Can eccentric arterial plaques alone cause flow stagnation points and favour thrombus incorporation?

被引:1
作者
Beneli, Cristina T. [1 ]
Barbosa, Priscila F. [1 ]
Floriano, Elaine M. [1 ]
Abreu, Monica A. [1 ]
Ramalho, Fernando S. [2 ]
Elias Junior, Jorge [3 ]
Rossi, Marcos A. [1 ]
Ramos, Simone G. [1 ]
机构
[1] Univ Sao Paulo, Dept Pathol, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP, Brazil
[2] Univ Sao Paulo, Dept Surg & Anat, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP, Brazil
[3] Univ Sao Paulo, Dept Radiol, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
atherosclerosis; blood flow; neointima; stenosis; WALL SHEAR-STRESS; CORONARY ATHEROSCLEROSIS; COMPENSATORY ENLARGEMENT; LIPID DEPOSITION; HORSESHOE VORTEX; CELLS; BIFURCATION; STENOSIS; PATHOGENESIS; EXPRESSION;
D O I
10.1111/j.1365-2613.2008.00630.x
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
We have used an experimental model of aorta stenosis, with a Plexiglas plug, simulating a stable atheromatous plaque that promotes local turbulence and thrombosis. With animal survival of more than 24 h, we followed the partial fibrinolysis of the thrombus as well as its posterior organization and incorporation to the arterial wall as a neointima for up to 30 days. The mushroom plug form permitted the development of recirculation and stasis areas around it, favouring this evolution. Despite noted limitations, this study demonstrates that thrombus incorporation can contribute to plaque extension, as it can promote recirculation and stasis areas.
引用
收藏
页码:295 / 310
页数:16
相关论文
共 51 条
[1]   TOLUIDINE BLUE-BASIC FUCHSIN STAIN FOR GLYCOLMETHACRYLATE EMBEDDED TISSUE [J].
ABREU, MA ;
BAROZA, LGV ;
ROSSI, MA .
JOURNAL OF HISTOTECHNOLOGY, 1993, 16 (02) :139-140
[2]  
BADIMON L, 1992, CIRCULATION, V86, P74
[3]   Gene expression profiling of human aortic endothelial cells exposed to disturbed flow and steady laminar flow [J].
Brooks, AR ;
Lelkes, PI ;
Rubanyi, GM .
PHYSIOLOGICAL GENOMICS, 2002, 9 (01) :27-41
[4]   Relation between non-uniform hemodynamics and sites of altered permeability and lesion growth at the rabbit aorto-celiac junction [J].
Buchanan, JR ;
Kleinstreuer, C ;
Truskey, GA ;
Lei, M .
ATHEROSCLEROSIS, 1999, 143 (01) :27-40
[5]   COMBINATION HEMATOXYLIN-EOSIN-ROSE BENGAL AND RESORCINOL-FUCHSIN CONNECTIVE-TISSUE STAIN FOR GLYCOLMETHACRYLATE EMBEDDED SECTIONS [J].
CANNON, MS ;
STUTH, NR .
JOURNAL OF HISTOTECHNOLOGY, 1993, 16 (02) :141-142
[6]   ARTERIAL WALL SHEAR AND DISTRIBUTION OF EARLY ATHEROMA IN MAN [J].
CARO, CG ;
FITZGERA.JM ;
SCHROTER, RC .
NATURE, 1969, 223 (5211) :1159-&
[7]   Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling - Molecular, cellular, and vascular behavior [J].
Chatzizisis, Yiannis S. ;
Coskun, Ahmet Umit ;
Jonas, Michael ;
Edelman, Elazer R. ;
Feldman, Charles L. ;
Stone, Peter H. .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2007, 49 (25) :2379-2393
[8]   Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress [J].
Cheng, Caroline ;
Tempel, Dennie ;
van Haperen, Rien ;
van der Baan, Arjen ;
Grosveld, Frank ;
Daemen, Mat J. A. P. ;
Krams, Rob ;
de Crom, Rini .
CIRCULATION, 2006, 113 (23) :2744-2753
[9]   MEDIAL THINNING IN ATHEROMA [J].
CRAWFORD, T ;
LEVENE, CI .
JOURNAL OF PATHOLOGY AND BACTERIOLOGY, 1953, 66 (01) :19-&
[10]   The role of shear stress in the pathogenesis of atherosclerosis [J].
Cunningham, KS ;
Gotlieb, AI .
LABORATORY INVESTIGATION, 2005, 85 (01) :9-23