Dexamethasone-Eluting Stent in Acute Coronary Syndrome to Prevent Restenosis

The major obstacle of the long- termed success of percutaneous coronary intervention (PCI) is the restenosis. Restenosis results from complex pathophysiological response of the vascular tissue to the balloon injury. In the pre-stent era, 80% of it was attributed to vascular recoil. However, by way of the mechanical support of metallic stent, recoil is no more the major reason of restenosis. About 80 % of In-stent restenosis resulted from intimal hyperplasia. The mechanism of the Intra-stent restenosis included 4 stages. First stage comprised the first 3 days after balloon injury, when the inflammatory reaction is most severe throughout the course. At that time, anti-inflammatory drug as steroid wuold be helpful to prevent the course of restenosis. Until the end of the third week, smooth muscle cells migrate and then proliferate in the second and the third stage, and the key effort to prevent restenosis right now is inhibition of cell cycle. Intravascular radiotherapy (so called Brachytherapy) and stent-based drug elution target upon them. Among them, rapamycin and paclitaxel proved to be effective both in animal and human experience. The last stage is re-epithelization, estrogen could promote the process and was considered to be effective in this stage. Stent-based elution of corticosteroid, despite of its feasibility and safety, was not as effective as other anti-proliferation agent ( eg. Rapamycin etc). The major reason might be the patient group with coronary artery disease is a heterogenous one. We believe if we applied corticosteroid over the patient with elevated inflammatory parameters, i.e. acute coronary syndrome (ACS) the effect of anti-restenosis would be obvious. In this study, by a special-designed, phosphorylcholine-coated stent, dexamethasone could be readily absorbed and then gradually released locally even 4 weeks after deployment. We expected a reduction of In-stent restenosis in ACS patient by the method with no or few systemic adverse effect