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Cardiovascular Research Advance Access first published online on April 14, 2008
This version [Corrected Proof] published online on May 2, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn096
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Targeting the prevention of plaque rupture as a new strategy for prevention of acute arterial cardiovascular events

Marcel Levi* and Erik Stroes

Department of Vascular Medicine and Internal Medicine (F-4), Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

* Corresponding author. Tel: +31 20 5662171; fax: +31 20 6919658. E-mail address: m.m.levi@amc.uva.nl

This editorial refers to ‘Differential effects of PARP inhibition on vascular cell survival and ACAT-1 expression favoring atherosclerotic plaque stability’{dagger} by C.P. Hans et al., pp. 429–439, this issue.

The first 10% of the full text of this article appears below.

Acute arterial cardiovascular disease is usually caused by the sudden thrombotic occlusion of a vessel that is critical for maintaining adequate tissue perfusion and that contains an atherosclerotic plaque. Due to a myriad of processes within this plaque, rupture of its fibrous cap may occur, thereby exposing highly procoagulant material to the circulating blood, leading to occlusive thrombus formation and subsequent ischemia or infarction. In particular, inflammatory cells bearing tissue factor at their surface play a pivotal role in this mechanism, as tissue factor has been found to be . . . [Full Text of this Article]


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Related articles in Cardiovasc Res:

Differential effects of PARP inhibition on vascular cell survival and ACAT-1 expression favouring atherosclerotic plaque stability
Chetan P. Hans, Mourad Zerfaoui, Amarjit S. Naura, Andrew Catling, and A. Hamid Boulares
Cardiovasc Res 2008 78: 429-439. [Abstract] [FREE Full Text]  

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Differential effects of PARP inhibition on vascular cell survival and ACAT-1 expression favouring atherosclerotic plaque stability
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