Levels and value of platelet activity in patients with severe internal carotid artery stenosis.

ABSTRACT

BACKGROUND: Turbulent blood flow caused by arterial stenosis can induce platelet activation and aggregation, which subsequently participate in arterial thromboembolic events. OBJECTIVE: To test the hypothesis that platelet activation (expressed by CD62p) is enhanced in cerebral vs systemic circulation in patients with severe internal carotid artery (ICA) stenosis. METHODS: Platelet CD62p expression was prospectively measured using flow cytometry in 35 consecutive symptomatic patients with severe ICA stenosis and in 20 at-risk control subjects who underwent both coronary and cerebral angiographic studies due to angina pectoris and suspicious vertebral artery or intracranial artery stenosis. The CD62p expression was also evaluated in 20 healthy subjects. Blood samples were first drawn from the right internal jugular vein (cerebral circulation) and right femoral vein (systemic circulation) before extra- and intracerebral angiographic examination of both patients and at-risk control subjects and again at 40 minutes after ICA stenting. Clopidogrel was administered to the patients following the second blood sampling. RESULTS: Systemic CD62p expression was higher in patients than in both the healthy and at-risk control subjects (both p < 0.0001). Additionally, cerebral CD62p expression was higher in patients than in at-risk control subjects (p < 0.0001) prior to intervention. Moreover, CD62p expression was higher in cerebral circulation than in systemic circulation in the patients (p < 0.0001) before ICA stenting. However, CD62p expression was less enhanced in cerebral circulation than in systemic circulation after ICA stenting (p < 0.0001). Furthermore, CD62p expression was decreased after 3 months of follow-up (p < 0.0001). CONCLUSIONS: Compared to systemic CD62p expression, cerebral CD62p expression was more enhanced prior to ICA stenting and was less enhanced after ICA stenting in patients with severe ICA stenosis.