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European Heart Journal Advance Access originally published online on June 27, 2009
European Heart Journal 2009 30(15):1821-1823; doi:10.1093/eurheartj/ehp266
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org

The unstable plaque: a broken balance

Filippo Crea* and Felicita Andreotti

Institute of Cardiology, Catholic University, Rome

* Corresponding author. Tel: +39 06 305 11 66, Fax: +39 (06) 305 5535, E-mail: filippo.crea@rm.unicatt.it

This editorial refers to ‘Enhanced expression of haemoglobin scavenger receptor in accumulated macrophages of culprit lesions in acute coronary syndromes’{dagger}, by K. Yunoki et al., on page 1844

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

Atherogenesis is traditionally traced to endothelial dysfunction, secondary to the interaction between intravascular factors and the luminal vessel surface. Dyslipidaemia, hypertension, smoking, inflammatory cytokines, and advanced glycation endproducts are thought to negatively modify blood and, consequently, the vascular intima. Ensuing endothelial activation and dysfunction are characterized by reduced nitric oxide bioavailability, generation of reactive oxygen species (ROS), expression of prothrombotic and leukocyte adhesion molecules, subendothelial lipid, mononuclear and smooth muscle cell accumulation, and impaired oxygen diffusion from the bloodstream into a thickened and ailing intima.1 Plaque rupture is also traditionally linked to events within the vascular intima, including fibrous cap thinning, necrotic core expansion, weakened shoulder regions, and sudden bursts of proteases by resident inflammatory cells.2

Yet, a large part of the vessel wall is represented by the media and adventitia, perfused by vasa vasorum that supply the outer layers. Proliferation of these . . . [Full Text of this Article]


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