The success of percutaneous coronary intervention (PCI) has historically been limited by a relatively high rate of restenosis, a response of the coronary artery to trauma induced during PCI. Bare-metal stents, by providing a supportive intravascular scaffolding, have significantly reduced the incidence of restenosis compared with traditional balloon PCI. However, significant loss of lumen within the bare-metal device (instent restenosis) occurs in 10-30% of patients within 6 months of the procedure. The recent introduction of drug-eluting stents, permitting local delivery of high concentrations of immunosuppressive or anti-proliferative agents, promises to prevent the processes underlying restenosis. Although these devices have been successful in providing an incremental reduction in rates of restenosis, they are expensive. To date, clinical trials of pharmacologic treatment have failed to demonstrate a clinically significant impact on restenosis. Recently, results of the Cilostazol for Restenosis (CREST) trial, a randomized, double-blind study, show that cilostazol reduces the risk of restenosis in patients who receive bare-metal stents, including high-risk patients. Effective adjunct pharmacologic therapy to prevent in-stent restenosis, therefore, remains desirable, particularly in patients receiving bare-metal stents, and potentially in patients receiving drug-eluting stents who are at high risk for restenosis (i.e., those with diabetes, long lesions, and small vessels). (c) 2005 Elsevier Ireland Ltd. All rights reserved.