Ascending thoracic aorta 18F-FDG PET-CT uptake in hypertensive breast cancer patients: a marker for vascular disease?

Background High blood pressure (HBP) is a known cardiovascular risk factor (CVRF) linked to atherosclerosis and thoracic aorta aneurysms, potentially driven by pro-inflammatory metabolism induced by the oscillating shear stress. Fluorodeoxyglucose (18F-FDG), a glucose analogue, is used for breast cancer (BC) stating and treatment monitoring. We hypothesized that patients with HBP, but no thoracic aorta disease may exhibit increased thoracic aortic 18F-FDG uptake, indicating vascular inflammation. Purpose To evaluate thoracic aortic 18F-FDG uptake as a marker of vascular inflammation in BC patients with HBP but no thoracic aorta disease. Methods Single-centre retrospective observational study of consecutive women under 55 years with BC, who underwent staging with 18F-FDG PET/CT prior to treatment between 2018 and 2021. 18F-FDG vascular uptake was obtained as tissue-to-background ratio (TBR) by measuring maximum standard uptake value (SUV) in the aorta, avoiding spill over from adjacent structures. The lesion maximum SUV was corrected for blood pool activity by dividing it by right atrium mean SUV. 18F-FDG tumour uptake was obtained as metabolic tumour volume (MTV). Total lesion glycolysis (TLG) was the product of MTV and tumour medium SUV. Primary endpoint was the evidence of increased vascular thoracic aorta metabolism in patients with BC and HBP. Data was collected through revision of informatized clinical files. Statistical analysis used Kolmogorov-Smirnov, T Student test, and non-parametric equivalents. Results 45 women with BC were included. Mean age was 43.3±7.59 years, 4 (8.89%) had HBP. Mean follow-up time was 47±14.9 months. Mean ascending thoracic aorta TBR was 1.75±0.57, median aortic cross TBR was 1.68±0.73 and mean descending thoracic aorta TBR was 2.11±0.64. A statistically significant relation between HBP and TBR was showed for the ascending thoracic aorta (p-value=0.039) but not for the aortic cross (p-value=0.093) nor the descending thoracic aorta (p-value=0.383). All patients had normal-sized ascending thoracic aorta, with a median dimension of 31.0 (±4.50) mm. Correlation between ascending thoracic aorta TBR and both MTV (p-value=0.811) and TLG (p-value=0.856) was not statistically significant. All-cause mortality was 22.2% (n=10), with no cardiovascular (CV) mortality or significant CV events. Conclusion In BC patients with HBP, increased 18F-FDG uptake in the ascending thoracic aorta suggests vascular inflammation, potentially contributing to atherosclerosis and thoracic aortic aneurysms. Larger prospective studies with extended follow-up are required to confirm if this inflammation predisposes to cardiovascular events.