Non-specific binding of [ 18 F]FDG to calcifications in atherosclerotic plaques: experimental study of mouse and human arteries

Purpose [ 18 F]FDG has been used as an inflammation marker and shown to accumulate in inflammatory atherosclerotic plaques. The aim of this study was to investigate the uptake and location of [ 18 F]FDG in atherosclerotic plaque compartments. Methods The biodistribution of intravenously administered [ 18 F]FDG was analysed in atherosclerotic LDLR/ApoB48 mice ( n =11) and control mice ( n =9). Digital autoradiography was used to detect the ex vivo distribution in frozen aortic sections. In vitro binding of [ 18 F]FDG in human atherosclerotic arteries was also examined. Results The uptake of [ 18 F]FDG was significantly higher in the aorta of atherosclerotic mice as compared with the control mice. Autoradiography of excised arteries showed higher [ 18 F]FDG uptake in the plaques than in the healthy vessel wall (mean ratio ±SD 2.7±1.1). The uptake of [ 18 F]FDG in the necrotic, calcified sites of the advanced atherosclerotic lesions was 6.2±3.2 times higher than that in the healthy vessel wall. The in vitro studies of human arterial sections showed marked binding of [ 18 F]FDG to the calcifications but not to other structures of the artery wall. Conclusion In agreement with previous studies, we observed [ 18 F]FDG uptake in atherosclerotic plaques. However, prominent non-specific binding to calcified structures was found. This finding warrants further studies to clarify the significance of this non-specific binding in human plaques in vivo.