Effect of Atorvastatin on Vascular Inflammation in Type 2 Diabetes

The early detection of vulnerable plaques is clinically important for risk stratification and also to provide early treatment. Inflammation is important in the both pathogenesis and outcome of atherosclerosis. Plaques containing numerous inflammatory cells, particular macrophages, have a high risk of rupture. Diabetes is a major risk factor for the development of atherosclerosis. Lipid-lowering therapy with statins significantly decreases cardiovascular morbidity and mortality in primary and secondary prevention. Statin exert their benefits through the inhibition of de novo cholesterol synthesis, resulting in significant reductions in plasma low-density lipoprotein cholesterol (LDL-C) levels. It remains controversial whether LDL-C lowering is the only mechanism for the observed beneficial effects. Many LDL-C-independent pleiotropic effects have been postulated. Moreover, Lipid lowering therapy may affect atherosclerosis also through the inhibition of inflammatory marker. These evidences highlight the possibility of statins could be have great impact on plaque inflammation. 18FDG is a glucose analogue that is taken up by cells in proportion to their metabolic activity. Several papers have reported the potential roles of metabolic imaging in the assessment of inflammatory vascular diseases, especially in large vessels. If so, FDG-PET can monitor the direct effect of statins on vascular inflammation. Additionally, monitoring the vascular inflammation by FDG-PET may be useful for determining the risk stratification of atherosclerotic patients. The investigators hypothesize that statins-induced attenuation of vascular inflammation could be monitored clinically by use of FDG-PET approach, and providing information of early efficacy statins therapy caused by stabilization of vulnerable plaque without affecting the lumen size.