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Stimulation of cardiac myosin adenosine triphosphatase in thyrotoxicosis.

THE striking cardiovascular manifestations of thyrotoxicosis have attracted the interest of clinicians and researchers for many years. Caleb H. Parry (1785) probably was the first to note an association between enlargement of the thyroid and enlargement or palpitations of the heart. It is now known that excess thyroid hormone, either produced endogenously or administered exogenously, produces hypermetabolism and thus places greater demand on the heart for tissue perfusion. The resulting increases in coronary blood flow, myocardial oxygen consumption, total cardiac output, and work are well documented (Rowe et al., 1956; Graettinger et al., 1959). In addition to the requirements placed on the heart by the peripheral tissues, the metabolism of the heart itself is directly stimulated by thyroid hormone. Oxygen consumption (Skelton et al., 1970) and protein synthesis (Michels et al., 1963; Cohen et al., 1966) are elevated in excised cardiac tissue in response to thyroxine. The metabolic changes in thyrotoxicosis are accompanied by augmentation of the contractile performance of the heart (Buccino et al., 1967). The basis for these effects of thyroid hormone is unclear, but new biochemical evidence has appeared recently that may explain the augmentation in myocardial performance, that is, an increase in myosin ATPase activity. Preliminary reports (Thyrum et al. 1970; Kucznski, 1973) of increased cardiac myosin ATPase activity in thyrotoxic animals have been confirmed and extended (Yazaki and Raben, 1975; Katagiri et al., 1975; Banerjee et al., 1976). In