Inflammation is a key mechanism in atherogenesis and the rapid progression of coronary artery disease. Tissue lesion occasions the release of chemical mediators, cytokines, accompanied by an increase in the blood concentrations of acute phase reactants, such as fibrinogen, C-reactive protein, serum amyloid A protein, sialic acid and ceruloplasmin and a reduction
of those of albumin. It has been observed that these proteins are higher in patients with is-chemic heart disease and, furthermore, who have a higher tendency to present adverse cardiovascular incidents [1]. On the other hand, the inflammation appears
to be directly linked to the ‘vulnerability’ or ‘instability’ of the atheromatous plaques that pre-dispose to disruption and acute coronary incidents. The inflammatory mechanism, therefore, can repre-sent the final common connection channel of chronic infection between atherogenesis and the clinical manifestations of coronary artery disease [2].
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