ABSTRACT
The pathogenesis of restenosis after coronary angioplasty is a complex process and it includes early recoil, thrombus formation, arterial remodeling, and neointimal hyperplasia.1 Neointimal hyperplasia is the sole mediator of in-stent restenosis and is the result of smooth muscle cell activation, proliferation, and migration, and extracellular matrix synthesis, beginning as early as 48 hours after stent implantation,2-4 and is predominant within the first 30 days.5,6 Strategies to inhibit restenosis involve the targeting of one or a combination of these reparative processes (Figure 3.1). Systemic delivery of drugs to reduce restenosis is limited by their systemic toxicity.7 A controlled, local delivery of antiproliferative agents using a stent platform should increase the drug concentration at the target site while minimizing the systemic effects of the drugs. Various modalities of stent-based drug delivery are being used
or are under evaluation (Figure 3.2). Indeed, clinical trials have confirmed the efficacy of this strategy in reducing clinical and angiographic restenosis in clinical practice.8-10 In this chapter, the pharmacology of various antiproliferative agents and the polymer for drug-eluting stent technology will be reviewed.
