Key result
Levothyroxine-treated women with Hashimoto thyroiditis had significantly higher pulsatility indexes in the common and internal carotid arteries than untreated euthyroid patients (adjusted P<0.05).
Why the study?
Does levothyroxine replacement therapy increase carotid pulsatility index in women with Hashimoto thyroiditis?
Case-Control (n=57)
Does levothyroxine replacement therapy increase carotid pulsatility index in women with Hashimoto thyroiditis?
p-value: p=0.0224 (PI CCA) and 0.0477 (PI ICA)
Women with Hashimoto thyroiditis on levothyroxine replacement therapy have increased pulsatility index in common and internal carotid arteries compared to nontreated euthyroid patients, suggesting hypothyroidism influences arterial stiffness.
Increased carotid PI in L-T4-treated HT women suggests possible hemodynamic effects; leaves open whether therapy or residual factors drive stiffness in this observational data.
The aim of this case-control study was to evaluate carotid hemodynamic variables and traditional cardiovascular risk factors in women with Hashimoto thyroiditis (HT). The study group consisted of 31 females with HT on levothyroxine (L-T4) and 26 euthyroid women with HT without L-T4 matched for age and body mass index (BMI) as controls. Carotid intima-media thickness (CIMT), carotid extra-media thickness (CEMT), and pulsatility indexes in common carotid artery (PI CCA) and in internal carotid artery (PI ICA) were measured. BMI, waist circumference, lipid profile, fasting glucose and insulin levels, and parameters of thyroid function [TSH, free thyroxine (FT4) and antithyroperoxidase antibodies (TPOAbs)] were assessed. The study and the control groups did not differ in age, BMI, waist circumference, lipid profile, fasting glucose, and insulin levels. Results are expressed as median (IQR). Treated HT group had higher FT4 levels than nontreated [17.13 (5.11) pmol/l vs. 14.7 (2.27) pmol/l; p=0.0011] and similar TSH [1.64 (2.08) IU/ml vs. 2.07 (3.14) IU/ml; p=0.5915]. PI CCA and PI ICA were higher in the study group than in controls (p=0.0224 and p=0.0477, respectively). The difference remained statistically significant for PI ICA and PI CCA after adjustment for other variables (coefficient=0.09487; standard error=0.04438; p=0.037 and coefficient=0.1786; standard error=0.0870; p=0.0449, respectively). CIMT and CEMT were similar in both groups (p=0.8746 and p=0.0712, respectively). Women with HT on L-T4 replacement therapy have increased PI in common and internal carotid arteries than nontreated euthyroid HT patients. Therefore, it seems that hypothyroidism, but not autoimmune thyroiditis per se, influences arterial stiffness.
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Owecki et al. (2015) conducted a case-control in Hashimoto thyroiditis (n=57). Levothyroxine (L-T4) treatment vs. Euthyroid women with Hashimoto thyroiditis without L-T4 was evaluated on Pulsatility indexes in common carotid artery (PI CCA) and internal carotid artery (PI ICA) (p=0.0224 (PI CCA) and 0.0477 (PI ICA)). Levothyroxine-treated women with Hashimoto thyroiditis had significantly higher pulsatility indexes in the common and internal carotid arteries than untreated euthyroid patients (adjusted P<0.05).
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