Institute of Nuclear Medicine, University College London, London, UK.
J Nucl Med. 2011 Nov;52(11):1698-703. doi: 10.2967/jnumed.111.093724. Epub 2011 Oct 11.
Inflammation and angiogenesis are hypothesized to be important factors contributing to plaque vulnerability, whereas calcification is suggested to confer stability. To investigate this in vivo, we combined CT angiography and PET and compared the findings with immunohistochemistry for patients undergoing carotid endarterectomy.
Twenty-one consecutive patients (18 men, 3 women; mean age ± SD, 68.3 ± 7.3) undergoing carotid endarterectomy were recruited for combined carotid (18)F-FDG PET/CT angiography. Plaque (18)F-FDG uptake was quantified with maximum standardized uptake value, and CT angiography quantified percentage plaque composition (calcium and lipid). Surgical specimens underwent ex vivo CT aiding image registration, followed by immunohistochemical staining for CD68 (macrophage density) and vascular endothelial growth factor (angiogenesis). Relationships between imaging and immunohistochemistry were assessed with Spearman rank correlation and multivariable regression.
The mean (±SD) surgically excised carotid plaque (18)F-FDG metabolism was 2.4 (±0.5) versus 2.2 (±0.3) contralaterally (P = 0.027). There were positive correlations between plaque (18)F-FDG metabolism and immunohistochemistry with CD68 (ρ = 0.55; P = 0.011) and vascular endothelial growth factor (ρ = 0.47; P = 0.031). There was an inverse relationship between plaque (18)F-FDG metabolism and plaque percentage calcium composition on CT (ρ = -0.51; P = 0.018) and between calcium composition and immunohistochemistry with CD68 (ρ = -0.57; P = 0.007). Regression showed that maximum standardized uptake value and calcium composition were independently significant predictors of angiogenesis, and calcium composition was a predictor of macrophage density.
We provide in vivo evidence that increased plaque metabolism is associated with increased biomarkers of angiogenesis and inflammation, whereas plaque calcification is inversely related to PET and histologic biomarkers of inflammation.
炎症和血管生成被认为是导致斑块易损性的重要因素，而钙化被认为赋予斑块稳定性。为了在体内研究这一点，我们结合 CT 血管造影和 PET，比较了接受颈动脉内膜切除术的患者的免疫组织化学检查结果。
连续招募了 21 名接受颈动脉内膜切除术的患者（18 名男性，3 名女性；平均年龄±标准差，68.3±7.3 岁）进行颈动脉（18）F-FDG PET/CT 血管造影检查。采用最大标准化摄取值定量斑块（18）F-FDG 摄取，CT 血管造影定量斑块成分（钙和脂质）百分比。手术标本行离体 CT 辅助图像配准，然后进行 CD68（巨噬细胞密度）和血管内皮生长因子（血管生成）的免疫组织化学染色。采用 Spearman 秩相关和多变量回归评估影像学和免疫组织化学之间的关系。
手术切除的颈动脉斑块（18）F-FDG 代谢平均值（±标准差）为 2.4（±0.5）与对侧 2.2（±0.3）相比（P=0.027）。斑块（18）F-FDG 代谢与 CD68（ρ=0.55；P=0.011）和血管内皮生长因子（ρ=0.47；P=0.031）的免疫组织化学呈正相关。斑块（18）F-FDG 代谢与 CT 斑块百分比钙成分呈负相关（ρ=-0.51；P=0.018），钙成分与 CD68 的免疫组织化学呈负相关（ρ=-0.57；P=0.007）。回归分析显示，最大标准化摄取值和钙成分是血管生成的独立显著预测因子，钙成分是巨噬细胞密度的预测因子。
我们提供了体内证据表明，斑块代谢增加与血管生成和炎症的生物标志物增加有关，而斑块钙化与 PET 和炎症的组织学生物标志物呈负相关。
