This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mach, F. Search for Related Content PubMed PubMed Citation Articles by Mach, F. Related Collections Remodeling Restenosis Restenosis

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1699.)
© 2000 American Heart Association, Inc.

Editorials

Toward New Therapeutic Strategies Against Neointimal Formation in Restenosis

François Mach

From the Division of Cardiology, Foundation for Medical Research, University Hospital, Geneva Medical School, Geneva, Switzerland.

Correspondence to François Mach, MD, Cardiology Division, Foundation for Medical Research, 64 Avenue Roseraie, 1211 Geneva 14, Switzerland. E-mail machf@cmu.unige.ch

Key Words: Editorials • restenosis • inflammation • therapeutic

Physiopathology of Restenosis

Percutaneous transluminal coronary angioplasty (PTCA) has become the treatment of choice for severe cases of coronary artery atherosclerosis, and currently, >1 million PTCA interventions are performed each year worldwide.¹ However, despite its overall value in achieving an immediate increase in lumen diameter, PTCA often triggers local arterial renarrowing (restenosis). This occurs in 20% to 50% of cases within 3 to 6 months and represents a major clinical and economic problem.² Although several drugs have been shown capable of preventing or reducing the proliferative healing response after arterial injury in experimental animal models, only stenting has proved effective in reducing postinterventional restenosis in humans.³ Prevention of restenosis is therefore a major challenge, which highlights the need to better understand the interplay of the various components responsible for restenotic lesions.

Arterial restenosis after balloon angioplasty is a complex and multifactorial wound healing process that involves several redundant and overlapping mechanisms. Schematically, one distinguishes 4 interrelated issues.^{4 5} First, a vessel wall "elastic recoil" (vasoconstriction due to endothelial disruption) occurs, which tends to present within 24 hours of PTCA and which may be of predictive value for subsequent restenosis. Second, a mural thrombus forms, which occurs within 2 to 3 weeks and involves local platelet activation and thrombin secretion; an increase in smooth muscle cell activation, proliferation, and migration; and leukocyte recruitment at the site of balloon injury. This complex process then induces neointimal hyperplasia. Already beginning 48 hours after balloon injury, the major wave of neointimal growth occurs over the ensuing . . . [Full Text of this Article]

This article has been cited by other articles:

				E. Ilkay, L. Tirikli, I. Ozercan, M. Yavuzkir, I. Karaca, A. Rahman, and N. Arslan Oral Mycophenolate Mofetil Prevents In-Stent Intimal Hyperplasia Without Edge Effect Angiology, October 1, 2006; 57(5): 577 - 584. [Abstract] [PDF]

				T. A. Batyraliev, I. V. Pershukov, Z. A. Niyazova-Karben, A. Karaus, O. Calenici, N. Guler, B. Eryonucu, A. Temamogullari, S. Ozgul, F. Akgul, et al. Current Role of Laser Angioplasty of Restenotic Coronary Stents Angiology, January 1, 2006; 57(1): 21 - 32. [Abstract] [PDF]

				H. C. Lowe, S. N. Oesterle, and L. M. Khachigian Coronary in-stent restenosis: Current status and future strategies J. Am. Coll. Cardiol., January 16, 2002; 39(2): 183 - 193. [Abstract] [Full Text] [PDF]