Effects of Prostaglandin E1, Dobutamine and Placebo on Hemodynamic, Renal and Neurohumoral Variables in Patients with Advanced Heart Failure
Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin El (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was pe...
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Published in | Japanese Heart Journal Vol. 40; no. 3; pp. 321 - 334 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Tokyo
International Heart Journal Association
01.05.1999
Japanese Heart Journal Association |
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Abstract | Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin El (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m2) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 ± 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 ± 1 μg/kg/min, range 2.5 to 5 μg/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE 1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1. |
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AbstractList | Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin E1 (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m2) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 +/- 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 +/- 1 micrograms/kg/min, range 2.5 to 5 micrograms/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1. Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin El (PGE1), a balanced i.v. vasodilator, was shown to elicit favorable hemodynamic and clinical effects in this cohort. A prospective randomized parallel group trial was performed to evaluate acute, intermediate and chronic changes in hemodynamic, neurohumoral and renal variables in response to PGE1, dobutamine and placebo. Thirty patients with class III and IV heart failure and low cardiac index (mean 1.9 l/min/m2) two hours after oral drugs including high dose enalapril were included. A 7-day-infusion of PGE1 (16.5 ± 5 ng/kg/min, range 10 to 20 ng/kg/min, group A n = 10), dobutamine (4.5 ± 1 μg/kg/min, range 2.5 to 5 μg/kg/min, group B n = 10) or placebo (saline, group C n = 10) was administered via a central venous access line after stepwise titration until intolerable side effects developed with PGE1 or a 20% increase in cardiac index occurred with dobutamine, which was continued on this dose throughout while PGE 1 was maintained on 50% peak dose. Hemodynamic data were collected at baseline, at peak dosages, after 12 hours and after 7 days. Of neurohumoral variables plasma norepinephrine, big endothelin (Big ET) and atrial natriuretic peptide (ANP) were simultaneously evaluated using RIA methods. Renal plasma flow (by paraaminohippurate clearance) and glomerular filtration rate (by iothalamate clearance) was measured prior to and during the infusions (after 12 hours and after 7 days). At peak dose and at 12 hours significant drops from baseline of mean pulmonary artery pressure, pulmonary capillary wedge pressure and systemic vascular resistance were observed which were accompanied by a rise in cardiac output with both PGE1 and dobutamine. These changes were maintained through 7 days when pulmonary vascular resistance levels also fell with both active drugs. Blood pressure did not change throughout, but PGE1 increased heart rate slightly at 12 hrs. Both PGE1 and dobutamine enhanced renal plasma flow after 7 days, but only PGE1 decreased glomerular filtration fraction significantly. Glomerular filtration rate did not change with either drug. PGE1 decreased ANP levels at 12 hrs, and dobutamine increased big ET levels at peak, but decreased big ET at 7 days. Norepinephrine levels were unaffected throughout. Except a slight decrease in right atrial pressure after 7 days placebo did not change any measured variable significantly. Taken together, these data suggest that treatment with PGE1 is as efficacious as low-dose dobutamine in improving cardiac performance and renal perfusion in advanced heart failure. Of importance, no deleterious neurohumoral counterregulation was observed with PGE1. |
Author | STANEK, Brigitte WIMMER, Andreas KUBECOVA, Lea PACHER, Richard FREY, Bernhard SPINAR, Jindrich HARTTER, Engelbert VITOVEC, Jiri KOS, Thomas YILMAZ, Nilgryn |
Author_xml | – sequence: 1 fullname: WIMMER, Andreas organization: Department of Cardiology, University of Vienna, Austria – sequence: 2 fullname: STANEK, Brigitte organization: Department of Cardiology, University of Vienna, Austria – sequence: 3 fullname: KUBECOVA, Lea organization: Department of Internal Medicine, University of Brno, Czech Republic – sequence: 4 fullname: VITOVEC, Jiri organization: Department of Internal Medicine, University of Brno, Czech Republic – sequence: 5 fullname: SPINAR, Jindrich organization: Department of Internal Medicine, University of Brno, Czech Republic – sequence: 6 fullname: YILMAZ, Nilgryn organization: Department of Nephrology, University of Vienna, Austria – sequence: 7 fullname: KOS, Thomas organization: Department of Cardiology, University of Vienna, Austria – sequence: 8 fullname: HARTTER, Engelbert organization: Department of Occupational Medicine and Ludwig Boltzmann Institute of Experimental Endocrinology, University of Vienna, Austria – sequence: 9 fullname: FREY, Bernhard organization: Department of Cardiology, University of Vienna, Austria – sequence: 10 fullname: PACHER, Richard organization: Department of Cardiology, University of Vienna, Austria |
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Keywords | Human Heart failure Pharmacologic test Cardiotonic agent Renal function Vasodilator agent Dobutamine Cardiovascular disease Prostaglandin E1 Heart disease Advanced stage Neurohormone Hemodynamics |
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Snippet | Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin El (PGE1), a balanced i.v.... Excessive neurohumoral activity remains a major burden to the circulation of patients with advanced heart failure. Prostaglandin E1 (PGE1), a balanced i.v.... |
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SubjectTerms | Advanced heart failure Alprostadil - therapeutic use Atrial Natriuretic Factor - blood Biological and medical sciences Blood Pressure - drug effects Cardiology. Vascular system Cardiotonic Agents - therapeutic use Dobutamine Dobutamine - therapeutic use Endothelins - blood Female Glomerular filtration rate Glomerular Filtration Rate - drug effects Heart Heart Failure - blood Heart Failure - drug therapy Heart Failure - physiopathology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart Rate - drug effects Hemodynamics Hemodynamics - drug effects Humans Male Medical sciences Middle Aged Norepinephrine - blood Prospective Studies Prostaglandin E1 Renal Circulation - drug effects Renal plasma flow Vasodilator Agents - therapeutic use |
Title | Effects of Prostaglandin E1, Dobutamine and Placebo on Hemodynamic, Renal and Neurohumoral Variables in Patients with Advanced Heart Failure |
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ispartofPNX | Japanese Heart Journal, 1999, Vol.40(3), pp.321-334 |
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