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Circulation. 2003;107:2635-2637
doi: 10.1161/01.CIR.0000071083.31270.C3
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(Circulation. 2003;107:2635.)
© 2003 American Heart Association, Inc.


Editorials

Endothelial Recovery

The Next Target in Restenosis Prevention

Douglas W. Losordo, MD; Jeffrey M. Isner, MD{dagger}; Larry J. Diaz-Sandoval, MD

From the Division of Cardiovascular Research, St Elizabeth’s Medical Center, Tufts University School of Medicine, Boston, Mass.

Correspondence to Douglas W. Losordo, MD, Chief, Cardiovascular Research, St Elizabeth’s Medical Center, Tufts University School of Medicine, 736 Cambridge St, Boston, MA 02135. E-mail douglas.losordo@tufts.edu


Key Words: Editorials • gene therapy • restenosis • endothelium • angioplasty


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

In this world there are only two tragedies. One is not getting what one wants and the other is getting it.

— —Oscar Wilde

By most accounts, the field of interventional cardiology appears to have achieved one of its most elusive milestones, the virtual eradication of restenosis. In the present issue of Circulation, however, Hedman and colleagues1 report the results of a pilot study of gene therapy with vascular endothelial growth factor (VEGF) for restenosis prevention. Are these authors attempting to develop a treatment for a disease that no longer exists? Or is it possible that the mounting exuberance anticipating the release of drug-eluting stents is ignoring a major liability of these otherwise promising therapies?

See p 2677

Percutaneous transluminal coronary angioplasty (PTCA) has been used to relieve symptoms and ischemia in patients with coronary disease for more than 2 decades. Despite an initial success rate of well over 90%, coronary arterial renarrowing of initially revascularized sites, or restenosis, constitutes the principal major complication of PTCA.

The pathogenesis of restenosis has classically been regarded as involving either reactive constriction of the artery wall or neointimal thickening. The former, termed remodeling,2 has been successfully addressed to a large extent by the development of endovascular stents: Two landmark clinical trials3,4 established stents as the first mechanical intervention to have a favorable impact on restenosis.

Neointimal thickening has been inferred to result most often from vascular smooth muscle cell (VSMC) proliferation.5,6 Indeed, histological inspection of lesions retrieved by directional atherectomy from . . . [Full Text of this Article]


Related Article:

Safety and Feasibility of Catheter-Based Local Intracoronary Vascular Endothelial Growth Factor Gene Transfer in the Prevention of Postangioplasty and In-Stent Restenosis and in the Treatment of Chronic Myocardial Ischemia: Phase II Results of the Kuopio Angiogenesis Trial (KAT)
Marja Hedman, Juha Hartikainen, Mikko Syvänne, Joachim Stjernvall, Antti Hedman, Antti Kivelä, Esko Vanninen, Hanna Mussalo, Esa Kauppila, Sakari Simula, Outi Närvänen, Arto Rantala, Keijo Peuhkurinen, Markku S. Nieminen, Markku Laakso, and Seppo Ylä-Herttuala
Circulation 2003 107: 2677-2683. [Abstract] [Full Text]



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