Abstract / Summary
Abstract Background Childhood obesity predisposes to early cardiovascular risk, and subclinical hypothyroidism — elevated thyroid-stimulating hormone with normal free thyroxine — is more prevalent in obese children and may compound vascular risk. We aimed to evaluate its association with echocardiographic aortic elasticity in obese children aged 5–18 years. We hypothesized that subclinical hypothyroidism would be associated with reduced aortic elasticity. Methods In this prospective cross-sectional study, 82 obese children (5–18 years) presenting to the Pediatric Endocrinology and Pediatric Cardiology clinics of Kütahya Health Sciences University City Hospital (March 2024–March 2025) were enrolled: 41 with mild subclinical hypothyroidism (thyroid-stimulating hormone 4.5–10 mIU/mL) and 41 euthyroid controls. Aortic strain, distensibility, stiffness index, and pressure–strain elastic modulus were calculated from M-mode echocardiography. Results Aortic elasticity parameters did not differ between the subclinical hypothyroidism and control groups (all p>0.05). Aortic diastolic diameter, glucose, and aspartate aminotransferase were significantly higher in children with thyroid-stimulating hormone of 7 mIU/mL or higher (p = 0.042, 0.036, and 0.026). In an exploratory, Bonferroni-corrected regression analysis, systolic blood pressure was the only independent predictor of aortic elasticity; thyroid-stimulating hormone showed no independent association with any parameter. Conclusions Subclinical hypothyroidism was not associated with measurable changes in aortic elasticity, refuting our hypothesis. A thyroid-stimulating hormone threshold of 7 mIU/mL or higher identified a subgroup with increased aortic diastolic diameter and metabolic perturbation, though this was not confirmed within the subclinical hypothyroidism group alone and did not survive Bonferroni correction. Systolic blood pressure, not thyroid-stimulating hormone, emerged as the independent correlate of aortic elasticity.