Quantitative morphologic study of intimal thickening at the human carotid bifurcation: II. The compensatory enlargement response and the role of the intima in tensile support

1994 ◽  
Vol 107 (2) ◽  
pp. 147-155 ◽  
Author(s):  
Nobuhide Masawa ◽  
Seymour Glagov ◽  
Christopher K. Zarins
1998 ◽  
Vol 4 (1_suppl) ◽  
pp. 183-186
Author(s):  
T. Yokouchi ◽  
S. Iwabuchi ◽  
A. Tomiyama ◽  
H. Samejima ◽  
K. Takahashi ◽  
...  

We performed balloon dilatation in the carotid artery of WHHL rabbits and examined subsequent morphological alteration over time. The balloon was inserted as far as the carotid bifurcation and observations were made on the morphological alteration after dilatation in the atherosclerotic intimal thickening from immediately after balloon dilatation over a period of ten months. Immediately after balloon dilatation, endothelial cells came of circularly and stretching, fragmentation off elastic fibers and coming off of smooth muscle cells of the media were confirmed. No change in the degree of thickening after dilatation was seen in the atherosclerotic intimal thickening of the carotid bifurcation. Three weeks later, endothelium covering except some parts, circular neointima and fibrosis of the media were observed; foamy cells had accumulated in the upper layer of the atherosclerotic intimal thickening, and that region was not yet covered with endothelial cells. The progress of fibrous intimal thickening so as to keep the lumen smooth was seen up to six months later, but foamy cells were not found in the neointima.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mihaela G Ionita ◽  
Gerard Pasterkamp ◽  
Dominique deKleijn

Objectives : Atherosclerosis is a chronic, complex inflammatory process and is the underlying cause of stroke and myocardial infarction due to rupture of the atherosclerotic plaque leading to acute occlusion of the artery in the brain or heart. Macrophages, infiltrating atherosclerotic lesions, abundantly express Mrp8 and Mrp14. Recently Mrp8, Mrp14 and the complex Mrp8/14 have been identified as endogenous ligands of Tlr-4.The role of Tlr-4 in the development and progression of the atherosclerotic plaque is well recognized and it is associated with a rupture-prone plaque phenotype. Expression of Mrps in human plaques and its relation to plaque phenotype is unknown. For this, we investigated the levels of Mrp8, Mrp14 and Mrp8/14 complex in a large number of human atherosclerotic plaques. Methods and results : Mrp8, Mrp14 and Mrp8/14 were quantified by ELISAs in human carotid endarterectomy specimens (186 patients) and plaque phenotype was determined by immunohistochemistry. Mrp levels were higher in the unstable (58 fibro-atheromatous, 64 atheromatous) compared to the stable (64 fibrous) plaques: Mrp8 p = 0.001 ; Mrp14 p = 0.001 ; Mrp8/14 p = 0.01 . Concomitantly, Mrp8, Mrp14 and Mrp8/14 were associated with characteristics of unstable plaques: more macrophages ( p = 0.024; p = 0.002; p = 0.076 ), less smooth muscle cells ( p = 0.041; p = 0.001; p = 0.074 ), larger lipid core ( p = 0.001; p = 0.001; p=0.004 ), less collagen ( p = 0.440; p = 0.011; p = 0.372 ). Furthermore, Mrp plaque levels were positively correlated with the pro-inflammatory cytokines (IL-6 and IL-8) and matrix metalloproteinsases (MMP2, MMP8 and MMP9) plaque levels. EDA, marker of stable plaques, was negatively associated with Mrps plaque levels. Histological analysis revealed that Mrps are expressed by a subgroup of plaque macrophages localized in the plaque cap and shoulder, the most rupture-prone sites of an atherosclerotic plaque. Conclusions: We show that Mrp8, Mrp14 and Mrp8/14 are strongly associated with the histological characteristics and inflammatory status of human rupture-prone plaques and identify Mrps as a potential marker for rupture-prone plaques.


Author(s):  
F.W. Saunders ◽  
P. Shedden

ABSTRACT:The role of the carotid siphon as a source of embolic material has had limited morphological or clinical study. The morphologic data available suggests that the siphon plays only a small role in embolic cerebrovascular disease. Clinical studies, however, suggest that it has a significant ischemic potential. To clarify this apparent discrepancy, we have designed a scanning electron microscope study of the carotid siphon. Eighty percent of the specimens from the carotid bifurcation and 30% of the siphon specimens showed evidence of damaged endothelium with attached red cell and platelet debris. The embolic potential of the siphon is estimated to be between ⅓ to ½ that of the carotid bifurcation. This supports the most recent clinical studies.


Author(s):  
D. P. Giddens ◽  
C. K. Zarins ◽  
S. Glagov ◽  
B. K. Bharadvaj ◽  
D. N. Ku

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