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 4.9Ϯ0.8 times more platelets accumulated downstream from coil stents than were formed downstream from tube stents (PϽ0.01), 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␣, 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. Key Words: stent thrombosis Ⅲ platelets Ⅲ glycoproteins Ⅲ flow chamber Ⅲ von Willebrand factor C oronary stent implantation is now an established procedure for the prevention of abrupt occlusion after unsuccessful coronary interventions. 1 However, thrombotic occlusion of the coronary arteries 2-4 (even though the incidence has been greatly reduced by high-pressure inflation and appropriate antithrombotic therapy) 5 and restenosis occurring later in Ϸ15% of patients 6 are unresolved issues regarding the use of stents. The results of clinical trials have clearly demonstrated that therapy with antiplatelet drugs, a combination of aspirin and ticlopidine, was more effective than persistent powerful anticoagulation with an oral anticoagulant, [3][4][5]7 suggesting an important role of platelets in the onset of stent thrombosis. Platelet accumulation around the stent is also believed to play a role in the later event of restenosis via local release of bioactive materials, such as platelet-derived growth factor 8,9 or recruitment of leukocytes, 10 although there are, as yet, no convincing clinical data showing the effects of antiplatelet agents on restenosis. 11 Nevertheless, it is reasonable to speculate that inhibition of the platelet accumulation around stents would facilitate reducing not only acute vascular events but also the subsequent event, restenosis. Indeed, clinical experiences and animal experiments have suggested that patient factors, 12 vascular factors (such as small vessel diameter), 13 and ...