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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:701.)
© 2007 American Heart Association, Inc.

Editorials

Small Is Beautiful

A Miniature Stent Model

Mark J. Post; Johannes Waltenberger

From the Departments of Physiology (M.J.P.) and Cardiology (J.W.), CARIM, Maastricht University, and the Department of Biomedical Engineering (M.J.P.), Technical University Eindhoven, The Netherlands.

Correspondence to Mark J. Post, MD, PhD, Department of Physiology, Maastricht University, PO Box 626, 6200 MD, Maastricht, The Netherlands. E-mail m.post@fys.unimaas.nl

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

Recent successes by drug eluting stents in the battle against restenosis have boosted the volume of stent related research. The goal of this research is to further reduce restenosis rates by improving stent and polymer design and by testing and modifying drugs from various classes. The novel mouse model described by Ali et al,¹ offers new opportunities to study fundamental and perhaps applied aspects of vascular biology related to stent implantation. In the absence of in vitro models of vascular healing that eventually may replace animal experiments, small animal models are especially welcome. The first mouse model of vascular healing was developed by Lindner and coworkers more than 10 years ago.² They injured the carotid artery with a guide wire and observed the same sequence of apoptosis, invasion of leukocytes, smooth muscle cell migration, and proliferation and reendothelialization as found in rabbits, pigs, and humans. Animal models of diseases and related therapies serve two purposes: to increase the understanding of pathobiology and to evaluate new therapies down to the histopathologic level. Models are simplifications of reality, and animal models are no exception. The predictive value of a model depends on a largely empirical framework that links animal behavior with clinical experience. Fortunately, animal models of vascular healing in various species and arterial beds have already provided a solid reference for this novel stent model. Most of these models, however, especially in rats, lack preexistent pathology such as atherosclerosis, which may explain some of the false-positive results with pharmacological inhibition of . . . [Full Text of this Article]

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