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      Hypothyroidism and Heart Failure: Epidemiology, Pathogenetic Mechanisms & Therapeutic Rationale

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          Abstract

          Heart Failure (HF) is a major public health problem and a major cause of morbidity and mortality worldwide. Thyroid hormones (TH) have multiple effects on the heart and cardiovascular system. In recent years, studies have shown that hypothyroidism, including subclinical hypothyroidism, is associated with an increased risk for developing and worsening of HF. This review addresses the relationship between HF and hypothyroidism by highlighting the epidemiology, pathophysiology and management.

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          Most cited references32

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          Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases.

          The goal of this review is to place the exciting advances that have occurred in our understanding of the molecular biology of the types 1, 2, and 3 (D1, D2, and D3, respectively) iodothyronine deiodinases into a biochemical and physiological context. We review new data regarding the mechanism of selenoprotein synthesis, the molecular and cellular biological properties of the individual deiodinases, including gene structure, mRNA and protein characteristics, tissue distribution, subcellular localization and topology, enzymatic properties, structure-activity relationships, and regulation of synthesis, inactivation, and degradation. These provide the background for a discussion of their role in thyroid physiology in humans and other vertebrates, including evidence that D2 plays a significant role in human plasma T(3) production. We discuss the pathological role of D3 overexpression causing "consumptive hypothyroidism" as well as our current understanding of the pathophysiology of iodothyronine deiodination during illness and amiodarone therapy. Finally, we review the new insights from analysis of mice with targeted disruption of the Dio2 gene and overexpression of D2 in the myocardium.
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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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              The Colorado thyroid disease prevalence study.

              The prevalence of abnormal thyroid function in the United States and the significance of thyroid dysfunction remain controversial. Systemic effects of abnormal thyroid function have not been fully delineated, particularly in cases of mild thyroid failure. Also, the relationship between traditional hypothyroid symptoms and biochemical thyroid function is unclear. To determine the prevalence of abnormal thyroid function and the relationship between (1) abnormal thyroid function and lipid levels and (2) abnormal thyroid function and symptoms using modern and sensitive thyroid tests. Cross-sectional study. Participants in a statewide health fair in Colorado, 1995 (N = 25 862). Serum thyrotropin (thyroid-stimulating hormone [TSH]) and total thyroxine (T4) concentrations, serum lipid levels, and responses to a hypothyroid symptoms questionnaire. The prevalence of elevated TSH levels (normal range, 0.3-5.1 mIU/L) in this population was 9.5%, and the prevalence of decreased TSH levels was 2.2%. Forty percent of patients taking thyroid medications had abnormal TSH levels. Lipid levels increased in a graded fashion as thyroid function declined. Also, the mean total cholesterol and low-density lipoprotein cholesterol levels of subjects with TSH values between 5.1 and 10 mIU/L were significantly greater than the corresponding mean lipid levels in euthyroid subjects. Symptoms were reported more often in hypothyroid vs euthyroid individuals, but individual symptom sensitivities were low. The prevalence of abnormal biochemical thyroid function reported here is substantial and confirms previous reports in smaller populations. Among patients taking thyroid medication, only 60% were within the normal range of TSH. Modest elevations of TSH corresponded to changes in lipid levels that may affect cardiovascular health. Individual symptoms were not very sensitive, but patients who report multiple thyroid symptoms warrant serum thyroid testing. These results confirm that thyroid dysfunction is common, may often go undetected, and may be associated with adverse health outcomes that can be avoided by serum TSH measurement.
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                Author and article information

                Journal
                101737788
                48175
                Int J Clin Res Trials
                Int J Clin Res Trials
                International journal of clinical research & trials
                2456-8007
                9 June 2020
                1 June 2020
                2020
                02 July 2020
                : 5
                : 1
                : 146
                Affiliations
                Department of Medicine, SUNY-Downstate Health Science University, Brooklyn, New York, USA
                Author notes
                [* ] Corresponding Author: Prof. Samy I. McFarlane, College of Medicine, Department of Medicine, Division of Endocrinology, Internal Medicine Residency Program Director, State University of New York, Downstate Medical Center, 450 Clarkson Ave, Box 50, Brooklyn, New York, USA, Tel 718-270-6707, Fax 718-270-4488; smcfarlane@ 123456downstate.edu
                Article
                NIHMS1600817
                10.15344/2456-8007/2020/146
                7331968
                32617437
                ca17826d-b79c-4073-968b-6eaa6401740c

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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                Categories
                Article

                heart failure,hypothyroidism,subclinical hypothyroidism,pathogenesis

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