Mechanisms involved in altering left ventricular (LV) diastolic properties during angina were studied in 10 chloralose-anesthetized dogs with chest and pericardium open. Proximal coronary artery stenoses of >90% were created in both left anterior descending and circumflex coronary arteries to abolish reactive hyperemia, and the heart was paced at nearly twice its resting rate (115 ± 4 to 200 ± 5 beats/min). After pacing, increases occurred in LV end-diastolic pressure (EDP, 10 ± 2 to 21 ± 2 mm Hg, P< 0.001), LV minimum diastolic pressure (5 ± 1 to 13 ± 2 mm Hg, P< 0.001), LV end-diastolic volume (55 ± 3 to 60 ± 2 ml,P< 0.001), LV end-systolic volume (28 ± 2 to 33 ± 2 ml,P< 0.001), right ventricular (RV) systolic pressure (RVP, 27 ± 2 to 32 ± 2 mm Hg,P< 0.01), RVEDP (5 ± 1 to 6 ± 1 mm Hg,P< 0.05), and time constant (T) of LV pressure fall in diastole (35 ± 4 to 53 ±4 msec,P< 0.001). Decreases occurred in LV peak systolic pressure (121 ± 5 to 102 ± 5 mm Hg, P< 0.001), LV maximum negative dp/dt (2300 ± 158 to 1319 ± 154 mm Hg/sec, P< 0.001), and LV ejection fraction (0.49 ± 0.02 to 0.44 ± 0.03, NS), whereas heart rate was not significantly different. LV diastolic pressure-volume curves were shifted upward for each dog; at any diastolic volume, pressure was higher than control. In four dogs, the pulmonary artery was abruptly constricted, and saline was infused to produce an acute increase in RV loading (RVP, 29 ± 1/6 ± 1 to 67 ± 5/11 ± 1 mm Hg,P< 0.001/P< 0.001), and the effect on the LV diastolic pressure-volume relation was examined. Only minor changes in this relation could be detected in contrast to the changes with pacing-induced ischemia. Since the upward shift in the LV diastolic pressure-volume curve in our ischemia model occurred in the absence of the pericardium and was associated with only small changes in RVEDP, we conclude that altered myocardial diastolic properties play an important role in this phenomenon. Circ Res 46: 430-439, 1980