Acute Platelet Inhibition With Abciximab Does Not Reduce In-Stent Restenosis
To the Editor:
We read with great interest the recent article by the Evaluation of ReoPro and Stenting to Eliminate Restenosis (ERASER) Investigators, in which it was reported that potent platelet inhibition with abciximab does not reduce in-stent restenosis.1 Abciximab is an effective antithrombotic agent because of its ability to bind to glycoprotein IIb/IIIa (αIIb/β3) and to inhibit platelet aggregation. Abciximab also binds to a related integrin, αvβ3, which is also known as the vitronectin receptor. The functions of this receptor include cell adhesion, proliferation, and migration and platelet-mediated thrombin generation. Thus, abciximab is expected to provide platelet-mediated effects and αvβ3-mediated effects in vivo.2
Previously, we investigated changes in coagulation and platelet activation in the coronary circulation induced by stent implantation.3 Both aspirin and ticlopidine were administered to patients before stent implantation. Blood samples were drawn from the coronary sinus immediately before, immediately after, and 4 and 24 hours after stent implantation. Plasma levels of prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin III complex (TAT), which are markers of coagulation activation, and levels of β-thromboglobulin (β-TG) and platelet factor 4 (PF4), which are markers of platelet disruption and activation, were measured. We found that F1+2 and TAT levels in blood from the coronary sinus increased significantly 24 hours after stent implantation (F1+2, from 0.73±0.05 to 1.00±0.10 ng/mL; TAT, from 5.01±0.64 to 10.7±2.26 ng/mL). However, no significant changes in β-TG and PF4 levels were observed after stent implantation (β-TG, from 60.1±8.6 to 63.8±9.2 ng/mL; PF4, from 27.6±5.0 to 19.9±6.3 ng/mL).
Gregorini et al4 also reported that the combined use of aspirin and ticlopidine effectively inhibited platelet activation in patients who underwent angioplasty. In the ERASER study, all patients received aspirin before coronary intervention and ticlopidine use was left to the investigator’s discretion. Therefore, we speculate that these combined therapies sufficiently inhibit platelet activation in the coronary circulation and that any additional effects of abciximab on platelets and, thus, in-stent restenosis were not observed in the ERASER study.
- Copyright © 2000 by American Heart Association
The ERASER Investigators. Acute platelet inhibition with abciximab does not reduce in-stent restenosis. Circulation. 1999;100:799–806.
Tam SH, Sassoli PM, Jordan RE, et al. Abciximab demonstrates equivalent affinity and functional blockade of glycoprotein IIb/IIIa and αvβ3 integrins. Circulation. 1998;98:1085–1091.