title: Cardiovascular hemodynamics and exercise tolerance in thyroid disease.
abstract: The heart is an organ sensitive to the action of thyroid hormone, and measurable changes in cardiovascular performance are detected with small variations in thyroid hormone serum concentrations. Most patients with thyroid disease experience cardiovascular manifestations, and the most serious complications of thyroid dysfunction occur as a result of cardiac involvement. The increased metabolic state and oxygen consumption that occur in hyperthyroid patients require an increased supply of oxygen and removal of metabolic products from the periphery. This is accomplished by increasing the cardiac output to meet the needs of the periphery. Circulation time is decreased in hyperthyroid patients, and a lowered arterial resistance and increased venous resistance promote the return of blood to the heart. Thyroid hormones may significantly decrease the strength of respiratory and skeletal muscles and affect regulatory mechanisms of adaptation to incremental effort. In hyperthyroidism, cardiovascular exercise testing and analysis of respiratory gas exchange demonstrate low efficiency of cardiopulmonary function as well as impaired chronotropic, contractile, and vasodilatatory reserves, which are reversible when euthyroidism is restored. During exercise, the increment (delta) of minute ventilation (respiratory rate x tidal volume), and oxygen pulse (oxygen uptake per heart beat) are significantly lower in dysthyroidism versus euthyroidism. Especially in older patients with thyroid dysfunction, markedly reduced workload, delta ejection fraction, and delta heart rate, both at the anaerobic threshold as well as at maximal exercise, are observed. In thyrotoxicosis, mitochondria oxidative dysfunction during exercise mostly causes intracellular acidosis, whereas in hypothyroidism, inadequate cardiovascular support appears to be one of the principal factors involved. These abnormalities partly explain why subjects with dysthyroidism are intolerant to exertion. Thus, in thyroid disease, both cardiac structures and function may remain normal at rest, however impaired cardiovascular and respiratory adaptation to effort becomes unmasked during exercise.
authors.affiliation: Department of Endocrinology/Metabolism, Gutenberg-University Hospital, Mainz, Germany. gkahaly@mail.uni-mainz.de
authors.forename: George J
authors.initials: GJ
authors.lastname: Kahaly
authors.forename: Christoph
authors.initials: C
authors.lastname: Kampmann
authors.forename: Susanne
authors.initials: S
authors.lastname: Mohr-Kahaly
mesh_terms: D000367:Age Factors; D000818:Animals; D002320:Cardiovascular Physiological Phenomena; D005080:Exercise Test / Q000379:methods; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D006321:Heart / Q000502:physiology; D006801:Humans; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D012143:Respiratory Physiological Phenomena; D013318:Stroke Volume / Q000502:physiology; D013959:Thyroid Diseases / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D014284:Triiodothyronine / Q000097:blood; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D014284:Triiodothyronine