F-18-FDG Uptake and Calcifications in the Thoracic Aorta on Positron Emission Tomography/Computed Tomography Examinations Frequency and Stability on Serial Scans
Journal of Thoracic Imaging. Philadelphia: Lippincott Williams & Wilkins, v. 26, n. 1, p. 54-62, 2011.
Portes Meirelles, Gustavo Souza [UNIFESP]
Strauss, Harry William
Purpose: Vascular F-18-2-fluoro-2-deoxy-D-glucose (F-18-FDG) uptake has been suggested as a means of identifying metabolically active atheroma, whereas vascular calcification is accepted as an indicator of atherosclerosis. This investigation describes the frequency and stability of F-18-FDG uptake and vascular calcification in the thoracic aorta on serial F-18-FDG positron emission tomography/computed tomography (PET/CT) studies and correlates the findings with clinical data and risk factors for cardiovascular disease (CVD).Materials and Methods: Serial F-18-FDG-PET/CT scans of 100 cancer patients who had at least 2 PET/CT studies were reviewed. Sites of aortic F-18-FDG uptake and calcifications were identified. Results were compared to assess the frequency and stability of the vascular findings and their correlation with clinical data.Results: F-18-FDG aortic uptake was seen in 70% of the patients on the initial scan and changed on the second scan in 55% of the patients. Calcifications were often seen in patients with F-18-FDG uptake, but calcification and F-18-FDG uptake were present at the same site in only 2 cases. Both calcification and F-18-FDG uptake correlated with age. Patients with diabetes, hypertension, hyperlipidemia, or a history of CVD had significantly more calcifications. No correlation was seen between F-18-FDG uptake and calcification stability and the interval between scans, age, risk factors, or history of CVD.Conclusions: F-18-FDG vascular uptake was common on PET/CT and correlated with vascular calcifications, although the specific sites rarely overlapped. Calcifications were stable over time, but F-18-FDG uptake changed in more than half of the patients, supporting the postulate that inflammation in atheroma is a waxing and waning inflammatory process.