Abstract
Papillary thyroid carcinoma (PTC) may contribute to cardiovascular (CV) morbidity through pro-inflammatory signaling and endothelial dysfunction, yet subclinical myocardial effects remain poorly characterized. While cardiovascular morbidity in papillary thyroid carcinoma (PTC) patients has largely been attributed to treatment-related factors such as TSH suppression, the potential contribution of the disease itself to early, subclinical cardiovascular vulnerability has not been well defined. To address this knowledge gap, we examined treatment-naïve PTC patients for evidence of subclinical cardiovascular dysfunction. This case-control study included 36 untreated PTC patients and 20 benign nodular goiter controls. Comprehensive cardiac assessment utilized transthoracic echocardiography, tissue Doppler imaging, and two-dimensional speckle-tracking echocardiography. Serum integrin αvβ3 and tumor necrosis factor-alpha (TNF-α) levels were quantified via enzyme-linked immunosorbent assay. Central thyroid hormone sensitivity was assessed using the Thyroid Feedback Quantile-based Index (TFQI). Compared with controls, patients with PTC exhibited evidence of subclinical myocardial functional alterations. Circulating integrin αvβ3 and TNF-α levels were significantly higher in patients with PTC. Integrin αvβ3 levels were associated with impaired GLS and diastolic dysfunction, whereas TNF-α showed no direct association with echocardiographic parameters. In addition, TFQI(FT4) levels were increased in PTC group and demonstrated a positive correlation with circulating integrin αvβ3 levels, as well as an association with impaired GLS. Treatment-naive, euthyroid patients with PTC exhibit early subclinical myocardial dysfunction despite preserved ejection fraction. Impairment in GLS, derived from echocardiographic assessment, is associated with circulating integrin αvβ3 and altered central thyroid hormone sensitivity, reflecting early CV alterations that warrant confirmation in longitudinal studies.