M. Sakakibara, S. Goto, K. Eto, N. Tamura, T. Isshiki, S. Handa
{"title":"Application of Ex Vivo Flow Chamber System for Assessment of Stent Thrombosis","authors":"M. Sakakibara, S. Goto, K. Eto, N. Tamura, T. Isshiki, S. Handa","doi":"10.1161/01.ATV.0000027102.53875.47","DOIUrl":null,"url":null,"abstract":"Objective—Factors influencing platelet accumulation around stents were to be investigated by an ex vivo flow chamber system. Methods and Results—Platelet accumulations on collagen surfaces under flow conditions were augmented in the presence of stents, especially at sites downstream from coil stents. Densitometric analysis revealed that 4.9±0.8 times more platelets accumulated downstream from coil stents than were formed downstream from tube stents (P <0.01), suggesting that stent morphology is an important determinant factor of its thrombogenicity. Platelet accumulations around stents were significantly inhibited by a combination of ticlopidine and aspirin, whereas aspirin alone produced only modest inhibition. Anti–glycoprotein IIb/IIIa (abciximab) inhibited platelet accumulation around stents in a dose-dependent manner, whereas the antibody blocking von Willebrand factor binding to glycoprotein Ib&agr;, which had been shown to inhibit platelet thrombus formation under high shear rates, did not inhibit the accumulation downstream from the coil stents. Our results suggest that the important characteristics of in vivo stent thrombosis, ie, augmented platelet accumulation with coil stents and the strong antithrombotic effect of the combination antiplatelet agents and an anti–glycoprotein IIb/IIIa, can be reproduced in ex vivo perfusion model. Conclusions—We conclude that an ex vivo perfusion system is useful in the assessment of the thrombogenicity of various stents and in the screening of effective antiplatelet agents.","PeriodicalId":8418,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","volume":"33 1","pages":"1360-1364"},"PeriodicalIF":0.0000,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"21","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/01.ATV.0000027102.53875.47","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 21
Abstract
Objective—Factors influencing platelet accumulation around stents were to be investigated by an ex vivo flow chamber system. Methods and Results—Platelet accumulations on collagen surfaces under flow conditions were augmented in the presence of stents, especially at sites downstream from coil stents. Densitometric analysis revealed that 4.9±0.8 times more platelets accumulated downstream from coil stents than were formed downstream from tube stents (P <0.01), suggesting that stent morphology is an important determinant factor of its thrombogenicity. Platelet accumulations around stents were significantly inhibited by a combination of ticlopidine and aspirin, whereas aspirin alone produced only modest inhibition. Anti–glycoprotein IIb/IIIa (abciximab) inhibited platelet accumulation around stents in a dose-dependent manner, whereas the antibody blocking von Willebrand factor binding to glycoprotein Ib&agr;, which had been shown to inhibit platelet thrombus formation under high shear rates, did not inhibit the accumulation downstream from the coil stents. Our results suggest that the important characteristics of in vivo stent thrombosis, ie, augmented platelet accumulation with coil stents and the strong antithrombotic effect of the combination antiplatelet agents and an anti–glycoprotein IIb/IIIa, can be reproduced in ex vivo perfusion model. Conclusions—We conclude that an ex vivo perfusion system is useful in the assessment of the thrombogenicity of various stents and in the screening of effective antiplatelet agents.