New insight of functional molecular imaging into the atheroma biology: 18F-NaF and 18F-FDG in symptomatic and asymptomatic carotid plaques after recent CVA. Preliminary results

Summary Aim The identification of the vulnerable atheroma plaque could allow a more effective treatment of cerebrovascular accident (CVA). Active calcification and inflammation of the carotid atheroma were assessed and compared in symptomatic and asymptomatic plaques by 18F‐NaF and 18F‐FDG PET/CT. Methods Nine patients investigated for recent CVA and no preventive treatment with statins were enrolled. In each patient, at least one atheroma plaque was detected by CT angiogram. In total, 18 plaques were available: 9 symptomatic and 9 asymptomatic. 18F‐NaF uptake and 18F‐FDG uptake by each plaque were assessed visually and semiquantitatively by calculating target/background ratios (TBRs) and TBR indexes (TBR symptomatic/TBR asymptomatic and 18F‐NaF TBR/18F‐FDG TBR within each of the 2 clinical groups of plaques). Results All plaques showed 18F‐NaF and 18F‐FDG uptake, and semiquantitation showed higher 18F‐NaF uptake by 11 of the 18 plaques, 6 symptomatic and 5 asymptomatic. In the symptomatic group, the mean 18F‐NaF TBR was 2·12 ± 0·44, and in the asymptomatic group, it was 1·85 ± 0·46. The 18F‐NaF/18F‐FDG showed that, overall, 18F‐NaF uptake is higher than 18F‐FDG. In the symptomatic plaques, the 18F‐NaF was higher for the low calcium content and the lowest for the high. Conclusion Active calcification and inflammation are simultaneous processes in the symptomatic and asymptomatic carotid atheroma. However, active calcification seems predominant over inflammation in both groups. In the symptomatic plaques, the highest 18F‐NaF uptake does not correspond with the largest calcium content. These patterns open new insights on the role of 18F‐NaF in the study of calcification and in the identification of the vulnerable carotid atheroma.