Dunphy Mark P S, Freiman Alvin, Larson Steven M, Strauss H William
Nuclear Medicine Service, Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
J Nucl Med. 2005 Aug;46(8):1278-84.
Both calcification and FDG uptake have been advocated as indicators of atheroma. Atheromas calcify as cells in the lesion undergo apoptosis and necrosis during evolution of the lesion and at the end stage of the lesion. FDG concentrates in lesions due to the relatively dense cellularity in regions of inflammation of active atheromas. This investigation examines the geographic relationship of focal vascular (18)F-FDG uptake, as a marker of atherosclerotic inflammation, to arterial calcification detected by contemporaneous CT.
We reviewed PET/CT images from 78 patients who were referred for tumor staging for the presence of vascular (18)F-FDG uptake and vascular calcification. Arterial wall (18)F-FDG accumulation greater than adjacent blood-pool activity was considered inflammation. Arterial attenuation of >130 Hounsfield units was considered calcification. Sites in the ascending and descending aorta, the carotid and iliac arteries, and the coronary territories were examined on the emission, CT, and fusion images on a point-by-point basis. When lesions were seen, we evaluated whether they were overlapping or discrete.
The (18)F-FDG arterial distribution was consistent with established atherosclerotic topography, with increased uptake in the thoracic aorta, at the carotid bifurcation, and in the proximal coronary vessels. Arteries typically displayed a patchwork of normal vessel, focal inflammation, or calcification; inflammation and calcification overlapped in <2% of cases. Arterial inflammation preceded calcification, in terms of mean patient age. Coronary inflammation was more prevalent in patients with more cardiovascular risk factors.
Vascular calcification and vascular metabolic activity rarely overlap, suggesting these findings represent different stages in the evolution of atheroma.
钙化和氟代脱氧葡萄糖（FDG）摄取均被认为是动脉粥样硬化的指标。在病变发展过程及病变末期，随着病变部位的细胞发生凋亡和坏死，动脉粥样硬化会发生钙化。由于活动性动脉粥样硬化炎症区域细胞相对密集，FDG会在病变部位聚集。本研究旨在探讨作为动脉粥样硬化炎症标志物的局灶性血管（18）F-FDG摄取与同期CT检测到的动脉钙化之间的空间关系。
我们回顾了78例因肿瘤分期而接受检查的患者的PET/CT图像，以确定是否存在血管（18）F-FDG摄取和血管钙化。动脉壁（18）F-FDG积聚大于相邻血池活性被视为炎症。动脉衰减大于130亨氏单位被视为钙化。在发射图像、CT图像和融合图像上逐点检查升主动脉和降主动脉、颈动脉和髂动脉以及冠状动脉区域的部位。发现病变时，我们评估它们是重叠还是离散。
（18）F-FDG的动脉分布与既定的动脉粥样硬化形态一致，在胸主动脉、颈动脉分叉处和冠状动脉近端摄取增加。动脉通常表现为正常血管、局灶性炎症或钙化的拼凑；炎症和钙化重叠的病例不到2%。就平均患者年龄而言，动脉炎症先于钙化出现。在心血管危险因素较多的患者中，冠状动脉炎症更为普遍。
血管钙化和血管代谢活性很少重叠，表明这些发现代表了动脉粥样硬化发展的不同阶段。
