Abstract
The aim of this study is to document the impact of thyroid hormones on pulmonary hypertension (PH). In two groups of hyperthyroid patients, one with Graves� disease and other with non-autoimmune aetiology, we have determined, by means of echocardiography, the estimated systolic pulmonary artery pressure (PAPs). We have documented an increased incidence of PH and statistically significant correlations between PAPs levels and free thyroxine (FT4), thyroid stimulating hormone (TSH) and TSH receptor antibodies (TRAb) and with the duration of hyperthyroidism. The severity of PH correlates with the severity and duration of hyperthyroidism. PAPs levels declined gradually, under specific therapy.
Highlights
The aim of this study is to document the impact of thyroid hormones on pulmonary hypertension (PH)
To limit the influence of other factors on the apparition of group 5 PH, we excluded all patients with haematological, systemic, metabolic or other diseases or chronic renal failure that could induce this form of PH, as well as all subjects treated with vasoactive drugs
1.Right atrial (RA), right ventricle (RV) diameter and tricuspid regurgitation (TR) velocity (TRV); 2.Estimated systolic pulmonary artery pressure (PAPs) (PAPs); in this study we considered that PAPs values ≥ 35 mmHg, indicates PH (3, 10) with severity ranging from mild (35-49 mmHg), to moderate (50-69 mmHg) and severe (≤70mmHg) [14, 15]
Summary
The aim of this study is to document the impact of thyroid hormones on pulmonary hypertension (PH). In two groups of hyperthyroid patients, one with Graves’ disease and other with non-autoimmune aetiology, we have determined, by means of echocardiography, the estimated systolic pulmonary artery pressure (PAPs). Hormones exert their effects on myocytes by genomic and nongenomic mechanisms. Their excess induces tachycardia and increased inotropism, leading to high cardiac output, elevated circulatory volume [8], followed by left ventricular (LV) hypertrophy, diastolic and systolic dysfunction. In some pathologies (Graves’ and Hashimoto disease) there are autoimmune processes, involving thyroid stimulating hormone (TSH) receptor antibodies (TRAb) that could mediate endothelial cells injury [9] and vascular remodelling, leading to aggravation of PH [10, 11]. Evidencing PH could be difficult and assessing mean PAP and PVR implies right heart catheterization, but echocardiography offers the possibility to estimate them accurately without the risks of invasive procedures [14, 15]
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