68Ga-FAPI PET visualize heart failure: from mechanism to clinic.

Purpose: Heart failure (HF) is a chronic progressive clinical syndrome associated with structural and/or functional heart abnormalities. Active fibroblasts and ventricular remodelling play an essential role in HF progression. 68Ga-labelled fibroblast activation protein (FAP) inhibitor (68Ga-FAPI) bi...

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Publicado en:European Journal of Nuclear Medicine & Molecular Imaging Vol. 50; no. 2; pp. 475 - 486
Autores principales: Song, Wenyu, Zhang, Xiao, He, ShuKun, Gai, Yongkang, Qin, Chunxia, Hu, Fan, Wang, Yan, Wang, Zhaohui, Bai, Peng, Wang, Jing, Lan, Xiaoli
Formato: Journal Article
Publicado: Springer Nature Jan2023
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jan2023
      vid: 50
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      pub: Springer Nature
      place: New York, New York
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        159782499
        10.1007/s00259-022-05994-4
        161159499
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        atl: 68Ga-FAPI PET visualize heart failure: from mechanism to clinic.
      aug:
        au:
          Song, Wenyu
          Zhang, Xiao
          He, ShuKun
          Gai, Yongkang
          Qin, Chunxia
          Hu, Fan
          Wang, Yan
          Wang, Zhaohui
          Bai, Peng
          Wang, Jing
          Lan, Xiaoli
        affil: Department of Nuclear Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      sug:
      ab: Purpose: Heart failure (HF) is a chronic progressive clinical syndrome associated with structural and/or functional heart abnormalities. Active fibroblasts and ventricular remodelling play an essential role in HF progression. 68Ga-labelled fibroblast activation protein (FAP) inhibitor (68Ga-FAPI) binds to FAP. This study aimed to examine the feasibility of using 68Ga-FAPI positron emission tomography (PET)/computed tomography (CT) to visualize changes in cardiac fibrosis and function over time in the HF setting. Methods: After establishing an isoproterenol (ISO)-induced HF rat model (14 consecutive days of intraperitoneal ISO injections), echocardiography and 68Ga-FAPI PET/CT were performed weekly in experimental and control groups. Rat hearts were examined weekly for biodistribution analysis; autoradiography; and haematoxylin and eosin, FAP immunofluorescence and Masson's trichrome staining analysis. Rat blood was sampled weekly for enzyme-linked immunosorbent assay analysis of various plasma indicators. A preliminary clinical study was also performed in seven HF patients who underwent both 13N-amino (NH3) perfusion and 68Ga-FAPI cardiac PET imaging. Results: In the animal experiments, myocardial 68Ga-FAPI uptake, expression of FAP and myocardial contractility peaked on day 7 after the initial ISO injection. Only slight fibrotic changes were observed on histopathological examination. 68Ga-FAPI uptake and ventricular wall motion decreased over time as cardiac fibrosis and degree of myocardial injury gradually increased. In the human HF patient study, 68Ga-FAPI PET imaging identified varying degrees of 68Ga-FAPI uptake in the myocardium that did not precisely match with 13N-NH3 myocardial perfusion. Conclusion: As HF progresses, 68Ga-FAPI uptake is high in the early stages and then gradually decreases. Although preliminary, our findings suggest that 68Ga-FAPI PET can be used to demonstrate active myocardial fibrosis. Active myocardial FAP expression is followed by myocardial remodelling and fibrosis. Detection of early active FAP expression may assist treatment decision making in HF patients. Clinical Trial Registration: NCT04982458
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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