| Literature DB >> 12615660 |
Paul Cullen1, Roberta Baetta, Stefano Bellosta, Franco Bernini, Giulia Chinetti, Andrea Cignarella, Arnold von Eckardstein, Andrew Exley, Martin Goddard, Marten Hofker, Eva Hurt-Camejo, Edwin Kanters, Petri Kovanen, Stefan Lorkowski, William McPheat, Markku Pentikäinen, Jürgen Rauterberg, Andrew Ritchie, Bart Staels, Benedikt Weitkamp, Menno de Winther.
Abstract
By its very nature, rupture of the atherosclerotic plaque is difficult to study directly in humans. A good animal model would help us not only to understand how rupture occurs but also to design and test treatments to prevent it from happening. However, several difficulties surround existing models of plaque rupture, including the need for radical interventions to produce the rupture, lack of direct evidence of rupture per se, and absence of convincing evidence of platelet- and fibrin-rich thrombus at the rupture site. At the present time, attention should therefore focus on the processes of plaque breakdown and thrombus formation in humans, whereas the use of animal models should probably be reserved for studying the function of particular genes and for investigating isolated features of plaques, such as the relationship between cap thickness and plaque stability.Entities:
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Year: 2003 PMID: 12615660 DOI: 10.1161/01.ATV.0000060200.73623.F8
Source DB: PubMed Journal: Arterioscler Thromb Vasc Biol ISSN: 1079-5642 Impact factor: 8.311