Contractile Properties of Cardiac Muscle in Hyperthyroidism

Right ventricular papillary muscles from hyperthyroid and normal cats were studied in vitro at 30°C, at contraction frequencies of 12, 30 and 60/min. At 12/min the contractility of hyperthyroid muscles was significantly greater than normal, as indicated by greater velocity of isotonic shortening, isometric tension development, and rate of tension development. Isotonically contracted muscle lengths were smaller and time to peak isometric tension less. At 60/min, velocity of shortening was still greater and time to peak tension less in hyperthyroid muscles, but isometric developed tension, rate of tension development, and isotonically contracted muscle lengths and shortening were not different. Increasing frequency from 12/min to 60/min resulted in immediate positive inotropic responses in both groups, but a smaller response in hyperthyroid than normal muscles. Over subsequent minutes, a slight decrease in contractility occurred in normal muscles but the decrease was significantly greater in hyperthyroid muscles. The difference in response to increasing frequency is attributed to more profound hypoxia in hyperthyroid muscles at high contraction frequencies. Predisposition of the muscle to hypoxia induced by hyperthyroidism then becomes an important determinant of the net effect of hyperthyroidism on myocardial contractility. The experimental situation is analogous to the coexistence, in vivo, of thyrotoxicosis and other conditions predisposing to coronary insufficiency, such as coronary artery disease or ventricular hypertrophy; that hyperthyroidism does not then augment contractile state in respect to tension development or muscle shortening helps explain the occurrence of thyrotoxic heart failure in response to the body's increased requirements for blood flow.