Matrix Metalloproteinases and Vulnerable Atheromatous Plaque

Author(s): Konstantinos Toutouzas, Andreas Synetos, Charalampia Nikolaou, Eleutherios Tsiamis, Dimitris Tousoulis, Christodoulos Stefanadis.

Journal Name: Current Topics in Medicinal Chemistry

Volume 12 , Issue 10 , 2012

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Abstract:

Atherosclerotic coronary artery disease, the underlying basis for ischemic heart disease, is the leading cause of death and disability in the USA and recent trends indicate that coronary artery disease is also becoming a major public health problem in developing countries [1]. Atherosclerosis is a continuous process that is initiated early in life, which gradually progresses with potentially devastating consequences: atherosclerotic plaque rupture is the most common underlying pathological mechanism creating acute ischemic coronary syndromes [2]. This term refers to the process of disruption of the endothelial surface and the exposure of the underlying prothrombotic vessel wall to circulating platelets and coagulation factors. In order to identify the high-risk plaque we need to recognize its specific morphological and functional characteristics. The morphological characteristics have been identified in several human histopathological and in vivo studies, and include: 1) a large lipid core (≥40% plaque volume) composed of free cholesterol crystals, cholesterol esters, and oxidized lipids impregnated with tissue factor, 2) a thin fibrous cap depleted of smooth muscle cells and collagen, 3) an outward (positive) remodeling, 4) inflammatory cell infiltration of fibrous cap and adventitia (mostly monocyte- macrophages, activated T cells and mast cells), and 5) increased neovascularization. The terms vulnerable, unstable or ‘high-risk’ are now widely used to describe plaques that exhibit such features, irrespective of whether rupture of the fibrous cap is present [3].

Keywords: Vulnerable plaque, matrix metalloproteinases, inflammation, Atherosclerotic coronary artery disease, atherosclerotic plaque rupture, ischemic heart disease, pathological mechanism, acute ischemic coronary syndromes, endothelial surface, in vivo studies, smooth muscle cells, inflammatory cell infiltration, neovascularization, inflammatory cell infiltration

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Article Details

VOLUME: 12
ISSUE: 10
Year: 2012
Page: [1166 - 1180]
Pages: 15
DOI: 10.2174/1568026611208011166
Price: $58

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