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European Heart Journal 2003 24(4):291-293; doi:10.1016/S0195-668X(02)00876-X
Copyright © 2003 by the European Society of Cardiology.
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Editorial

Atheromatous plaque location and arterial remodelling

J.C. Kaski*

Coronary Artery Disease Research Unit, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK

* Tel.: +44-208-725-5901; fax: +44-208-725-3328
jkaski@sghms.ac.uk

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

See doi:10.1016/S1095-668X(02)00426-8for the article to which this editorial refers.

Atherosclerosis is associated with a number of structural and functional changes in the arterial wall. Endothelial dysfunction, oxidised-LDL accumulation, increased concentrations of macrophages, neutrophils and T-cells as well as smooth muscle cell migration are some of the most relevant changes that take place during atherogenesis and coronary artery disease progression. It has been shown that the presence of a space-occupying plaque is commonly associated with the expansion of the arterial wall (‘vessel remodelling’).1 The mechanisms responsible for this phenomenon are speculative.

1. Positive and negative vessel remodelling

The majority of coronary artery atheromatous plaques are eccentric and tend to grow towards the adventitia before encroaching upon the lumen of the artery. This was shown initially by Glagov et al.1 in a pioneering study, which demonstrated thatleft main coronary . . . [Full Text of this Article]


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