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J Am Coll Cardiol, 2002; 40:2072-2081
© 2002 by the American College of Cardiology Foundation
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CLINICAL STUDY

Enhanced extracellular matrix accumulation in restenosis of coronary arteries after stent deployment

Ick-M. o Chung, MD*, Herman K. Gold, MD{ddagger}, Stephen M. Schwartz, MD, PhD*, Yuji Ikari, MD§, Michael A. Reidy, PhD* and Thomas N. Wight, PhD*{dagger},*

* Department of Pathology, University of Washington, Seattle, Washington, USA
{dagger} Hope Heart Institute, Seattle, Washington, USA
{ddagger} Division of Cardiology, Massachusetts General Hospital, Harvard University, Boston, Massachusetts, USA
§ Division of Cardiology, Mitsui Memorial Hospital, Tokyo, Japan

Manuscript received January 9, 2002; revised manuscript received August 22, 2002, accepted August 29, 2002.

* Reprint requests and correspondence: Dr. Thomas N. Wight, Vascular Biology, The Hope Heart Institute, 1124 Columbia Street, Suite 783, Seattle, Washington 98104, USA.
twight{at}hopeheart.org

OBJECTIVES: The goal of this study was to evaluate the cellular and extracellular composition of human coronary arterial in-stent restenosis after various periods of time following stent deployment.

BACKGROUND: Neointimal in-growth rather than stent recoil is thought to be important for coronary arterial in-stent restenosis. There is only limited data on the cellular and extracellular composition changes with time after stent deployment.

METHODS: We analyzed 29 coronary arterial in-stent restenotic tissue samples (14 left anterior descending coronary artery, 10 right coronary artery, and 5 left circumflex artery) retrieved by using directional coronary atherectomy from 25 patients at 0.5 to 23 (mean, 5.7) months after deployment of Palmaz-Schatz stents employing histochemical and immunocytochemical techniques.

RESULTS: Cell proliferation was low (0% to 4%). Myxoid tissue containing extracellular matrix (ECM) enriched with proteoglycans was found in 69% of cases and decreased over time after stenting. Cell-depleted areas were found in 57% of cases and increased with time after stenting. Versican, biglycan, perlecan, and hyaluronan were present with varying individual distributions in all samples. Positive transforming growth factor-ß1 staining was found in 80% of cases. Immunostaining with alpha-smooth muscle actin identified the majority of cells as smooth muscle cells with occasional macrophages present (≤12 cells per section).

CONCLUSIONS: These data suggest that enhanced ECM accumulation rather than cell proliferation contribute to later stages of in-stent restenosis. Balloon angioplasty of in-stent restenosis may, therefore, fail due to ECM changes during: 1) additional stent expansion, 2) tissue extrusion out of the stent, or 3) tissue compression.

Abbreviations and Acronyms
  ECM
  extracellular matrix
  HABP
  hyaluronan binding protein
  PBS
  phosphate buffered saline
  PCNA
  proliferating cell nuclear antigen
  SMC
  smooth muscle cell
  TGF-ß1
  transforming growth factor-ß1




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