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Objectives: The objective of this study was to evaluate whether baseline 18F-fluorodeoxyglucose (FDG) uptake is associated with carotid plaque progression.Methods: A total of 156 subjects with carotid plaque were enrolled and underwent carotid magnetic resonance imaging (MRI) (at baseline and the 12-month follow-up) and positron emission tomography-computed tomography (PET-CT) (baseline). Carotid plaque progression was evaluated by two indices (the incidence of plaque progression and percentage of plaque increase) with three-dimensional (3D) imaging, while the 18F-FDG uptake was evaluated by the 18F-FDG uptake levels and 18F-FDG uptake velocity. The association between plaque progression and 18F-FDG uptake was investigated by the trend test and multivariate logistic regression analysis.Results: Of the 156 subjects, 80 (51.3%) showed carotid plaque progression during the 12-month follow-up. Firstly, no association was found between 18F-FDG uptake levels and plaque progression. Secondly, significant differences in the incidence of plaque progression were observed among the groups with different uptake velocities, showing a significant decreasing trend ranging from high to intermediate to low (p = 0.002, trend test). After adjusting for covariates, an adequate prediction of the 18F-FDG uptake velocity for the incidence of plaque progression was revealed (OR = 0.682, p < 0.05). In addition, no association was found between the 18F-FDG uptake velocity and the percentage of plaque increase in the subjects with plaque progression (p = 0.757, trend test).Conclusions: Our findings suggest 18F-FDG uptake velocity is independently associated with the incidence of carotid plaque progression. Additionally, the 18F-FDG uptake velocity, as another important parameter of PET-CT, warrants further study in future clinical research.Key Points: • The18F-FDG uptake levels were not associated with the carotid plaque progression. • The18F-FDG uptake velocity could predict the incidence of carotid plaque progression. • The18F-FDG uptake velocity with related factors warrants more attention in future clinical research. [ABSTRACT FROM AUTHOR]

Abstract Accelerated atherosclerosis often occurs in patients with antiphospholipid syndrome (APS), and auto-antibodies to β 2 glycoprotein I (anti-β 2 GPI) are confirmed as pathogenic antibodies to APS. Our previous studies have demonstrated that the conversion of mouse peritoneal macrophages into foam cells could be enhanced by co-existence of β 2 GPI and anti-β 2 GPI IgG, but this phenomenon has not been explored in vivo. Here, we present a mouse model to observe the effect of anti-β 2 GPI IgG in the development of atherosclerosis. Male ApoE-deficient mice were intraperitoneally injected with anti-β 2 GPI IgG (100 μg/mouse) and homologous control IgG (100 μg/mouse) every week for 16 weeks. Plasma lipid composition, magnetic resonance imaging (MRI) and histological staining were used to evaluate vascular inflammation, lumen stenosis and plaque stability. The results showed that the levels of total cholesterol, triglycerol and low-density lipoprotein-cholesterol in plasma were not changed in all mice fed with high-fat diet, but the level of high-density lipoprotein-cholesterol was lower and the atherosclerosis index was significantly increased in HD + anti-β 2 GPI group than in other high-fat diet groups. In addition, compared with NR IgG-treated mice, anti-β 2 GPI IgG-treated mice showed more lipid deposition in the carotid artery, markedly narrowed arteriolar lumen as well as higher MMP-9 expression, more macrophages and fewer collagen fibers in the aortic arch root. Furthermore, the aortic mRNA levels of TNF-α, IL-1β, and MCP-1 were significantly increased in anti-β 2 GPI IgG-treated mice. Together, these data indicate that anti-β 2 GPI IgG increases vascular inflammation, aggravates atherosclerosis and promotes the formation of vulnerable plaque in ApoE-deficient mice. Highlights • Anti-β 2 GPI IgG treatment can interfere with lipid metabolism. • Anti-β 2 GPI IgG treatment aggravate lipid deposition and markedly narrow arteriolar lumen. • Anti-β 2 GPI IgG treatment aggravates vascular inflammation. • Anti-β 2 GPI IgG treatment increases atherosclerotic plaque vulnerability. [ABSTRACT FROM AUTHOR]