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, 18F-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.