RT Journal Article SR Electronic T1 PET/CT Imaging of Unstable Carotid Plaque with 68Ga-Labeled Somatostatin Receptor Ligand JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 774 OP 780 DO 10.2967/jnumed.116.181438 VO 58 IS 5 A1 Ming Young Simon Wan A1 Raymond Endozo A1 Sofia Michopoulou A1 Robert Shortman A1 Manuel Rodriguez-Justo A1 Leon Menezes A1 Syed Yusuf A1 Toby Richards A1 Damian Wild A1 Beatrice Waser A1 Jean Claude Reubi A1 Ashley Groves YR 2017 UL http://jnm.snmjournals.org/content/58/5/774.abstract AB 68Ga-labeled somatostatin receptor ligand PET imaging has recently been shown in preclinical and early human studies to have a potential role in the evaluation of vulnerable arterial plaques. We prospectively evaluated carotid plaque 68Ga-DOTATATE uptake in patients with recent carotid events, assessed inter- and intraobserver variability of such measurements, and explored the mechanism of any plaque DOTATATE activity with immunohistochemistry in resected specimens. Methods: Twenty consecutively consenting patients with recent symptomatic carotid events (transient ischemic attack, stroke, or amaurosis fugax), due for carotid endarterectomy, were prospectively recruited. 68Ga-DOTATATE PET/CT of the neck was performed before surgery. 68Ga-DOTATATE uptake was measured by drawing regions of interest along the carotid plaques and contralateral plaques/carotid arteries by an experienced radionuclide radiologist and radiographer. Two PET quantification methods with inter- and intraobserver variability were assessed. Resected carotid plaques were retrieved for somatostatin receptor subtype-2 (sst2) immunohistochemical staining. Results: The median time delay between research PET and surgery was 2 d. SUVs and target-to-background ratios for the symptomatic plaques and the asymptomatic contralateral carotid arteries/plaques showed no significant difference (n = 19, P > 0.10), regardless of quantification method. The intraclass correlation coefficient was greater than 0.8 in all measures of carotid artery/plaque uptake (SUV) and greater than 0.6 in almost all measures of target-to-background ratio. None of the excised plaques was shown to contain cells (macrophages, lymphocytes, vessel-associated cells) expressing sst2 on their cell membrane. Conclusion: 68Ga-DOTATATE activity on PET in recently symptomatic carotid plaques is not significantly different from contralateral carotids/plaques. Any activity seen on PET is not shown to be from specific sst2 receptor–mediated uptake in vitro. It is therefore unlikely that sst2 PET/CT imaging will have a role in the detection and characterization of symptomatic carotid plaques.