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Longitudinal [18F]FDG PET/MR Assessment of Arterial Inflammation in Patients With Prostate Cancer Undergoing Androgen
Song Xue1, Chenming Hu2, Lianghua Li3
1Division of Nuclear Medicine, Department of Biomedical Imaging and Image-guided Therapy, Vienna General Hospital (S.X., H.E., M.H., X.L.), Medical University of Vienna, Austria.
Background:
Androgen deprivation therapy (ADT) improves outcomes in advanced prostate cancer but is associated with increased cardiovascular morbidity and mortality. Arterial inflammation, measurable by [18F]fluorodeoxyglucose positron emission tomography, may represent an intermediate pathway linking ADT to cardiovascular risk. We quantified intraindividual changes in arterial inflammation on [18F]fluorodeoxyglucose positron emission tomography/magnetic resonance across ADT exposure, characterized their temporal trajectory, and explored associated clinical factors.
Methods:
Forty-three men with prostate cancer underwent 2 longitudinal [18F]fluorodeoxyglucose positron emission tomography/magnetic resonance examinations across the course of ADT exposure. The maximum standardized uptake value was measured in the common carotid arteries, aortic arch, ascending and descending thoracic aorta, abdominal aorta, and common iliac arteries. Arterial inflammation was expressed as the maximum target-to-background ratio (TBRmax) by normalizing arterial (maximum standardized uptake value) to the venous blood-pool mean standardized uptake value. Segmental values were aggregated into all-artery, aorta, and branch composite measures. Paired changes were assessed using paired tests, and longitudinal trajectories were modeled using linear mixed-effects models.
Results:
ADT was associated with significant intraindividual increases in TBRmax in the carotid arteries (1.54±0.32 to 1.75±0.31; P<0.001), abdominal aorta (1.89±0.39 to 2.19±0.36; P<0.001), common iliac arteries (1.88±0.45 to 2.24±0.54; P<0.001), aortic arch (P=0.005), and ascending aorta (P=0.02). All-artery, aorta, and branch composite TBRmax increased significantly (all P<0.001). Longitudinal models showed progressive, time-dependent rises in TBRmax, with the largest monthly increments in iliac arteries (0.0205/mo; P<0.001), carotid arteries (0.0123/mo; P<0.001), and abdominal aorta (0.0098/mo; P=0.038).
Conclusions:
In patients with prostate cancer, ADT is associated with consistent and progressive arterial inflammation, most prominently in carotid, iliac, and abdominal aortic regions. These findings support arterial inflammation as a potential imaging phenotype of ADT-associated cardiovascular risk.
