STATE-OF-THE-ART PAPER
Role of the endothelium in modulating neointimal formation
Vasculoprotective approaches to attenuate restenosis after percutaneous coronary interventions
Nicholas Kipshidze, MD, PhD, FACC*,*,
George Dangas, MD, PhD, FACC*,
Mykola Tsapenko, MD, PhD ,
Jeffrey Moses, MD, FACC*,
Martin B. Leon, MD, FACC*,
Michael Kutryk, MD and
Patrick Serruys, MD, PhD, FACC
* Lenox Hill Heart and Vascular Institute and Cardiovascular Research Foundation, New York, New YorkUSA
St. Michael's Hospital, Toronto, Canada
Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands
Veterans Administration Hospital, Bronx, New YorkUSA
Manuscript received February 20, 2004;
revised manuscript received April 10, 2004,
accepted April 27, 2004.
* Reprint requests and correspondence: Dr. Nicholas Kipshidze, Lenox Hill Heart and Vascular Institute, 130 East 77th Street, New York, New York 10021 (Email: NKipshidze{at}Lenoxhill.net).
Restenosis at the site of an endoluminal procedure remains a significant problem in the practice of interventional cardiology. We present current data on intimal hyperplasia, which identify the major role of endothelial cells (ECs) in the development of restenosis. Considering endothelial denudation as one of the most important mechanisms contributing to restenosis, we focus more attention on methods of accelerating restoration of endothelial continuity. Prevention of restenosis may be achieved by promoting endothelial regeneration through the use of growth factors, EC seeding, vessel reconstruction with autologous EC/fibrin matrix, and the use of estrogen-loaded stents and stents designed to capture progenitor ECs.
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Abbreviations and Acronyms
| | EC = endothelial cell | | LPLI = low-power laser irradiation | | NO = nitric oxide | | PTCA = percutaneous transluminal coronary angioplasty | | SMC = smooth muscle cell | | VEGF = vascular endothelial growth factor |
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