Molecular forms of natriuretic peptides in heart failure and their implications
- 1Department of Hospital Medicine, Cleveland Clinic, Cleveland, Ohio, USA
- 2Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, USA
- 3Department of Nephrology/Hypertension, Cleveland Clinic, Cleveland, Ohio, USA
- Correspondence to Dr Ye Olivia Xu-Cai, Department of Hospital Medicine, Cleveland Clinic, 9500 Euclid Avenue/Mail Stop S-70, Cleveland, OH 44195, USA; caio{at}ccf.org
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Contributors YOX-C was responsible for the acquisition, analysis and interpretation of data and drafting of the manuscript. QW was responsible for analysis and interpretation of data, study concept and design and critical revision of the manuscript.
- Accepted 28 April 2009
- Published Online First 17 May 2009
Abstract
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important biomarkers in the diagnosis and risk stratification for heart failure (HF). These peptides are synthesised as inactive precursors, pro-ANP and pro-BNP, which are converted to biologically active 28 amino acid ANP and 32 amino acid BNP, respectively. Most immunoassays currently used in the clinical setting, however, do not determine precise molecular forms of these natriuretic peptides, which may vary depending on the pathophysiological state of HF. Analysis from chromatography-based studies reveals that in HF inactive pro-ANP and pro-BNP forms often predominate. This indicates that the bioactive forms of natriuretic peptides may not be processed proportionally in patients with advanced HF. Distinguishing the bioactive natriuretic peptides from their inactive forms in plasma may help to define the role of these peptides in the pathogenesis of HF and provide new insights into the treatment of the disease.
- Atrial natriuretic peptide
- B-type or brain natriuretic peptide
- biomarker
- cardiomyopathy dilated
- heart failure
Footnotes
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Funding This work is supported in part by grants from the Research Program Committee of the Cleveland Clinic, the National Institutes of Health (R01 HL089298), the Ralph Wilson Medical Research Foundation and the Bakken Heart–Brain Institute.
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Competing interests None.
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Provenance and peer review Not commissioned; externally peer reviewed.









