2003
DOI: 10.1161/01.cir.0000070544.15890.0e
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Cerebral Microembolism Is Blocked by Tirofiban, a Selective Nonpeptide Platelet Glycoprotein IIb/IIIa Receptor Antagonist

Abstract: 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 Ͼ6per hour on initial transcranial Doppler ultrasonography recording r… Show more

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Cited by 75 publications
(55 citation statements)
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“…Microembolus signals detected with TCD include blood clots, platelet aggregated particles, arteriosclerosis plaque particles (platelets, fibrinogen, cholesterol), and fat or air. However, the majority of microemboli from artery cerebral infarction were particles enriched in platelets that were caused by the rupture of atherosclerosic unstable plaques (Goertler et al, 2002;Junghans and Siebler, 2003). Sitzer et al (1995) found that atherosclerotic plaques and intraluminal thrombus from carotid ulcerations were the main source of microemboli.…”
Section: Discussionmentioning
confidence: 99%
“…Microembolus signals detected with TCD include blood clots, platelet aggregated particles, arteriosclerosis plaque particles (platelets, fibrinogen, cholesterol), and fat or air. However, the majority of microemboli from artery cerebral infarction were particles enriched in platelets that were caused by the rupture of atherosclerosic unstable plaques (Goertler et al, 2002;Junghans and Siebler, 2003). Sitzer et al (1995) found that atherosclerotic plaques and intraluminal thrombus from carotid ulcerations were the main source of microemboli.…”
Section: Discussionmentioning
confidence: 99%
“…7,10 Tirofiban is a fast-acting, fast-deactivated, highly selective nonpeptide gpIIb/IIIa antagonist approved by the Food and Drug Administration for the treatment of acute coronary syndrome up to 48 hours after onset. 11,12 Pilot studies in a small number of patients with stroke showed that tirofiban abolished cerebral microemboli in patients with symptomatic carotid lesions 13,14 and reduced infarct lesions as assessed with MR perfusion imaging and diffusion-weighted imaging. 15 However, to test the efficacy of tirofiban in a multicenter acute stroke trial with a longer time window, it is necessary to assess the safety of tirofiban.…”
mentioning
confidence: 99%
“…Therefore, their measurement may be used as a surrogate marker for evaluating anti-platelet effect (Wong 2005). Glycoprotein IIb/IIIa receptor antagonist such as tirofiban infusion has shown to reduce the rate of microemboli and the effect was reversible with the cessation of infusion (Junghans and Siebler 2003). Administration of intravenous and oral acetylsalicyclic acid (ASA) has shown to reduce the frequency of microemboli rapidly (Goertler, Baeumer et al 1999;Goertler, Blaser et al 2001).…”
Section: Assessing Efficacy Of Secondary Prophylaxismentioning
confidence: 99%