Imaging of vulnerable atherosclerotic plaques with FDG-microPET: No FDG accumulation
Abstract Background Non-invasive methods of evaluating atherosclerosis in humans and experimental animals are needed. Studies indicate that FDG-PET has a potential to detect vulnerable, inflamed atherosclerotic lesions. Methods Nine atherosclerotic apoE-deficient mice were PET scanned. Four to deter...
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Veröffentlicht in: | Atherosclerosis 2007-06, Vol.192 (2), p.275-282 |
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Zusammenfassung: | Abstract Background Non-invasive methods of evaluating atherosclerosis in humans and experimental animals are needed. Studies indicate that FDG-PET has a potential to detect vulnerable, inflamed atherosclerotic lesions. Methods Nine atherosclerotic apoE-deficient mice were PET scanned. Four to determine optimal timing for imaging, and five post mortem after 1 h redistribution of FDG and again after sequential removal of the interscapular brown fat and the atherosclerotic aortic arch. Uptake in various tissues in fasting ( n = 13) and non-fasting ( n = 7) apoE-deficient mice, including atherosclerotic and non-atherosclerotic aorta, was measured. Finally, accelerated atherosclerosis was induced by carotid ligation ( n = 12), and FDG-uptake was measured. Results FDG accumulation initially thought to correspond to the atherosclerotic aortic arch was recorded. Removal of interscapular brown fat, but not atherosclerotic aortic arch, removed the signal. The aortic arch accumulated less FDG than the non-atherosclerotic thoracic aorta both in fasting (ratio 0.5, p = 0.008) and non-fasting (ratio 0.33, p = 0.02) conditions. Carotid atherosclerosis likewise failed to increase FDG-uptake compared to the non-ligated artery (ratio 1.03). Conclusion Spontaneously developed advanced atherosclerotic lesions in aorta were, paradoxically, associated with reduced FDG uptake, and accelerated carotid atherosclerosis also failed to increase FDG-uptake. The results seriously question the potential of FDG-PET for imagining of advanced, vulnerable atherosclerotic lesions. |
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ISSN: | 0021-9150 1879-1484 |
DOI: | 10.1016/j.atherosclerosis.2006.07.019 |