Para-[18F]fluorobenzylguanidine kinetics in a canine coronary artery occlusion model.

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.