[⁶⁸Ga]Ga-NODAGA-Arg-Gly-Asp (RGD) is a PET tracer targeting α_vβ₃ integrin, which is upregulated during angiogenesis soon after acute myocardial infarction (AMI). We prospectively evaluated determinants of myocardial uptake of [⁶⁸Ga]Ga-NODAGA-RGD and its associations with left ventricular (LV) function in patients after AMI.

Methods: Myocardial blood flow and [⁶⁸Ga]Ga-NODAGA-RGD uptake (60 min after injection) were evaluated by PET in 31 patients 7.7 ± 3.8 d after primary percutaneous coronary intervention for ST-elevation AMI. Transthoracic echocardiography of LV function was performed on the day of PET and at the 6-mo follow-up.

Results: PET images showed increased uptake of [⁶⁸Ga]Ga-NODAGA-RGD in the ischemic area at risk (AAR), predominantly in injured myocardial segments. The SUV in the segment with the highest uptake (SUV_max) in the ischemic AAR was higher than the SUV_mean of the remote myocardium (0.73 ± 0.16 vs. 0.51 ± 0.11, P < 0.001). Multivariable predictors of [⁶⁸Ga]Ga-NODAGA-RGD uptake in the AAR included high peak N-terminal pro–B-type natriuretic peptide (P < 0.001), low LV ejection fraction, low global longitudinal strain (P = 0.01), and low longitudinal strain in the AAR (P = 0.01). [⁶⁸Ga]Ga-NODAGA-RGD uptake corrected for myocardial blood flow and perfusable tissue fraction in the AAR predicted improvement in global longitudinal strain at follow-up (P = 0.002), independent of peak troponin, N-terminal pro–B-type natriuretic peptide, and LV ejection fraction.

Conclusion: [⁶⁸Ga]Ga-NODAGA-RGD uptake shows increased α_vβ₃ integrin expression in the ischemic AAR early after AMI that is associated with regional and global systolic dysfunction, as well as increased LV filling pressure. Increased [⁶⁸Ga]Ga-NODAGA-RGD uptake predicts improvement of global LV function 6 mo after AMI.