INFLAMMATION IN HIGH-GRADE CAROTID STENOSIS - A POSSIBLE ROLE FOR MACROPHAGES AND T-CELLS IN PLAQUE DESTABILIZATION

Background and Purpose-Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis, In this study, we investigated w hether the extent of inflammatory infiltration in high-grade stenoses of the internal carotid artery (ICA) correlates to clinical features o f plaque destabilization. Methods-Endarterectomy specimens from 37 con secutive patients undergoing surgery for high-grade ICA stenosis were stained immunocytochemically for macrophages (CD68) and T cells (CD3), The staining was quantified by planimetry of immunostained areas (CD6 8) or counting individual cells (CD3), Clinical evidence of plaque ins tability was provided by the preoperative assessment of recent ischemi c symptoms attributable to the stenosis and of the occurrence of cereb ral microembolism in transcranial Doppler ultrasound monitoring of the ipsilateral middle cerebral artery. Results-The percentage of macroph age-rich areas and number of T cells per mm(2) section area were large r in recently symptomatic patients than in asymptomatic patients (macr ophages: 18+/-10% versus 11+/-4%, P=0.005; T cells: 71.2+/-34.4 versus 40.5+/-31.4 mm(2), P=0.005). The presence of microembolism was associ ated with an increase in macrophage-rich areas (P=0.011). Macrophage ( 19+/-10% versus 9+/-3%, P=0.0009) and T cell (71.5+/-39.0 versus 46.4/-22 mm2, P=0.045) infiltration were more pronounced in predominantly atheromatous than in fibrous plaques, but did not correlate significan tly to the presence of surface ulceration or luminal thrombosis. Concl usions-Our data suggest a role of plaque-infiltrating macrophages and T cells in the clinical destabilization of high-grade ICA stenoses. In flammatory mechanisms may be a therapeutic target in patients with sym ptomatic ICA disease.