. Salicylate may be used as the lipophilic carrier, transporting more iron into hepatocytes. In this study, we examined the effect of the combined administration of these compounds on plasma lipid profile and lipoprotein composition, as well as on hepatic lipid concentration. Male Spraque-Dawley rats were injected i.p. with Fe (15 mg/kg weight). This injection was repeated 24 h later with a gavage of sodium salicylate (700 mg/kg). Control rats received 0.9% NaCl only. The peroxidation indices TBARS (P < 0.001) and conjugated dienes (P < 0.05) significantly increased in the blood (50 and 122%, respectively) and liver (333 and 101%, respectively) of Fe salicylate-treated rats. Concomitantly, blood and liver arachidonic acid content was diminished by iron treatment. In parallel, the plasma lipid profile was markedly affected in Fe-salicylate treated-rats. Lower plasma concentrations of total cholesterol (25%, P < 0.0001) cholesteryl ester, (34%, P < 0.001) and high-density lipoprotein-cholesterol (50%, P < 0.001) were observed. Lipoprotein composition analysis revealed enrichment of free cholesterol and depletion of cholesterol ester in very low-density, intermediate-density, low-density and high-density (HDL2, HDL3) lipoproteins. Furthermore, SDS-polyacrylamide gel electrophoresis revealed several alterations in the apolipoprotein distribution of these lipoproteins. The activity of lecithin:cholesterol acyltransferase was unchanged and could not account for the reduction of cholesterol esterification. As for the plasma, the liver exhibited a significant (P < 0.001) decrease in total cholesterol (2.42 +/- 0.07 versus 1.89 +/- 0.06 mg/g liver), essentially due to a reduction in cholesteryl ester (0.93 +/- 0.07 versus 0.51 +/- 0.03 mg/g, P < 0.001). Again, the activity of ACAT (dpm/mg microsomal protein) was not lower (12,700 +/- 1250) than that of controls (9650 +/- 1080). Thus, the iron-salicylate was able to induce peroxidation and to profoundly affect the intravascular and intrahepatic lipid, and plasma lipoprotein metabolism. Additional work is needed to elucidate the mechanisms involved in the underlying lipid and lipoprotein abnormalities.
Atherosclerosis 1997 Mar 21
PMID:Iron-salicylate complex induces peroxidation, alters hepatic lipid profile and affects plasma lipoprotein composition. 910 57

Oxidation of low density lipoprotein (LDL) by glucose-derived radicals may play a role in the aetiology of atherosclerosis in diabetes. Salicylate was shown to scavenge certain radicals. In the present study, aspirin, salicylate and its metabolites 2,5- and 2, 3-dihydroxybenzoic acid (DHBA) were tested for their ability to impair LDL oxidation by glucose. Only the DHBA derivatives, when present during LDL modification, inhibited LDL oxidation and the increase in endothelial tissue factor synthesis induced by glucose oxidised LDL. The LDL glycation reaction was not affected by DHBA. The antioxidative action of DHBA may be attributed to free radical scavenging and/or chelation of transition metal ions catalysing glucose autoxidation.
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PMID:The salicylate metabolite gentisic acid, but not the parent drug, inhibits glucose autoxidation-mediated atherogenic modification of low density lipoprotein. 1072 43


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