Abciximab treatment in vitro after aspirin treatment in vivo has additive effects on platelet aggregation, ATP release, and P-selectin expression

To prevent arterial thrombosis, abciximab is administered together with asp irin. However, whether or not there are benefits to combine abciximab with aspirin is not yet well defined. Healthy volunteers were studied for the ef fect of aspirin+abciximab using sodium arachidonate and adenosine diphospha te (ADP) alone or in combination to induce platelet activation/aggregation. Abciximab produced complete inhibition of platelet aggregation induced wit h ADP but only 40% inhibition of aggregation induced by 0.75-mmol/l sodium arachidonate. Abciximab added in vitro to platelet-rich plasma (PRP) from p latelets from aspirin-treated donors produced an almost complete inhibition of platelet aggregation. Aspirin, and abciximab alone, did not inhibit ade nosine triphosphate (ATP) release as thoroughly as aspirin+abciximab did. A bciximab (35 5 mug/ml) produced inhibition of P-selectin expression induced with 5 (from 46.2 +/- 6.0% to 27.4 +/- 7.0%, P = .002) and 20-mu mol/l ADP (from 53.1 +/- 8.1% to 35.1 +/- 11.0%, P = .019), but no effect was observ ed when 0.75-mmol/l sodium arachidonate was used (P = .721). Aspirin dimini shed P-selectin expression in sodium arachidonate-stimulated platelets (fro m 77.7 +/- 11.8% to 40.2 +/- 3.6%, P < .0001) in non-aspirinated and platel ets from aspirin-treated donors, respectively. Abciximab (3, 4, and 5 <mu>g /ml) added to platelets from aspirin-treated donors decreased P-selectin ex pression in platelets stimulated with sodium arachidonate from 40.2 +/- 8.6 % to 25.6 +/- 11.5% (P = .027), to 20.5 +/- 3.5% (P < .0001), and to 22.5 < plus/minus> 1.8% (P < .0001). We concluded that the antiplatelet effect of abciximab is greatly increased by aspirin. (C) 2000 Elsevier Science Ltd. A ll rights reserved.