Review
Gene therapy for coronary restenosis: is the enthusiasm justified?
M O'Sullivan, M R BennettDivision 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
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Introduction |
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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
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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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