Secretion of prohormone of b-type natriuretic peptide, proBNP1-108: Is increased in heart failure

Lisa C. Costello-Boerrigter, Harald Lapp, Guido Boerrigter, Amir Lerman, Alexander Bufe, Fima Macheret, Denise M. Heublein, Catherine Larue, John C Jr. Burnett

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Objectives: Using a novel, specific assay for proBNP1-108, this study tested the hypotheses that proBNP1-108 is secreted by both nonfailing and failing human hearts and that proBNP1-108 secretion is increased in failing hearts. Background: The prohormone of B-type natriuretic peptide (proBNP1-108) is a 108-amino acid peptide produced primarily by the heart and cleaved into biologically active BNP1-32 and the biologically inactive NT-proBNP1-76. It is unknown to what extent increased cardiac proBNP1-108 secretion compared to reduced peripheral processing is responsible for elevated proBNP1-108 levels in patients with heart failure (HF) compared to subjects without HF. Methods: The transcardiac gradient of proBNP1-108 was determined by collecting arterial blood and blood from the coronary sinus (CS). Samples from subjects without overt heart disease (n = 9) were collected during cardiac catheterization after coronary artery disease had been excluded. Samples from HF patients (n = 21) were collected during implantation of a biventricular pacemaker. ProBNP1-108 was measured with a new assay. Values are medians (25th/75th percentiles). Results: The gradient of proBNP1-108 across the nonfailing hearts was 8 (2/20) ng/l (aorta: 15 [1/25] ng/l; CS: 24 [8/41] ng/l; p = 0.018). The transcardiac gradient of proBNP1-108 in the failing hearts was 326 (96/482) ng/l (arterial: 381 [201/586] ng/l; CS: 709 [408/1,087] ng/l; p<0.001). The transcardiac gradient was greater in failing than nonfailing hearts (p = 0.001). Conclusions: ProBNP1-108 is secreted by nonfailing and failing human hearts, but more so in the latter. It remains to be established where peripheral processing of proBNP1-108 occurs and how this is affected by disease.

Original languageEnglish (US)
Pages (from-to)207-212
Number of pages6
JournalJACC: Heart Failure
Volume1
Issue number3
DOIs
StatePublished - Jun 2013

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Natriuretic Peptides
Heart Failure
Coronary Sinus
Pro-BNP1-108
Brain Natriuretic Peptide
Cardiac Catheterization
Aorta
Coronary Artery Disease
Heart Diseases
Amino Acids

Keywords

  • Biomarker
  • Heart failure
  • Natriuretic peptides
  • ProBNP

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Secretion of prohormone of b-type natriuretic peptide, proBNP1-108 : Is increased in heart failure. / Costello-Boerrigter, Lisa C.; Lapp, Harald; Boerrigter, Guido; Lerman, Amir; Bufe, Alexander; Macheret, Fima; Heublein, Denise M.; Larue, Catherine; Burnett, John C Jr.

In: JACC: Heart Failure, Vol. 1, No. 3, 06.2013, p. 207-212.

Research output: Contribution to journalArticle

Costello-Boerrigter, LC, Lapp, H, Boerrigter, G, Lerman, A, Bufe, A, Macheret, F, Heublein, DM, Larue, C & Burnett, JCJ 2013, 'Secretion of prohormone of b-type natriuretic peptide, proBNP1-108: Is increased in heart failure', JACC: Heart Failure, vol. 1, no. 3, pp. 207-212. https://doi.org/10.1016/j.jchf.2013.03.001
Costello-Boerrigter, Lisa C. ; Lapp, Harald ; Boerrigter, Guido ; Lerman, Amir ; Bufe, Alexander ; Macheret, Fima ; Heublein, Denise M. ; Larue, Catherine ; Burnett, John C Jr. / Secretion of prohormone of b-type natriuretic peptide, proBNP1-108 : Is increased in heart failure. In: JACC: Heart Failure. 2013 ; Vol. 1, No. 3. pp. 207-212.
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abstract = "Objectives: Using a novel, specific assay for proBNP1-108, this study tested the hypotheses that proBNP1-108 is secreted by both nonfailing and failing human hearts and that proBNP1-108 secretion is increased in failing hearts. Background: The prohormone of B-type natriuretic peptide (proBNP1-108) is a 108-amino acid peptide produced primarily by the heart and cleaved into biologically active BNP1-32 and the biologically inactive NT-proBNP1-76. It is unknown to what extent increased cardiac proBNP1-108 secretion compared to reduced peripheral processing is responsible for elevated proBNP1-108 levels in patients with heart failure (HF) compared to subjects without HF. Methods: The transcardiac gradient of proBNP1-108 was determined by collecting arterial blood and blood from the coronary sinus (CS). Samples from subjects without overt heart disease (n = 9) were collected during cardiac catheterization after coronary artery disease had been excluded. Samples from HF patients (n = 21) were collected during implantation of a biventricular pacemaker. ProBNP1-108 was measured with a new assay. Values are medians (25th/75th percentiles). Results: The gradient of proBNP1-108 across the nonfailing hearts was 8 (2/20) ng/l (aorta: 15 [1/25] ng/l; CS: 24 [8/41] ng/l; p = 0.018). The transcardiac gradient of proBNP1-108 in the failing hearts was 326 (96/482) ng/l (arterial: 381 [201/586] ng/l; CS: 709 [408/1,087] ng/l; p<0.001). The transcardiac gradient was greater in failing than nonfailing hearts (p = 0.001). Conclusions: ProBNP1-108 is secreted by nonfailing and failing human hearts, but more so in the latter. It remains to be established where peripheral processing of proBNP1-108 occurs and how this is affected by disease.",
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T1 - Secretion of prohormone of b-type natriuretic peptide, proBNP1-108

T2 - Is increased in heart failure

AU - Costello-Boerrigter, Lisa C.

AU - Lapp, Harald

AU - Boerrigter, Guido

AU - Lerman, Amir

AU - Bufe, Alexander

AU - Macheret, Fima

AU - Heublein, Denise M.

AU - Larue, Catherine

AU - Burnett, John C Jr.

PY - 2013/6

Y1 - 2013/6

N2 - Objectives: Using a novel, specific assay for proBNP1-108, this study tested the hypotheses that proBNP1-108 is secreted by both nonfailing and failing human hearts and that proBNP1-108 secretion is increased in failing hearts. Background: The prohormone of B-type natriuretic peptide (proBNP1-108) is a 108-amino acid peptide produced primarily by the heart and cleaved into biologically active BNP1-32 and the biologically inactive NT-proBNP1-76. It is unknown to what extent increased cardiac proBNP1-108 secretion compared to reduced peripheral processing is responsible for elevated proBNP1-108 levels in patients with heart failure (HF) compared to subjects without HF. Methods: The transcardiac gradient of proBNP1-108 was determined by collecting arterial blood and blood from the coronary sinus (CS). Samples from subjects without overt heart disease (n = 9) were collected during cardiac catheterization after coronary artery disease had been excluded. Samples from HF patients (n = 21) were collected during implantation of a biventricular pacemaker. ProBNP1-108 was measured with a new assay. Values are medians (25th/75th percentiles). Results: The gradient of proBNP1-108 across the nonfailing hearts was 8 (2/20) ng/l (aorta: 15 [1/25] ng/l; CS: 24 [8/41] ng/l; p = 0.018). The transcardiac gradient of proBNP1-108 in the failing hearts was 326 (96/482) ng/l (arterial: 381 [201/586] ng/l; CS: 709 [408/1,087] ng/l; p<0.001). The transcardiac gradient was greater in failing than nonfailing hearts (p = 0.001). Conclusions: ProBNP1-108 is secreted by nonfailing and failing human hearts, but more so in the latter. It remains to be established where peripheral processing of proBNP1-108 occurs and how this is affected by disease.

AB - Objectives: Using a novel, specific assay for proBNP1-108, this study tested the hypotheses that proBNP1-108 is secreted by both nonfailing and failing human hearts and that proBNP1-108 secretion is increased in failing hearts. Background: The prohormone of B-type natriuretic peptide (proBNP1-108) is a 108-amino acid peptide produced primarily by the heart and cleaved into biologically active BNP1-32 and the biologically inactive NT-proBNP1-76. It is unknown to what extent increased cardiac proBNP1-108 secretion compared to reduced peripheral processing is responsible for elevated proBNP1-108 levels in patients with heart failure (HF) compared to subjects without HF. Methods: The transcardiac gradient of proBNP1-108 was determined by collecting arterial blood and blood from the coronary sinus (CS). Samples from subjects without overt heart disease (n = 9) were collected during cardiac catheterization after coronary artery disease had been excluded. Samples from HF patients (n = 21) were collected during implantation of a biventricular pacemaker. ProBNP1-108 was measured with a new assay. Values are medians (25th/75th percentiles). Results: The gradient of proBNP1-108 across the nonfailing hearts was 8 (2/20) ng/l (aorta: 15 [1/25] ng/l; CS: 24 [8/41] ng/l; p = 0.018). The transcardiac gradient of proBNP1-108 in the failing hearts was 326 (96/482) ng/l (arterial: 381 [201/586] ng/l; CS: 709 [408/1,087] ng/l; p<0.001). The transcardiac gradient was greater in failing than nonfailing hearts (p = 0.001). Conclusions: ProBNP1-108 is secreted by nonfailing and failing human hearts, but more so in the latter. It remains to be established where peripheral processing of proBNP1-108 occurs and how this is affected by disease.

KW - Biomarker

KW - Heart failure

KW - Natriuretic peptides

KW - ProBNP

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