[68Ga]Pentixafor PET/MR imaging of chemokine receptor 4 expression in the human carotid artery
[68Ga]Pentixafor PET/MR imaging of chemokine receptor 4 expression in the human carotid artery
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[68 Ga] Pentixa用于人颈动脉中趋化因子受体4表达的PET/MR成像
DOI：
10.1007/s00259-019-04322-7
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发表时间：
2019-07-01
影响因子：
9.1
通讯作者：
Hacker, Marcus
中科院分区：
文献类型：
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作者：
Li, Xiang;Yu, Wei;Hacker, Marcus
目的趋化因子受体4（CXCR 4）在动脉粥样硬化（AS）过程中对免疫细胞迁移起重要作用。我们的目的是评估[Ga-68]喷替沙的正电子发射断层扫描（PET）结合磁共振成像（MRI）在体内定量CXCR 4表达在颈动脉plaque.MethodsSeventy-two淋巴瘤患者进行了前瞻性的全身[Ga-68]喷替沙的PET/MRI与一个额外的T2加权颈动脉序列。沿颈动脉分叉区域沿着绘制感兴趣区域（VOI），并计算[Ga-68]喷替卡松摄取的最大组织-血液比（TBR）。病变分为非偏心性（n=27），轻度偏心性（n=67），中度（n=41）和重度（n=19）偏心性颈动脉粥样硬化。另一组有症状的颈动脉狭窄患者（n=10）计划进行血栓动脉内膜切除术（TEA），分别采用3 T MRI和专用斑块序列（飞行时间、T1和T2加权）进行成像。MRI结果与完整颈动脉斑块的组织化学评估相关。结果在混合PET/MRI中，我们观察到轻度脑梗死患者的[Ga-68]喷替沙星摄取显著增加，（平均TBRmax=1.570.27，平均SUVmax=2.51 +/- 0.39），中度（平均TBRmax=1.64 +/- 0.37，平均SUVmax=2.61 +/- 0.55）和严重偏心性颈动脉（平均TBRmax=1.55 +/- 0.26，平均SUVmax=2.40 +/- 0.44）与非偏心性颈动脉（平均TBRmax=1.29 +/- 0.21，平均SUVmax=1.77 +/- 0.42）相比（p <0.05）。TEA的组织学结果证实，突出的CXCR 4表达位于发炎的动脉粥样硬化和动脉粥样硬化前。结论应用[Ga-68] PentixaforPET/MRI技术在颈动脉粥样硬化斑块中检测CXCR 4的表达是可行的。在动脉粥样硬化斑块组织中，CXCR 4的表达可能被用作炎性动脉粥样硬化的替代标志物。
PurposeType 4 chemokine receptor (CXCR4) plays an important role in immune cell migration during the atherosclerosis progression. We aimed to evaluate [Ga-68]Pentixafor positron emission tomography (PET) in combination magnetic resonance imaging (MRI) for in vivo quantification of CXCR4 expression in carotid plaques.MethodsSeventy-two patients with lymphoma were prospectively scheduled for whole body [Ga-68]Pentixafor PET/MRI with an additional T2-weighted carotid sequence. Volumes of interest (VOIs) were drawn along the carotid bifurcation regions, and the maximum tissue-to-blood ratios (TBR) of [Ga-68]Pentixafor uptake were calculated. Lesions were categorized into non-eccentric (n=27), mild eccentric (n=67), moderately (n=41) and severely (n=19) eccentric carotid atherosclerosis. A different cohort of symptomatic patients (n=10) with carotid stenosis scheduled for thrombendarterectomy (TEA) was separately imaged with 3T MRI with dedicated plaque sequences (time of flight, T1-, and T2-weighted). MRI findings were correlated with histochemical assessment of intact carotid plaques.ResultsAt hybrid PET/MRI, we observed significantly increased [Ga-68]Pentixafor uptake in mildly (mean TBRmax=1.570.27, mean SUVmax=2.51 +/- 0.39), moderately (mean TBRmax=1.64 +/- 0.37, mean SUVmax=2.61 +/- 0.55) and severely eccentric carotids (mean TBRmax=1.55 +/- 0.26, mean SUVmax=2.40 +/- 0.44) as compared to non-eccentric carotids (mean TBRmax=1.29 +/- 0.21, mean SUVmax=1.77 +/- 0.42) (p0.05). Histological findings from TEA confirmed that prominent CXCR4 expression was localized within inflamed atheromas and preatheromas. Co-localization of cellular CXCR4 and CD68 expression in the plaque was observed by immunofluorescence staining.Conclusions p id=Par4 In vivo evaluation of CXCR4 expression in carotid atherosclerotic lesions is feasible using [Ga-68]Pentixafor PET/MRI. In atherosclerotic plaque tissue, CXCR4 expression might be used as a surrogate marker for inflammatory atherosclerosis.