Diet-Modulated Lipoprotein Metabolism and Vascular Inflammation Evaluated by F-18-fluorodeoxyglucose Positron Emission Tomography

Abstract

Vascular inflammation plays a central role in atherosclerosis, from initiation and progression to acute thrombotic complications. Modified low-density lipoproteins (LDLs) and apoB-containing particles stimulate plaque inflammation by interacting with macrophages. Loss of function of high-density lipoprotein (HDL) for preventing LDL particles from oxidative modification in dyslipidemic states may amplify modified LDL actions, accelerating plaque inflammation. Diets are one of the most important factors that can affect these processes of lipoprotein oxidation and vascular inflammation. Recently, F-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) has emerged as a reliable noninvasive imaging modality for identifying and quantifying vascular inflammation within atherosclerotic lesions based on the high glycolytic activity of macrophages infiltrating active atherosclerotic plaques. Vascular inflammation evaluated by FDG PET has been positively related to metabolic syndrome components and traditional risk factors of cardiovascular disease, including high-sensitivity C-reactive protein, body mass index, and insulin resistance. A positive association of vascular inflammation with endothelial dysfunction, resistin levels, pericardial adipose tissue, and visceral fat area has also been reported. In contrast, HDL cholesterol and adiponectin have been inversely related to vascular inflammation detected by FDG PET. Because of its reproducibility, serial FDG PET shows potential for tracking the effects of dietary interventions and other systemic and local antiatherosclerotic therapies for plaque inflammation.