The oxygen supply of the human heart ∗

Abstract

The factors involved in oxygenation of the human heart have been discussed and illustrated in normal subjects and in common forms of heart disease. Within all groups at rest, significant variability in ventricular performance, myocardial oxygen requirements and oxygen supply patterns exists, suggesting that individual resting observations are of little value in detecting abnormalities of the coronary circulation. An exception appears to exist in low cardiac output congestive heart failure where functional coronary insufficiency is postulated due to coronary participation in peripheral vasoconstriction. During exercise, increased myocardial oxygen requirements are met by elevated coronary blood flow in normal coronary subjects, allowing maintenance of resting myocardial oxygen tension. Coronary vascular reserve is inadequate in coronary arterial disease, and a compensatory elevation of myocardial oxygen extraction lowers exercise coronary venous oxygen saturation and, presumably, myocardial oxygen tension. In congestive heart failure, markedly elevated exercise myocardial oxygen requirements place extraordinary demands on the coronary circulation, and in some instances may precipitate insufficiency of the anatomically normal or mildly diseased coronary circulation. An important consequence of coronary insufficiency appears to be compensatory elevation of myocardial oxygen extraction and reduction of myocardial oxygen tension during exercise. These studies demonstrate no relationship between absolute coronary venous oxygen values and angina pectoris, although the precipitation of this symptom may be related to the degree of reduction in coronary venous oxygenation during exercise. Analysis of myocardial lactate, pyruvate and catecholamine metabolism reveals no causal relationship to angina pectoris or coronary vasodilatation. Of the study subjects having angina pectoris, 82 per cent have detectable oxygen supply abnormalities, an incidence in close agreement with that of diffuse versus localized coronary arterial disease. The role of inefficient energy utilization has been suggested in the precipitation of coronary insufficiency in congestive heart failure and obliterative coronary arterial disease. Conversely, reduced myocardial oxygen tension secondary to coronary insufficiency may impair ventricular performance and result in myocardial damage. These problems require further evaluation of the biochemical events associated with coronary insufficiency, and an examination of myocardial energy production and utilization in coronary arterial disease.