Abstract. The intrinsic contractile properties of isolated cat papillary muscles and myocardial high energy phosphate stores were examined at three levels of thyroid activity and correlated with hemodynamic measurements in the intact animal. In addition, the relationship of thyroid state to endogenous norepinephrine stores and myocardial responsiveness to certain inotropic in-.terventions were studied. In muscles from hyperthyroid cats, the velocity of shortening and the rate of tension development were markedly augmented, while duration of active state was decreased, compared to euthyroid muscles. These findings occurred in the presence and absence of intact norepinephrine stores and over a wide range of temperature and contraction frequency. The opposite changes occurred in muscles from hypothyroid cats. Isometric tension was slightly higher in muscles from hyperthyroid and lower in muscles from hypothyroid cats. The inotropic response to both norepinephrine and strophanthidin varied inversely with the level of thyroid state and allowed all three groups of muscles to reach a common ceiling of isometric tension regardless of thyroid state. Creatine phosphate and adenosine triphosphate stores were intact at all three levels of thyroid state. Thus, the level of thyroid activity profoundly affects the intrinsic contractile state of cardiac muscle, independent of both norepinephrine stores and alterations in high energy phosphate stores, and, in addition, modifies the responsiveness of cardiac muscle to inotropic agents.

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Four apparently healthy young adults with vague chest symptoms during the day, two of whom had infrequent syncope while ambulatory at night, had periods of asystole up to nine seconds in duration occurring repeatedly during rapid-eye-movement (REM) sleep. Extensive evaluations, including electrophysiologic studies in two patients, were normal. It is therefore suggested that the underlying pathophysiology involved autonomic dysfunction. REM sleep-related sinus arrests such as these, which may occur in apparently healthy subjects but are undetected, may explain some cases of sudden, unexpected death during sleep. Polygraphic monitoring during sleep may be helpful in delineating the pathophysiology of the sleep-related arrhythmia in persons with daytime cardiac arrhythmias thought to be secondary to abnormal vagal tone. The possibility of nocturnal asystole should be considered in patients such as those described here.

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