Molecular Imaging of Fibroblast Activity After Myocardial Infarction Using a 68Ga-Labeled Fibroblast Activation Protein Inhibitor, FAPI-04
Ex vivo
DOI:
10.2967/jnumed.119.226993
Publication Date:
2019-08-12T18:29:05Z
AUTHORS (14)
ABSTRACT
Heart failure remains a major source of late morbidity and mortality after myocardial infarction (MI). The temporospatial presence activated fibroblasts in the injured myocardium predicts quality cardiac remodeling MI. Therefore, monitoring is great interest for studying Fibroblast activation protein (FAP) expression upregulated fibroblasts. This study investigated feasibility imaging with new <sup>68</sup>Ga-labeled FAP inhibitor (<sup>68</sup>Ga-FAPI-04) PET fibroblast preclinical model <b>Methods:</b> MI sham-operated rats were scanned <sup>68</sup>Ga-FAPI-04 PET/CT (1, 3, 6, 14, 23, 30 d MI) <sup>18</sup>F-FDG (3 MI). Dynamic blocking studies performed on 7 coronary ligation. After vivo scans, animals euthanized their hearts harvested ex analyses. Cryosections prepared autoradiography, hematoxylin eosin (H&E), immunofluorescence staining. <b>Results:</b><sup>68</sup>Ga-FAPI-04 uptake peaked day 6 tracer accumulated intensely territory, as identified by decreased confirmed PET/MR H&E Autoradiography staining cross-sections revealed that mainly at border zone infarcted myocardium. In contrast, there was only minimal infarct blocked rats, comparable to remote noninfarcted (PET image–derived ratio uptake: ± 2). Immunofluorescence FAP-positive myofibroblasts Morphometric analysis whole-heart sections demonstrated 3- 8-fold higher density than center area, respectively. <b>Conclusion:</b><sup>68</sup>Ga-FAPI-04 represents promising radiotracer post-MI activation. Noninvasive may have significant diagnostic prognostic value, which could aid clinical management patients
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