Abstract
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Objectives Atherosclerosis is well known as a basic pathogenesis of many diseases; including cerebro- and cardiovascular disease, aortic aneurysm / dissection and arteriosclerosis obliterans. However, the mechanism of atherosclerosis has not been fully revealed. Recently, 18F-sodium fluoride (18F-NaF) is developed as a non- invasive examination for coronary arteriosclerosis and aortosclerosis. To our knowledge, there have been few reports that evaluated the temporal changes of the calcified plaque with or without 18F-NaF uptake. For the quantitative analyses of arterial 18F-NaF uptake, the maximum target-to-background ratio (TBRmax) has been commonly used, however, it was known that TBRmax was greatly affected by blood activity. Recently, Blomberg et al. showed that the maximum blood-subtracted 18F-NaF activity (bsNaFmax) didn’t rely on blood activity in healthy subjects (J Nucl Med 2015). In this study, we investigated a correlation between the 18F-NaF uptake and the growth of calcified plaque in the aorta using standardized uptake value (SUV), TBRmax and bsNaFmax.
Methods The patient populations included 18 oncologic patients [ 9 women : 9 men ; mean age ± S.D. 62.5 ± 8.7 years; age range 48-78 years ] who had been enrolled for whole-body 18F-NaF PET/CT scan and follow-up unenhanced CT scan between August 2007 and February 2011. Image analyses of PET, CT and fusion images were evaluated visually and quantitatively using 3D volume analysis software (SYNAPSE VINCENT, FUJIFILM Medical, Tokyo, Japan). A quantitative analysis was performed using the maximum SUV (SUVmax), TBRmax, bsNaFmax. For the analysis of focal lesions, regions of interest (ROIs) were placed on the calcified plaques using the fusion images of PET and CT. The maximum and mean CT values (CTmax and CTmean; Hounsfield units (HU)) were evaluated at the sites of calcification in the aortic wall, which was defined as high attenuated lesions (>130 HU) or 18F-NaF-avid sites without high attenuation. CTmax, CTmean, and calcification volumetric score (mm3) were evaluated for each site. The follow-up CT performed one year after 18F-NaF PET were carried out by the same method. The increase of CTmax, CTmean and calcification volumetric score were calculated, and were expressed as ΔCTmax, ΔCTmean and Δcalcification volumetric score, respectively. Then, we assessed relationship between NaF uptake and calcified plaque volume obtained 1 year later.
Results We detected and analyzed 144 sites with high attenuation (>130 HU) or 18F-NaF uptake without high attenuation. Surprisingly, bsNaFmax and TBRmax had no correlation with CTmax, CTmean and calcification volumetric score. However, bsNaFmax showed a mild correlation with Δcalcification volumetric score (R2=0.245, P value<0.001) (Figure.1). The bsNaFmax had no significant correlation with ΔCTmax or ΔCTmean. Moreover, TBRmax didn’t correlate with Δcalcification volumetric score, ΔCTmax or ΔCTmean.
Conclusions TBRmax and bsNaFmax did not show significant relationships with CTmax, CTmean, and calcification volumetric score. However, only bsNaFmax showed a significant relationship with Δcalcification volumetric score. From our results, bsNaFmax was thought to be a good predictor of calcified atherosclerotic plaque growth and progression of atherosclerosis in the aorta.