Dexamethasone: effects on neointimal hyperplasia and vessel integrity.

The clinical success of balloon angioplasty is limited by restenosis, which occurs in up to 50% of patients. Lumen compromise and restenosis are caused by acute elastic recoil and late constrictive remodeling and to a lesser degree by neointimal hyperplasia [1,2]. The application of bare metal stents (BMS) has revolutionized percutaneous coronary interventions by reducing the rate of clinical complications and the need for target vessel revascularization. Although BMS mechanically prevent the decrease of total vessel area caused by constrictive remodeling, in-stent restenosis still reduces the clinical success rate of BMS substantially. In contrast to restenosis after balloon angioplasty, after stent implantation restenosis is caused exclusively by ingrowth of a thickened neointima as the result of increased migration and proliferation of vascular smooth muscle cells (SMC) [3,4]. The invasion of inflammatory blood cells with the concomitant release of cytokines and growth factors positively correlates with the degree of in-stent stenosis [5]. In addition to the cellular component of the stent neointima, the accumulation of extracellular matrix (ECM) components such as proteoglycans and collagens has been recognized to be a key factor, since the ECM determines SMC phenotype, thrombogenic properties, and volume expansion [6,7]. Since in-stent restenosis is determined by the extent of neointimal hyperplasia, the application of anti-proliferative, anti-migratory, or anti-inflammatory drugs locally at the target lesion has become an attractive possibility to further enhance the long-term patency of stented vessels. Indeed,