HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kipshidze, N. Articles by Serruys, P. Search for Related Content PubMed PubMed Citation Articles by Kipshidze, N. Articles by Serruys, P.

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

View larger version (28K): [in a new window]   Figure 1 Proposed mechanism of restenosis.

View larger version (31K): [in a new window]   Figure 2 Impact of the stent implantation on the vessel wall. EC = endothelial cell.

View larger version (11K): [in a new window]   Figure 3 Relationship between severity of the vessel wall injury (by injury score) and endothelial cell (EC) regeneration (%).

View larger version (17K): [in a new window]   Figure 4 Time course of endothelial cell regeneration after percutaneous coronary interventions in different animal models.

View larger version (57K): [in a new window]   Figure 5 Severity ofthe vessel wall injury and activated mechanisms in the development of restenosis. EEL = external elastic lamina; IEL = internal elastic lamina.

View larger version (36K): [in a new window]   Figure 6 Time course of endothelial progenitor cell (EPC) capture. (A) Endothelial progenitor cells originate in the bone marrow and circulate postnatally in peripheral blood at concentrations of 3 to 10 cells/mm3. (B) Anti-CD34 antibody-coated stents, once deployed, have the ability to bind EPCs to their surface. (C) Over time, EPCs bound to the endoluminal surface of the stent proliferate and migrate to fill the intra strut spaces establishing a confluent, functional endothelial cell monolayer on the stented arterial segment.

View larger version (112K): [in a new window]   Figure 7 In vivo endothelial progenitor cell (EPC) capture at 1 h after deployment. All stents were deployed into the coronary arteries of Yorkshire Swine. (A to C) anti-CD34-coated stents. (D to F) bare stainless-steel stents. (A) and (D), low-magnification scanning electron micrographs (x220) of stented arterial segments. (B) and (E), high-magnification scanning electron micrographs (x2,500). (C) and (F), Confocol microscopy images (x200) of immunohistochemical staining for the endothelial cell (EC) marker (ulex europaeus agglutinin 1). Cells were counted after staining with propidium iodine, a nuclear marker that stains all cells red. All EC marker-positive cells appear green/yellow. Anti-CD34 antibody-coated stents showed >70% cell surface coverage with EC marker-positive cells 1 h after stent deployment. Stainless-steel stents showed little to no cell coverage after 1 h.