Coronary Vascular Reserve Research Articles

Mechanisms of angina in aortic stenosis.

The pathophysiology of cardiac pain in pure aortic stenosis has primarily been ascribed to an augmented left ventricular demand outstripping energy supply. This report provides evidence that not only is the energy demand increased but the supply in terms of coronary vascular reserve may be impaired, particularly in response to stress. Hemodynamic and coronary circulatory changes were studied in 18 patients with aortic stenosis during standard isoproterenol infusion. It was not possible to differentiate any patient with or without angina pectoris or patients with or without coronary artery disease on a basis of change in any measure of left ventricular dynamics. On the other hand, differences did occur in the mechanisms of energy delivery during isoproterenol stress: (1) In group A (aortic stenosis without angina or coronary artery disease), coronary flow increased normally, myocardial oxygen extraction decreased, and myocardial lactate production occurred in only one of seven patients. This suggested that energy supply was, generally, adequate to demand. (2) In group B (critical aortic stenosis with angina but no coronary disease), coronary flow rose insignificantly, myocardial oxygen extraction actually increased in three of five patients, and abnormal glycolysis occurred in all patients. This suggested that little or no reserve for increased coronary flow existed and that compensatory mechanisms had to be summoned. (3) In group C (aortic stenosis with angina and coronary artery disease), coronary flow rose normally, myocardial oxygen extraction decreased normally, but abnormal lactate metabolism occurred in most patients. This suggested adequate overall coronary reserve but evidence of regional ischemia.

The oxygen supply of the human heart ∗

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.