ATVB In Focus |
From the Institute of Arteriosclerosis Research (P.C., S.L., J.R., B.W.), University of Münster, Germany; Institute of Pharmacology and Pharmacognosy (R.B., F.B., A.C.), University of Parma, Italy; Institute of Pharmacological Sciences (S.B.), University of Milan, Italy; Institut Pasteur de Lille (G.C., B.S.), Lille, France; Institute of Clinical Chemistry (A.v.E., A.E.), Zürich University Hospital, Switzerland; Papworth Hospital (M.G., A.R.), Cambridge, UK; Molecular Genetics Group (M.K., E.K., M.d.W.), Maastricht University, The Netherlands; AstraZeneca (E.H.-C., W.M.), Mölndal, Sweden; and Wihuri Institute (P.K., M.P.), Helsinki, Finland.
Correspondence to Dr. Paul Cullen, Institute of Arteriosclerosis Research, Domagkstrasse 3, D-48149 Muenster, Germany. E-mail cullen{at}uni-muenster.de
Previous Brief Review in this Series:
Pennacchio LA, Rubin EM. Apolipoprotein A5, a newly identified gene that affects plasma triglyceride levels in humans and mice. 2003;23:529534.
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.
Key Words: atherosclerosis plaque rupture pathophysiology animal models
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