The observation that platelet-platelet interaction and thrombosis are ultim
ately regulated by the glycoprotein (GP) IIb/IIIa receptor complex, trigger
ed the development of agents capable of interfering with this platelet rece
ptor complex. Several large clinical trials have demonstrated the effective
ness of this class of agents. The first of these agents to show beneficial
effects after coronary interventions was the mouse/human chimeric Fab fragm
ent antibody c7E3 (abciximab; ReoPro), This study analyzes whether the addi
tion of heparin to the GP IIb/IIIa antagonist abciximab would enhance the a
ntithrombotic effect. Blood drawn directly from patients on aspirin who und
erwent interventional procedures perfused an ex vivo perfusion chamber cont
aining a severely injured arterial wall at local theologic conditions of a
mildly stenosed coronary artery. Blood was perfused directly from patients
at baseline and following administration of heparin, abciximab, or both, Th
e antithrombotic effects of the 3 treatments were assessed by reduction of
the thrombus formation on the perfused specimens. Thrombus formation at bas
eline was not significantly modified by the administration of heparin (13,8
97 +/- 1,316 vs 11,917 +/- 1,519 mu m(2)). Abciximab produced a 58% reducti
on in thrombus formation (11,631 +/- 861 vs 4,925 +/- 585 mu m(2); p < 0.00
1). The addition of heparin to abciximab did not further reduce thrombus ar
ea versus abciximab alone (5,651 +/- 581 vs 4,925 +/- 585 mu m(2)). Thus, o
ur data show that abciximab dramatically decreases mural thrombus formation
and that combining heparin with abciximab did not add any additional antit
hrombotic effect to abciximab alone. (C) 2000 by Excerpta Medico, Inc.