With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH-64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.LEFT ventricular hypertrophy (LVH) may impair cardiac function but the mechanisms for this change are not clear. Hypertrophy alters excitation-contraction coupling, energy utilization, and contractile proteins, 1 but it is not known whether these changes are primary or secondary to other mechanisms. One of those other mechanisms, myocardial ischemia, could occur in two ways: Roberts and Wearn 2 showed that in rabbits with left ventricular Original manuscript received February 28, 1977; accepted for publication March 7, 1978. hypertrophy the capillary-fiber ratio remained at its normal value of 1:1 so that the mean diffusion distance must have increased; these findings have been confirmed in man. 3 ' 4 Then Linzbach 3 and Woods 5 reported that, although the main coronary arteries increased in diameter in people with LVH, this increase in diameter did not match the increased heart weight. They therefore inferred that in hypertrophy there might be a reduced coronary vascular reserve that might impair cardiac function. However, no one has shown that the increased diffusion distance for oxygen does impair cardiac function nor that coronary vascular reserve is reduced in hypertrophy.We wished to test another hypothesis that involves myocardial blood flow, one which also fits in with the known vulnerability of the subendocardial muscle to is-