Global and regional left ventricular function was assessed at rest, during spontaneous angina pectoris and after nitroglycerin therapy in 14 patients with ischemic heart disease. Cardiac output, left ventricular pressure and left ventricular volume were measured when patients experienced spontaneous angina pectoris during cardiac catheterization. In every patient control measurements had already been made; further measurements were made after nitroglycerin had relieved pain. Subsequent coronary angiography showed significant two or three vessel disease in all 14 patients. The S-T segment was depressed in every patient during pain (average 0.26 + 0.04 mV; mean + standard error of the mean [SEM]). During spontaneous angina, there was a significant increase in left ventricular end-diastolic pressure (17 ± 2 to 35 ± 2 mm Hg, p < 0.001), left ventricular end-diastolic volume (77 ± 6 to 88 ± 8 ml/m2, p < 0.005) and left ventricular end-systolic volume (35 ± 4 to 52 ± 7 ml/m2, p < 0.001). Concomitantly stroke index decreased from 42 ± 2 to 36 ± 3 ml/beat per m2 (p < 0.01) and ejection fraction from 56 ± 4 to 44 ± 4 percent (p < 0.001). Assessment of regional left ventricular performance during spontaneous angina revealed either development of new areas or extension of already existing areas of abnormal wall motion in all patients. Nitroglycerin restored global and regional left ventricular function to a normal state. In six individual patients there was an excellent correlation between the S-T depression (V5) and left ventricular end-diastolic pressure during spontaneous angina (correlation coefficient [r] = 0.88 to 0.96) and after nitroglycerin therapy (r = 0.76 to 0.84). For the group, there was a good correlation between change in S-T depression and changes in left ventricular end-diastolic pressure (r = 0.87) and left ventricular end-diastolic volume (r = 0.78). Thus, these data indicate marked systolic and diastolic dysfunction of the left ventricle during spontaneous angina pectoris, characterized by decreases in stroke index and ejection fraction and increases in left ventricular end-systolic and end-diastolic volumes and left ventricular filling pressure.