The Impact of Rosiglitazone on Regression of Atherosclerosis

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. The discovery of the peroxisome proliferator-activated receptor γ (PPARγ) gene led to the hope of favorably influencing the insulin resistance syndrome. The administration of PPARγ agonists have been shown to reduce insulin resistance, to reduce the expression of leptin, to lower plasma free fatty acid level and to lower blood pressure. Moreover, beyond the glucose effect, PPARγ agonists may theoretically affect atherosclerosis also through the inhibition of inflammatory cytokines secreted from the macrophage, such as IL-6, IL-1β, TNF-α, etc. These evidences highlight the possibility of PPARγ agonists could be have great impact on plaque regression.

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. However, PET has limited spatial resolution. Recently, a combined PET/CT is emerged as a promising modality which could provide both anatomical and functional information. We hypothesize that PPARγ agonists-induced plaque regression could be monitored clinically by use of 18FDG PET/CT approach, and providing information of early efficacy PPARγ treatment caused by stabilization of vulnerable plaque without affecting the lumen size.