TY - JOUR
T1 - Hemodynamic effects of intravenous prostacyclin in stable angina pectoris
AU - Firth, Brian G.
AU - Winniford, Michael D.
AU - Campbell, William B.
AU - Hillis, L. David
N1 - Funding Information:
From the Departments of Internal Medicine (Cardiology Division) and pharmacology, Lhtiversityo f Texas Health Science Center, and Parkland Memorial Hospital, Dallas, Texas. Dr. Winniford was supported by National Heart, Lung, and Blood InstiMe Training Grant HL 07360. Bethesda, Maryland, Dr. Hillis is an Established Investigator of the American Heart Association, and Dr. Campbell is the recipient of a Research Career Development Award from the National InstiMes of Health (K04-H_-00801). These studies were supported by grants from the National Heart, Lung, and Blood InstiMe (K-25471), Bethesda. krytand, and the American HE& Association, Dallas, Texas (with funds contributed in part by the Palm Seach County Chapter). Manuscript received March 14, 1983; revised manuscript received May 31, 1983, accepted June 3, 1983.
PY - 1983/9/1
Y1 - 1983/9/1
N2 - 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 <0.001) and cardiac index (2.88 ± 0.65 to 3.97 ± 1.17 liters/min/m2, p <0.001) and a decrease in mean femoral arterial pressure (96 ± 18 to 86 ± 11 mm Hg, p <0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p <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 <0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1α (the stable metabolite of PGI2) concentrations in both arterial (42 ± 29 to 567 ± 216 pg/ml, p <0.001) and venous (46 ± 31 to 604 ± 229 pg/ml, p <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.
AB - 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 <0.001) and cardiac index (2.88 ± 0.65 to 3.97 ± 1.17 liters/min/m2, p <0.001) and a decrease in mean femoral arterial pressure (96 ± 18 to 86 ± 11 mm Hg, p <0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p <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 <0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1α (the stable metabolite of PGI2) concentrations in both arterial (42 ± 29 to 567 ± 216 pg/ml, p <0.001) and venous (46 ± 31 to 604 ± 229 pg/ml, p <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.
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U2 - 10.1016/0002-9149(83)90003-6
DO - 10.1016/0002-9149(83)90003-6
M3 - Article
C2 - 6351580
AN - SCOPUS:0020599773
VL - 52
SP - 439
EP - 443
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 5
ER -