Impaired cardiac PGI2 and PGE2 biosynthesis in patients with angina pectoris

Thirty-four patients with unstable angina and 14 patients with stable effort angina were investigated for cardiac prostacyclin and prostaglandin E 2 (PGE 2 ) biosynthesis, under resting conditions and after cold pressor testing. Twenty-seven patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were studied as a control group. Prostacyclin (as 6-keto-PGF 1α ) and PGE 2 were measured by specific radioimmunoassay of blood from the coronary sinus and aorta. During resting conditions no significant differences in plasma 6-keto-PGF 1α and PGE 2 concentrations were found between coronary sinus and aortic blood, and no transcardiac gradient existed either in control subjects or in patients with stable and unstable angina, respectively. In control subjects cold pressor testing induced a significant increase in 6-keto-PGF 1α and PGE 2 levels in blood from the different sampling sites, and a significant transcardiac gradient occurred (+11.2 ± 6.4 pg/ml for 6-keto-PGF 1α and +5.1 ± 3.4 pg/ml for PGE 2 ). However, in angina patients no significant increase in 6-keto-PGF 1α and PGE 2 plasma levels was found and no transcardiac gradient was formed after cold pressor testing. These results indicate impaired cardiac prostacyclin and PGE 2 biosynthesis both in patients with stable and unstable effort angina.