Hemodynamic and angiographic effects of prostaglandin E1 in coronary artery disease

The effects of prostaglandin E1 (PGE1) were assessed in 24 patients with coronary artery disease. Quantitative coronary angiography was performed in 15 patients. PGE1 was found to produce dilation of coronary stenoses (6 +/- 12% to intravenous PGE1, difference not significant, 19 +/- 22% to intracoronary PGE1, p less than 0.05), but usually no change in the diameter of angiographically normal segments. In these patients intracoronary nitroglycerin consistently dilated the normal segments not altered with PGE1 and often led to further dilation of the stenoses. In 9 other patients who were undergoing coronary angioplasty, hemodynamics and the time to ischemia induced by coronary occlusion were measured. In both patient groups PGE1 led to decreases in aortic, pulmonary artery and pulmonary arterial wedge pressures and an increase in heart rate (all p less than 0.05). Before coronary occlusion PGE1 produced coronary vasodilation manifested by preservation in coronary sinus flow (130 +/- 41 to 126 +/- 42 ml/min, difference not significant); as aortic pressure declined coronary resistance decreased (0.9 +/- 0.3 to 0.8 +/- 0.3 mm Hg/ml/min, p less than 0.05). During coronary occlusion residual flow to the affected region was usually similar to control occlusions (37 +/- 20 to 36 +/- 25 ml/min, difference not significant) and collateral resistance was decreased (3.2 +/- 2.9 to 2.9 +/- 2.6 mm Hg/ml/min, p less than 0.05). However, time to ischemia usually remained unchanged. PGE1 shows an interesting angiographic and hemodynamic profile in patients with coronary artery disease. Although no obvious clinical benefit was seen, PGE1 was safely administered both intravenously and directly into narrowed coronary arteries.