Optimizing 18F-FDG PET/CT imaging of vessel wall inflammation: the impact of 18F-FDG circulation time, injected dose, uptake parameters, and fasting blood glucose levels.

PURPOSE: (18)F-FDG PET is increasingly used for imaging of vessel wall inflammation. However, limited data are available on the impact of methodological variables, i.e. prescan fasting glucose, FDG circulation time and injected FDG dose, and of different FDG uptake parameters, in vascular FDG PET imaging. METHODS: Included in the study were 195 patients who underwent vascular FDG PET/CT of the aorta and the carotids. Arterial standardized uptake values (meanSUVmax), target-to-background ratios (meanTBRmax) and FDG blood-pool activity in the superior vena cava (SVC) and the jugular veins (JV) were quantified. Vascular FDG uptake values classified according to the tertiles of prescan fasting glucose levels, the FDG circulation time, and the injected FDG dose were compared using ANOVA. Multivariate regression analyses were performed to identify the potential impact of all variables described on the arterial and blood-pool FDG uptake. RESULTS: Tertile analyses revealed FDG circulation times of about 2.5 h and prescan glucose levels of less than 7.0 mmol/l, showing a favorable relationship between arterial and blood-pool FDG uptake. FDG circulation times showed negative associations with aortic meanSUVmax values as well as SVC and JV FDG blood-pool activity, but positive correlations with aortic and carotid meanTBRmax values. Prescan glucose levels were negatively associated with aortic and carotid meanTBRmax and carotid meanSUVmax values, but were positively correlated with SVC blood-pool uptake. The injected FDG dose failed to show any significant association with vascular FDG uptake. CONCLUSION: FDG circulation times and prescan blood glucose levels significantly affect FDG uptake in the aortic and carotid walls and may bias the results of image interpretation in patients undergoing vascular FDG PET/CT. The injected FDG dose was less critical. Therefore, circulation times of about 2.5 h and prescan glucose levels less than 7.0 mmol/l should be preferred in this setting.

Arterial and fat tissue inflammation are highly correlated: a prospective 18F-FDG PET/CT study.

PURPOSE: There is evidence that the link between obesity and cardiovascular disease might relate to inflammation in both fat tissue and the arterial wall. (18)F-FDG uptake on PET is a surrogate marker of vessel wall inflammation. The aim of the study was to measure FDG uptake in both regions using PET and identify links between adipose and arterial inflammation. METHODS: Included in the study were 173 cardiovascular patients who were prospectively imaged with FDG PET/CT. Arterial FDG uptake was measured in the carotid arteries and ascending aorta. The same was done in fat tissue in the neck, the presternal region (both subcutaneous) and the pericardium. FDG uptake was quantified as average maximal target-to-background ratio (mean TBR max). Multivariate regression analyses were performed to identify significant associations between arterial and adipose tissue FDG uptake and clinical variables as given by the standardized correlation coefficient (ß). RESULTS: FDG uptake values in all fat tissue regions were highly predictive of vascular FDG uptake in both the carotids (ß 0.262, p < 0.0001, in the neck subcutaneous region) and aorta (ß 0.22, p = 0.008, in the chest pericardial region; ß 0.193, p = 0.019, in the chest subcutaneous region). Obesity was significantly associated with elevated FDG uptake in adipose tissue (ß 0.470, p < 0.0001, in the neck subcutaneous region; ß 0.619, p = 0.028, in the chest subcutaneous region; ß 0.978, p = 0.035, in the chest pericardial region). CONCLUSION: FDG uptake in diverse fat tissue regions was significantly associated with arterial FDG uptake, a reasonable surrogate of inflammation. Increasing body weight significantly predicted the level of fatty inflammation. FDG PET therefore provides imaging evidence of an inflammatory link between fat tissue and the vasculature in patients with cardiovascular disease.

Impact of noninsulin-dependent type 2 diabetes on carotid wall 18F-fluorodeoxyglucose positron emission tomography uptake.

OBJECTIVES: In this study, the impact of noninsulin-dependent type 2 diabetes mellitus on carotid wall (18)F-fluorodeoxyglucose (FDG) uptake in patients with documented or suspected cardiovascular disease was evaluated. BACKGROUND: Inflammation is a pivotal process in the progression of atherosclerosis, which can be noninvasively imaged by FDG positron emission tomography (FDG-PET). METHODS: Carotid artery wall FDG uptake was quantified in 134 patients (age 60.2 ± 9.7 years; diabetic subjects, n = 43). The pre-scan glucose (gluc) level corrected mean of the maximum standardized uptake value (SUV) values ((mean)SUV(gluc)), mean of the maximum target-to-background ratio ((mean)TBR(gluc)), and single hottest segment (SHS(gluc)) of FDG uptake in the artery wall were calculated. Associations between FDG uptake, the presence of risk factors for atherosclerosis, and diabetes were then assessed by multiple regression analysis with backward elimination. RESULTS: The study demonstrated a significant association between diabetes and FDG uptake in the arterial wall (diabetes (mean)SUV(gluc) ß = 0.324, (mean)TBR(gluc) ß = 0.317, and SHS(gluc) ß = 0.298; for all, p < 0.0001). In addition, in diabetic patients, both body mass index ≥ 30 kg/m(2) ((mean)SUV(gluc) ß = 0.4, (mean)TBR(gluc) ß = 0.357, and SHS(gluc) ß = 0.388; for all, p < 0.015) and smoking ((mean)TBR(gluc), ß = 0.312; SHS(gluc), ß = 0.324; for all, p < 0.04) were significantly associated with FDG uptake. CONCLUSIONS: Type 2 diabetes was significantly associated with carotid wall FDG uptake in patients with known or suspected cardiovascular disease. In diabetic patients, obesity and smoking add to the risk of increased FDG uptake values.

Prevalence and risk factors of carotid vessel wall inflammation in coronary artery disease patients: FDG-PET and CT imaging study.

OBJECTIVES: We investigated the prevalence and clinical risk factors of carotid vessel wall inflammation by means of 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) in a population consisting of coronary artery disease (CAD) patients. BACKGROUND: The atherosclerotic disease process is characterized by infiltration and retention of oxidized lipids in the artery wall, triggering a disproportionate inflammatory response. Efforts have been made to use noninvasive imaging to quantify this inflammatory response in the vessel wall. Recently, carotid FDG-PET has been shown to reflect the metabolic rate of glucose, a process known to be enhanced in inflamed tissue. METHODS: Carotid inflammation was quantified in 82 CAD patients (age 62 ± 10 years) as the maximum target-to-background ratio ((wholevessel)TBR(max)). Furthermore, we assessed the maximal standardized uptake value values ((wholevessel)SUV(max)), the single hottest segment (SHS), and the percent active segments (PAS) of the FDG uptake in the artery wall, measured by FDG-PET. RESULTS: Whole-vessel TBR(max) >1.8 was present in 67%, >2.0 in 39%, >2.2 in 23%, and >2.4 in 12% of the population. Multiple linear regression analysis with backward elimination revealed that body mass index (BMI) ≥30 kg/m2 (p < 0.0001), age >65 years (p = 0.01), smoking (p = 0.02), and hypertension (p = 0.01) were associated with (wholevessel)TBR(max). The number of components of the metabolic syndrome was also associated with (wholevessel)TBR(max) (p = 0.02). In similar analyses, (wholevessel)SUV(max) was associated with BMI ≥30 kg/m2 (p < 0.0001), age >65 years (p = 0.004), male gender (p = 0.02), and hypertension (p = 0.04); SHS with BMI ≥30 kg/m2 (p < 0.0001), age >65 years (p = 0.02), smoking (p = 0.04), and hypertension (p = 0.05); PAS with BMI ≥30 kg/m2 (p = 0.001), smoking (p = 0.03), and hypertension (p = 0.01). CONCLUSIONS: Carotid inflammation as revealed by FDG-PET is highly prevalent in the CAD population and is associated with obesity, age over 65 years, history of hypertension, smoking, and male gender. Artery wall FDG uptake increased when components of the metabolic syndrome clustered.