Atherosclerosis complicated by plaque rupture or disruption and thrombosis is primarily responsible for the development of acute coronary syndromes. Plaques with a large extracellular lipid-rich core, thin fibrous cap due to reduced collagen content and smooth muscle density, and increased numbers of activated macrophages and mast cells, appear to be vulnerable to rupture. Plaque disruption tends to occur at points at which the plaque surface is weakest and most vulnerable, which coincide with points at which stresses, resulting from biomechanical and hemodynamic forces acting on plaques, are concentrated. Reduced matrix synthesis as well as increased matrix degradation predisposes vulnerable plaques to rupture in response to extrinsic mechanical or hemodynamic stresses. Modification of endothelial dysfunction and reduction of vulnerability to plaque rupture and thrombosis may lead to plaque stabilization. The broad concept of plaque stabilization, although attractive, has not yet been rigorously validated in humans. This article reviews the mechanism of atherosclerosis development and the pathophysiology of acute coronary syndromes in order to provide a molecular and cellular basis for understanding how plaque passivation might be accomplished in clinical medicine.
Keywords: ulceration, Vascular Injury, oxidized LDL, Nitric Oxide, Phosphodiesterase, monocyte chemo-attractant molecules (MCP-1), VCAM expression, Advanced Atheroma, Turbulence
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