Aortic stenosis in man, which produces pressure overload hypertrophy of the left ventricle, is often associated with angina pectoris. This suggests myocardial ischemia and occurs even in the presence of normal coronary arteries. An abnormality in coronary blood flow associated with hypertrophy has been proposed as a cause of such ischemia. Experimental studies of coronary blood flow in pressure overload hypertrophied ventricles have shown reduced subendocardial blood flow. These experiments, however, used supracoronary banding techniques to simulate aortic stenosis. These models produce severe pressure overload hypertrophy of the ventricle but differ from true aortic stenosis in that the coronaries are exposed to higher than normal systolic pressure. Coronary hypertension could affect coronary blood flow. Indeed, anatomic alterations of the coronary arteries in supracoronary models have been shown. The effects of such alteration on blood flow in unknown. It is possible that changes in blood flow in experimental supracoronary aortic stenosis may not reflect those seen in subcoronary aortic stenosis in patients. Contractile function may be depressed in some patients with aortic stenosis. Experimental studies of this issue in animals have yielded conflicting results. One source of conflict is that most experimental models have imposed a sudden pressure overload on the ventricle. This is not analogous to gradually occurring pressure overload ot human aortic stenosis and may damage the myocardium. Thus, interpretation of results obtained from sudden pressure overload models are difficult to evaluate. Knowledge of coronary blood flow and muscle contractile function in aortic stenosis would be advanced by study of a model in which a subcoronary stenosis produced gradual but severe pressure overload hypertrophy. This would obviate the confounding influences of coronary artery systolic hypertension seen in supracoronary models as well as possible myocardial damage created by suddenly imposed pressure overload. We propose to study coronary blood flow and ventricular muscle contractile function in a dog model of gradually applied subcoronary aortic stenosis.
