Mechanism of late in-stent restenosis after implantation of a paclitaxel derivate-eluting polymer stent system in humans

Renu Virmani, Francesco Liistro, Goran Stankovic, Carlo Di Mario, Matteo Montorfano, Andrew Farb, Frank D. Kolodgie, Antonio Colombo

Research output: Contribution to journalArticlepeer-review

Abstract

Background - We recently reported delayed angiographic restenosis in 15 patients who received 7-hexanoyltaxol (QP2)-eluting polymer stents (QuaDS) for the treatment of in-stent restenosis. This study presents the histological findings of atherectomy specimens from a subset of these patients receiving implants. Methods and Results - Between October and December 2001, 5 patients treated with QuaDS-QP2 stents underwent directional coronary atherectomy at 11.2±1.0 months for recurrent in-stent restenosis. Restenotic lesion composition was assessed with special stains, immunohistochemistry with quantitative image analysis, and, in one specimen, transmission electron microscopy. Atherectomy specimens contained fibrin interspersed in a smooth muscle cell-rich neointima with proteoglycan matrix. In 2 of 5 specimens, large aggregates of macrophages and T-lymphocytes were noted. These areas of active inflammation demonstrated a relatively high proliferation index by Ki-67 antibody staining, whereas the proliferation index in smooth muscle cell-rich restenotic areas was low. Conclusion - Restenotic lesions from QuaDS-QP2-eluting stents at 12 months show persistent fibrin deposition with varying degrees of inflammation. These pathological changes, representing delayed healing, are usually observed up to only 3 months in human coronary arteries with stainless steel balloon-expandable stents. The nonreabsorbable polymer alone may have induced chronic inflammation.

Original languageEnglish
Pages (from-to)2649-2651
Number of pages3
JournalCirculation
Volume106
Issue number21
DOIs
Publication statusPublished - Nov 19 2002

Keywords

  • Fibrin
  • Inflammation
  • Restenosis
  • Stents

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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