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Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
Abnormal endothelial function in female patients with hypothyroidism and borderline thyroid function
Anna G Dagre1, John P Lekakis, Athanassios D Protogerou
1Vascular Laboratory, Department of Clinical Therapeutics, Alexandra University Hospital, 23 Ikarias Street, 14578 Ekali, Athens, Greece. annadagre@hotmail.com
Insights
Hypothyroidism is linked to endothelial dysfunction, impacting blood vessel health. Treatment for hypothyroidism normalizes this function, suggesting a role in cardiovascular disease prevention.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Vascular Biology
Background:
- Hypothyroidism is a potential risk factor for cardiovascular disease.
- Endothelial function is crucial for vascular health and NO-dependent vasodilation.
- Assessing endothelial function in hypothyroidism can elucidate cardiovascular risk pathways.
Purpose of the Study:
- To evaluate nitric oxide-dependent endothelial function in resistance arteries of individuals with varying degrees of hypothyroidism.
- To investigate the relationship between thyroid-stimulating hormone (TSH) levels and endothelial function.
- To determine if L-thyroxine therapy improves endothelial function in hypothyroidism.
Main Methods:
- Ninety-six female subjects were categorized into five groups based on TSH levels, including controls, upper normal TSH, subclinical hypothyroidism, overt hypothyroidism, and treated hypothyroidism.
- Forearm blood flow response during reactive hyperemia was measured using venous occlusion strain-gauge plethysmography to assess endothelial function.
- Statistical analysis, including ANOVA, was employed to compare groups and assess correlations.
Main Results:
- Duration of reactive hyperemia, a measure of endothelial function, significantly differed among the hypothyroidism groups (p<0.001).
- Endothelial function was impaired in subjects with upper normal TSH and subclinical hypothyroidism compared to controls, and significantly worse in overt hypothyroidism.
- A significant negative linear correlation was observed between duration of reactive hyperemia and TSH levels (r=-0.383, p<0.001).
Conclusions:
- Endothelial dysfunction is present in the microvasculature of patients with hypothyroidism, worsening with increased TSH levels.
- This endothelial dysfunction may contribute to the increased cardiovascular disease risk associated with hypothyroidism.
- Effective L-thyroxine therapy for hypothyroidism appears to restore normal endothelial function.
Background:
It has been suggested that hypothyroidism is associated with an increased risk for cardiovascular disease. The aim of this study was to assess non-invasively NO-dependent endothelial function of resistance arteries in subjects with hypothyroidism of varying severity.
Methods:
Ninety-six female subjects (aged: 42+/-13 years) comprised the study population. Subjects were divided into five groups based on TSH levels at presentation: Group 0 (n=23) with TSH: 0.3-2.0 microU/ml, Group 1 (n=22) with TSH: 2.1-4.0 microU/ml (upper normal), Group 2 (n=18) with TSH: 4.1-10 microU/ml (subclinical hypothyroidism), Group 3 (n=22) with TSH >10 microU/ml (overt hypothyroidism). One additional group with well-controlled hypothyroidism on L-thyroxine therapy (Group 4, n=11, TSH: 0.3-2.0 microU/ml) was also studied. Endothelial function of resistance arteries was assessed by measuring forearm blood flow response during reactive hyperemia utilizing venous occlusion strain-gauge plethysmography.
Results:
Duration of reactive hyperemia was significantly different among groups of subjects with varying hypothyroidism (83.7+/-58.3 s, 53.2+/-35.7 s, 52.8+/-47.5 s, 12.9+/-13.3 s and 69.5+/-26.2 s in Groups 0, 1, 2, 3 and 4, respectively, p<0.001, ANOVA). Duration of reactive hyperemia was significantly shorter in subjects with upper normal TSH values (Group 1) compared to controls (53.2+/-35.7 s vs. 83.7+/-58.3 s, p=0.013), while it was comparable to that of subjects with subclinical hypothyroidism (Group 2) (52.8+/-47.5 s). However, duration of reactive hyperemia in Group 1 was significantly longer compared to Group 3 (overt hypothyroidism) (53.2+/-35.7 s vs. 12.9+/-13.3 s, p=0.002). Similarly, duration of reactive hyperemia in subjects with subclinical hypothyroidism was significantly longer compared to subjects with overt hypothyroidism (52.8+/-47.5 s vs. 12.9+/-13.3 s, p=0.003). Duration of reactive hyperemia in Group 4 (well-controlled hypothyroidism on L-thyroxine therapy) did not differ significantly compared to controls. There was a highly significant linear correlation between duration of reactive hyperemia and TSH (r=-0.383, p<0.001).
Conclusion:
Endothelial dysfunction was detected in the microvasculature of patients with hypothyroidism. Duration of reactive hyperemia decreased with increasing TSH levels. Since endothelial dysfunction is a factor leading to atherosclerosis, this abnormality may partly explain predisposition of patients with thyroid failure to cardiovascular disease.
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