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In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
Published on: November 3, 2015
Extracellular matrix changes in stented human coronary arteries.
Andrew Farb1, Frank D Kolodgie, Jin-Yong Hwang
1Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
Circulation
|August 11, 2004
Summary
The extracellular matrix in human coronary stents takes over 18 months to heal, after which neointimal retraction occurs. ECM contraction could be a target for preventing stent restenosis.
Area of Science:
- Cardiovascular Research
- Biomaterials Science
- Histopathology
Background:
- Restenosis after stenting involves smooth muscle cell (SMC) and extracellular matrix (ECM) accumulation.
- The ECM constitutes over 50% of neointimal volume, but its human in-stent composition is poorly understood.
Purpose of the Study:
- To characterize the composition of extracellular matrix within human coronary stents over time.
- To investigate the temporal changes in ECM components and their relation to neointimal hyperplasia and stent restenosis.
Main Methods:
- Histological assessment of postmortem human coronary arteries (n=45) with stents.
- Analysis of neointimal proteoglycans, hyaluronan, collagen types I and III, SMCs, and CD44.
- Categorization of stents into three groups based on implantation duration (3-9 months, 9-18 months, >18 months).
Main Results:
- Neointimal versican and hyaluronan were high in early stents (3-18 months) and decreased later.
- Decorin, type I collagen, and type III collagen showed increased deposition over time.
- SMC density and stenosis were reduced in stents >18 months old.
- CD44 staining correlated with macrophages and increased neointimal thickness.
Conclusions:
- The extracellular matrix in human coronary stents exhibits characteristics of a wound that heals incompletely before 18 months.
- Neointimal retraction occurs after 18 months, suggesting a dynamic healing process.
- ECM contraction presents a potential therapeutic target for preventing stent restenosis.
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