Restenosis following implantation of bare metal coronary stents: pathophysiology and pathways involved in the vascular response to injury

Abstract

This review summarizes the restenotic process that occurs after the implantation of bare metal coronary stents. The pathology of in-stent restenosis is distinct from that seen after balloon angioplasty and is characterized by neointimal proliferation and extracellular matrix deposition. The degree of neointimal proliferation is proportional to the amount of injury, the intensity of the inflammatory infiltrate and the association of stent struts with lipid-filled plaque. In-stent restenosis also appears to be associated with systemic markers of inflammation. Shear stress has an important influence on restenosis as does the presence and adhesiveness of vascular progenitor cells. Clinical predictors (e.g., artery size, stent length, diabetes, and gender) may affect the incidence of restenosis seen after stent placement. A number of catheter-based interventions have been used to treat in-stent restenosis. Although preliminary data suggest that the use of drug-eluting stents may be effective, only intracoronary radiation has shown consistent efficacy in randomized trials.