Hyperthyroidism and Pulmonary Hypertension: An Important Association

Vallabhajosula, Sailaja; Radhi, Saba; Alalawi, Raed; Raj, Rishi; Nugent, Kenneth; Çevik, Cihan

doi:10.1097/maj.0b013e31821790f4

Cited by 42 publications

(39 citation statements)

References 50 publications

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“…Although hyperthyroidism has been associated with pulmonary hypertension in adults,8 neonatal thyrotoxicosis presenting with PPHN is extremely rare, and to the best of our knowledge, there are only two such cases reported in the literature to date. Markham and Stevens3 reported an infant born at 34 weeks gestation, who developed neonatal thyrotoxicosis with PPHN and was managed with propranolol and oxygen.…”

Section: Discussionmentioning

confidence: 96%

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Neonatal thyrotoxicosis presenting as persistent pulmonary hypertension

et al. 2012

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Section: Discussionmentioning

confidence: 96%

“…Proposed mechanisms include high cardiac output-induced endothelial injury, impaired production and increased metabolism of intrinsic pulmonary vasodilating substances (NO, prostacylcin, etc), and decreased clearance of pulmonary artery vasoconstrictors (serotonin, endothelin-1 and thromboxane) 4 8…”

Section: Discussionmentioning

confidence: 99%

Neonatal thyrotoxicosis presenting as persistent pulmonary hypertension

et al. 2012

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“…47 One small observational study of 63 patients with PAH found that approximately half of these patients had concomitant autoimmune thyroid disease. 46 One case report noted a prevalence of 6.7% of thyroid-stimulating immunoglobulin-negative thyrotoxicosis in patients with preexisting PAH being treated with epoprostenol.…”

Section: Introductionmentioning

confidence: 99%

“…Case reports support that the treatment of hyperthyroidism by antithyroid medications, radioactive iodine, surgery or a combination is associated with decreased pulmonary artery pressure. 47 The potential effects of calcium blockers, endothelin receptor blockers, phosphodiesterase 5 inhibitors, or prostacyclins in patients with PH and thyroid disease are not known.…”

Section: Introductionmentioning

confidence: 99%

Group 5 Pulmonary Hypertension

Kalantari

Gomberg‐Maitland

2016

Cardiology Clinics

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“…7 Pulmonary artery hypertension (PAH) is an increase in mean pulmonary arterial pressure ≥ 25 mm Hg at rest. 4 Higher pressure in the left atrium increases pressure in the pulmonary veins, which stimulates baroreceptors and causes a reflex contraction in the arterioles.…”

Section: Pulmonary Hypertensionmentioning

confidence: 99%

Hypothyroidism and the Heart

Osuna

Udovcic

Sharma

2017

Methodist DeBakey Cardiovascular Journal

131

123

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Thyroid hormones greatly impact energy homeostasis in the heart, and excess thyroid hormone leads to a hypermetabolic state. The thyroid gland produces two hormones, thyroxine (T4) and triiodothyronine (T3). The major form of thyroid hormone is thyroxine, which acts mostly as a prohormone. 1 The set point for thyroid hormone production and secretion by the thyroid gland is regulated by the hypothalamic thyrotropin-releasing hormone (TRH), which stimulates the production and secretion of thyroid stimulating hormone (TSH) that, in turn, controls thyroid hormone concentrations. Most of T4 is converted to biologically active T3 through the removal of an iodide by deiodinases. While there are three types of deiodinases, most of the circulating T3 is derived from Type 1; Type 1 activates thyroid hormone by converting T4 to active T3, and it deactivates thyroid hormone by converting T4 to inactive reverse T3 (rT3) or to T2.2 It is important to note that there is no significant intracellular deiodinase activity in cardiac cells; therefore, the heart relies mainly on the action of T3 since that is the hormone transported into the myocyte.3 Both T4 and T3 circulate in the blood almost entirely (> 95%) bound to thyroxine-binding globulin and a family of other hormone-binding proteins. The remaining unbound T3 is transported through a variety of membrane transport proteins and subsequently to the cell nucleus to regulate expression of selected genes. 4 Molecular Mechanisms of Thyroid Hormone ActionThe intracellular cardiac effects of thyroid hormone are exerted by two mechanisms: genomic and nongenomic. Several of the main effects are exerted through genomic actions, which consist of T3 linking to nuclear receptors that bind to thyroid-responsive elements (TREs) in the promoter of target genes. 5 There are several key myocyte-specific genes regulated by this mechanism (Table 1). 3 Binding of thyroid hormone to these TREs can either activate or repress gene expression, thereby regulating the expression of specific messenger RNA and translated proteins and producing different tissue-specific responses. Importantly, thyroid hormone-regulated genes are also involved in structural and regulatory proteins, and long-term exposure to high T3 levels can increase the synthesis of cardiac proteins, leading to cardiac hypertrophy and dysfunction. Extranuclear nongenomic activities provoke rapid changes in the cardiac myocyte plasma membrane and cytoplasmic organelles. These include changes in sodium, potassium, and calcium ion channels; changes in actin cytoskeleton polymerization; and changes to the intracellular signaling pathways in the heart and smooth muscle cells.Both genomic and nongenomic mechanisms act together to regulate cardiac function and cardiovascular hemodynamics.2 For example, they upregulate expression of the sarcoplasmic reticulum calcium-activated ATPase and downregulate phospholamban expression, thereby enhancing myocardial relaxation. They also increase expression of the more rapid contractile isoforms of the myo...

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Hyperthyroidism and Pulmonary Hypertension: An Important Association

Cited by 42 publications

References 50 publications

Neonatal thyrotoxicosis presenting as persistent pulmonary hypertension

Neonatal thyrotoxicosis presenting as persistent pulmonary hypertension

Group 5 Pulmonary Hypertension

Hypothyroidism and the Heart

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