Carotid angioplasty and stenting (CAS) is gaining popularity as an alternative method for treatment of carotid stenosis, particularly in high-risk surgical patients. A limitation of CAS is the periprocedural risk of temporary or permanent ischemic neurological deficits. In a review of 14 studies reporting upon 834 patients who underwent CAS, 1 73 (8.8%) patients experienced thromboembolic events: transient ischemic attacks (TIA) in 26 and ischemic stroke in 47. Most of these deficits resulted from local thrombosis and distal embolization. Platelet adhesion and aggregation following CAS occur as a result of damage to the vessel wall and local exposure of the subendothelium. 2 Platelets have specific membrane glycoproteins (GPs) that bind to exposed proteins in the subendothelial layers. 2 Platelet adhesion is followed by platelet activation, which causes morphological changes in the shape of platelets and activation of membrane GP IIb/IIIa receptors. These activated GP IIb/IIIa receptors bind to fibrinogen molecules, which subsequently form bridges between adjacent platelets to facilitate platelet aggregation and subsequent thrombus formation.A novel approach that has demonstrated great promise after extensive clinical evaluation in coronary interventions 3,4 involves the use of platelet inhibitors that block the platelet GP IIb/IIIa receptors. Unlike aspirin, this new class of drugs prevents the binding of fibrinogen to these receptors, thereby inhibiting platelet aggregation irrespective of the metabolic pathway responsible for the initiation of platelet aggregation. 2 Because of similarities between angioplasty and stent placement and subsequent vascular response in the coronary and carotid arteries, investigators have used GP IIb/IIIa inhibitors as adjunctive therapy during CAS. 5 Most reports of GP IIb/IIIa inhibition during CAS feature the use of abciximab, an antibody-immunoglobulin compound. Intravenously administered abciximab is a short-acting agent with a half-life of 10 minutes, but its effect on platelets last for almost 48 hours. 2 Another compound, eptifibatide, a cyclic peptide that may be a more specific inhibitor of GP IIb/IIIa receptors, has recently undergone preliminary clinical evaluation for CAS. 6 Experience with nonpeptide inhibitors of GP IIb/ IIIa receptors, i.e., lamifiban and tirofiban, is very limited.The majority of studies on GP IIb/IIIa inhibition during CAS involve nonrandomized series of patients treated with intravenous abciximab. 7 Kapadia et al. 8 reported upon 128 patients who were administered intravenous abciximab (bolus followed by infusion) during and immediately after CAS. The ischemic event rate was significantly lower in the abciximab-treated group compared with 23 historical controls (1.6% versus 8%). The only major stroke was observed in the control group. In another prospective observational study, 9 37 high-risk patients were treated with intravenous abciximab (bolus followed by infusion); another 33 low-risk patients not re-