An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 ± 12 vs 70 ± 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 39 vs 222 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 ± 7 vs 28 ± 8 mm Hg, p < .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 ± 5 to 51 ± 7 msec (p < .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 ± 5 vs 75 ± 5 msec, p = .06). High-quality two-dimensional targeted M mode echocardiograms in the control and postpacing periods were available in four patients; left ventricular end-diastolic and end-systolic dimensions and percent fractional shortening were unchanged. The left ventricular diastolic pressure-volume relationship and pressure-wall thickness relationship were shifted upward during angina in these patients. We conclude that angina in patients with aortic stenosis is accompanied by a substantial and reversible increase in left ventricular end-diastolic pressure; this increase appears to be due in part to an impairment of diastolic distensibility of the left ventricle and left ventricular relaxation. These findings, which are similar to those observed during pacing-induced angina in patients with coronary stenoses, suggest that the increase in left ventricular end-diastolic pressure that occurs during angina is a manifestation of demand ischemia per se, and does not depend on the presence of dyssynergistic contraction of ischemic and nonischemic regions.