Since Gruentzig performed the first PTCA since 1977, the early results of percutaneous revascularization have improved greatly with advances in catheterization techniques, operator experience, support systems, imaging equipment, and adjunctive medications. The success rate of the procedure exceeds 90% and complications are less than 5%. Despite this success, the long-term results of this technique are still plagued by restenosis. Approximately 100,000 patients in the United States require repeat target lesion revascularization each year, which entails additional risk and increases healthcare costs by$2 billion annually. Initially, restenosis was thought to be caused by endothelial hyperplasia alone. Current data suggest that restenosis is a complex process that includes elastic regression, intimal hyperplasia, and vascular remodeling. Elastic retraction Elastic retraction refers to the difference between the lumen diameter at balloon dilation and the minimum lumen diameter after withdrawal of pressure. The degree of retraction depends on the elastic changes of the atheromatous plaque and the elastic characteristics of the arterial wall. Most of the elastic retraction occurs within 30 minutes (up to 24 hours) after balloon withdrawal, which can reduce the lumen cross-sectional area by 50%. 2. Endothelial hyperplasia Endothelial hyperplasia is a common response of blood vessels to vascular injury caused by PTCA and other interventional methods. Autopsy of excised plaque specimens supports the nature of restenosis as cellular hyperplasia. 3. Arterial remodeling Pilot studies and clinical intravascular ultrasound follow-up studies have shown a progressive reduction in vessel geometry after coronary interventions, resulting in a loss of lumen diameter, i.e., negative remodeling. Stenting significantly reduces late negative arterial remodeling, and this ability is an important factor in its ability to reduce restenosis rates. Restenosis usually occurs 3-6 months after PTCA and is rare 1 month and 1 year after surgery. Current efforts for restenosis prevention include pharmacological interventions, mechanical interventions and radiological interventions. In the past 10 years, a large number of drugs have been used in clinical trials for restenosis intervention, including fish oil, corticosteroids, cell growth inhibitors, calcium channel blockers, lipid-lowering drugs, ACE inhibitors, low-molecular heparin, prostaglandin inhibitors, high-dose vitamin E, and growth inhibitor analogs. The results show that only calcium channel blockers and fish oil appear to have some benefit for restenosis. Two recent randomized trials suggest that c7E3 (a platelet GPIIb/IIIa inhibitor) and vasopeptide (a growth inhibitor analogue) significantly reduce restenosis. Laboratory studies suggest that gene therapy of the vasculature may be effective. Mechanical interventions include recent studies confirming the Palmaz-Schatz stent as the only stent that reduces restenosis. A large number of clinical trials are currently exploring optimal plaque removal to reduce restenosis. Drug-coated stents have recently received much attention for restenosis prevention, and several clinical trials are now achieving impressive results (<5% restenosis rate) using rapamycin and paclitaxel-coated stents. Early animal studies and clinical data suggest that local radiation therapy of vascular lesions may have a beneficial effect on remodeling and intimal hyperplasia, but the effect of radiation therapy is complicated by complications such as marginal effects, high thrombosis rates, and the lack of satisfactory results in clinical trials of radioactive stents. For restenosis treatment, PTCA, stenting and coronary plaque rotation can be performed again, but the high restenosis rate limits the clinical use.