Subclinical hypothyroidism and risk to carotid atherosclerosis

Valentina, Velkoska Nakova; Bosevski, Marijan; Chedo, Dimitrovski; Branka, Krstevska

doi:10.1590/s0004-27302011000700007

Cited by 50 publications

(41 citation statements)

References 26 publications

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“…Overt and subclinical hypothyroidism are well-established risk factors for atherosclerosis. 1,2 Patients with subclinical hypothyroidism are more likely to have an increased CIMT and a higher prevalence of carotid plaques, 1,17 and levothyroxine replacement therapy in these patients reduced CIMT and improved cardiovascular risk factor levels and endothelial function. 18,19 Studies of the association between thyroid hormone levels in the euthyroid range and atherosclerosis, however, have been inconsistent.…”

Section: Discussionmentioning

confidence: 99%

Thyroid Hormones and Coronary Artery Calcification in Euthyroid Men and Women

Zhang

Kim

Chang

et al. 2014

ATVB

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Objective— Overt and subclinical hypothyroidism are risk factors for atherosclerosis. It is unclear whether thyroid hormone levels within the normal range are also associated with atherosclerosis measured by coronary artery calcium (CAC). Approach and Results— We conducted a cross-sectional study of 41 403 apparently healthy young and middle-aged men and women with normal thyroid hormone levels. Free thyroxin, free triiodothyronine, and thyroid-stimulating hormone levels were measured by electrochemiluminescent immunoassay. CAC score was measured by multidetector computed tomography. The multivariable adjusted CAC ratios comparing the highest versus the lowest quartile of thyroid hormones were 0.74 (95% confidence interval, 0.60–0.91; P for trend <0.001) for free thyroxin, 0.81 (0.66–1.00; P for trend=0.05) for free triiodothyronine, and 0.78 (0.64–0.95; P for trend=0.01) for thyroid-stimulating hormone. Similarly, the odds ratios for detectable CAC (CAC >0) comparing the highest versus the lowest quartiles of thyroid hormones were 0.87 (0.79–0.96; P for linear trend <0.001) for free thyroxin, 0.90 (0.82–0.99; P for linear trend=0.02) for free triiodothyronine, and 0.91 (0.83–1.00; P for linear trend=0.03) for thyroid-stimulating hormone. Conclusions— In a large cohort of apparently healthy young and middle-aged euthyroid men and women, low-normal free thyroxin and thyroid-stimulating hormone were associated with a higher prevalence of subclinical coronary artery disease and with a greater degree of coronary calcification.

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Section: Discussionmentioning

confidence: 99%

Thyroid Hormones and Coronary Artery Calcification in Euthyroid Men and Women

Zhang

Kim

Chang

et al. 2014

ATVB

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“…The traditional theory held that insufficient thyroid hormone (TH) caused AS (Ichiki 2010). However, subclinical hypothyroidism (SCH) has also been related with AS (Valentina et al 2011). TH is maintained at normal levels in patients with SCH, whereas thyroid-stimulating hormone (TSH) is increased.…”

Section: Introductionmentioning

confidence: 99%

Effects of TSH on the function of human umbilical vein endothelial cells

Tian¹,

Zhang²,

Liu³

et al. 2014

Journal of Molecular Endocrinology

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Recent studies have reported that subclinical hypothyroidism (SCH) is associated with atherosclerosis (AS). Thyroid hormone is maintained at normal levels in patients with SCH, whereas TSH is increased. However, the pathogenesis of AS in association with SCH is only partially understood. In addition, endothelial dysfunction plays an important role in the development of AS. The purpose of the present research was to study the direct effect of TSH on human umbilical vein endothelial cells (HUVECs). The expression of some genes associated with endothelial dysfunction after treatment with TSH was evaluated by real-time PCR and western blotting respectively. At first, we showed that the TSH receptor (TSHR) is expressed in HUVECs. We also provide evidence indicating that TSH treatment promotes tumor necrosis factor a-induced endothelial cells interactions by upregulating the expression of the adhesion molecules intercellular adhesion molecule-1. Furthermore, the expression of endothelial nitric oxide synthase (eNOS) and prostacyclin (PGI 2 ) was significantly attenuated following treatment with TSH in dose-and time-dependent manner. Conversely, the results indicated that TSH upregulated endothelin-1 (ET1) mRNA and protein expression in HUVECs, similar effects were observed for plasminogen activator inhibitor-1 (PAI1) after treatment with various concentrations of TSH. Taken together, these results demonstrate that elevated TSH can promote endothelial dysfunction by altering gene expression in HUVECs.

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“…However, studies investigating the systolic and diastolic function of the heart in ScH showed controversial results. Some studies demonstrate mild diastolic dysfunction in patients with ScH [4][5][6][7][8][9], but not in others [10][11][12][13]. Diastolic dysfunction increases morbidity, leading to no effort tolerance and occurrence of heart failure.…”

Section: Introductionmentioning

confidence: 99%