Oj. De Boer et al., Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization?, CARDIO RES, 41(2), 1999, pp. 443-449
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective: Microvessels in atherosclerotic plaques provide an alternative p
athway for the recruitment of leucocytes in the lesions. The present study
was designed to investigate the potential role of these microvessels in cre
ating vulnerable sites in atherosclerotic plaques. Methods: Thirty-four ath
erosclerotic plaques were obtained from 25 patients undergoing carotid enda
rtherectomy (n=16), femoral endartherectomy (n=6) and aortic surgery (n=12)
. Plaques were histologically classified as either lipid-rich (rupture pron
e, n=21) or fibrous (stable, n=13). Serial cryostat sections were immunohis
tochemically investigated using monoclonal antibodies against endothelial c
ells (ULEX-E and F-VIII), vascular endothelial growth factor (VEGF), endoth
elial adhesion molecules (ICAM-1,VCAM-1, E-Selectin, CD40) and inflammatory
cells (macrophages (CD68) and T lymphocytes (CD3). Results: The microvesse
l density in lipid-rich plaques was significantly increased as compared to
fibrous plaques. Most of these vessels were located in the shoulder-region
of the plaque and at the base of the atheroma. Microvessels in lipid-rich p
laques also expressed increased levels of ICAM-1,VCAM-1, E-Selectin and CD3
0. Moreover, inflammation was most abundantly present in the proximity of m
icrovessels. VEGF was only observed on vessels and mononuclear cells in lip
id-rich plaques, suggesting that this factor may play a role in microvessel
s formation. Conclusions: Neovascularisation and expression of adhesion mol
ecules by microvessels at sires of vulnerable lipid-rich plaques may sustai
n the influx of inflammatory cells and hence, could contribute to plaque de
stabilization. (C) 1999 Elsevier Science B;V. All rights reserved.