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Heart 2001;86:491-493; doi:10.1136/heart.86.5.491
Copyright © 2001 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2001;86:491-493 ( November )

Review

Gene therapy for coronary restenosis: is the enthusiasm justified?

M O'Sullivan, M R Bennett

Division of Cardiovascular Medicine, University of Cambridge Department of Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK

Correspondence to: Dr M O'Sullivan mo222@cam.ac.uk

The first 150 words of the full text of this article appear below.

    Introduction

Despite dramatic technological advances in coronary intervention, restenosis following percutaneous coronary intervention remains an important cause of morbidity with major financial implications.1 By six months postprocedure, some 16-32% of highly selected patients receiving optimal treatment within the privileged context of a clinical trial have developed restenosis, necessitating target vessel revascularisation in 9-15% of patients. The development of antirestenotic treatments is therefore an area of intense research activity. The failure of conventional pharmacological agents to inhibit restenosis, along with concern over the long term safety and efficacy of intracoronary brachytherapy, has fostered the belief that gene therapy may be the future of antirestenotic treatments.2 3 Furthermore, the focal nature of restenosis makes it a highly attractive target for locally delivered genetic material that may have toxic effects if administered systemically. However, the important question remains: can research in this field translate into clinically useful treatment or is our enthusiasm for antirestenotic gene . . . [Full text of this article]


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This article has been cited by other articles:

  • O'Sullivan, M., Scott, S. D, McCarthy, N., Figg, N., Shapiro, L. M, Kirkpatrick, P., Bennett, M. R (2003). Differential cyclin E expression in human in-stent stenosis smooth muscle cells identifies targets for selective anti-restenosis therapy. Cardiovasc Res 60: 673-683 [Abstract] [Full Text]  

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