Atherosclerosis

Atherosclerosis is the most common cause of death in western countries; Ath erosclerosis can be considered as a chronic inflammation of the intimal par t of large arteries. It results from an initial endothelial dysfunction clu e to several risk factors, leading to an accumulation of modified lipoprote ins, monocyte-derived macrophages and T cells interacting with the normal c ellular components of the arterial wall and inducing foam cell and necrotic core formation. In many cases, the development of these atherosclerotic pl aques is limited by a fibrous cap surrounding the necrotic core and mainly composed of extra-cellular matrix;proteins and smooth muscle cells. All the se events lead to the development of atherosclerotic plaques, which can pro trude into :the arterial lumen and induce such clinical manifestation as an gina pectoris. One of the main complications of the atherosclerosis is the plaque rupture leading to vessel occlusion and acute clinical syndromes suc h as myocardial infarction or stroke. The plaque rupture results mainly fro m the acute accumulation of macrophages leading:to the: local secretion of metalloproteinases, extracellular matrix degradation and smooth muscle cell apoptosis inducing significant thinning and rupture of the fibrous cap. Th e plaque rupture expose lipids, apoptotic bodies and tissue factor accumula ted in necrotic core to blood components, initiating the coagulation cascad e, platelet activation and thrombosis. Considering this process as a whole, biologists and physicians have to prevent, detect and treat the atheroscle rotic lesions at each step of their evolution: the isolated risk factors, t he initial endothelial dysfunction, the chronic inflammatory process respon sible of atherosclerotic progression and the plaque rupture and thrombosis.