Apelin: A new plasma marker of cardiopulmonary disease

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Standard

Apelin : A new plasma marker of cardiopulmonary disease. / Goetze, Jens Peter; Rehfeld, Jens F.; Carlsen, Jørn; Videbaek, Regitze; Andersen, Claus B.; Boesgaard, Soeren; Friis-Hansen, Lennart.

I: Regulatory Peptides, Bind 133, Nr. 1-3, 15.01.2006, s. 134-138.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Goetze, JP, Rehfeld, JF, Carlsen, J, Videbaek, R, Andersen, CB, Boesgaard, S & Friis-Hansen, L 2006, 'Apelin: A new plasma marker of cardiopulmonary disease', Regulatory Peptides, bind 133, nr. 1-3, s. 134-138. https://doi.org/10.1016/j.regpep.2005.09.032

APA

Goetze, J. P., Rehfeld, J. F., Carlsen, J., Videbaek, R., Andersen, C. B., Boesgaard, S., & Friis-Hansen, L. (2006). Apelin: A new plasma marker of cardiopulmonary disease. Regulatory Peptides, 133(1-3), 134-138. https://doi.org/10.1016/j.regpep.2005.09.032

Vancouver

Goetze JP, Rehfeld JF, Carlsen J, Videbaek R, Andersen CB, Boesgaard S o.a. Apelin: A new plasma marker of cardiopulmonary disease. Regulatory Peptides. 2006 jan. 15;133(1-3):134-138. https://doi.org/10.1016/j.regpep.2005.09.032

Author

Goetze, Jens Peter ; Rehfeld, Jens F. ; Carlsen, Jørn ; Videbaek, Regitze ; Andersen, Claus B. ; Boesgaard, Soeren ; Friis-Hansen, Lennart. / Apelin : A new plasma marker of cardiopulmonary disease. I: Regulatory Peptides. 2006 ; Bind 133, Nr. 1-3. s. 134-138.

Bibtex

@article{c06a85410f0647d6b9f85c6a3dffcb43,
title = "Apelin: A new plasma marker of cardiopulmonary disease",
abstract = "Objectives: Dyspnea is a major symptom of both parenchymal lung disease and chronic heart failure. Underlying cardiac dysfunction can be assessed by measurement of cardiac-derived B-type natriuretic peptide or its precursor in plasma. However, no specific endocrine marker of the lung parenchyma has so far been identified. We therefore examined whether plasma concentrations of apelin, a novel inotropic hormone, is affected in patients with chronic parenchymal lung disease without cardiac dysfunction. Methods and results: Patients with severe chronic parenchymal lung disease and normal cardiac function (n = 53), idiopathic pulmonary hypertension with increased right ventricular pressure (n = 10), and patients with severe left ventricular systolic dysfunction (n = 22) were enrolled. Plasma apelin-36 and proBNP concentrations were measured with radioimmunoassays. While proBNP plasma concentrations were unaffected in chronic parenchymal lung disease patients compared to normal subjects, the apelin-36 concentration was reduced 3.3-fold (median 35 pmol/l (0-162 pmol/l) vs. 117 pmol/l (55-232 pmol/l), P < 0.001). Moreover, the apelin-36 concentration was decreased in chronic heart failure patients (2.1-fold, P < 0.01) and in patients with idiopathic pulmonary hypertension (4.0-fold, P < 0.001). In contrast, the proBNP concentration was highly increased in both chronic heart failure and idiopathic pulmonary hypertension patients. Conclusion: Plasma concentrations of apelin-36, a novel inotropic peptide, are decreased in patients with chronic parenchymal lung disease and preserved cardiac function. Combined measurement of apelin-36 and proBNP may be a new diagnostic approach in distinguishing pulmonary from cardiovascular causes of dyspnea.",
keywords = "Apelin, BNP, Dyspnea, Heart failure, proBNP",
author = "Goetze, {Jens Peter} and Rehfeld, {Jens F.} and J{\o}rn Carlsen and Regitze Videbaek and Andersen, {Claus B.} and Soeren Boesgaard and Lennart Friis-Hansen",
year = "2006",
month = jan,
day = "15",
doi = "10.1016/j.regpep.2005.09.032",
language = "English",
volume = "133",
pages = "134--138",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",
number = "1-3",

}

RIS

TY - JOUR

T1 - Apelin

T2 - A new plasma marker of cardiopulmonary disease

AU - Goetze, Jens Peter

AU - Rehfeld, Jens F.

AU - Carlsen, Jørn

AU - Videbaek, Regitze

AU - Andersen, Claus B.

AU - Boesgaard, Soeren

AU - Friis-Hansen, Lennart

PY - 2006/1/15

Y1 - 2006/1/15

N2 - Objectives: Dyspnea is a major symptom of both parenchymal lung disease and chronic heart failure. Underlying cardiac dysfunction can be assessed by measurement of cardiac-derived B-type natriuretic peptide or its precursor in plasma. However, no specific endocrine marker of the lung parenchyma has so far been identified. We therefore examined whether plasma concentrations of apelin, a novel inotropic hormone, is affected in patients with chronic parenchymal lung disease without cardiac dysfunction. Methods and results: Patients with severe chronic parenchymal lung disease and normal cardiac function (n = 53), idiopathic pulmonary hypertension with increased right ventricular pressure (n = 10), and patients with severe left ventricular systolic dysfunction (n = 22) were enrolled. Plasma apelin-36 and proBNP concentrations were measured with radioimmunoassays. While proBNP plasma concentrations were unaffected in chronic parenchymal lung disease patients compared to normal subjects, the apelin-36 concentration was reduced 3.3-fold (median 35 pmol/l (0-162 pmol/l) vs. 117 pmol/l (55-232 pmol/l), P < 0.001). Moreover, the apelin-36 concentration was decreased in chronic heart failure patients (2.1-fold, P < 0.01) and in patients with idiopathic pulmonary hypertension (4.0-fold, P < 0.001). In contrast, the proBNP concentration was highly increased in both chronic heart failure and idiopathic pulmonary hypertension patients. Conclusion: Plasma concentrations of apelin-36, a novel inotropic peptide, are decreased in patients with chronic parenchymal lung disease and preserved cardiac function. Combined measurement of apelin-36 and proBNP may be a new diagnostic approach in distinguishing pulmonary from cardiovascular causes of dyspnea.

AB - Objectives: Dyspnea is a major symptom of both parenchymal lung disease and chronic heart failure. Underlying cardiac dysfunction can be assessed by measurement of cardiac-derived B-type natriuretic peptide or its precursor in plasma. However, no specific endocrine marker of the lung parenchyma has so far been identified. We therefore examined whether plasma concentrations of apelin, a novel inotropic hormone, is affected in patients with chronic parenchymal lung disease without cardiac dysfunction. Methods and results: Patients with severe chronic parenchymal lung disease and normal cardiac function (n = 53), idiopathic pulmonary hypertension with increased right ventricular pressure (n = 10), and patients with severe left ventricular systolic dysfunction (n = 22) were enrolled. Plasma apelin-36 and proBNP concentrations were measured with radioimmunoassays. While proBNP plasma concentrations were unaffected in chronic parenchymal lung disease patients compared to normal subjects, the apelin-36 concentration was reduced 3.3-fold (median 35 pmol/l (0-162 pmol/l) vs. 117 pmol/l (55-232 pmol/l), P < 0.001). Moreover, the apelin-36 concentration was decreased in chronic heart failure patients (2.1-fold, P < 0.01) and in patients with idiopathic pulmonary hypertension (4.0-fold, P < 0.001). In contrast, the proBNP concentration was highly increased in both chronic heart failure and idiopathic pulmonary hypertension patients. Conclusion: Plasma concentrations of apelin-36, a novel inotropic peptide, are decreased in patients with chronic parenchymal lung disease and preserved cardiac function. Combined measurement of apelin-36 and proBNP may be a new diagnostic approach in distinguishing pulmonary from cardiovascular causes of dyspnea.

KW - Apelin

KW - BNP

KW - Dyspnea

KW - Heart failure

KW - proBNP

UR - http://www.scopus.com/inward/record.url?scp=29244471763&partnerID=8YFLogxK

U2 - 10.1016/j.regpep.2005.09.032

DO - 10.1016/j.regpep.2005.09.032

M3 - Journal article

C2 - 16263185

AN - SCOPUS:29244471763

VL - 133

SP - 134

EP - 138

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

IS - 1-3

ER -

ID: 310768294