Acute and chronic tissue response to coronary stent implantation: Pathologic findings in human specimen

Citation
Ph. Grewe et al., Acute and chronic tissue response to coronary stent implantation: Pathologic findings in human specimen, J AM COL C, 35(1), 2000, pp. 157-163
Citations number
33
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
35
Issue
1
Year of publication
2000
Pages
157 - 163
Database
ISI
SICI code
0735-1097(200001)35:1<157:AACTRT>2.0.ZU;2-Q
Abstract
OBJECTIVES The aim of our study was to analyze the cellular components of n eointimal tissue regeneration after coronary stenting. BACKGROUND High restenosis rates are a major limiting factor of coronary st enting. To reduce the occurrence of restenoses, more insights into the mech anisms 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 thro mbus. Alpha-actin-positive smooth muscle cells (SMCs) are found as the main cellular component of the neointimal tissue. Later (>6 weeks) extracellula r matrix increases and fewer SMCs can be found. In every phase the SMC laye rs are loosely infiltrated by inflammatory cells (T lymphocytes). In the ea rly postinterventional phase all endothelial cells are destroyed. The borde rline between the vessel lumen and the vascular wall is constituted by a th in, membranous thrombus. Six weeks after stenting, SMCs form the vessel sur face. Complete reendothelialization is first found 12 weeks after stenting. CONCLUSIONS Stent integration is a multifactorally triggered process with p roliferating SMCs generating regenerative tissue. In the early phase predom inantly thrombotic material can be observed at the site of stenting, follow ed by the invasion of SMCs, T lymphocytes and macrophages. The incidence of delayed reendothelializations and the occurrence of deep dissections may b e associated with excessive SMC hyperplasia. (C) 1999 by the American Colle ge of Cardiology.