Non-specific binding of [18F]FDG to calcifications in atherosclerotic plaques: experimental study of mouse and human arteries
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[18F]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 [18F]FDG in atherosclerotic plaque compartments.
The biodistribution of intravenously administered [18F]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 [18F]FDG in human atherosclerotic arteries was also examined.
The uptake of [18F]FDG was significantly higher in the aorta of atherosclerotic mice as compared with the control mice. Autoradiography of excised arteries showed higher [18F]FDG uptake in the plaques than in the healthy vessel wall (mean ratio ±SD 2.7±1.1). The uptake of [18F]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 [18F]FDG to the calcifications but not to other structures of the artery wall.
In agreement with previous studies, we observed [18F]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.
KeywordsAtherosclerosis PET [18F]FDG Plaque Calcification
This work was funded by the Ida Montin Foundation, the Finnish Cultural Foundation, the Finnish Foundation for Cardiovascular Research, the Paulo Foundation and the Hospital District of Southwest Finland.
The authors would like to thank Sanna Suominen, Tarja Marttila, Hannele Ylipahkala and Mervi Oikonen for technical assistance.
- 11.Leppänen P, Koota S, Kholova I, Koponen J, Fieber C, Eriksson U, et al. Gene transfers of vascular endothelial growth factor-A, vascular endothelial growth factor-B, vascular endothelial growth factor-C, and vascular endothelial growth factor-D have no effects on atherosclerosis in hypercholesterolemic low-density lipoprotein-receptor/apolipoprotein B48-deficient mice. Circulation 2005;112:1347–1352PubMedCrossRefGoogle Scholar