Abnormal Left Ventricular Function in Hyperthyroidism Evidence for a Possible Reversible Cardiomyopathy

• Published in: The New England journal of medicine Vol. 307; no. 19; pp. 1165 - 1170
• Main Authors: Forfar, John Colin, Muir, Alexander Laird, Sawers, Stewart Allison, Toft, Anthony Douglas
• Format: Journal Article
• Language: English
• Published: United States Massachusetts Medical Society 04.11.1982
• Subjects: Adrenergic receptors; Adult; Blood Pressure; Cardiac Output; Cardiology; Cardiomyopathies - etiology; Cardiomyopathy; Female; Heart - physiopathology; Heart failure; Heart Rate; Heart Ventricles - diagnostic imaging; Humans; Hyperthyroidism; Hyperthyroidism - complications; Hyperthyroidism - physiopathology; Male; Middle Aged; Patients; Physical Exertion; Physical training; Plasma; Propranolol; Propranolol - pharmacology; Radionuclide Imaging; Space life sciences; Stroke Volume; Thyroid diseases; Thyroid hormones; Ventricle; Workloads
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM198211043071901

We assessed the effects of exercise and beta-adrenoceptor blockade on left ventricular ejection fraction (LVEF) measured by radionuclide ventriculography in nine patients with uncomplicated hyperthyroidism. Patients were studied in both the hyperthyroid and euthyroid states. The hyperthyroid state was characterized by a high LVEF at rest but — paradoxically — by a significant fall (P<0.01) in LVEF during exercise. At the same workload and at the same heart rate, patients had a restoration of the normal rise in LVEF during exercise when they were euthyroid. The LVEF was greater during exercise (P<0.02) when the patients were euthyroid than when they were hyperthyroid. Pretreatment with propranolol caused similar reductions in resting LVEF in the hyperthyroid and euthyroid states; the drug attenuated the rise in LVEF during exercise when the patients were euthyroid, but did not influence the exercise-induced reduction in LVEF in hyperthyroidism. The abnormal left ventricular function observed during exercise in hyperthyroidism suggests a reversible functional cardiomyopathy, independent of beta-adrenoceptor activation, that is presumably a direct effect of an excess in circulating thyroid hormones. (N Engl J Med. 1982; 307:1165–70.) The mechanism of altered myocardial function in hyperthyroidism has been the subject of clinical and experimental investigation over several decades. 1 Despite the striking similarities between the effects of excessive circulating thyroid hormones and those of enhanced sympathoadrenal activity, recent investigations have failed to demonstrate adrenergic hypersensitivity or excess circulating catecholamines in hyperthyroid states. 2 3 4 5 However, the demonstrations of increased beta-adrenoceptor density in the hearts of hyperthyroid animals 6 and of augmented cyclic AMP responses to hypoglycemia in hyperthyroid patients 7 suggest the possibility of increased catecholamine responsiveness in this condition. Nonspecific cardiac symptoms such as fatigue and dyspnea on exertion are common in . . .