title: Eptifibatide and abciximab exhibit equivalent antiplatelet efficacy in an experimental model of stenting in both healthy volunteers and patients with coronary artery disease.
abstract: Platelet deposition and aggregation are the major determinants of acute thrombosis in coronary stents. We aimed to compare the antiplatelet efficacy of different treatments--glycoprotein (Gp) IIb/IIIa inhibitors and conventional antiaggregants--in an experimental model for stenting. Blood samples were obtained from patients with coronary artery disease (n = 15) and healthy volunteers (n = 8) and incubated either with eptifibatide (2.0 microg/ml), abciximab (3.0 microg/ml), indomethacin (15 microg/ml), or saline. Platelet adenosine diphosphate-induced aggregation in whole blood was assessed for all groups. Blood was also tested in an experimental circulation model containing metallic probes, on which platelet deposition in shear flow conditions was assessed by means of fluorescent-labeled platelet-specific (anti-GpIIIa and Ib) antibodies. Eptifibatide and abciximab, in comparison with indomethacin and no treatment, significantly reduced platelet aggregation (0, 0, 4, and 3 arbitrary units [AU], respectively; p < 0.001), anti-GpIIIa (2.25, 1.83, 11.24, and 13.42 counts per second [cps]/mg, respectively; p < 0.001), and anti-GpIb binding (0.61, 0.61, 1.00, and 1.83 cps/mg, respectively; p < 0.001). Anti-GpIIIa and anti-GpIb binding were significantly correlated (R = 0.36; p < 0.01). Patients showed a higher anti-GpIIIa, but not anti-GpIb binding, than controls (8.43 versus 3.33 cps/mg; p < 0.01), irrespective of treatment. In conclusion, eptifibatide and abciximab show equivalent in vitro antiplatelet efficacy, superior to that of indomethacin. Given the occurrence of GpIIb/IIIa platelet overexpression in the course of coronary artery disease, an extended use of GpIIb/IIIa inhibitors may be proposed to prevent acute thrombosis during routine coronary stenting.
authors.affiliation: Department of Cardiology, Thoraxcenter, University Hospital of Groningen, The Netherlands. gioamor@hotmail.com
authors.forename: G
authors.initials: G
authors.lastname: Amoroso
authors.forename: A J
authors.initials: AJ
authors.lastname: van Boven
authors.forename: D J
authors.initials: DJ
authors.lastname: van Veldhuisen
authors.forename: R A
authors.initials: RA
authors.lastname: Tio
authors.forename: C P
authors.initials: CP
authors.lastname: Baljé-Volkers
authors.forename: A S
authors.initials: AS
authors.lastname: Petronio
authors.forename: W
authors.initials: W
authors.lastname: van Oeveren
mesh_terms: D000077284:Abciximab; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000378:metabolism*; D000077542:Eptifibatide; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology*; D010455:Peptides / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects* / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D018709:Statistics, Nonparametric; D015607:Stents; D013810:Therapeutic Equivalency
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D000077542:Eptifibatide; D000077284:Abciximab