Two distinct mechanisms are involved in stent thrombosis under flow conditions.
The mechanism of stent thrombosis was evaluated by a flow chamber model. A Palmaz-Schatz stent was placed on glass surfaces coated with type I collagen in a parallel-plate flow chamber. Platelets were rendered fluorescent with mepacrine and whole blood was perfused through the chamber. Platelet thrombi formed around the implanted stents were continuously recorded by epi-fluorescent video-microscopy. Platelet thrombi appeared on the collagen surface within a few minutes in the absence of function blocking monoclonal antibodies. Antibody blocking vWF interaction with GP Ib alpha completely inhibited the platelet thrombi around the stent, but had no effect on platelet thrombus formation in the space between the stents and collagen, while both were inhibited by anti-GP IIb/IIIa. Our results suggest that two distinct mechanisms, one mediated by vWF interaction with GP Ib alpha occurring at high shear rates, and the other mediated exclusively by GP IIb/IIIa occurring at low shear rates, are involved in the process of platelet thrombus formation in the presence of stents.
Eto
K
K
Division of Cardiology, Department of Medicine, Tokai University School of Medicine, Kanagawa, Japan.
Goto
S
S
Shimazaki
T
T
Sakakibara
M
M
Yoshida
M
M
Isshiki
T
T
Handa
S
S
D000818:Animals; D002478:Cells, Cultured; D003094:Collagen; D006801:Humans; D051379:Mice; D010974:Platelet Aggregation; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D015607:Stents
D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D003094:Collagen