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.