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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, 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.
Highlights
Atherosclerotic cardiovascular disease (ASCVD), manifested as various forms of fatal diseases including myocardial infarction, ischemic stroke, and peripheral artery occlusive disease, is the leading cause of morbidity and mortality [1]
The main aim of this review is to describe the interactions between lipoprotein and macrophages leading to vascular inflammation
The main aim of this review is to describe the interactions between lipoprotein and macrophages leading effects to vascular inflammation atherosclerosis, effectsand of diets duringofthis during atherosclerosis, of diets during thisduring process of inflammation, evaluation this
Summary
Atherosclerotic cardiovascular disease (ASCVD), manifested as various forms of fatal diseases including myocardial infarction, ischemic stroke, and peripheral artery occlusive disease, is the leading cause of morbidity and mortality [1]. Activated macrophages can express tissue factors, which act as the main procoagulants and induce thrombosis in plaques [3]. Modified low-density lipoproteins (LDLs) trigger plaque positron emission tomography (PET). Modified low-density lipoproteins (LDLs) trigger plaque inflammation by interacting with macrophages. High-density lipoproteins (HDLs) protect LDLs from oxidative modification and inhibit by decreasing decreasingthe theexpression expressionofof modification and inhibitmonocyte monocyteadhesion adhesion to to the the endothelium endothelium by adhesion molecules in endothelial cells Loss of this protective function of HDL in dyslipidemic states may accelerate plaque inflammation, amplifying the role of modified LDLs. The high glycolytic activity of infiltrated macrophages enables visualization of vascular inflammation in atherosclerotic lesions by. Data from experimental and clinical studies indicate that statins lower low-density lipoproteins (LDLs) and reduce plaque inflammation and affect plaque stability [3,9]. The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) CRP substudy suggested that CRP screening can be conducted to improve the targeting of statin therapy adjunctively with lipid testing [3,19]
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