Systemic hemodynamic, neurohormonal, and renal effects of a steady- state infusion of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure

William T. Abraham, Brian D. Lowes, Deborah A. Ferguson, John Odom, Jin K. Kim, Alastair D. Robertson, Michael R. Bristow, Robert W. Schrier

Research output: Contribution to journalArticle

221 Citations (Scopus)

Abstract

Background: Human brain natriuretic peptide (hBNP) is a promising agent for the treatment of decompensated cardiac failure. However, the systemic hemodynamic, neurohormonal, and renal effects of hBNP have been incompletely studied in human heart failure. Methods and Results: The effects of a continuous 4-hour infusion of hBNP were determined in 16 decompensated heart failure patients in an invasive, randomized, double-blind, placebo-controlled study. Patients were evaluated during three 4-hour study periods: baseline, treatment (placebo [n = 4] versus hBNP 0.025 or 0.05 μg/kg/min [n = 12]), and post-treatment. Urinary volume losses were replaced hourly to separate the vasodilatory and diuretic effects of hBNP. Two patients in the hBNP group were excluded from the analysis because of adverse events. hBNP significantly (P < .001) reduced right atrial pressure and pulmonary capillary wedge pressure by approximately 30% and 40%, respectively. hBNP also significantly lowered systemic vascular resistance from 1722 ± 139 to 1101 ± 83 dynes · s · cm-5 (P < .05). These unloading effects of hBNP produced a 28% increase in cardiac index (P < .05) with no change in heart rate. Compared to placebo, hBNP decreased plasma norepinephrine and aldosterone. Renal hemodynamics were unaffected by hBNP; however, most patients were resistant to its natriuretic effect. Conclusions: 1) The predominant hemodynamic effects of hBNP were a decrease in cardiac preload and systemic vascular resistance. 2) hBNP also improved cardiac output without increasing heart rate. 3) Plasma norepinephrine and aldosterone levels decreased during hBNP infusion. 4) hBNP is pharmacologically active and has potential in the therapy for decompensated heart failure.

Original languageEnglish (US)
Pages (from-to)37-44
Number of pages8
JournalJournal of Cardiac Failure
Volume4
Issue number1
DOIs
StatePublished - Mar 1998

Fingerprint

Brain Natriuretic Peptide
Heart Failure
Hemodynamics
Kidney
Placebos
Aldosterone
Vascular Resistance
Norepinephrine
Heart Rate
Natriuretic Agents
Pulmonary Wedge Pressure
Atrial Pressure
Therapeutics
Diuretics
Cardiac Output

Keywords

  • Hemodynamics
  • Kidney
  • Sodium excretion

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Systemic hemodynamic, neurohormonal, and renal effects of a steady- state infusion of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure. / Abraham, William T.; Lowes, Brian D.; Ferguson, Deborah A.; Odom, John; Kim, Jin K.; Robertson, Alastair D.; Bristow, Michael R.; Schrier, Robert W.

In: Journal of Cardiac Failure, Vol. 4, No. 1, 03.1998, p. 37-44.

Research output: Contribution to journalArticle

Abraham, William T. ; Lowes, Brian D. ; Ferguson, Deborah A. ; Odom, John ; Kim, Jin K. ; Robertson, Alastair D. ; Bristow, Michael R. ; Schrier, Robert W. / Systemic hemodynamic, neurohormonal, and renal effects of a steady- state infusion of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure. In: Journal of Cardiac Failure. 1998 ; Vol. 4, No. 1. pp. 37-44.
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abstract = "Background: Human brain natriuretic peptide (hBNP) is a promising agent for the treatment of decompensated cardiac failure. However, the systemic hemodynamic, neurohormonal, and renal effects of hBNP have been incompletely studied in human heart failure. Methods and Results: The effects of a continuous 4-hour infusion of hBNP were determined in 16 decompensated heart failure patients in an invasive, randomized, double-blind, placebo-controlled study. Patients were evaluated during three 4-hour study periods: baseline, treatment (placebo [n = 4] versus hBNP 0.025 or 0.05 μg/kg/min [n = 12]), and post-treatment. Urinary volume losses were replaced hourly to separate the vasodilatory and diuretic effects of hBNP. Two patients in the hBNP group were excluded from the analysis because of adverse events. hBNP significantly (P < .001) reduced right atrial pressure and pulmonary capillary wedge pressure by approximately 30{\%} and 40{\%}, respectively. hBNP also significantly lowered systemic vascular resistance from 1722 ± 139 to 1101 ± 83 dynes · s · cm-5 (P < .05). These unloading effects of hBNP produced a 28{\%} increase in cardiac index (P < .05) with no change in heart rate. Compared to placebo, hBNP decreased plasma norepinephrine and aldosterone. Renal hemodynamics were unaffected by hBNP; however, most patients were resistant to its natriuretic effect. Conclusions: 1) The predominant hemodynamic effects of hBNP were a decrease in cardiac preload and systemic vascular resistance. 2) hBNP also improved cardiac output without increasing heart rate. 3) Plasma norepinephrine and aldosterone levels decreased during hBNP infusion. 4) hBNP is pharmacologically active and has potential in the therapy for decompensated heart failure.",
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T1 - Systemic hemodynamic, neurohormonal, and renal effects of a steady- state infusion of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure

AU - Abraham, William T.

AU - Lowes, Brian D.

AU - Ferguson, Deborah A.

AU - Odom, John

AU - Kim, Jin K.

AU - Robertson, Alastair D.

AU - Bristow, Michael R.

AU - Schrier, Robert W.

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AB - Background: Human brain natriuretic peptide (hBNP) is a promising agent for the treatment of decompensated cardiac failure. However, the systemic hemodynamic, neurohormonal, and renal effects of hBNP have been incompletely studied in human heart failure. Methods and Results: The effects of a continuous 4-hour infusion of hBNP were determined in 16 decompensated heart failure patients in an invasive, randomized, double-blind, placebo-controlled study. Patients were evaluated during three 4-hour study periods: baseline, treatment (placebo [n = 4] versus hBNP 0.025 or 0.05 μg/kg/min [n = 12]), and post-treatment. Urinary volume losses were replaced hourly to separate the vasodilatory and diuretic effects of hBNP. Two patients in the hBNP group were excluded from the analysis because of adverse events. hBNP significantly (P < .001) reduced right atrial pressure and pulmonary capillary wedge pressure by approximately 30% and 40%, respectively. hBNP also significantly lowered systemic vascular resistance from 1722 ± 139 to 1101 ± 83 dynes · s · cm-5 (P < .05). These unloading effects of hBNP produced a 28% increase in cardiac index (P < .05) with no change in heart rate. Compared to placebo, hBNP decreased plasma norepinephrine and aldosterone. Renal hemodynamics were unaffected by hBNP; however, most patients were resistant to its natriuretic effect. Conclusions: 1) The predominant hemodynamic effects of hBNP were a decrease in cardiac preload and systemic vascular resistance. 2) hBNP also improved cardiac output without increasing heart rate. 3) Plasma norepinephrine and aldosterone levels decreased during hBNP infusion. 4) hBNP is pharmacologically active and has potential in the therapy for decompensated heart failure.

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