Lowie E G W Vanfleteren1, Aniek M G van Meerendonk2, Frits M Franssen3, Emiel F M Wouters3, Felix M Mottaghy4, Marinus J van Kroonenburgh5, Jan Bucerius6. 1. CIRO+, Center of Expertise in Chronic Organ Failure, Horn, The Netherlands; Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. Electronic address: lowievanfleteren@ciro-horn.nl. 2. Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 3. CIRO+, Center of Expertise in Chronic Organ Failure, Horn, The Netherlands; Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 4. Department of Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands; Department of Nuclear Medicine, University Hospital, RWTH Aachen, Aachen, Germany. 5. Department of Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands. 6. Department of Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands; Department of Nuclear Medicine, University Hospital, RWTH Aachen, Aachen, Germany; Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, The Netherlands.
Abstract
BACKGROUND: Fat tissue, and particularly visceral fat, is known to play a role in low grade systemic inflammation in COPD, and is likely to contribute to the excess cardiovascular comorbidity in COPD. Therefore, we aimed to study (18)FDG-PET-assessed inflammation of the aorta and the (visceral) fat, and evaluate its interrelations and differences in subjects with and without COPD. METHODS: We retrospectively identified 42 patients (71% male, 48% current smokers, mean age 66.6 ± 8.3 years, mean BMI 25.1 ± 4.3 kg/m(2)), who underwent (18)F-FDG-PET/CT for suspected early stage bronchus carcinoma. COPD-diagnosis was based on spirometry and defined as FEV1/FVC < lower limit of normal. Inflammatory status of aortic and fat regions was defined as the average of obtained maximum target-to-background ratios (meanTBRmax). The TBR is the standardized uptake value (SUV) normalized to (18)F-FDG blood pool activity. RESULTS: Compared to controls, patients with COPD (n = 19; 45%) had increased meanTBRmax of both the abdominal aorta (1.31 ± 0.14 vs. 1.49 ± 0.31; p = 0.02) and the abdominal visceral fat (0.28 ± 0.09 vs. 0.38 ± 0.18; p = 0.047), while inflammatory activity of the abdominal subcutaneous fat failed to show statistically significant differences (0.21 ± 0.09 vs. 0.24 ± 0.09; p = 0.345). In all patients, meanTBRmax of abdominal visceral fat was correlated with meanTBRmax of the abdominal aorta, independently of age and BMI (β = 0.590, p = 0.002). CONCLUSION: Metabolic activity of the abdominal aorta and visceral fat is increased in COPD patients compared to peers. The degree of visceral fat metabolic activity is associated with aortic inflammation. More prospective research is warranted concerning the role of visceral fat in the development of vascular comorbidity in COPD.
BACKGROUND: Fat tissue, and particularly visceral fat, is known to play a role in low grade systemic inflammation in COPD, and is likely to contribute to the excess cardiovascular comorbidity in COPD. Therefore, we aimed to study (18)FDG-PET-assessed inflammation of the aorta and the (visceral) fat, and evaluate its interrelations and differences in subjects with and without COPD. METHODS: We retrospectively identified 42 patients (71% male, 48% current smokers, mean age 66.6 ± 8.3 years, mean BMI 25.1 ± 4.3 kg/m(2)), who underwent (18)F-FDG-PET/CT for suspected early stage bronchus carcinoma. COPD-diagnosis was based on spirometry and defined as FEV1/FVC < lower limit of normal. Inflammatory status of aortic and fat regions was defined as the average of obtained maximum target-to-background ratios (meanTBRmax). The TBR is the standardized uptake value (SUV) normalized to (18)F-FDG blood pool activity. RESULTS: Compared to controls, patients with COPD (n = 19; 45%) had increased meanTBRmax of both the abdominal aorta (1.31 ± 0.14 vs. 1.49 ± 0.31; p = 0.02) and the abdominal visceral fat (0.28 ± 0.09 vs. 0.38 ± 0.18; p = 0.047), while inflammatory activity of the abdominal subcutaneous fat failed to show statistically significant differences (0.21 ± 0.09 vs. 0.24 ± 0.09; p = 0.345). In all patients, meanTBRmax of abdominal visceral fat was correlated with meanTBRmax of the abdominal aorta, independently of age and BMI (β = 0.590, p = 0.002). CONCLUSION: Metabolic activity of the abdominal aorta and visceral fat is increased in COPDpatients compared to peers. The degree of visceral fat metabolic activity is associated with aortic inflammation. More prospective research is warranted concerning the role of visceral fat in the development of vascular comorbidity in COPD.
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