From the Department of Pathology, Osaka City University Medical School
(R.K., M.U.); the Department of Cardiology, Osaka City General Hospital
(T.N.); the Department of Food and Nutrition, Faculty of Human Life Science,
Osaka City University (A.K.), Osaka, Japan; and the Department of
Cardiovascular Pathology, Academic Medical Center, University of Amsterdam,
the Netherlands (A.E.B.).
Correspondence to Dr Makiko Ueda, Department of Pathology, Osaka City University Medical School, 1–4-54 Asahi-machi, Abeno-ku, Osaka, 545, Japan.
Background—Experimental animal
studies have shown that coronary stenting induces
neointimal proliferation. However, the histopathological
events after coronary stenting in humans have not been
studied systematically.
Methods and Results—We investigated 11 stented coronary
arteries (9 Palmaz-Schatz stents, 1 Wiktor stent, and 1 ACS Multi-Link
stent) obtained from 11 patients who had died 2 days to 21 months after
stenting. We focused on gross, histological, and
immunohistochemical aspects of the repair processes. Two patients
developed symptoms of restenosis. Serial sections were stained
with antibodies against smooth muscle cells (SMCs),
macrophages, and endothelial cells. At 9 and 12
days after stenting, the stent sites showed thrombus formation with
early formation of neointima composed of abundant
macrophages and
Conclusions—These observations strongly support the concept that
neointimal proliferation in humans is a process of staged
redifferentiation of SMCs, which may cause in-stent stenosis.
Moreover, the exuberant neointimal proliferation with
accumulation of macrophages and extensive neovascularization at
sites of stent restenosis suggests a role for organization of
mural thrombus.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Neointimal Tissue Response at Sites of Coronary Stenting in Humans
Macroscopic, Histological, and Immunohistochemical Analyses
-actin–negative spindle cells. From 64 days
on, all sites with stenting showed a distinct layer of
neointima, albeit to varying degrees. In
nonrestenotic lesions, neointimal thickening was
markedly less than in restenotic lesions but without
qualitative differences; the neointima contained
macrophages but was composed predominantly of
-actin-positive SMCs.
Key Words: stents • restenosis • coronary disease • immunohistochemistry
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