01.02.2015 | Original Article
Targeting post-infarct inflammation by PET imaging: comparison of 68Ga-citrate and 68Ga-DOTATATE with 18F-FDG in a mouse model
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 2/2015
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Imaging of inflammation early after myocardial infarction (MI) is a promising approach to the guidance of novel molecular interventions that support endogenous healing processes. 18F-FDG PET has been used, but may be complicated by physiological myocyte uptake. We evaluated the potential of two alternative imaging targets: lactoferrin binding by 68Ga-citrate and somatostatin receptor binding by 68Ga-DOTATATE.
Methods
C57Bl/6 mice underwent permanent coronary artery ligation. Serial PET imaging was performed 3 – 7 days after MI using 68Ga-citrate, 68Ga-DOTATATE, or 18F-FDG with ketamine/xylazine suppression of myocyte glucose uptake. Myocardial perfusion was evaluated by 13N-ammonia PET and cardiac geometry by contrast-enhanced ECG-gated CT.
Results
Mice exhibited a perfusion defect of 30 – 40 % (of the total left ventricle) with apical anterolateral wall akinesia and thinning on day 7 after MI. 18F-FDG with ketamine/xylazine suppression demonstrated distinct uptake in the infarct region, as well as in the border zone and remote myocardium. The myocardial standardized uptake value in MI mice was significantly higher than in healthy mice under ketamine/xylazine anaesthesia (1.9 ± 0.4 vs. 1.0 ± 0.1). 68Ga images exhibited high blood pool activity with no specific myocardial uptake up to 90 min after injection (tissue-to-blood contrast 0.9). 68Ga-DOTATATE was rapidly cleared from the blood, but myocardial SUV was very low (0.10 ± 0.03).
Conclusion
Neither 68Ga nor 68Ga-DOTATATE is a useful alternative to 18F-FDG for PET imaging of myocardial inflammation after MI in mice. Among the three tested approaches, 18F-FDG with ketamine/xylazine suppression of cardiomyocyte uptake remains the most practical imaging marker of post-infarct inflammation.
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