Skip Navigation

Cardiovascular Research 2004 63(1):22-30; doi:10.1016/j.cardiores.2004.02.001
© 2004 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sindermann, J. R
Right arrow Articles by Hendry, J. H
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sindermann, J. R
Right arrow Articles by Hendry, J. H
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2004, European Society of Cardiology

Biological aspects of radiation and drug-eluting stents for the prevention of restenosis

Jürgen R Sindermanna, Vitali Verinb, John W Hopewellc, Hans Peter Rodemannd and Jolyon H Hendry*,e

aDepartment of Cardiology and Angiology, and Institute for Arteriosclerosis Research, University of Münster, Münster, Germany
bCardiology Center, University Hospital, Geneva, Switzerland
cDepartment of Clinical Oncology, The Churchill Hospital, Oxford, UK
dSection of Radiobiology and Molecular Environmental Research, Dept. of Radiation Oncology, Eberhard-Karls University, Tübingen, Germany
eApplied Radiobiology and Radiotherapy Section, Division of Human Health, International Atomic Energy Agency, Wagramer Strasse 5, PO Box 100, A-1400, Vienna 48149, Austria

*Corresponding author. Tel.: +43-1-260-021667; fax: +43-1-26007-21667. Email address: j.hendry{at}iaea.org

Based on recent advances, this article aims to review the biological basis for the use of either radiation or drug-eluting stents for the prevention of restenosis, and to elucidate the complementary role that they may play in the future. Vascular restenosis is a multifactorial process primarily driven by the remodeling of the arterial wall, as well as by the hyperproliferation of smooth muscle cells (SMC). These pathophysiological features are the target of therapeutic strategies aimed at inhibiting constrictive remodeling as well as inhibiting SMC proliferation. The success of radiation as well as anti-proliferative drugs such as paclitaxel and sirolimus lies in the primary and/or multifactorial inhibition of cell proliferation. Radiation has the additional feature of preventing constrictive remodeling while sirolimus has the potential property of being anti-inflammatory, which may be a desirable feature. The effects of radiation are not reliant on any uptake and "metabolism" by the target cells, as in the case with drugs, and thus radiation potentially may be more effective as a result of its more-direct action. However, radiation does have some significant drawbacks compared to drug-eluting stents, including a much delayed re-endothelialization resulting in the need for prolonged anti-platelet therapy. Based on recent clinical data, drug-eluting stents have been shown to markedly reduce the likelihood of restenosis, which actually favors this approach for the prevention of restenosis. From a biological perspective, drug-eluting stents and radiation have certain differences, which are reviewed in this article.

KEYWORDS Restenosis; Stents; Angioplasty; Smooth muscle; Remodeling

Time for primary review 24 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
H. Murayama, M. Takahashi, M. Takamoto, Y. Shiba, H. Ise, J. Koyama, Y.-i. Tagawa, Y. Iwakura, and U. Ikeda
Deficiency of tumour necrosis factor-{alpha} and interferon-{gamma} in bone marrow cells synergistically inhibits neointimal formation following vascular injury
Cardiovasc Res, November 1, 2008; 80(2): 175 - 180.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.