Physiopathologie de l'athérosclérose et marqueurs précoces

Atherosclerosis is a chronic progressive disease characterized by the accumulation of lipids and fibrous elements in large arteries. Over the two past decades, investigations clearly showed that atherosclerosis is a chronic inflammation process that can be converted into an acute clinical event by plaque rupture and thrombosis. The process is initiated when atherogenic lipoproteins penetrate the endothelium and are retained in the intima where they undergo oxidative modifications. The oxidized lipoproteins (mainly oxidized LDL) activate endothelial cells and induce the expression of adhesion molecules and chemotactic factors promoting recruitment of monocytes and T cells which migrate into the subendothelial space. Monocytes differentiate into macrophages expressing scavenger receptors which mediate lipoproteins internalisation leading to foam cells formation. The secretion of pro-inflammatory cytokines, proteases, vasoactive molecules and growth factors contribute to intensify local inflammation and growth of the plaque. Plaque can become increasingly complex with calcification, ulceration at the luminal surface and haemorrhage from small vessels into the lesion. Recent observations have highlighted the important role of the plaque composition rather than plaque size or stenosis severity in the plaque instability leading to plaque rupture and thrombosis. The purpose of this review is to summarise current understanding of the pathogenesis and progression of atherosclerosis and to underline the evidence supporting the role of potential new clinical and biological markers in predicting primary cardiovascular events.