Apelin: A new plasma marker of cardiopulmonary disease
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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.
In: Regulatory Peptides, Vol. 133, No. 1-3, 15.01.2006, p. 134-138.Research output: Contribution to journal › Journal article › peer-review
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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