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PG I2 stimulating plasma factor was measured in patients with ischemic heart disease and age-matched controls. The plasma factor measured by bioassay using rat aorta was 3.2 +/- 0.6 (n = 21), 2.7 +/- 0.8 (n = 7), 1.6 +/- 1.5*** (n = 18) and 2.2 +/- 0.06** (n = 3) PG I2 ng/mg rat aorta (mean +/- SD; * p less than 0.05, ** p less than 0.01, *** p less than 0.001) in control, angina pectoris, acute myocardial infarction and old myocardial infarction with angina pectoris groups, respectively. The plasma factor measured by radioimmunoassay was 43.5 +/- 19.5 (n = 11), 35.4 +/- 13.1 (n = 4), 38.5 +/- 18.0 (n = 9), 26.0 +/- 20.1* (n = 7) and 59.5 +/- 31.2 (n = 5) ng/mg rat aortic protein/15 min in control, variant angina, stable angina, acute myocardial infarction and old myocardial infarction groups, respectively. The factor in deproteinized plasma of the acute myocardial infarction group was also smaller than that of the control group. PG I2 synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A2. The plasma factor was not inactivated by heating. The results indicate that a heat-stable plasma factor which acts on phospholipase A2 or on its surrounding reaction systems is deficient in the early stage of acute myocardial infarction. A decrease in the factor may cause PG I2 deficiency, resulting in coronary thrombosis or vasospasm and consequently in acute myocardial infarction.

A decrease in plasma factor which stimulates prostaglandin I2 synthesis in patients with acute myocardial infarction.