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Published on: December 2, 2014
Aortic stiffness and left ventricular function in patients with differentiated thyroid cancer
A Gazdag1, E V Nagy2, A Erdei2
1Division of Endocrinology, Department of Medicine, Faculty of Medicine, University of Debrecen, P.O.B. 19, Debrecen, 4012, Hungary. annamaria.gazdag@gmail.com.
Thyroxine therapy in differentiated thyroid cancer patients increases aortic stiffness due to subclinical hyperthyroidism and hypothyroidism. Minimizing TSH suppression is advised, especially for those with cardiovascular conditions.
Area of Science:
- Cardiology
- Endocrinology
- Oncology
Background:
- Differentiated thyroid cancer (DTC) patients undergo total thyroidectomy and radioiodine ablation.
- Thyroxine (L-T4) therapy is used for TSH suppression, potentially leading to subclinical hyperthyroidism or hypothyroidism.
- Cardiovascular impact of these thyroid states requires investigation.
Purpose of the Study:
- To assess aortic stiffness and left ventricular (LV) function in DTC patients.
- To compare cardiovascular effects during TSH-suppressive L-T4 therapy versus after L-T4 withdrawal.
- To evaluate the impact of subclinical hyperthyroidism and overt hypothyroidism on cardiovascular parameters.
Main Methods:
- Studied 24 DTC patients on L-T4 therapy and after withdrawal.
- Measured aortic stiffness, LV dimensions, ejection fraction, and diastolic function (E'/A') via echocardiography.
- Assessed thyroid function, lipids, vWF, and fibrinogen, comparing to 22 healthy controls.
Main Results:
- Aortic stiffness was significantly increased in both hypothyroidism and subclinical hyperthyroidism compared to controls.
- Subclinical hyperthyroidism demonstrated a more pronounced increase in aortic stiffness.
- LV dimensions and ejection fractions remained similar; E'/A' was reduced in both thyroid states versus controls.
Conclusions:
- Long-term TSH suppression in DTC patients adversely affects the arterial wall.
- Cardiovascular risks associated with TSH suppression warrant careful consideration.
- Minimize TSH suppression to the lowest effective level, balancing benefits and risks, particularly in patients with cardiovascular comorbidities.
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