The duration of the systolic time intervals in nondigitalized patients with heart failure was determined from simultaneous fast speed recordings of the electrocardiogram, phonocardiogram, and carotid arterial pulsation. These were compared with the systolic time intervals corrected for heart rate and sex in 211 normal subjects. The failing left ventricle is characterized by a prolongation in the systolic pre-ejection period and a diminution in the left ventricular ejection time while total electromechanical systole remains relatively unaltered. Both components of the pre-ejection period, the Q-1 interval and the isovolumic contraction time, were prolonged. These alterations in the phases of systole occur in the absence of a measurable change in ventricular depolarization time. The prolongation in the pre-ejection period is well correlated with the reduced stroke volume and cardiac output in heart failure and is independently augmented by high levels of arterial pressure. The abbreviation in left ventricular ejection time is also correlated significantly with the stroke volume and cardiac output. It is postulated that a defect in the mechanical performance of the heart is responsible for the abnormal systolic time intervals in human heart failure.

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Summary. We have investigated the possibility that alterations in -the duration of the systolic preejection period can be used to estimate adrenergic influences on the human left ventricle. The preejection period was determined from high speed, simultaneous recordings of the phonocardiogram, carotid pulse tracing, and electrocardiogram. The preejection period was shortened by isoproterenol, epinephrine, and moderate doses of norepinephrine-all of which activate beta adrenergic receptors-and by cedilanid-D. It was unaltered by changes in heart rate induced by atropine and right atrial electrical pacing. Beta adrenergic receptor blockade by propranolol abolished the shortening effects of the three catecholamines but did not inhibit that due to cedilanid-D. Vasoconstriction, both alpha adrenergic (epinephrine and norepinephrine after propranolol) and nonadrenergic (angiotensin), prolonged the preejection period. Most of the shortening of the preejection period by beta adrenergic receptor activating agents and cedilanid-D and all of the prolongation accompanying pharmacologic vasoconstriction occurred after the onset of the first heart sound, thereby excluding changes in eiectrical-mechanical delay as a major factor in the observed preejection period responses. Shortening of the preejection period by beta adrenergic activity induced with isoproterenol was dose-related. Increasing doses of propranolol produced parallel shifts to the right in the isoproterenol dose-response curve.In 37 normal resting subjects intravenous propranolol (10 mg) prolonged the preejection period an average of 10 (SE + 1) msec. In six patients with psychogenic sinus tachycardia and a patient with a pheochromocytoma the presence of excessive beta adrenergic influences on the left ventricle was demonstrated by the finding of an initially short preejection period which responded with an abnormally great prolongation to beta adrenergic receptor blockade. IntroductionThe duration of the preejection period of left ventricular systole can be determined easily and

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