Molecular mechanisms of in-stent restenosis and approach to therapy with eluting stents

Restenosis is the principal drawback of percutaneous coronary procedures. Until now, the only widely accepted way to reduce restenosis rate has been the stent. However, clinical restenosis still represents the major limitation of this technology. This article summarizes recent laboratory and clinical investigations concerning the mechanisms responsible for the transmission of mitogenic signals from plasma membrane to the nucleus in vascular smooth muscle cells that determine neointima formation after stent deployment. Recent experimental data on the impact of diabetes and physical exercise on restenosis also is reviewed. Finally, the new concept of local drugs that elute directly to the site of vascular injury from coated stents and the available clinical results obtained with rapamycin or paclitaxel-eluting stents are discussed.