We investigated the relation of carotid 18 F-FDG uptake to high-sensitivity C-reactive protein (hsCRP) and Framingham risk score (FRS) in a large cohort of asymptomatic adults. Methods: Carotid artery 18 F-FDG uptake was measured on the PET/CT scans of 1,181 asymptomatic subjects, and maximum target-to-background ratio (M-TBR) and intima-media thickness (IMT) were compared with clinical risk factors and hsCRP. The estimated 10-y risk for general cardiovascular disease was calculated by FRS. Results: FRS increased from 11.5% 6 7.8% to 14.8% 6 10.5% in subjects with an M-TBR $ 1.7, compared with , 1.7, and the odds ratio for an FRS $ 10% was 1.9 (95% confidence interval [CI], 1.4-2.5). Adjusting for age confirmed a significant association of M-TBR and IMT with FRS. Independent determinants of high M-TBR were abdominal fat (b coefficient [B], 1.1040; P , 0.0001), low-density lipoprotein (LDL) (B, 0.0006; P , 0.05), and FRS (B, 0.0025; P , 0.05) for subjects , 50 y and abdominal fat (B, 0.9740; P , 0.0001), age (B, 0.0040; P 5 0.0001), LDL (B, 0.0008; P 5 0.0001), and IMT (B, 0.1097; P , 0.01) for subjects $ 50 y. Although hsCRP also stratified subjects for FRS-based risk, no correlation was found between hsCRP and M-TBR or IMT, suggesting that they may have different inferences. Importantly, in the low-hsCRP (14.2% 6 9.7% vs. 11.3% 6 7.4%) and high-hsCRP groups (18.8% 6 14.3% vs. 13.3% 6 10.2%), FRS was significantly greater for subjects with high M-TBR than for those with low M-TBR. The odds ratio for FRS $ 10% between subjects with high and low M-TBR was 1.20 (95% CI, 0.90-1.60; P 5 0.209) in the low-hsCRP group and 2.95 (95% CI, 1.48-5.86; P 5 0.002) in the high-hsCRP group. Conclusion: High carotid 18 F-FDG uptake in asymptomatic adults is associated with increased clinical risk factors and FRS. Furthermore, it appears to reflect aspects of atherosclerotic inflammation distinct from hsCRP concentration and may offer incremental information regarding cardiovascular risk.

High carotid FDG uptake predicts cardiovascular events independent of traditional risk factors and CIMT in asymptomatic adults and may add to risk stratification beyond the FRS and CIMT.

We assessed the association between nonalcoholic fatty liver disease (NAFLD) and carotid artery inflammation measured by (18)F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography. Participants were 755 consecutive otherwise healthy adult males who underwent a general health screening program. Carotid FDG uptake, represented as maximum target-to-background ratio, was increased with mild (n = 237; 1.61 ± 0.14; P = .033) and moderate NAFLD (n = 145; 1.63 ± 0.16; P = .005) compared with controls (n = 373; 1.58 ± 0.15). In patients aged >50 years, moderate NAFLD was the only independent risk factor for high carotid FDG uptake (odds ratio, 2.12; 95% confidence interval, 1.10-4.07; P = .001). Apparently healthy adult males with NAFLD have elevated carotid FDG uptake as well as increased carotid intima-media thickness, suggesting that they may be at an increased risk of having inflammatory atherosclerotic plaques in the carotid arteries.

This exploratory study suggests that high-hepatic FDG uptake may be a useful prognostic factor for cardiovascular events in individuals with NAFLD.

Hepatic FDG uptake is closely associated with elevated TG and GGT regardless of the presence of FLD. Thus, inflammation response may play a major role in increased hepatic glucose uptake.