[⁶⁸Ga]Ga-NODAGA-E[(cRGDyK)]₂ Angiogenesis PET/MR in a Porcine Model of Chronic Myocardial Infarction

Angiogenesis is crucial in tissue repair and prevents scar tissue formation following an ischemic event such as myocardial infarction. The ischemia induces formation of new capillaries, which have high expression of integrin α_vβ₃. [⁶⁸Ga]Ga-NODAGA-E[(cRGDyK)]₂ ([⁶⁸Ga]Ga-RGD) is a promising PET-radiotracer reflecting angiogenesis by binding to integrin α_vβ₃. A Göttingen mini-pig underwent transient catheter-induced left anterior descending artery (LAD) occlusion for 120 min, and after 8 weeks was imaged on a Siemens mMR 3T PET/MR system. A large antero-septal infarction was evident by late gadolinium enhancement (LGE) on the short axis and 2-4 chamber views. The infarcted area corresponded to the area with high [⁶⁸Ga]Ga-RGD uptake on the fused PET/MR images, with no uptake in the healthy myocardium. To support the hypothesis that [⁶⁸Ga]Ga-RGD uptake reflects angiogenesis, biopsies were sampled from the infarct border and healthy myocardium. Expression of α_vβ₃ was evaluated using immunohistochemistry. The staining showed higher α_vβ₃ expression in the capillaries of the infarct border compared to those in the healthy myocardium. These initial data confirm in vivo detection of angiogenesis using [⁶⁸Ga]Ga-RGD PET in a translational model, which overall support the method applicability when evaluating novel cardio-protective therapies.