Petteri Rinne1, Sanna Hellberg1, Max Kiugel1, Jenni Virta1, Xiang-Guo Li1, Meeri Käkelä1, Kerttuli Helariutta2, Pauliina Luoto1, Heidi Liljenbäck1,3, Harri Hakovirta4, Maria Gardberg5, Anu J Airaksinen2, Juhani Knuuti1, Antti Saraste1,6, Anne Roivainen7,8. 1. Turku PET Centre, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, FI-20520, Turku, Finland. 2. Laboratory of Radiochemistry, Department of Chemistry, University of Helsinki, Helsinki, Finland. 3. Turku Center for Disease Modeling, University of Turku, Turku, Finland. 4. Department of Surgery, University of Turku, Turku, Finland. 5. Department of Pathology, Turku University Hospital and University of Turku, Turku, Finland. 6. Heart Center, Turku University Hospital and University of Turku, Turku, Finland. 7. Turku PET Centre, Turku University Hospital and University of Turku, Kiinamyllynkatu 4-8, FI-20520, Turku, Finland. anne.roivainen@utu.fi. 8. Turku Center for Disease Modeling, University of Turku, Turku, Finland. anne.roivainen@utu.fi.
Abstract
PURPOSE: Rupture-prone atherosclerotic plaques are characterized by accumulation of macrophages, which have shown to express somatostatin type 2 receptors. We aimed to investigate whether somatostatin receptor-targeting positron emission tomography (PET) tracers, [(68)Ga]DOTANOC, [(18)F]FDR-NOC, and [(68)Ga]DOTATATE, can detect inflamed atherosclerotic plaques. PROCEDURES: Atherosclerotic IGF-II/LDLR(-/-)ApoB(100/100) mice were studied in vivo and ex vivo for tracer uptake into atherosclerotic plaques. Furthermore, [(68)Ga]DOTANOC and [(68)Ga]DOTATATE were compared in a head-to-head setting for in vivo PET/X-ray computed tomography (CT) imaging characteristics. RESULTS: Ex vivo uptake of [(68)Ga]DOTANOC and [(68)Ga]DOTATATE in the aorta was higher in atherosclerotic mice compared to control C57Bl/6N mice, while the aortic uptake of [(18)F]FDR-NOC showed no genotype difference. Unlike [(18)F]FDR-NOC, [(68)Ga]DOTANOC and [(68)Ga]DOTATATE showed preferential binding to atherosclerotic plaques with plaque-to-wall ratio of 1.7 ± 0.3 and 2.1 ± 0.5, respectively. However, the aortic uptake and aorta-to-blood ratio of [(68)Ga]DOTANOC were higher compared to [(68)Ga]DOTATATE in in vivo PET/CT imaging. CONCLUSION: Our results demonstrate superior applicability for [(68)Ga]DOTANOC and [(68)Ga]DOTATATE in the detection of atherosclerotic plaques compared to [(18)F]FDR-NOC.
PURPOSE: Rupture-prone atherosclerotic plaques are characterized by accumulation of macrophages, which have shown to express somatostatin type 2 receptors. We aimed to investigate whether somatostatin receptor-targeting positron emission tomography (PET) tracers, [(68)Ga]DOTANOC, [(18)F]FDR-NOC, and [(68)Ga]DOTATATE, can detect inflamed atherosclerotic plaques. PROCEDURES: AtheroscleroticIGF-II/LDLR(-/-)ApoB(100/100) mice were studied in vivo and ex vivo for tracer uptake into atherosclerotic plaques. Furthermore, [(68)Ga]DOTANOC and [(68)Ga]DOTATATE were compared in a head-to-head setting for in vivo PET/X-ray computed tomography (CT) imaging characteristics. RESULTS: Ex vivo uptake of [(68)Ga]DOTANOC and [(68)Ga]DOTATATE in the aorta was higher in atheroscleroticmice compared to control C57Bl/6N mice, while the aortic uptake of [(18)F]FDR-NOC showed no genotype difference. Unlike [(18)F]FDR-NOC, [(68)Ga]DOTANOC and [(68)Ga]DOTATATE showed preferential binding to atherosclerotic plaques with plaque-to-wall ratio of 1.7 ± 0.3 and 2.1 ± 0.5, respectively. However, the aortic uptake and aorta-to-blood ratio of [(68)Ga]DOTANOC were higher compared to [(68)Ga]DOTATATE in in vivo PET/CT imaging. CONCLUSION: Our results demonstrate superior applicability for [(68)Ga]DOTANOC and [(68)Ga]DOTATATE in the detection of atherosclerotic plaques compared to [(18)F]FDR-NOC.
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