title: Thyroid Hormone and Cardioprotection.
abstract: The heart is a major target of thyroid hormones, with maintenance of euthyroid hormone balance critical for proper function. In particular, chronic low thyroid function can eventually lead to dilated heart failure with impaired coronary blood flow. New evidence also suggests that heart diseases trigger a reduction in cardiac tissue thyroid hormone levels, a condition that may not be detectible using serum hormone assays. Many animal and clinical studies have demonstrated a high prevalence of low thyroid function in heart diseases with worse outcomes from this condition. Animal and human studies have also demonstrated many benefits from thyroid hormone treatment of heart diseases, particularly heart failure. Nonetheless, this potential treatment has not yet translated to patients due to a number of important concerns. The most serious concern involves the potential of accidental overdose leading to increased arrhythmias and sudden death. Several important clinical studies, which actually used excessive doses of thyroid hormone analogs, have played a major role in convincing the medical community that thyroid hormones are simply too dangerous to be considered for treatment in cardiac patients. Nonetheless, this issue has not gone away due primarily to overwhelmingly positive evidence for treatment benefits and a new understanding of the cellular and molecular mechanisms underlying those benefits. This review will first discuss the clinical evidence for the use of thyroid hormones as a cardioprotective agent and then provide an overview of the cellular and molecular mechanisms underlying beneficial changes from thyroid hormone treatment of heart diseases. © 2016 American Physiological Society. Compr Physiol 6:1199-1219, 2016.
authors.affiliation: Department of Biomedical Sciences, New York Institute of Technology, College of Osteopathic Medicine, Old Westbury, New York, USA.
authors.forename: Anthony Martin
authors.initials: AM
authors.lastname: Gerdes
authors.affiliation: The Feinstein Institute for Medical Research, Manhasset, New York, USA.|Department of Molecular Medicine, Hofstra North Shore-LIJ School of Medicine, Hempstead, New York, USA.
authors.forename: Kaie
authors.initials: K
authors.lastname: Ojamaa
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002316:Cardiotonic Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications / Q000503:physiopathology; D007037:Hypothyroidism / Q000150:complications / Q000503:physiopathology; D013963:Thyroid Hormones / Q000009:adverse effects / Q000494:pharmacology / Q000502:physiology / Q000627:therapeutic use*; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D013963:Thyroid Hormones