CLINICAL INVESTIGATION Endogenous biosynthesis of prostacyclin during cardiac catheterization and angiography in man

ABSTRACT The potent platelet inhibitory and vasodilator properties of prostacyclin suggest that levels of this substance may be of relevance to drug action and pathologic processes in the coronary vascular bed. Attempts to estimate the coronary secretion rate of prostacyclin have relied on measure-ments of metabolites obtained via cardiac catheter, usually as an adjunct to coronary angiography. To test the hypothesis that such procedures might themselves perturb endogenous biosynthesis of prostacy-clin we used mass spectrometry to measure plasma levels of 6-keto-prostaglandin (PG) F,, across the coronary vascular bed, as well as to assess the excretion of a major urinary metabolite, 2,3-dinor-6-keto-PGF,, (PGI-M), in patients undergoing cardiac catheterization. PGI-M excretion increased vari-ably from a median 100 to 205 pg/mg creatinine (p <.01) during catheterization with angiography and remained elevated 2 to 4 hr after initiation of the procedure. However, cardiac catheterization without angiography also stimulated metabolite excretion, perhaps reflecting catheter-induced vascular trauma. The direct effect of radiocontrast media on vascular release of prostacyclin was indicated by increased PGI-M excretion in healthy volunteers administered intravenous radiocontrast and by studies of the canine coronary artery and jugular vein in vitro. Measurement of plasma 6-keto-PGF, after left heart catheterization showed that levels in aortic (21 +- 8 pg/ml) and coronary sinus (14 ± 2 pg/ml) blood were increased compared with peripheral venous levels (c 4 + 1 pg/ml) determined before this procedure. The aortic and coronary sinus concentrations of 6-keto-PGF,, both increased markedly in one of the five patients after injection of radiocontrast but an aortic coronary sinus gradient of 6-keto-PGF, was undetectable before or after angiography. These results indicate that cardiac catheterization and angiography are associated with an increase in prostacyclin formation in vivo