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      The role of thyroid hormones in acute coronary syndromes: Prognostic value of alterations in thyroid hormones : Prognostic value of alterations in thyroid hormones

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          Abstract

          <p class="first" id="clc22689-para-0001">The prognosis of acute coronary syndromes ( <span style="fixed-case">ACS</span>) is affected by many factors. Normal thyroid homeostasis is known to alter during various critical illnesses, a condition that has been shown to correlate with the severity of the disease and increased mortality. The purpose of this article is to review literature to emphasize the considerable association of thyroid function with the cardiovascular system and summarize all existing evidence with regard to the role of thyroid hormones alterations during <span style="fixed-case">ACS</span>. The electronic databases of <span style="fixed-case">PubMed</span>, Medline, Scopus, and Cochrane were searched for relevant literature and studies. Alterations in thyroid hormone plasma concentrations, especially low triiodothyronine ( <span style="fixed-case">T3</span>) levels, represent a hormonal imbalance that is not uncommon among patients suffering an acute coronary event. Many studies have identified this abnormal thyroid hormonal status to be related to worse prognosis. Although further large‐scale clinical trials are needed, the low <span style="fixed-case">T3</span> syndrome manifesting in patients during <span style="fixed-case">ACS</span> might be useful in prognostic stratification. </p>

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          Most cited references31

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          Thyroid disease and the heart.

          The cardiovascular signs and symptoms of thyroid disease are some of the most profound and clinically relevant findings that accompany both hyperthyroidism and hypothyroidism. On the basis of the understanding of the cellular mechanisms of thyroid hormone action on the heart and cardiovascular system, it is possible to explain the changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm disturbances that result from thyroid dysfunction. The importance of the recognition of the effects of thyroid disease on the heart also derives from the observation that restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics. In the present review, we discuss the appropriate thyroid function tests to establish a suspected diagnosis as well as the treatment modalities necessary to restore patients to a euthyroid state. We also review the alterations in thyroid hormone metabolism that accompany chronic congestive heart failure and the approach to the management of patients with amiodarone-induced alterations in thyroid function tests.
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            Thyroid hormone action in the heart.

            The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiac function in patients with hypo- or hyperthyroidism. T(3)-induced changes in cardiac function can result from direct or indirect T(3) effects. Direct effects result from T(3) action in the heart itself and are mediated by nuclear or extranuclear mechanisms. Extranuclear T(3) effects, which occur independent of nuclear T(3) receptor binding and increases in protein synthesis, influence primarily the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T(3) effects are mediated by the binding of T(3) to specific nuclear receptor proteins, which results in increased transcription of T(3)-responsive cardiac genes. The T(3) receptor is a member of the ligand-activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. T(3) also leads to an increase in the speed of diastolic relaxation, which is caused by the more efficient pumping of the calcium ATPase of the sarcoplasmic reticulum. This T(3) effect results from T(3)-induced increases in the level of the mRNA coding for the sarcoplasmic reticulum calcium ATPase protein, leading to an increased number of calcium ATPase pump units in the sarcoplasmic reticulum.
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              Mechanisms behind the non-thyroidal illness syndrome: an update.

              The mechanisms behind the changes in serum triiodothyronine (T(3)), thyroxine (T(4)) and TSH that occur in the non-thyroidal illness syndrome (NTIS) are becoming clearer. Induction of a central hypothyroidism occurs due to a diminution in hypothalamic thyrotropin-releasing hormone. This can be signalled by a decrease in leptin caused by malnutrition and possibly a localised increase in hypothalamic T(3) catalyzed by altered expression of hypothalamic iodothyronine deiodinases D2 and D3. Data from D1 and D2 knockout mice suggest that these enzymes may have little contribution to the low serum T(3) found in acute illness. The decline in serum T(3) and T(4) in models of acute illness precedes the fall in hepatic D1, suggesting that much of the initial fall in these hormones may be attributable to an acute phase response giving rise to a reduction in the thyroid hormone binding capacity of plasma. When measured by reliable methods, changes in serum free T(4) and free T(3) are modest in comparison to the fall seen in total thyroid hormone. Thyroid hormone transporter expression is up-regulated in many models of the NTIS, thus if diminished tissue uptake of hormone occurs in vivo, it is likely to be the result of impaired transporter function caused by diminished intracellular ATP or plasma inhibitors of transporter action. In man, chronic illness leads to an upregulation of thyroid hormone receptor (THR) expression at least in liver and renal failure. In contrast, human and animal models of sepsis and trauma indicate that expression of THRs and their coactivators are decreased in acute illness.
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                Author and article information

                Journal
                Clinical Cardiology
                Clin Cardiol
                Wiley
                01609289
                August 2017
                August 2017
                March 10 2017
                : 40
                : 8
                : 528-533
                Affiliations
                [1 ]National and Kapodistrian University of Athens; Medical School, MSc “Cardiopulmonary Resuscitation,”; Athens Greece
                [2 ]Department of Cardiology; General Hospital of Nikea; Piraeus Greece
                [3 ]Department of Cardiology; Evangelismos General Hospital of Athens; Athens Greece
                [4 ]Intensive Care Unit; KAT Hospital; Athens Greece
                [5 ]European University Cyprus; School of Medicine; Nicosia Cyprus
                Article
                10.1002/clc.22689
                6490650
                28295435
                bbf9c652-2c74-4846-96d6-79ea9ade5fe6
                © 2017

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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