Abstract WMP114: Imaging of 68Ga-prgd2 Pet/ct for Integrin αvß3 in Cerebral Small Vascular Disease
Background: Angiogenesis was identified in severe intracranial artery stenosis/occlusion patient. The purpose of this study was to identify endogenous angiogenesis in SVD patients.
Methods: We measured expression of integrin αvß3 using 68Ga-S-2-(isothiocyanatobenzyl)-1, 4, 7-triazacyclononane-1, 4, 7-triacetic acid-PEG3-E[c(RGDyK)]2 (68Ga-PRGD2) PET in 9 patients with SVD. Additionally, all patients underwent18F-FDG PET and 13N-Amonia PET to evaluate the metabolism and cerebral blood flow. 8 patients underwent Mini-Mental State Examination (MMSE). All patients were given informed consent.
Results: 68Ga-PRGD2 uptake was indentified around white matter lesion and subcortical infarcts as punctiform in 9 patients, and the maximum standardized uptake values (SUVmax) of 68Ga-PRGD2 around lesions were significantly higher than those in the normal brain (0.18±0.067 vs 0.06±0.029, mean±SD, P<0.001). Cerebral blood flow has a positive correlation with cerebral metabolism and negative correlation with MMSE score, no significant correlation with 68Ga-PRGD2 uptake (r=-0.368, P=0.092)
Conclusion: The present study shows that there is angiogenesis in human cerebral SVD for the first time. No significant correlation between CBF and angiogenesis suggests complicated mechanisms of angiogenesis in SVD, which needs further investigation.
Figure 1. MRI FLAIR showed diffuse white matter lesions( A).. 68Ga-PRGD2 uptake was identified as punctiform around the WMLs (B.). 13N-Amonia PET image(C) , 18F-FDG PET image(D).
Figure 2. Correlation between 68Ga-PRGD2, 18F-FDG and 13N-Amonia
Author Disclosures: S. Shu: None. Z. Zhu: None. Y. Zhu: None. J. Ni: None. L. Zhou: None. M. Yao: None. L. Cui: None. F. Li: None. B. Peng: None.
- © 2016 by American Heart Association, Inc.