RESUMEN
Coronary balloon angioplasty was first used in 1977; since then, indications for percutaneous coronary intervention have expanded. However, despite significant advances in reducing the incidence of acute complications, chronic restenosis of dilated lesions remains a serious and frequent problem. The mechanisms of restenosis can be described as a combination of effects involving three main components: vessel recoil and remodeling, hemostatic activation and thrombus formation, and neointimal hyperplasia. Thrombosis is associated with vascular and plaque injury. In animal models thrombus at the injury site is a major determinant of intimal hyperplasia and restenosis. Although the introduction of coronary stenting has limited the effect of vessel recoil and remodeling, no effective therapy is yet available to prevent restenosis. This article reviews the potential role of the hemostatic system in restenosis and those drugs and techniques that may inhibit its effect on the restenotic process.
