doi: 10.1161/01.CIR.0000038982.49640.70
(Circulation. 2002;106:2734.)
© 2002 American Heart Association, Inc.
Special Review |
Coated Stents for the Prevention of Restenosis: Part I
From the Division of Cardiology, Montreal General Hospital/McGill University (M.N.B.), and the Divisions of Cardiology and Clinical Epidemiology, Jewish General Hospital/McGill University (M.J.E.), Montreal, Quebec, Canada.
Correspondence to Mark J. Eisenberg, MD, MPH, Associate Professor of Medicine, Divisions of Cardiology and Clinical Epidemiology, Jewish General Hospital/McGill University, 3755 Cote-St-Catherine Rd, Suite A-118, Montreal, Quebec H3T 1E2, Canada. E-mail marke@epid.jgh.mcgill.ca
Key Words: restenosis • stents • drugs
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Over the past decade, the use of endoluminal metallic stents has become common practice during percutaneous coronary intervention (PCI), especially after clinical trials showed evidence of decreased restenosis rates when compared with balloon angioplasty alone.1–3 Although stents significantly reduce restenosis when compared with balloon angioplasty, restenosis rates in patients who receive stents are still 20% to 40% at 6 months.1–6 Recently, the concept of using stents coated with agents that could potentially inhibit neointimal hyperplasia has emerged. These agents include biocompatible materials, anticoagulants, corticosteroids, and antimitotic agents. This 2-part article reviews animal studies, human observational studies, and results from randomized clinical trials investigating coated stents. Part I discusses the pathophysiology of in-stent restenosis, as well as animal studies investigating coated stents. Part II discusses human studies investigating coated stents.
Pathophysiology of In-Stent Restenosis
In-stent restenosis is primarily due to neointimal hyperplasia.7–13 Vessel injury by an angioplasty balloon or stent struts leads to the activation of platelets and mural thrombus formation.13–16 The presence of vascular injury, mural thrombus, and a metallic foreign body activates circulating neutrophils and tissue macrophages.12,13,17,18 These cellular elements release cytokines and growth factors that activate smooth muscle cells.19–23 Upregulation and expression of genes such as c-myc that regulate cell division ensues, leading to cell proliferation.24,25 Production of matrix metalloproteinases is also upregulated, leading to remodeling of the extracellular matrix, and initiating smooth muscle cell migration.26–28 The end result of this cascade of events is the uncontrolled proliferation of smooth muscle cells around the vessel intima and the deposition of extracellular matrix
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