The hemodynamic effects of corwin were evaluated in 9 patients with coronary artery disease and without clinical signs of heart failure at rest, during submaximal exercise and during exercise-induced angina pectoris before and after administration of corwin. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina pectoris; hemodynamic data were also recorded at this higher exercise capacity (+16%: p less than 0.001). At rest, corwin increased heart rate (from 80 to 84 beats/min) and pressure-rate product. During submaximal exercise, heart rate decreased from 105 to 96 beats/min, and pressure-rate product and ST-segment depression also decreased after corwin. The prevention of angina pectoris in all patients was accompanied by a lower heart rate (from 132 to 117 beats/min), pressure-rate product and ST-segment depression. At rest and during exercise, the cardiac output was unchanged and the pulmonary capillary wedge pressure was slightly decreased after corwin (from 12.5 to 10 mm Hg; p less than 0.001). At the 16% greater exercise capacity after corwin, angina pectoris recurred at the same values of cardiac output, pulmonary wedge pressure and ST-segment depression; maximal heart rate decreased from 132 to 124 beats/min, and the pressure-rate product was lower. Thus, corwin is an active antianginal drug. Its effects are likely due to a decrease in pressure-rate product and myocardial oxygen requirements during exercise. In contrast to beta-antagonists devoid of partial agonist activity, corwin does not depress left ventricular function either at rest or during exercise.