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Coronary blood flow was measured by the nitrous oxide method, and cardiac output was measured by the Fick principle, in a series of 31 human subjects with the clinical diagnosis of angina pectoris. Coronary arteriography was carried out on the same subjects as a part of the same procedure, and the extent and severity of the coronary artery lesions was determined. A numerical value was assigned to the severity of the coronary artery disease, an attempt was made to correlate the severity of coronary artery disease with the measured coronary blood flow and with various hemodynamic parameters which traditionally describe the systemic and pulmonary circulation. There was no correlation between any of the parameters measured and the severity of coronary artery disease demonstrated by angiography. It is concluded, therefore, that the nitrous oxide method for measuring coronary blood flow is not helpful in separating subjects with normal coronary arteries from those with coronary artery disease, nor are resting hemodynamic observations helpful.Maximum flow through the coronary arteries of the dog heart was measured by postmortem perfusion. This flow rate is sufficient to provide a considerable factor of safety as far as constriction of the major coronary arteries is concerned. If these data are extrapolated to the coronary vessels of man, it would seem that a very large "safety factor" exists, and this may explain why severe coronary disease is not revealed by studies of coronary blood flow. Additional Indexing Words: Myocardial metabolismCardiac cathet A LTHOUGH many reports are available on the determination of myocardial blood flow by the nitrous oxide method in subjects prone to have angina pectoris,'-8 there are few in which the coronary arteries were studied by angiography. We have found no study in which an attempt has been made to correlate the severity of coronary artery disease as demonstrated by coronary arteriography with coronary flow as determined by the nitrous oxide method, although some ob-

The systemic and coronary hemodynamic effects of relatively large doses of propranolol have been studied following its infusion into intact anesthetized dogs at rest and during simulated exercise. At rest, the administration of propranolol was associated with decreased cardiac output and ventricular work and increased peripheral, pulmonary, and coronary vascular resistances. Coronary blood flow and coronary sinus oxygen content decreased while myocardial oxygen consumption and the index of cardiac efficiency were unchanged. The usual hemodynamic response to mild exercise was obtained, with increased cardiac output, cardiac work, body oxygen consumption, and a modest but insignificant increase in coronary blood flow. When propranolol was given and the same exercise continued, body oxygen consumption, cardiac output, and left ventricular work significantly decreased. Insignificant decreases occurred in coronary blood flow, left ventricular oxygen usage, and coronary sinus oxygen content. The present observations are consistent with the thesis that beta-adrenergic blockade induced by propranolol decreases cardiac work at rest and reduces the cardiovascular response to exercise.

Summary:The purpose of this investigation was to determine if echocardiographic measures of ventricular structure and function ascribed to aerobic training might be an artifact of heart rate (HR) differences between trained and untrained subjects. Comparisons were made at rest, of 10 young, male, aerobically well-trained athletes [(V02)max 65>ml/kg/min] and 10 young, healthy controls [( VO2),,,<56ml/kg/min].Additionally, the echocardiographic responses to low (HR=80 beats/min) and moderate intensity (HR= 120 beats/min) supine cycling exercise were analyzed. Echocardiographic measures were made as described by Sahn et al. (1978). Results of echocardiographic comparisons between groups, both during supine rest and at a constant heart rate of 80 beats/min during supine cycling confirmed that athletes had significantly greater left ventricular mass (LV mass) and end-diastolic size per square meter of body surface area (p<0.05). When supine cycling loads were increased to elevate HR to 120 beats/min in groups of 7 athletes and 5 controls, athletes exhibited a progressive and significant (p<0.05) enlargement of left ventricular end-diastolic size (LVEDS), while left ventricular end-systolic size (LVESS) showed negligible change. The control group showed little change in LVEDS, but decreased LVESS significantly (p<0.05).Contractility measures, i.e., estimated ejection fraction (EF) and velocity of circumferential shortening (~c F ) increased in both groups in a similar manner. It was concluded that echocardiographic differences in ventricular structure and function observed between aerobically trained and untrained subjects are not an artifact of heart rate differences. Clearly, aerobic training results in increased LV mass and diastolic size which allows for further dilitation with supine exercise, Aerobic training does not appear to alter indices of myocardial contractility.

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