Restenosis—an open file

Abstract The main procedural drawback to percutaneous coronary angioplasty is restenosis of the treated site within 6 months. Despite advances in equipment, technique, and adjunctive therapies, restenosis has occurred in approximately one‐third to one‐half of all patients. The biology of restenosis can be divided into plaque persistence and recoil, thrombus formation and transformation, and cellular proliferation and vascular remodeling. Animal models of restenosis have helped to elucidate these mechanisms of restenosis and provide a means to test pharmacologic and mechanical strategies to reduce stenosis recurrence. While numerous agents have been tested in animal models, until recently none has translated into benefit in large‐scale clinical trials. Two therapeutic “hopefuls” which have recently emerged in clinical practice are the potent platelet inhibitors, glycoprotein IIb/IIIa receptor antagonists, and intracoronary metallic stents. The IIb/IIIa receptor antagonists target thrombus formation at the angioplasty site, thereby minimizing abrupt vessel closure acutely and neointimal growth chronically, while intracoronary stents safely produce a large coronary arterial lumen acutely and prevent vessel recoil. Separately, these therapeutic strategies have been shown to reduce clinical restenosis 20‐30% at 6‐month follow‐up. With these encouraging results, the future will certainly provide more pharmacologic and mechanical therapies targeting restenosis. With increased understanding of the restenotic process and continued refinement of effective treatments, it may be possible one day to prevent stenosis recurrence.