Restenosis remains a frequent cause of late failure after initially successful coronary angioplasty occurring in as many as 20-40% of procedures performed. Loss of luminal diameter as a result of restenosis has been attributed to three physiologic mechanisms: passive elastic recoil of the vessel, geometric vessel remodeling and neointimal hyperplasia. Coronary stents provide mechanical scaffolding that reduces restenosis by limiting the extent of elastic recoil and late vascular remodeling. Despite these improvements, the incidence of restenosis following coronary stent implantation occurs in 20-40% of cases. Restenosis following stenting is primarily a result of neointimal hyperplasia.