Subclinical thyroid dysfunctions are defined by normal free-triiodothyronine (FT3) and free-thyroxine (FT4) concentrations in the presence of abnormal TSH, which is low-undetectable in subclinical hyperthyroidism (SH) and increased in subclinical hypothyroidism (Sh). The clinical significance of subclinical thyroid dysfunction is much debated (1-3). The presence of tissue effects, symptoms and signs of mild thyroid hormone excess or deficiency and the management and treatment of these conditions are controversial issues. Similarly, the TSH cut-off point that determines the effects of subclinical thyroid dysfunction remains to be established. The cardiovascular system, which is a major target of thyroid hormone, is sensitive to the effects of thyroid hormone excess or deficiency at the tissue level. Many symptoms and signs in patients with overt hypo- or hyperthyroidism are related to the reduced or increased action of thyroid hormone on cardiac function. Triiodothyronine (T3) affects the heart and vascular system through genomic and non-genomic mechanisms; it influences heart rate, systolic and diastolic function and systemic vascular resistance, and hence cardiac performance (4,5). In human overt hyperthyroidism, the increase in left ventricular performance is predominantly sustained by the increased preload that results in enhanced left ventricular diastolic function (6,7). The reduced systemic vascular resistance, coupled with increased venous return and preload, enhances cardiac output (6,7). The decreased cardiac output in hypothyroid patients at rest depends largely on altered diastolic relaxation and hemodynamic loading (5,8). The reduced cardiac preload, combined with bradycardia and slightly depressed myocardial contractility, accounts for a subnormal cardiac output in overt hypothyroidism, whereas peripheral vascular resistance is remarkably increased (4,5,8). Moreover, cardiovascular alterations have been found in individuals with subclinical thyroid disease (9). This review covers the data about the progression of subclinical thyroid dysfunctions and cardiovascular risk. It also deals with the cardiovascular risk and the need for treatment as estimated from epidemiological data on cardiovascular morbidity and mortality.

Cardiovascular consequences of subclinical hyper and hypothyroidism / Biondi, Bernadette. - In: HOT THYROIDOLOGY. - ISSN 2075-2202. - ELETTRONICO. - 2:(2004), pp. 1-7.

Cardiovascular consequences of subclinical hyper and hypothyroidism

BIONDI, BERNADETTE
2004

Abstract

Subclinical thyroid dysfunctions are defined by normal free-triiodothyronine (FT3) and free-thyroxine (FT4) concentrations in the presence of abnormal TSH, which is low-undetectable in subclinical hyperthyroidism (SH) and increased in subclinical hypothyroidism (Sh). The clinical significance of subclinical thyroid dysfunction is much debated (1-3). The presence of tissue effects, symptoms and signs of mild thyroid hormone excess or deficiency and the management and treatment of these conditions are controversial issues. Similarly, the TSH cut-off point that determines the effects of subclinical thyroid dysfunction remains to be established. The cardiovascular system, which is a major target of thyroid hormone, is sensitive to the effects of thyroid hormone excess or deficiency at the tissue level. Many symptoms and signs in patients with overt hypo- or hyperthyroidism are related to the reduced or increased action of thyroid hormone on cardiac function. Triiodothyronine (T3) affects the heart and vascular system through genomic and non-genomic mechanisms; it influences heart rate, systolic and diastolic function and systemic vascular resistance, and hence cardiac performance (4,5). In human overt hyperthyroidism, the increase in left ventricular performance is predominantly sustained by the increased preload that results in enhanced left ventricular diastolic function (6,7). The reduced systemic vascular resistance, coupled with increased venous return and preload, enhances cardiac output (6,7). The decreased cardiac output in hypothyroid patients at rest depends largely on altered diastolic relaxation and hemodynamic loading (5,8). The reduced cardiac preload, combined with bradycardia and slightly depressed myocardial contractility, accounts for a subnormal cardiac output in overt hypothyroidism, whereas peripheral vascular resistance is remarkably increased (4,5,8). Moreover, cardiovascular alterations have been found in individuals with subclinical thyroid disease (9). This review covers the data about the progression of subclinical thyroid dysfunctions and cardiovascular risk. It also deals with the cardiovascular risk and the need for treatment as estimated from epidemiological data on cardiovascular morbidity and mortality.
2004
Cardiovascular consequences of subclinical hyper and hypothyroidism / Biondi, Bernadette. - In: HOT THYROIDOLOGY. - ISSN 2075-2202. - ELETTRONICO. - 2:(2004), pp. 1-7.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/512021
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