Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization?

Citation
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
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
00086363 → ACNP
Volume
41
Issue
2
Year of publication
1999
Pages
443 - 449
Database
ISI
SICI code
0008-6363(199902)41:2<443:LRIRPR>2.0.ZU;2-W
Abstract
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.