Medical College of Wisconsin
CTSICores SearchResearch InformaticsREDCap

Hemodynamic effects of intravenous prostacyclin in stable angina pectoris. Am J Cardiol 1983 Sep 01;52(5):439-43 PMID: 6351580

Pubmed ID

6351580

Abstract

Prostacyclin (PGI2) is a naturally occurring vasodilator and inhibitor of platelet aggregation that produces vasodilatation of the systemic, pulmonary and coronary vascular beds in animal models. Because the endogenous production of PGI2 is reduced in those with coronary arterial disease (CAD), it may have a therapeutic role in patients with ischemic heart disease. To assess its safety and efficacy in this clinical setting, 17 patients with stable angina and CAD received an incremental intravenous infusion of either PGI2 (n = 10) to a maximum dose of 10 ng/kg/min (average 9.8 +/- 0.8 [mean +/- standard deviation]), or diluent buffer solution (placebo) (n = 7). All patients who received PGI2 became flushed, but experienced no other adverse effects PGI2 caused an increase in heart rate (66 +/- 11 to 80 +/- 11 beats/min, p less than 0.001) and cardiac index (2.88 +/- 0.65 to 3.97 +/- 1.17 liters/min/m2, p less than 0.001) and a decrease in mean femoral arterial pressure (96 +/- 18 to 86 +/- 11 mm Hg, p less than 0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p less than 0.001). In response to PGI2, mean coronary sinus blood flow did not change significantly (100 +/- 40 to 121 +/- 52 ml/min), but coronary vascular resistance decreased (1.07 +/- 0.40 to 0.83 +/- 0.36 U, p less than 0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1 alpha (the stable metabolite of PGI2) concentrations in both arterial (42 +/- 29 to 567 +/- 216 pg/ml, p less than 0.001) and venous (46 +/- 31 to 604 +/- 229 pg/ml, p less than 0.001) blood but no demonstrable change in plasma renin activity. Thus, intravenous PGI2 to a dosage of 10 ng/kg/min is a safe and effective systemic, pulmonary and coronary arterial vasodilator in patients with CAD and stable angina pectoris.

Author List

Firth BG, Winniford MD, Campbell WB, Hillis LD

Author

William B. Campbell PhD Chair, Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin




Scopus

2-s2.0-0020599773   12 Citations

MESH terms used to index this publication - Major topics in bold

6-Ketoprostaglandin F1 alpha
Angina Pectoris
Blood Pressure
Cardiac Output
Coronary Circulation
Dose-Response Relationship, Drug
Epoprostenol
Female
Heart Rate
Hemodynamics
Humans
Infusions, Parenteral
Male
Middle Aged
Prostaglandins
Random Allocation
Vascular Resistance
jenkins-FCD Prod-353 9ccd8489072cb19f5b9f808bb23ed672c582f41e