Eptifibatide and abciximab exhibit equivalent antiplatelet efficacy in an experimental model of stenting in both healthy volunteers and patients withcoronary artery disease

Platelet deposition and aggregation are the major determinants of acute thr ombosis in coronary stents. We aimed to compare the antiplatelet efficacy o f different treatments-glycoprotein (Gp) IIb/IIIa inhibitors and convention al antiaggregants-in an experimental model for stenting. Blood samples were obtained from patients with coronary artery disease (n = 15) and healthy v olunteers (n = 8) and incubated either with eptifibatide (2.0 mug/ml), abci ximab (3.0 mug/ml), indomethacin (15 mug/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 met allic probes, on which platelet deposition in shear flow conditions was ass essed by means of fluorescent-labeled platelet-specific (anti-GpIIIa and lb ) antibodies. Eptifibatide and abciximab, in comparison with indomethacin a nd no treatment, significantly reduced platelet aggregation (0, 0, 4, and 3 arbitrary units [AU], respectively; p < 0.001), anti-GpIIIa (2.25, 1.83, 1 1.24, and 13.42 counts per second [cps]/mg, respectively; p < 0.001), and a nti-GpIb binding (0.61, 0.61, 1.00, and 1.83 cps/mg, respectively; p < 0.00 1). 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 bind ing, than controls (8.43 versus 3.33 cps/mg; p < 0.01), irrespective of tre atment. In conclusion, eptifibatide and abciximab show equivalent in vitro antiplatelet efficacy, superior to that of indomethacin. Given the occurren ce of GpIIb/IIIa platelet overexpression in the course of coronary artery d isease, an extended use of GpIIb/IIIa inhibitors may be proposed to prevent acute thrombosis during routine coronary stenting.