PT - JOURNAL ARTICLE AU - Ziwei Zhu AU - Mingxin Gao AU - Mingkai Yun AU - Hongli Liu AU - Wenyuan Yu AU - Yang Yu AU - Xiang Li AU - Xiaoli Zhang TI - <strong>Clinical <sup>18</sup>F-NaF PET/CT imaging of coronary atherosclerosis in correlation with pathology and immunohistology: initial evidence</strong> DP - 2020 May 01 TA - Journal of Nuclear Medicine PG - 26--26 VI - 61 IP - supplement 1 4099 - http://jnm.snmjournals.org/content/61/supplement_1/26.short 4100 - http://jnm.snmjournals.org/content/61/supplement_1/26.full SO - J Nucl Med2020 May 01; 61 AB - 26Objectives: The role of 18F-NaF PET in atherosclerosis has been highly emphasized as a potential imaging marker of vulnerable plaques while the mechanism of 18F-NaF uptake in vulnerable plaques is still unclear. The aim of this study was to investigate the correlation between 18F-NaF uptake in coronary atherosclerosis and the immuno-pathological characteristics of atherosclerotic plaques. Methods: 71 coronary artery disease (CAD) patients who were referred to coronary artery bypass grafting (CABG) were prospectively recruited. Coronary endarterectomy was selectively performed. All patients underwent cardiac 18F-NaF PET/CT with acquisition for 20min after 2 hours of injection 18F-NaF (3.17Mbq/kg). Coronary lesions were precisely excised, which guided by CT and angiography’s landmarks. The corresponding target-to-background ratio (TBR) in individual lesion of coronary arteries was calculated by correcting the regional maximum standardized uptake value (SUVmax) by venous blood activity (SUVmean). Pathological (H&amp;E) and immunohistochemical (IHC) staining, including CD68 (monocyte/macrophages), osteogenetic biomarkers: osteopontin (OPN) and osteocalcin (OCN) were respectively conducted. All lesions were classified into stable and unstable plaques by two experienced pathologists. Correlation between atherosclerotic inflammatory expressed as mean IOD/area (5 views)and osteogenetic activity with 18F-NaF uptake were analyzed. Results: 37 coronary artery specimens (4 in D1 artery, 10 in LAD ,7 in OM, 4 in RCA, 10 in PDA) were collected for assessment (Lengthmean (cm)=1.67, range:0.30-7.30). TBR of 18F-NaF uptake was 1.80 (0.77-5.85). In comparison with stable plaques (n=10), intraplaque macrophage (CD68, %) was significantly increased in unstable plaques (n=27) (Mann-Whitney U test, 0.0064(0.0016-0.026) vs 0.0207(0.0055-0.0429), P = 0.04) while osteogenstic activity (OPN, OCN expression) was slightly increased in unstable plaques (P &gt; 0.05). (2) There was a significant correlation between CD68 and TBR of 18F-NaF uptake in all lesions (r = 0.437, P = 0.007), yet no significant correlation between osteogenesis and NaF uptake in all lesions (Fig.1).(3) Accordingly, lesions were classified into non-inflamed (&lt;0.02, n = 17) and inflamed lesion by the IOD/area of CD68 expression (:≥0.02, n = 20) , TBR in inflamed lesions was significantly higher than non-inflamed lesions (1.18 (1.00-1.70) vs. 1.69 (1.25-2.68), P = 0.013) (Fig.2). Conclusions: 18F-NaF uptake might be associated with inflammatory activity in coronary atherosclerotic plaques, but not correlated with the physiological activity of osteogenesis. Research Support: The Role of 18F-NaF PET/CT Imaging of Coronary Artery Calcification in CAD Patients, ChiCTR1900022527. This work was supported by National Natural Science Foundation of China [81871377, 81571717] and Capital Characteristic Clinical Application Research [Z181100001718071]