ABSTRACT
The focus of the treatment of restenosis over the last two decades has been through the application of pharmacologic active agents and mechanical approaches using a host of different devices. Unfortunately, with only a few exceptions, this frequent and costly complication of percutaneous revascularization techniques has proven refractory to all such therapies. Characteristic of the restenosis process is neointimal proliferation that involves the migration of vascular smooth muscle cells (SMCs) from the media and the adventitia and their intraluminal proliferation and vascular remodeling which potentially involves all three layers of the vessel wall. The inciting stimuli involved in restenosis include disruption of the endothelial barrier layer, mechanical factors which disrupt the medial smooth muscle layer and serve as stimuli for SMC proliferation and migration, and the contact of this disrupted layer with circulating blood factors and mitogens which serve as further stimuli to neointimal formation.
