Associations of Subclinical Microcalcification and Inflammation with Carotid Atheroma Development: a Dual-tracer PET/CT Study
Overview
Nuclear Medicine
Radiology
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Purpose: Carotid artery atherosclerosis, a significant manifestation of cardiovascular disease (CVD) and leading cause of stroke, develops through a gradual process of arterial inflammation and calcification. This study explores the relationship between arterial inflammation (18 F-FDG PET/CT) and vascular calcification (18 F-NaF PET/CT) in the left and right common carotid arteries (LCC/RCC) and their association with CVD and thromboembolic risk in patients with subclinical atherosclerosis.
Methods: A cohort of 115 subjects (73 healthy volunteers, 42 at-risk for CVD) underwent 18 F-NaF and 18 F-FDG PET/CT imaging. Radiotracer uptake was quantitatively assessed by measuring the average blood-pool-corrected mean standardized uptake value (aSUVmean).
Results: Relative to healthy volunteers, at-risk subjects had greater uptake of NaF and FDG (10-22% and 16-27% higher, respectively, in both arteries, p < 0.05). On multivariate regression, NaF aSUVmean correlated with age and BMI (p < 0.01), and FDG aSUVmean correlated with BMI (p ≤ 0.01), fibrinogen (p < 0.01 in LCC only), and total cholesterol (p = 0.02 in RCC only). NaF aSUVmean increased with elevated 10-year CVD risk (p = 0.003 in LCC only), while no significant trend was seen for FDG. NaF and FDG aSUVmean increased with elevated thromboembolic risk in both arteries (p < 0.05). No correlations between NaF and FDG aSUVmean were observed (p > 0.05).
Conclusion: 18 F-NaF PET/CT may serve as a prognostic tool for carotid microcalcification and subclinical atherosclerosis, while the utility of 18 F-FDG PET/CT remains uncertain.
Clinical Trial Registration: "Cardiovascular Molecular Calcification Assessed by 18F-NaF PET CT (CAMONA)", NCT01724749, https://clinicaltrials.gov/study/NCT01724749 .
Xie W, Cao L, Yu J, Tian A, Wang J, Lin R BMC Med Imaging. 2025; 25(1):81.
PMID: 40055673 PMC: 11889901. DOI: 10.1186/s12880-025-01617-0.