Rupture of the Atherosclerotic Plaque

Author:

Cullen Paul1,Baetta Roberta1,Bellosta Stefano1,Bernini Franco1,Chinetti Giulia1,Cignarella Andrea1,von Eckardstein Arnold1,Exley Andrew1,Goddard Martin1,Hofker Marten1,Hurt-Camejo Eva1,Kanters Edwin1,Kovanen Petri1,Lorkowski Stefan1,McPheat William1,Pentikäinen Markku1,Rauterberg Jürgen1,Ritchie Andrew1,Staels Bart1,Weitkamp Benedikt1,de Winther Menno1

Affiliation:

1. 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...

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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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