THYROTOXICOSIS AND THE HEART - 09/09/11
Résumé |
Cardiovascular manifestations are some of the most profound and characteristic symptoms and signs of hyperthyroidism. 16, 37 Since the first descriptions 200 years ago by Perry and Graves, clinicians have noted the finding of a hyperdynamic cardiovascular system resulting from excess thyroid hormone secretion by the thyroid gland. More recently, similar changes have been linked to treatment with l-thyroxine in dosages which suppress thyroid-stimulating hormone. 2 Understanding the mechanisms by which thyroid hormone affects the cardiovascular system provides a basis for the management of patients with thyrotoxic heart disease. This review examines these molecular mechanisms in naturally occurring thyroid disease states and the potential utility of thyroid hormone therapy in the management of patients with various forms of cardiovascular disease. 20, 22
The changes in cardiovascular hemodynamics that accompany thyrotoxicosis are summarized in Table 1. There are striking similarities between the clinical presentation of the hyperadrenergic state that accompanies pheochromocytoma and the cardiovascular hemodynamics of hyperthyroidism. 25, 45 This has led to the suggestion that thyrotoxicosis is associated with excessive catecholamine secretion. 37 Historically, observations relating to the clinical manifestations of hyperthyroidism emphasize the importance of heightened cardiovascular responses to exogenously administered catecholamines. These findings served as a basis for establishing one of the earliest diagnostic tests for hyperthyroidism. In 1918 Goetsch 12 reported marked cardioacceleration and blood pressure responses to injections of epinephrine in the hyperthyroid patient. The magnitude of these responses was observed to be less in euthyroid individuals.
Hyperthyroidism potentiates not only cardiovascular symptoms but other responses such as diaphoresis, tremor, and hepatic glycogenolysis normally associated with excessive catecholamine stimulation. 19, 27, 45 These findings led to the conclusion that hyperthyroidism was a bihormonal disease state involving both excessive thyroid hormone and catecholaminergic action. Although prior reports have proposed altered catecholamine sensitivity of the heart and other organs in hyperthyroidism, critical review of these studies does not support the pharmacologic concept of the enhanced biologic responsiveness. 25 When various measures such as heart rate or cardiac contractile response to exogenously administered catecholamines have been studied, no convincing evidence of a lower threshold or a shift in the dose-response relationship has been observed. 27 Studies in experimental animals and subhuman primates have confirmed that the metabolic and hemodynamic sensitivity to exogenous catecholamines is unaltered in experimental hyperthyroidism. 14
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| Address reprint requests to Irwin Klein, MD, Division of Endocrinology, North Shore University Hospital, 300 Community Drive, Manhasset, NY 11030 Supported in part by NIH grants HL41304, HL56804, and HL58840 to IK and KO. |
Vol 27 - N° 1
P. 51-62 - mars 1998 Retour au numéro
Article précédent
- SUBCLINICAL THYROTOXICOSIS
- Ellen Marqusee, Susan T. Haden, Robert D. Utiger
- THEORIES OF CAUSATION OF GRAVES' DISEASE : A Historical Perspective
- Clark T. Sawin
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