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J Am Coll Cardiol, 2000; 35:157-163 © 2000 by the American College of Cardiology Foundation |
* Department of Cardiology and Angiology, University Hospital "Bergmannsheil," Bochum, Germany
Institute of Pathology, University Hospital "Bergmannsheil," Bochum, Germany
Manuscript received August 26, 1998; revised manuscript received July 29, 1999, accepted September 14, 1999.
Reprint requests and correspondence: Dr. Peter H. Grewe, Department of Cardiology and Angiology, University Hospital "Bergmannsheil" Bochum, Bürkle-de-la-Camp-Platz 1, 44789 Bochum, Germany
PeterGrewe{at}AOL.com
OBJECTIVES
The aim of our study was to analyze the cellular components of neointimal tissue regeneration after coronary stenting.
BACKGROUND
High restenosis rates are a major limiting factor of coronary stenting. To reduce the occurrence of restenoses, more insights into the mechanisms leading to proliferation and expression of extracellular matrix are necessary.
METHODS
Twenty-one autopsy cases with coronary stents implanted 25 h to 340 days before death were studied. The stented vessel segments were analyzed postmortem by light microscopy and immunohistochemical staining.
RESULTS
In the initial phase stents are covered by a thin multilayered thrombus. Alpha-actin–positive smooth muscle cells (SMCs) are found as the main cellular component of the neointimal tissue. Later (>6 weeks) extracellular matrix increases and fewer SMCs can be found. In every phase the SMC layers are loosely infiltrated by inflammatory cells (T lymphocytes). In the early postinterventional phase all endothelial cells are destroyed. The borderline between the vessel lumen and the vascular wall is constituted by a thin, membranous thrombus. Six weeks after stenting, SMCs form the vessel surface. Complete reendothelialization is first found 12 weeks after stenting.
CONCLUSIONS
Stent integration is a multifactorally triggered process with proliferating SMCs generating regenerative tissue. In the early phase predominantly thrombotic material can be observed at the site of stenting, followed by the invasion of SMCs, T lymphocytes and macrophages. The incidence of delayed reendothelializations and the occurrence of deep dissections may be associated with excessive SMC hyperplasia.
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