Objective: Stent thrombosis and in-stent restenosis remain problematic in c
ertain patient sub-groups. c7E3-Fab (ReoPro(TM), abciximab) inhibits the pl
atelet glycoprotein IIb/IIIa receptor as well as the smooth muscle cell alp
ha(v)beta(3) receptor, and thus may influence both processes, especially if
high local concentrations could be achieved. We have studied the adsorptio
n and elution characteristics of c7E3-Fab on commercially available polymer
-coated stents. We have also investigated the effect of such antibody bindi
ng on platelet deposition in vitro, and on antibody deposition into ex vivo
human saphenous vein wall to assess whether such stents may influence sten
t thrombosis and restenosis. Methods and results: Adsorption was measured u
sing a radioisotope technique after immersing segments of polymer-coated st
ents in c7E3-Fab solutions. Uptake was dependent on antibody concentration
and duration of immersion of wire in the solution. After 22 h (at 5 mg ml(-
1)), 1146+/-101 ng cm(-1) wire was adsorbed. In an in vitro perfusion circu
it, the antibody eluted slowly, with 53% remaining after 12 days washing. T
o determine the value that such stents might have in clinical practise, ads
orption to balloon-mounted stents was assessed at room temperature, using c
ommercially available c7E3-Fab (2 mg ml(-1)). Efficacy of eluting c7E3-Fab
was determined by measuring deposition of (111)-Indium platelets. Immersing
stents in c7E3-Fab for 20 min inhibited platelet deposition by 82.3% compa
red to controls (P = 0.018). Deployment of treated stents in ex vivo saphen
ous vein resulted in the deposition of c7E3-Fab in the intima and media. Co
nclusions: c7E3-Fab can be passively adsorbed onto polymer-coated stents. I
t elutes slowly and in a predictable manner, significantly inhibiting plate
let deposition in vitro. These studies pave the way to developing stent-bas
ed delivery of a potent anti-platelet agent that may additionally affect sm
ooth muscle cell activity. (C) 2000 Elsevier Science B.V. All rights reserv
ed.