| Summary: | Ischemic vascular diseases are associated with elevated tissue expression of angiomotin (AMOT), a promising molecular target for PET imaging. On that basis, we developed an AMOT-targeting radiotracer, <sup>68</sup>Ga-sCD146 and performed the first in vivo evaluation on a myocardial infarction mice model and then, compared AMOT expression and α<sub>v</sub>β<sub>3</sub>-integrin expression with <sup>68</sup>Ga-sCD146 and <sup>68</sup>Ga-RGD<sub>2</sub> imaging. After myocardial infarction (MI) induced by permanent ligation of the left anterior descending coronary artery, myocardial perfusion was evaluated by Doppler ultrasound and by <sup>18</sup>F-FDG PET imaging. <sup>68</sup>Ga-sCD146 and <sup>68</sup>Ga-RGD<sub>2</sub> PET imaging were performed. In myocardial infarction model, heart-to-muscle ratio of <sup>68</sup>Ga-sCD146 imaging showed a significantly higher radiotracer uptake in the infarcted area of MI animals than in sham (* <i>p</i> = 0.04). Interestingly, we also observed significant correlations between <sup>68</sup>Ga-sCD146 imaging and delayed residual perfusion assessed by <sup>18</sup>F-FDG (* <i>p</i> = 0.04), with lowest tissue fibrosis assessed by histological staining (* <i>p</i> = 0.04) and with functional recovery assessed by ultrasound imaging (** <i>p</i> = 0.01). <sup>68</sup>Ga-sCD146 demonstrated an increase in AMOT expression after MI. Altogether, significant correlations of early post-ischemic <sup>68</sup>Ga-sCD146 uptake with late heart perfusion, lower tissue fibrosis and better functional recovery, make <sup>68</sup>Ga-sCD146 a promising radiotracer for tissue angiogenesis assessment after MI.
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