Apelin: A new plasma marker of cardiopulmonary disease

• Published in: Regulatory peptides Vol. 133; no. 1; pp. 134 - 138
• Main Authors: Goetze, Jens Peter, Rehfeld, Jens F., Carlsen, Jørn, Videbaek, Regitze, Andersen, Claus B., Boesgaard, Soeren, Friis-Hansen, Lennart
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15.01.2006; Amsterdam Elsevier
• Subjects: Aged; Apelin; Biological and medical sciences; Biomarkers - blood; Biomarkers - metabolism; BNP; Cardiology. Vascular system; Dyspnea; Female; Fundamental and applied biological sciences. Psychology; Heart; Heart failure; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Intercellular Signaling Peptides and Proteins - blood; Intercellular Signaling Peptides and Proteins - metabolism; Male; Medical sciences; Microscopy, Confocal; Middle Aged; Pneumology; proBNP; Pulmonary Heart Disease - blood; Pulmonary Heart Disease - diagnosis; Respiratory system : syndromes and miscellaneous diseases; Vertebrates: endocrinology; Heart failure; Dyspnea; BNP; Apelin; proBNP; Respiratory disease; Heart disease; Cardiovascular disease
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/j.regpep.2005.09.032

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. 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. 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.