Inflammatory State

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Inflammation has been related not only to acute CV events but also to initiation and progression of atherosclerosis. Several CV risk factors, including diabetes, may trigger an inflammatory state. Although white blood cells are commonly considered to be the principal mediators of inflammation, a key role of platelets in the inflammatory process has recently been demonstrated. The interaction between diabetes and inflammation appears complex.19 Although it is plausible that metabolic disturbances associated with this condition trigger vascular inflammation, the converse may also be true. Accordingly, C-reac-tive protein (CRP) has been shown to independently predict the risk of developing type 2 diabetes.20 Inflammatory parameters elevated in diabetes, and in the context of insulin resistance in the absence of overt diabetes, include high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a), and the circulating (soluble) form of CD40 ligand (sCD40L) (see Fig. 2-2). In addition, an increased expression of adhesion molecules, such as endothelial (E)-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intracellular adhesion molecule-1 (ICAM-1) has been detected. The morphologic substrate of increased vascular inflammatory activity can be derived by an analysis of coronary atherectomy specimens of patients with ACS: tissue from diabetic patients exhibits a larger content of lipid-rich atheroma and a more pronounced macrophage infiltration, compared with specimens from nondiabetic individuals.15 The receptor for AGE (RAGE) may play an important role in inflammatory processes and endothelial activation, most likely accelerating the processes of coronary atherosclerotic development, especially in diabetic patients. Recently, it has been demonstrated that CRP, a key pro-inflammatory cytokine in patients with atherosclerosis, upregulates RAGE expression in endothelial cells. These observations reinforce the mechanistic links in diabetes among inflammation, endothelial dysfunction, atherothrombosis, and, as detailed later, accelerated restenosis.

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