Angina pectoris is commonly attributed to a disproportion between the work demanded of the heart and the blood or oxygen supply available to it (1,2,3,4,5). That the heart's work increases during the attack of pain has been inferred from several well known facts. First, increased blood pressure is common during the period of pain, although there is no complete correlation between the degree and duration of pain and the change in blood pressure (6, 7). Second, situations which commonly induce anginal attacks, such as exercise, excitement, food, and cold, increase the cardiac output of normal subjects (8, 9).The duration of most spontaneous attacks of angina following effort is too brief to permit satisfactory estimations of cardiac output during the pain. Physicians have hesitated to induce attacks of cardiac pain of a duration sufficient to permit such estimations. Probably these reasons account for the lack of estimations of cardiac output in the huge literature on angina pectoris. Therefore the widely accepted view that angina is associated with increased heart work has never been verified by measurement.During a long series of estimations of cardiac output, carried out on patients during the last eight years, we had several unexpected opportunities to study angina pectoris. These opportunities were seized. Therefore we have secured satisfactory estimations of cardiac output, metabolic rate, blood pressure, pulse rate, and respiration, during cardiac pain in four patients. Comparable estimations, when the patients were free of pain, were secured also.Three of our patients had typical angina pectoris. Two have since died of their disease and in one a necropsy was secured. The fourth individual suffered from atypical cardiac pain apparently induced by digitalis.In two instances we secured data on the physiological changes which accompanied the relief of pain after the administration of nitroglycerine.In all of these patients the estimated work of the left ventricle was much larger during the pain than in its absence. Our one necropsy proved the coronary circulation to have been impeded. Therefore, our results support the generally accepted view of the causation of angina pectoris.
METHODSEstimations of cardiac output and metabolic rate were performed in the manner described (10, 11). Left ventricular work has been calculated by the formula:-Work = cardiac output X mean blood pressure X 13.6 (12). Patient W. B. had slight aortic regurgitation and in this case the estimation of work is too small, as the amount of blood leaking through the aortic valve is not included in the estimation of cardiac output. The increased blood pressure during pain would tend to increase the error and, although this would be somewhat offset by the decreased duration of diastole with the faster pulse rate, we believe that the actual increase of heart work during the pain must have been larger than our estimate of it.Criteria discussed before (13) have permitted us to evaluate the significance of differences in cardiac output estimations...