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(Circulation. 2002;106:2296.)
© 2002 American Heart Association, Inc.

Editorial

Systemic Drug Therapy for Restenosis

"Déjà Vu All Over Again"

David P. Faxon, MD

From the Section of Cardiology, University of Chicago, Chicago, Ill.

Correspondence to David P. Faxon, MD, Section of Cardiology, University of Chicago, 5841 South Maryland Ave, Room B-608, MC 6080, Chicago, IL 60637. E-mail dfaxon@medicine.bsd.uchicago.edu

Key Words: Editorials • restenosis • stents • drugs

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

The problem of restenosis, a major limitation of angioplasty since its introduction in 1978, may finally be under control. The rate of restenosis has fallen from 30% to 40% to 15% to 20% with the advent and widespread use of coronary stents. Now, with the introduction of intravascular radiation therapy, in-stent restenosis seems to be reduced by 50%, and with the almost unbelievable preliminary results of drug-eluting stents, the rate of restenosis may be reduced to less than 5% in de novo lesions. Although these outcomes are truly remarkable, both intravascular radiation therapy and drug-eluting stents have a number of significant limitations.

See p 2379

Radiation has safety issues and is limited by geographical miss, edge restenosis, and late stent thrombosis. Drug-eluting stents are likely to be expensive and are unproven in unfavorable anatomy. Even in optimal patients, restenosis can still occur with both types of treatment. A continued search for a simpler and effective means of controlling this problem seems reasonable given these limitations. In this issue of Circulation, Farb et al¹ present evidence that everolimus, an oral analog of rapamycin, can reduce neointimal thickness by more than 40% after stent placement in a rabbit model of restenosis. Rapamycin is a naturally occurring macrolide antibiotic produced by the actinomycete Streptomyces hygroscopicus found on Eastern Island. It has been shown to be a potent inhibitor of cytokine and growth factor-mediated cell-proliferation.² It is known to bind to a cellular receptor FKBP-12 and to inhibit the target of rapamycin (TOR), . . . [Full Text of this Article]

Related Article:

Oral Everolimus Inhibits In-Stent Neointimal Growth

Andrew Farb, Michael John, Eduardo Acampado, Frank D. Kolodgie, Margaret Forney Prescott, and Renu Virmani
Circulation 2002 106: 2379-2384. [Abstract] [Full Text]

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