Correlation of Inflammation Assessed by 18F-FDG PET, Active Mineral Deposition Assessed by 18F-Fluoride PET, and Vascular Calcification in Atherosclerotic Plaque: A Dual-Tracer PET/CT Study

Formation and progression of atherosclerotic plaque is a dynamic and complex process involving various pathophysiologic steps including inflammation and calcification. The purpose of this study was to compare macrophage activity as determined by F-18-FDG PET and ongoing mineral deposition as measured by F-18-sodium fluoride PET in atherosclerotic plaque and to correlate these findings with calcified plaque burden as assessed by CT. Methods: Forty-five patients were examined by whole-body F-18-FDG PET, F-18-sodium fluoride PET, and CT. Tracer uptake in various arterial segments was analyzed both qualitatively and semiquantitatively by measuring the blood-pool-corrected standardized uptake value (target-to-background ratio [TBR]). The pattern of tracer uptake in atherosclerotic lesions was compared after color-coded multistudy image fusion of PET and CT studies. The Fisher exact test and the Spearman correlation coefficient rs were used for statistical analysis of image-based results and cardiovascular risk factors. Intra-and interrater reproducibility were evaluated using the Cohen kappa. Results: F-18-sodium fluoride uptake was observed at 105 sites in 27 (60%) of the 45 study patients, and mean TBR was 2.3 +/- 0.7. F-18-FDG uptake was seen at 124 sites in 34 (75.6%) patients, and mean TBR was 1.5 +/- 0.3. Calcified atherosclerotic lesions were observed at 503 sites in 34 (75.6%) patients. Eighty-one (77.1%) of the 105 lesions with marked F-18-sodium fluoride uptake and only 18 (14.5%) of the 124 lesions with F-18-FDG accumulation were colocalized with arterial calcification. Coincident uptake of both F-18-sodium fluoride and F-18-FDG was observed in only 14 (6.5%) of the 215 arterial lesions with radiotracer accumulation. Conclusion: PET/CT with F-18-FDG and F-18-sodium fluoride may allow evaluation of distinct pathophysiologic processes in atherosclerotic lesions and might provide information on the complex interactions involved in formation and progression of atherosclerotic plaque.