Abstract 18807: Spatial Distribution of the Metabolically Active Pulmonary Circulation in Humans
Introduction: Human pulmonary perfusion is not homogeneously distributed. Analysis of pulmonary perfusion spatial distribution (SD) variations, could be useful in the evaluation of pulmonary disorders. We developed a new tracer called PulmoBind (PB), which binds to the adrenomedullin receptor abundantly expressed in the lung endothelium. Nowadays, all imagery methods rely on physical agents distributed within the pulmonary circulation and whose external signals are reflections of perfusion. There is no clinically validated imaging agent that relies on biologic functions of the endothelium properties and could quantitatively assess the spatial distribution of metabolic active pulmonary circulation (SDMAPC). The aim of this study was to determine the ability of the endothelial cell tracer PB to measure the SDMAPC in human.
Methods: Healthy subjects (n=20) were included in the PB phase I trial (NCT01539889). SPECT imaging was performed in the supine position 90 min after injection. SD was determined as mean activity as a function of cumulative voxels in the dorso-ventral (DV), caudo-cranial (CC) and saggital (S) axis.
Results: Mean peak PB uptake was 58±7% of the injected dose. Peak uptake indexed for body surface area correlated with age (-0.49, p=0.04) but not with creatinine clearance and respiratory function parameters. In the DV axis, vascular activity was greater in dorsal voxels with 18±2 % and 10±2% higher activity for the left (L) and right (R) lung respectively. There was more uniform activity in the CC axis but with a persistent gradient 15±1% (L) and 13±1% (R) higher in the caudal voxels. Finally, the analysis of S axis showed the presence of a gradient with 6±1% (L) and 8±1% (R) higher centro-peripheral activity.
Conclusion: PB SPECT imaging can be used to evaluate SDMAPC. As with other modalities, gravity-dependant and independent heterogeneity is suggested. Future trials are needed to evaluate the SD of PB and its variations in pulmonary vascular diseases.
Author Disclosures: X. Levac: None. F. Harel: None. V. Finnerty: None. Q. Nguyen: None. M. Letourneau: None. S. Marcil: None. A. Fournier: None. J. Dupuis: None.
- © 2014 by American Heart Association, Inc.