Longitudinal [18F]FDG PET/MR assessment of arterial inflammation in prostate cancer patients undergoing androgen deprivation therapy

Background Androgen deprivation therapy (ADT) improves outcomes in advanced prostate cancer, but it is associated with increased cardiovascular (CV) morbidity and mortality. Arterial inflammation, measurable by [¹⁸F]FDG PET, may represent an intermediate pathway linking ADT to CV risk. This study aimed to quantify intra-individual changes in arterial inflammation on [¹⁸F]FDG PET/MR before and after ADT, characterize their temporal trajectory, and identify associated clinical factors. Methods This retrospective, single-center study included men with histologically confirmed prostate cancer who underwent [¹⁸F]FDG PET/MR. Maximum standardized uptake value (SUVmax) 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 maximum target-to-background ratios (TBRmax) by normalizing arterial SUVmax to the blood-pool SUVmax of the superior vena cava (supradiaphragmatic) or inferior vena cava (infradiaphragmatic). Segmental values were aggregated into All-Artery, Aorta, and Branch (carotid and iliac) composite measures. Pre–post changes were tested using paired t-tests, and longitudinal trajectories were modeled with linear mixed-effects models. Subgroup analyses explored associations with age, diabetes, prior CV disease, and statin or antiplatelet therapy. Results Forty-three men with prostate cancer underwent [18F]FDG PET/MR before ADT and during ongoing therapy. ADT was associated with significant intra-individual 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 (1.64 ± 0.24 to 1.78 ± 0.25; p = 0.005), and ascending aorta (1.77 ± 0.28 to 1.97 ± 0.40; p = 0.02). The descending thoracic aorta showed a numerical increase that approached significance (1.82 ± 0.38 to 1.97 ± 0.40; p = 0.054). As a group, all-artery, aorta, and branch territories TBRmax composites increased significantly (all p < 0.001). Longitudinal models showed progressive, time-dependent rises in TBRmax in iliac arteries (0.0205/month; p < 0.001), carotid arteries (0.0123/month; p < 0.001), and abdominal aorta (0.0098/month; p = 0.038). Subgroup analyses indicate that ADT-associated vascular inflammation occurs broadly across age, diabetes, and CV disease strata. Patients on statins or antiplatelet therapy exhibited attenuated progression, particularly in the aortic arch group and the branch composite group. Conclusions In patients with prostate cancer, ADT is associated with consistent and progressive arterial inflammation, showing on intra-individual increases in large-artery [¹⁸F]FDG uptake, most prominently in carotid, iliac, and abdominal aortic regions. Statin or antiplatelet therapies may help to mitigate this vascular effect.