6533b82efe1ef96bd129268f

RESEARCH PRODUCT

Heart in Hypothyroidism

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description

The transition from the fetal to the adult phenotype heart depends on the increase in thyroid hormone (TH) in perinatal period (Liu and Gerdes, J Mol Cell Cardiol 22:1339–1348, 1990; Gerdes and Iervasi, Circulation 122:385–393, 2010). Moreover, T3 action is essential for preserving both cardiac morphology and performance in adult life because thyroid hormone controls the inotropic and lusitropic properties of the myocardium, cardiac growth, myocardial contractility, and vascular function (Liu and Gerdes, J Mol Cell Cardiol 22:1339–1348, 1990; Gerdes and Iervasi, Circulation 122:385–393, 2010; Fazio et al., Recent Prog Horm Res 59:31–50, 2002; Kahaly and Dillmann, Endocr Rev 26:704–728, 2005; Klein and Ojamaa, N Engl J Med 344:501–509, 2001; Biondi and Klein, Endocrine 24:1–13, 2004). Most patients with thyroid dysfunction experience cardiovascular (CV) manifestations, and the most serious complications of thyroid disease occur as a result of cardiac involvement (Fazio et al., Recent Prog Horm Res 59:31–50, 2002; Kahaly and Dillmann, Endocr Rev 26:704–728, 2005; Klein and Ojamaa, N Engl J Med 344:501–509, 2001; Biondi and Klein, Endocrine 24:1–13, 2004). Severe hypothyroidism or myxedema has a clinically relevant impact on the heart and on the cardiovascular system, and measurable changes in cardiovascular performance are detected even with small variations in thyroid hormone concentrations (Liu and Gerdes, J Mol Cell Cardiol 22:1339–1348, 1990; Gerdes and Iervasi, Circulation 122:385–393, 2010; Fazio et al., Recent Prog Horm Res 59:31–50, 2002; Kahaly and Dillmann, Endocr Rev 26:704–728, 2005; Klein and Ojamaa, N Engl J Med 344:501–509, 2001; Biondi and Klein, Endocrine 24:1–13, 2004).