TY - JOUR
T1 - Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization?
AU - de Boer, O. J.
AU - van der Wal, A. C.
AU - Teeling, P.
AU - Becker, A. E.
PY - 1999
Y1 - 1999
N2 - OBJECTIVE: Microvessels in atherosclerotic plaques provide an alternative pathway for the recruitment of leucocytes in the lesions. The present study was designed to investigate the potential role of these microvessels in creating vulnerable sites in atherosclerotic plaques. METHODS: Thirty-four atherosclerotic plaques were obtained from 25 patients undergoing carotid endartherectomy (n = 16), femoral endartherectomy (n = 6) and aortic surgery (n = 12). Plaques were histologically classified as either lipid-rich (rupture prone, n = 21) or fibrous (stable, n = 13). Serial cryostat sections were immunohistochemically investigated using monoclonal antibodies against endothelial cells (ULEX-E and F-VIII), vascular endothelial growth factor (VEGF), endothelial adhesion molecules (ICAM-1, VCAM-1, E-Selectin, CD40) and inflammatory cells (macrophages (CD68) and T lymphocytes (CD3). RESULTS: The microvessel 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 plaques also expressed increased levels of ICAM-1, VCAM-1, E-Selectin and CD40. Moreover, inflammation was most abundantly present in the proximity of microvessels. VEGF was only observed on vessels and mononuclear cells in lipid-rich plaques, suggesting that this factor may play a role in microvessels formation. CONCLUSIONS: Neovascularisation and expression of adhesion molecules by microvessels at sites of vulnerable lipid-rich plaques may sustain the influx of inflammatory cells and hence, could contribute to plaque destabilization
AB - OBJECTIVE: Microvessels in atherosclerotic plaques provide an alternative pathway for the recruitment of leucocytes in the lesions. The present study was designed to investigate the potential role of these microvessels in creating vulnerable sites in atherosclerotic plaques. METHODS: Thirty-four atherosclerotic plaques were obtained from 25 patients undergoing carotid endartherectomy (n = 16), femoral endartherectomy (n = 6) and aortic surgery (n = 12). Plaques were histologically classified as either lipid-rich (rupture prone, n = 21) or fibrous (stable, n = 13). Serial cryostat sections were immunohistochemically investigated using monoclonal antibodies against endothelial cells (ULEX-E and F-VIII), vascular endothelial growth factor (VEGF), endothelial adhesion molecules (ICAM-1, VCAM-1, E-Selectin, CD40) and inflammatory cells (macrophages (CD68) and T lymphocytes (CD3). RESULTS: The microvessel 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 plaques also expressed increased levels of ICAM-1, VCAM-1, E-Selectin and CD40. Moreover, inflammation was most abundantly present in the proximity of microvessels. VEGF was only observed on vessels and mononuclear cells in lipid-rich plaques, suggesting that this factor may play a role in microvessels formation. CONCLUSIONS: Neovascularisation and expression of adhesion molecules by microvessels at sites of vulnerable lipid-rich plaques may sustain the influx of inflammatory cells and hence, could contribute to plaque destabilization
U2 - https://doi.org/10.1016/S0008-6363(98)00255-7
DO - https://doi.org/10.1016/S0008-6363(98)00255-7
M3 - Article
C2 - 10341843
SN - 0008-6363
VL - 41
SP - 443
EP - 449
JO - Cardiovascular research
JF - Cardiovascular research
IS - 2
ER -