A Retrospective Case-Control Study Examining the Association of Thyroid-Stimulating Hormone Suppression and Vascular Wall Inflammation on [F]FDG-PET/CT.

This retrospective case-control study aimed to investigate the effects of thyroid-stimulating hormone (TSH) suppression on vascular wall inflammation, assessed by [F]-fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT). Vascular [F]FDG-uptake is highly correlated with arterial inflammation, which represents a major risk factor for atherosclerotic plaques. Forty patients with differentiated thyroid cancer underwent [F]FDG-PET/CTs under TSH suppression therapy following surgical removal of the thyroid and subsequent radioiodine ablation. The [F]FDG-uptake was measured in the carotid arteries, aortic arch, and the ascending, descending, and abdominal aorta. All measurements in the PET scans were normalized to body weight and corrected for blood pool activity in the superior vena cava, creating target-to-background ratios (TBRs). Twenty-five patients with euthyroid hormone status were used as a control group. In addition, to evaluate long-term changes, the follow-up PET/CTs of 24 thyroid carcinoma patients under continued TSH suppression therapy were analyzed. In patients with TSH suppression, significantly higher arterial [F]FDG-uptake ( < 0.001) was observed in the ascending aorta, aortic arch, abdominal aorta, carotid artery, and for all arterial vessels combined (mean TBR ± standard deviation [SD]: 1.8 ± 0.4, 1.8 ± 0.3, 1.9 ± 0.4, 1.4 ± 0.3, 1.7 ± 0.2, respectively) compared with the euthyroid control group (TBR ± SD: 1.4 ± 0.2, 1.4 ± 0.2, 1.4 ± 0.2, 1.1 ± 0.2, 1.3 ± 0.1, respectively). In the subgroup of patients who received an additional follow-up scan after a mean duration of 1.9 ± 1.1 years of continued TSH suppression therapy, no significant changes in arterial [F]FDG-uptake were found in the five arterial sites when both scans were compared over time ( > 0.05). Our study suggests that patients under TSH suppression may experience a significant increase in vascular [F]FDG-uptake, a marker of arterial inflammation, and, therefore, might be at higher risk for cardiovascular disease. Interestingly, the duration of TSH suppression was not significantly associated with vascular [F]FDG-uptake in our study, indicating that the observed increase in arterial inflammation may not be influenced by the duration of TSH suppression.