Meiqi Wu1, Jing Ning2, Jingle Li2, Zhichao Lai3, Ximin Shi1, Haiqun Xing1, Marcus Hacker2, Bao Liu3, Li Huo4, Xiang Li2. 1. Department of Nuclear Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Center for Rare Diseases Research, Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China. 2. Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria; and. 3. Department of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. 4. Department of Nuclear Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Center for Rare Diseases Research, Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China; huoli@pumch.cn.
Abstract
Increased expression of fibroblast-activating protein (FAP) in fibrous caps may contribute to progression of atherosclerotic plaques. Methods: Forty-one patients who underwent 68Ga-conjugated quinoline-based FAP inhibitor (68Ga-FAPI-04) PET/CT for noncardiovascular indications were retrospectively analyzed. Correlations were assessed between the uptake of 68Ga-FAPI-04 in large arterial walls (SUVmax and target-to-background ratio, TBR) and degree of calcification and cardiovascular risk factors. Results: Focal arterial uptake of 68Ga-FAPI-04 or calcification was detected in 1,177 arterial segments in all 41 patients. TBR was negatively correlated with the degree of calcification (Hounsfield units) (r = -0.27, P < 0.01). Mean TBR in higher-risk patients was greater than in lower-risk patients (2.2 ± 0.3 vs. 1.8 ± 0.3, P < 0.01). Immunohistochemical labeling of carotid plaques exhibited prominent FAP expression in a thin fibrous cap and moderate FAP expression in a thick cap. Conclusion: 68Ga-FAPI-04 PET/CT might have potential for imaging fibroblastic activation in the arterial wall.
Increased expression of fibroblast-activating protein (FAP) in fibrous caps may contribute to progression of atherosclerotic plaques. Methods: Forty-one patients who underwent 68Ga-conjugated quinoline-based FAP inhibitor (68Ga-FAPI-04) PET/CT for noncardiovascular indications were retrospectively analyzed. Correlations were assessed between the uptake of 68Ga-FAPI-04 in large arterial walls (SUVmax and target-to-background ratio, TBR) and degree of calcification and cardiovascular risk factors. Results: Focal arterial uptake of 68Ga-FAPI-04 or calcification was detected in 1,177 arterial segments in all 41 patients. TBR was negatively correlated with the degree of calcification (Hounsfield units) (r = -0.27, P < 0.01). Mean TBR in higher-risk patients was greater than in lower-risk patients (2.2 ± 0.3 vs. 1.8 ± 0.3, P < 0.01). Immunohistochemical labeling of carotid plaques exhibited prominent FAP expression in a thin fibrous cap and moderate FAP expression in a thick cap. Conclusion: 68Ga-FAPI-04 PET/CT might have potential for imaging fibroblastic activation in the arterial wall.
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