Laurberg Jacob Marsvin, Olsen Aage Kristian, Hansen Søren Baarsgaard, Bottcher Morten, Morrison Matthew, Ricketts Sally-Ann, Falk Erling
Department of Cardiology and Institute of Clinical Medicine, Aarhus University Hospital (Skejby), Aarhus, Denmark.
Atherosclerosis. 2007 Jun;192(2):275-82. doi: 10.1016/j.atherosclerosis.2006.07.019. Epub 2006 Aug 21.
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.
Nine atherosclerotic apoE-deficient mice were PET scanned. Four to determine optimal timing for imaging, and five post mortem after 1h 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.
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).
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.
需要用于评估人类和实验动物动脉粥样硬化的非侵入性方法。研究表明,FDG-PET有检测易损、炎症性动脉粥样硬化病变的潜力。
对9只动脉粥样硬化载脂蛋白E缺陷小鼠进行PET扫描。4只用于确定成像的最佳时机,5只在FDG重新分布1小时后进行尸检,并在依次切除肩胛间棕色脂肪和动脉粥样硬化主动脉弓后再次进行尸检。测量禁食(n = 13)和非禁食(n = 7)载脂蛋白E缺陷小鼠各种组织的摄取情况,包括动脉粥样硬化和非动脉粥样硬化主动脉。最后,通过颈动脉结扎诱导加速动脉粥样硬化(n = 12),并测量FDG摄取情况。
记录到最初认为与动脉粥样硬化主动脉弓相对应的FDG积聚。切除肩胛间棕色脂肪而非动脉粥样硬化主动脉弓后,信号消失。在禁食(比值0.5,p = 0.008)和非禁食(比值0.33,p = 0.02)条件下,主动脉弓积聚的FDG均少于非动脉粥样硬化胸主动脉。与未结扎动脉相比,颈动脉粥样硬化同样未能增加FDG摄取(比值1.03)。
矛盾的是,主动脉中自发形成的晚期动脉粥样硬化病变与FDG摄取减少相关,颈动脉加速动脉粥样硬化也未能增加FDG摄取。这些结果严重质疑了FDG-PET对晚期、易损动脉粥样硬化病变成像的潜力。