title: Novel approaches for the prevention of restenosis.
abstract: Restenosis, the re-narrowing of the lumen of the coronary artery, in the months following a successful percutaneous balloon angioplasty or stenting, remains the main limitation to percutaneous coronary revascularisation. Serial intravascular ultrasound studies have shown that restenosis after conventional balloon angioplasty represents a complex interplay between elastic recoil, smooth muscle proliferation and vascular remodelling, while restenosis after stent deployment is due almost entirely to smooth muscle hyperplasia and matrix proliferation. Despite intensive investigation in animal models and in clinical trials, most pharmacological agents have been found to be ineffective in preventing restenosis after percutaneous balloon angioplasty or stenting. Although studies frequently report success in the suppression of neointimal proliferation in animal models of balloon vascular injury, few of them have been successful in clinical trials. Lately, the advent of endovascular radiation, new antiproliferative agents, recombinant DNA, growth factor regulators and novel local drug delivery systems have shown promising results. In the past five years, intracoronary radiation with gamma- and beta-emitting sources has been evaluated intensively with very encouraging results. This is the first potent non-pharmacological approach that has been successful in a large number of patients in controlling excessive tissue proliferation. It is very likely that a combination of stents and pharmacological and/or non-pharmacological inhibition of neointimal hyperplasia will likely result in further reductions in the incidence if restenosis. The continued attractiveness of percutaneous coronary revascularisation, as an alternative to medical treatment or bypass surgery for patients with coronary artery disease, will depend upon our ability to control the restenotic process. Due to the vast literature on the subject, this review will focus mainly on clinical trials that show the most promise and will highlight those that warrant further investigation.
authors.affiliation: Cardiac Catheterization Laboratory, Washington Hospital Center, Washington, DC, USA. lxg6@mhg.edu
authors.forename: L
authors.initials: L
authors.lastname: Gruberg
authors.forename: R
authors.initials: R
authors.lastname: Waksman
authors.forename: L F
authors.initials: LF
authors.lastname: Satler
authors.forename: A D
authors.initials: AD
authors.lastname: Pichard
authors.forename: K M
authors.initials: KM
authors.lastname: Kent
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D003251:Constriction, Pathologic / Q000517:prevention & control; D003327:Coronary Disease / Q000517:prevention & control* / Q000628:therapy; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D015316:Genetic Therapy; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012008:Recurrence; D015607:Stents
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000970:Antineoplastic Agents; D005343:Fibrinolytic Agents; D000960:Hypolipidemic Agents; D010975:Platelet Aggregation Inhibitors