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A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Pathological analyses of long-term intracoronary Palmaz-Schatz stenting; Is its efficacy permanent?
Katsumi Inoue1, Kenichi Abe, Kenji Ando
1Department of Laboratory Medicine, Kokura Memorial Hospital, 1-1 Kifune-machi, Kokurakita-ku, Kitakyushu, 802-8555, Japan. kmhptca@nn.iij4u.or.jp
Insights
Late restenosis after stenting involves chronic inflammation around stent struts. Persistent inflammatory cells, particularly macrophages, contribute to plaque vulnerability and potential restenosis years after the procedure.
Area of Science:
- Cardiovascular Research
- Biomedical Engineering
- Pathology
Background:
- Late restenosis after coronary stenting is a significant clinical concern.
- Palmaz-Schatz stents show gradual lesion progression and restenosis in up to 28% of cases after 4 years.
- Understanding the pathogenesis of late restenosis is crucial for developing preventive strategies.
Purpose of the Study:
- To investigate the histopathological and immunohistochemical changes in stented coronary arteries over time.
- To elucidate the role of chronic inflammation in the development of late restenosis.
- To identify cellular and molecular mechanisms contributing to late stent failure.
Main Methods:
- Histopathological and immunohistochemical analysis of 19 human coronary arteries explanted 2-7 years post-stenting.
- Evaluation of inflammatory cell infiltration (T lymphocytes, macrophages, giant cells) around stent struts.
- Assessment of neointimal scar maturation, collagen deposition, and matrix metalloproteinase (MMP) activity.
Main Results:
- Chronic inflammatory cell infiltration around stent struts was observed even without restenosis.
- At 2 years, neovascularization and lymphocyte infiltration were noted.
- By 3-4 years, prominent infiltration by lipid-laden macrophages and high MMP activity were evident, with some cases showing strut disruption and thrombus formation.
Conclusions:
- Stainless steel stents induce a persistent foreign-body inflammatory reaction.
- Chronic peri-strut inflammation, particularly by macrophages, may promote late atherosclerotic changes.
- These inflammatory processes can lead to plaque vulnerability and late stent failure.
Background:
Angiographic regression of luminal narrowing occurs 6 months to 3 years poststenting. However, after 4 years lesions progressed gradually and late restenosis was observed in 28% of 179 Palmaz-Schatz-stented lesions during the past 10 years. Elucidating its pathogenesis is pivotal to developing preventive strategies.
Methods And Results:
Histopathological and immunohistochemical studies were performed in 19 stented coronary arteries obtained from 19 patients autopsied after noncardiac death 2-7 years poststenting. The quality/severity of chronic inflammatory cells (T lymphocytes, macrophages and multinucleated giant cells) infiltration around the stent struts that is observed even in the absence of restenosis depended on the time elapsed from stenting: a) 2 years postprocedure, in spite of angiographic regression during the first year and pathologically expressed as maturation of the neointimal scar, there was chronic inflammatory response evidence: neovascularization and lymphocyte infiltration, b) > or = 3 years: the neointimal smooth muscle cells were sparse with abundant proliferation of collagen fibers. Presence of slight helper/inducer T lymphocytes and mild macrophage infiltration around the stent struts was evident immunohistochemically, c) > or = 4 years: prominent infiltration by lipid-laden macrophages with strong collagen-degrading matrix metalloproteinase immunoreactivity was observed around the struts. In two of these arteries, the surface contacting the stent was focally disrupted and covered by nonocclusive mural thrombi.
Conclusions:
Stainless steel stents evoke a remarkable foreign-body inflammatory reaction to the metal. These persistent peri-strut chronic inflammatory cells may accelerate new indolent atherosclerotic changes and consequent plaque vulnerability.