ecent researches have shown that the atherosclerosis is a chronic inflammatory disease. In particular, chronic inflammation plays a key role in coronary artery plaque instability and subsequent occlusive thrombosis. Inflammatory and immune mechanisms, employing monocytes, innate receptors, cytokines are suggested to be involved in atherogenesis. Among the initiation pathways of atherogenesis are innate mechanisms, such as toll-like-receptors (TLRs). TLRs are expressed in the cardiovascular system and could thus be a key link between cardiovascular diseases and the immune system. Stimulation ofthese receptors results in the activation of a diversity of intracellular signal transduction pathways and the production of pro-inflammatory cytokines, which ultimately can contribute to atherosclerotic lesion development. Thus, bacterial endotoxin is a potential source of vascular inflammation and may be an important risk factor for atherosclerosis. Many prospective studies have shown independent associations between myocardial infarction and C-reactive protein, interleukin-6, fibrinogen, von Willebrandfactor, fibrin D-dimerand tissue plasminogen activator antigen. Numerous researches antiinflammatory therapies at an atherosclerosis, are inconsistent enough, however they allow to hope for success, in preventive maintenance and treatment cardiovascular events.

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