A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Non-specific binding of [F-18]FDG to calcifications in atherosclerotic plaques: experimental study of mouse and human arteries
Tekijät: Laitinen I, Marjamaki P, Haaparanta M, Savisto N, Laine VJO, Soini SL, Wilson I, Leppanen P, Yla-Herttuala S, Roivainen A, Knuuti J
Kustantaja: SPRINGER
Julkaisuvuosi: 2006
Journal: European Journal of Nuclear Medicine and Molecular Imaging
Tietokannassa oleva lehden nimi: EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
Lehden akronyymi: EUR J NUCL MED MOL I
Vuosikerta: 33
Numero: 12
Aloitussivu: 1461
Lopetussivu: 1467
Sivujen määrä: 7
ISSN: 1619-7070
DOI: https://doi.org/10.1007/s00259-006-0159-6
Tiivistelmä
Purpose: [F-18] 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 [F-18] FDG in atherosclerotic plaque compartments.Methods: The biodistribution of intravenously administered [F-18] 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 [F-18] FDG in human atherosclerotic arteries was also examined.Results: The uptake of [F-18] FDG was significantly higher in the aorta of atherosclerotic mice as compared with the control mice. Autoradiography of excised arteries showed higher [F-18] FDG uptake in the plaques than in the healthy vessel wall ( mean ratio +/- SD 2.7 +/- 1.1). The uptake of [F-18] 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 [F-18] FDG to the calcifications but not to other structures of the artery wall.Conclusion: In agreement with previous studies, we observed [F-18] 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.
Purpose: [F-18] 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 [F-18] FDG in atherosclerotic plaque compartments.Methods: The biodistribution of intravenously administered [F-18] 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 [F-18] FDG in human atherosclerotic arteries was also examined.Results: The uptake of [F-18] FDG was significantly higher in the aorta of atherosclerotic mice as compared with the control mice. Autoradiography of excised arteries showed higher [F-18] FDG uptake in the plaques than in the healthy vessel wall ( mean ratio +/- SD 2.7 +/- 1.1). The uptake of [F-18] 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 [F-18] FDG to the calcifications but not to other structures of the artery wall.Conclusion: In agreement with previous studies, we observed [F-18] 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.
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