ABSTRACT
In-stent restenosis, caused by neointimal formation, has been a vexing problem of coronary stenting intervention. Coronary stent implantation induces an important arterial injury at the stenting site, which initiates the cascade of in-stent restenosis. Although the molecular mechanism of in-stent restenosis is not completely understood, inflammatory response, smooth muscle cell dedifferentiation, migration and proliferation, and extracellular matrix formation within the intima have been known to play an important role in the development of neointimal hyperplasia.1,2 Stent-based drug delivery results in a high drug concentration and sustained drug release at the stenting site with low systemic side effects. Local delivery with antiinflammatory and/or antiproliferative agents has been shown to reduce neointimal hyperplasia in animal models and clinical trials.3-5 As the pathogenesis of in-stent restenosis is multifactorial and consists of elaboration of cytokines and growth factors, agents with both antiinflammatory and antiproliferative proper ties could have a potential advantage to suppress neointimal formation.
