Background: The kinetics of para-[18F]fluorobenzylguanidine ([18F]PFBG) were investigated in a canine coronary artery occlusion model.
Methods and results: Five dogs were imaged by positron emission tomography (PET) before and after complete surgical ligation of the left anterior descending coronary artery. PET studies included a 10-minute dynamic [13N]NH3 perfusion scan, followed 1 hour later by 3-hour dynamic [18F]PFBG scanning. [18F]PFBG and [13N]NH3 images demonstrated homogeneous myocardial uptake/perfusion before infarction. One hundred eighty minutes after [18F]PFBG administration, myocardial accumulation was decreased by 60% (day 2, 0.0065% +/- 0.0015% injected dose/ml) and 58% (day 16, 0.0069% +/- 0.003% injected dose/ml) compared with a similar myocardial region of interest from the preinfarction (0.016% +/- 0.005% injected dose/ml) study. Myocardial accumulation of [13N]NH3 at 9 minutes showed a 52% (day 2) and 7% (day 16) decrease compared with the preinfarction study. The accumulation of [18F]PFBG in the infarction was decreased significantly at 120 and 180 minutes on all postinfarction studies (p = 0.01). In three dogs a significant decrease in the myocardial norepinephrine concentration was documented in the area of infarction (237 +/- 94 ng/gm) versus the noninfarcted (1018 +/- 48 ng/gm) myocardium (p = 0.001).
Conclusions: A decreased accumulation of [18F]PFBG was observed in the area of myocardial infarct in this canine model. The magnitude of the decrease in [18F]PFBG was larger than that seen with [13N]NH3 on day 16 after infarction, suggesting reperfusion and persistent sympathetic neuronal dysfunction.