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March 1972

Cardiovascular Response in Hyperthyroidism: The Influence of Adrenergic-Receptor Blockade

Author Affiliations


From the departments of endocrinology and cardiology of Cook County Hospital and Hektoen Institute for Medical Research, and the departments of medicine of the University of Illinois College of Medicine and Northwestern University Medical School, Chicago.

Arch Intern Med. 1972;129(3):426-429. doi:10.1001/archinte.1972.00320030046003

Cardiac catheterization and measurements of phases of left ventricular systole were performed in seven hyperthyroid patients before and during the oral administration of propranolol hydrochloride, a betaadrenergic receptor blocking agent. The data suggest that the hyperdynamic circulatory state in hyperthyroidism results from the combination of the direct action of thyroxin on the myocardium and the activation of the beta-adrenergic receptors. Propranolol decreased heart rate, cardiac output, maximum first derivative of left ventricular pressure, mean systolic ejection rate, left ventricular work and left ventricular stroke power induced through the sympathetic nervous system. Caution is urged in its use because of an unexplained left ventricular end-diastolic pressure elevation in more than half of the subjects before treatment.

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