Abstract

Introduction: Up-regulation of somatostatin receptor subtype-2 (SST2) has been observed on the cell surface of activated macrophages, where it can potentially be exploited as a molecular imaging target to identify high-risk plaque. Hypothesis: We tested the hypothesis that SST2 vascular PET imaging with 68Ga-DOTATATE can reveal high-risk plaque in patients with atherosclerosis, and compared with 18F-FDG. Methods: Prospective sequential 68Ga-DOTATATE and 18F-FDG PET imaging plus CT angiography was performed in 39 patients with atherosclerosis. Results: A total of 36 carotid arteries and 40 coronary plaques were analyzed. Mean age 69.5 ± 9.5 yrs, 76.9% male. Median (IQR) 68Ga-DOTATATE TBRmax was significantly higher in recently symptomatic carotid arteries compared to: 1) the contralateral side [p=0.0013], 2) stable carotid plaques [p<0.0001] and 3) normal carotid arteries [p<0.0001] Figs A and B. 18F-FDG TBRmax was also higher on the symptomatic side [1.60 (1.44-1.88) vs. 1.56 (1.31-1.78), p=0.0024]. Unlike 18F-FDG, myocardial 68Ga-DOTATATE binding was sufficiently low to allow coronary artery analysis in all patients. Culprit coronary plaques imaged 33 (21-62) days post-ACS had higher 68Ga-DOTATATE TBRmax compared to both stable stented plaques [p = 0.04] and stable calcific plaques [p <0.0001]; however the highest signal occurred in relation to soft lipid-rich plaques. Conclusion: Measuring vascular inflammation with SST2 PET is feasible and differentiates high and low risk lesions. High target specificity, low myocardial binding and generator production offer potential advantages of 68Ga-DOTATATE over 18F-FDG and other tracers for imaging atherosclerosis.

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