Cerebral microembolism is blocked by tirofiban, a selective nonpeptide platelet glycoprotein IIb/IIIa receptor antagonist. Circulation 2003;107

Background—Microembolic signals (MES) as detected by transcranial Doppler ultrasound define an individual stroke risk in patients with carotid artery disease. To study the composition of MES in vivo, we used the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonist tirofiban, a highly selective platelet aggregation inhibitor. Methods and Results—Twenty-four patients with recent cerebral or retinal embolism of arterial origin and a MES rate 6 per hour on initial transcranial Doppler ultrasonography recording received the short-acting GPIIb/IIIa antagonist tirofiban. With tirofiban, the MES rate dropped from a median (range) of 38 (9 to 324) to zero in all patients. After cessation of infusion, the inhibitory effect of tirofiban was reversible, with a significant increase of MES (median 13.5; range, 0 to 35; n16; P0.001). Six patients received overlapping oral antiplatelet agents and remained MES-negative. Conclusions—Cerebral microembolism of arterial origin has the property of solid emboli, with platelet-fibrinogen units as predominant constituent parts. GPIIb/IIIa antagonists may have the potential to bridge the ischemic risk in patients with unstable carotid disease. (Circulation. 2003;107:2717-2721.) Key Words: atherosclerosis embolism receptors stroke platelets Circulating cerebral microemboli (MES) can be detectedby transcranial Doppler ultrasonography (TCD) in a considerable proportion of patients with recent cerebral or retinal ischemia.1,2 The clinical significance of these emboli