The data suggest that postmenopausal estrogen treatment reduces the risk for angiographically significant coronary artery disease.

Although the circulatory changes in various thyroid states are well known, the alterations of myocardial contractility of hypothyroidism and hyperthyroidism have remained controversial. The changes in the length of the ejection time (ET) and isovolumic contraction time (ICT) are used as indicative of alterations in inotropic state of the myocardium. Isovolumic contraction time, ejection time, and pre-ejection period were measured externally in 10 normal, 13 hyperthyroid, and five hypothyroid subjects. Cardiac outputs, mean rate of left ventricular ejection index, and predicted ejection times were calculated. More shortening of ICT and ET in hyperthyroid and more prolongation of these intervals in hypothyroid subjects than could be attributed to other factors were interpreted as indicative of increased and decreased myocardial contractility, respectively. Catecholamine depletion in hyperthyroid subjects with adequate administration of intramuscular reserpine induced no changes in cardiac output and oxygen consumption and caused no alteration in different phases of ventricular systole; consequently it had no effect on enhancement of hyperthyroid myocardial contractility.

A B T R A C T The effect of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time was studied in 11 normal male subjects. Methoxamine, a pressor amine of predominantly vasoconstrictor activity but lacking significant inotropic effect, was administered intravenously resulting in an average increase in mean arterial pressure of 27 mm Hg. Heart rate was held constant by high right atrial pacing, and there was no significant change in cardiac output. During methoxamine infusion, when stroke volume, heart rate, and inotropic state were held constant, left ventricular ejection time increased as mean arterial pressure increased. There was a highly significant correlation between the increase in mean systolic blood pressure and the prolongation of left ventricular ejection time (r = 0.870). In one subject, an increase in mean systolic pressure of 75 mm Hg prolonged left ventricular ejection time 55 msec, producing paradoxical splitting of the second heart sound. The prolongation of left ventricular ejection time during infusion was not blocked by the prior intravenous administration of atropine sulfate or propranolol hydrochloride, thus ruling out both vagal inhibition of the left ventricle and reflex withdrawal of sympathetic tone as its cause. In three subjects, left ventricular end diastolic pressure was mea-A partial report of this work appeared in abstract form. 1966. J. Clin. Res. 14: 261.Dr. Paley's present adress is the Mt. Zion Hospital, San Francisco, Calif.

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