title: Biological responses in stented arteries.
abstract: Vascular walls change their dimension and mechanical properties in response to injury such as balloon angioplasty and endovascular stent implantation. Placement of bare metal stents induces neointimal proliferation/restenosis which progresses through different phases of repair with time involving a cascade of cellular reactions. These phases just like wound healing comprise distinct steps consisting of thrombosis, inflammation, proliferation, and migration followed by remodelling. It is noteworthy that animals show a rapid progression of healing after stent deployment compared with man. During stenting, endothelial cells are partially to completely destroyed or crushed along with medial wall injury and stretching promoting activation of platelets, and thrombus formation accompanied by inflammatory reaction. Macrophages and platelets play a central role through the release of cytokines and growth factors that induce vascular smooth muscle cell accumulation within the intima. Smooth muscle cells undergo complex phenotypic changes including migration and proliferation from the media towards the intima, and transition from a contractile to a synthetic phenotype; the molecular mechanisms responsible for this change are highlighted in this review. Since studies in animals and man show that smooth muscle cells play a dominant role in restenosis, drugs like rapamycin and paclitaxel have been coated on stent with polymers to allow local slow release of drugs, which have resulted in dramatic reduction of restenosis that was once the Achilles' heel of interventional cardiologists.
authors.affiliation: Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Rue Michel Servet -1, 1211 Geneva 4, Switzerland.
authors.forename: Chiraz
authors.initials: C
authors.lastname: Chaabane
authors.forename: Fumiyuki
authors.initials: F
authors.lastname: Otsuka
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
authors.forename: Marie-Luce
authors.initials: ML
authors.lastname: Bochaton-Piallat
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000293:injuries / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001696:Biomechanical Phenomena; D002317:Cardiovascular Agents / Q000627:therapeutic use; D002465:Cell Movement; D049109:Cell Proliferation; D003251:Constriction, Pathologic; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D057510:Endovascular Procedures / Q000009:adverse effects / Q000295:instrumentation*; D006439:Hemodynamics; D006801:Humans; D040542:Mechanotransduction, Cellular; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D058426:Neointima; D010641:Phenotype; D012039:Regional Blood Flow; D015607:Stents; D013314:Stress, Mechanical; D057772:Vascular System Injuries / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology / Q000517:prevention & control; D014945:Wound Healing
chemical_list: D002317:Cardiovascular Agents
keywords: Endothelial cells; Extracellular matrix; Restenosis; S100A4; Smooth muscle cells