ANGIOGENESIS, MACROPHAGES AND MAST CELLSINFILTRATE ARE INVOLVED IN CAROTID PLAQUE INSTABILITY

Plaque rupture is more frequent in symptomatic than asymptomatic patients and in symptomatic patients in which the fibrous cap is thinner with greater inflammatory infiltrate. The aim of this study was to evaluate the role of major cardiovascular risk factors and histomorphological characteristics, in particular of macrophages and mast cells and of microvascular density, in atherosclerotic plaques collected from 33 consecutive symptomatic and asymptomatic patients undergoing carotid endoarterectomy for carotid disease. Patients were divided in two groups: symptomatic patients [defined according to the North American Symptomatic Carotid Endoarterectomy Trial Classification presenting with cerebrovascular TIAs or stroke within the last three months, and asymptomatic patients, exhibiting progressive ipsilateral internal carotid artery stenosis. Morphological analysis revealed an higher neovascularization in plaques from symptomatic patients, as compared to asymptomatic patients. New-formed blood vessels were located in the intima, interfacing the necrotic core, and at the shoulder area. In parallel, we found a significant increased number of CD68-positive macrophages and tryptase-positive mast cells in plaques from symptomatic patients, as compared to asymptomatic patients. Morphological evidence concerning microvascular density, CD68-positive macrophages and tryptase-postive mast cells have been confirmed by morphometric analysis. Increased plaque vascularity may contribute to lesion progression; being a source of nutrient, inflammatory cell recruitment, and intraplaque hemorrhage, which tends to weaken the plaque and predispose to plaque rupture with ensuing clinical sequelae, such as stroke.