Recent animal studies suggest that cardiac hypertrophy compromises the coronary circulation. Although flow per gram of ventricle in most animal models of hypertrophy is normal, coronary vasodilator responses to pharmacological or physiological stimuli are mildly impaired. Studies of regional perfusion indicate that the limitation of coronary vasodilator capacity in hypertrophied ventricles primarily affects the endocardium. In contrast to studies in animals, measurements of coronary reactive hyperemia in man suggest that coronary dilator responses are profoundly depressed in patients with severe left ventricular hypertrophy secondary to aortic stenosis. These studies in man demonstrate that alterations in the coronary circulation secondary to cardiac hypertrophy are of sufficient magnitude to contribute to the development of angina and heart failure (secondary to endocardial fibrosis) in patients with aortic stenosis.