The pathophysiology and burden of restenosis

Abstract

The introduction of percutaneous transluminal coronary angioplasty (PTCA) revolutionized the surgical treatment of coronary artery disease. However, despite increased surgical experience and technical breakthroughs, restenosis occurs in 30%-50% of patients undergoing simple balloon angioplasty and in 10%-30% of patients who receive an intravascular stent. Animal and human data indicate that restenosis is a response to injury incurred during PTCA. The need for reintervention in a high percentage of patients due to restenosis remains an important limitation to the long-term success of PTCA. Stenting reduces initial elastic recoil and limits negative arterial remodeling; however, bare-metal stents may promote intimal hyperplasia by eliciting an immune and proliferative response. Consistent with these data, clinical studies suggest that drug-eluting stents, coated with anti-inflammatory or antiproliferative agents, reduce the risk for restenosis. Stenting represents a considerable cost burden. Treatment strategy should focus on selective use of expensive drug-eluting stents in populations where they have been found to be more clinically effective than bare-metal stents--patients who are at high risk for restenosis or who develop restenosis with bare-metal stents. Recent studies suggest that the pharmacologic management of restenosis is now feasible. Together, the judicious use of stents and oral pharmacotherapy promise to reduce the risk for restenosis, even among high-risk patients.