salicylates has been researched along with Carotid-Stenosis* in 2 studies
1 review(s) available for salicylates and Carotid-Stenosis
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Triflusal.
Triflusal is an antiplatelet agent structurally related to the salicylate group of compounds, but it is not derived from aspirin (acetylsalicylic acid). Platelet antiaggregant properties of triflusal and its active 3-hydroxy-4-trifluoro-methylbenzoic acid metabolite are primarily mediated by specific inhibition of platelet arachidonic acid metabolism. Triflusal, compared with placebo for 6 months, significantly reduced the incidence of nonfatal myocardial infarction in patients with unstable angina. In patients with peripheral arteriopathy, total and pain free walking distances were markedly improved in triflusal compared with placebo recipients. The cumulative event rate for stroke, ischemic cardiopathy and vascular death was lower, but not significantly different, in patients with atherothrombotic stroke who received triflusal than in aspirin recipients. Differences were significant, and favoured triflusal, in a subgroup of patients with > 70% carotid stenosis. Prophylaxis with triflusal for 6 months after aortocoronary vein grafting reduced the number of new distal anastomosis occlusions and the graft attrition rate more than aspirin or placebo. The incidence of deep vein thrombosis or pulmonary embolism in more than 500 patients undergoing hip surgery was similar for these 3 treatments. The amount of blood transfused was significantly reduced in triflusal compared with aspirin recipients who underwent hip surgery. Risk of haemorrhage was also reduced in ischemic stroke patients receiving triflusal versus aspirin. Topics: Adult; Angina Pectoris; Animals; Aspirin; Carotid Stenosis; Humans; In Vitro Techniques; Middle Aged; Myocardial Infarction; Platelet Aggregation Inhibitors; Postoperative Complications; Pulmonary Embolism; Randomized Controlled Trials as Topic; Salicylates; Thrombophlebitis | 1998 |
1 other study(ies) available for salicylates and Carotid-Stenosis
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2-(4-Chlorobenzyl)-3-hydroxy-7,8,9,10-tetrahydrobenzo[H]quinoline-4-carboxylic acid (PSI-697): identification of a clinical candidate from the quinoline salicylic acid series of P-selectin antagonists.
P-selectin-PSGL-1 interaction causes rolling of leukocytes on the endothelial cell surface, which subsequently leads to firm adherence and leukocyte transmigration through the vessel wall into the surrounding tissues. P-selectin is upregulated on the surface of both platelets and endothelium in a variety of atherosclerosis-associated conditions. Consequently, inhibition of this interaction by means of a small molecule P-selectin antagonist is an attractive strategy for the treatment of atherosclerosis. High-throughput screening and subsequent analoging had led to the identification of compound 1 as the lead candidate. Herein, we report the continuation of this work and the discovery of a second-generation series, the tetrahydrobenzoquinoline salicylic acids. These compounds have improved pharmacokinetic properties, and a number of them have shown oral efficacy in mouse and rat models of atherogenesis and vascular injury. The lead 31 (PSI-697), is currently in clinical development for the treatment of atherothrombotic vascular events. Topics: Administration, Oral; Animals; Apolipoproteins E; Atherosclerosis; Carotid Stenosis; Dogs; Fibrinolytic Agents; Hydroxyquinolines; Indoles; Leukocyte Rolling; Male; Mice; Mice, Knockout; P-Selectin; Quinolines; Rats; Rats, Sprague-Dawley; Salicylates; Structure-Activity Relationship | 2007 |