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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, 68 Ga-sCD146 and performed the first in vivo evaluation on a myocardial infarction mice model and then, compared AMOT expression and α v β 3 -integrin expression with 68 Ga-sCD146 and 68 Ga-RGD 2 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 18 F-FDG PET imaging. 68 Ga-sCD146 and 68 Ga-RGD 2 PET imaging were performed. In myocardial infarction model, heart-to-muscle ratio of 68 Ga-sCD146 imaging showed a significantly higher radiotracer uptake in the infarcted area of MI animals than in sham (* p = 0.04). Interestingly, we also observed significant correlations between 68 Ga-sCD146 imaging and delayed residual perfusion assessed by 18 F-FDG (* p = 0.04), with lowest tissue fibrosis assessed by histological staining (* p = 0.04) and with functional recovery assessed by ultrasound imaging (** p = 0.01). 68 Ga-sCD146 demonstrated an increase in AMOT expression after MI. Altogether, significant correlations of early post-ischemic 68 Ga-sCD146 uptake with late heart perfusion, lower tissue fibrosis and better functional recovery, make 68 Ga-sCD146 a promising radiotracer for tissue angiogenesis assessment after MI.

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Comparison of a New 68Ga-Radiolabelled PET Imaging Agent sCD146 and RGD Peptide for In Vivo Evaluation of Angiogenesis in Mouse Model of Myocardial Infarction