You are here

Article Text

Article menu
Download PDFPDF
Education in Heart
Heart failure
Biomarkers in heart failure
  1. Wei-Chung Chen,
  2. Kimberly D Tran,
  3. Alan S Maisel
  1. Division of Cardiology, University of California at San Diego, Veteran Affairs San Diego Healthcare System, San Diego, California, USA
  1. Correspondence to Dr Alan S Maisel, VA San Diego Healthcare System, 3350 La Jolla Village Drive, Cardiology Section, MC 9111A, San Diego, CA 92161, USA; amaisel{at}ucsd.edu

https://doi.org/10.1136/hrt.2008.151639

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Cardiovascular disease has emerged as one of the most prominent causes of morbidity and mortality among adult populations. As medical advances have enabled more patients to survive post-myocardial insult, the prevalence of congestive heart failure (CHF) has exploded. It is now estimated that 5 million people in the USA live with CHF, and that approximately 550 000 new cases are diagnosed each year.1 Hospitalisations for heart failure have increased dramatically from 402 000 in 1979 to 1 101 000 in 2004 (National Hospital Discharge Survey), and the cost of CHF is now estimated at US$56 billion a year, 70% of which is due to hospitalisation.1 Among a variety of proposed heart failure treatment modalities, cardiac biomarkers have emerged as powerful adjuncts to standardised clinical care in the diagnosis, prognosis, and treatment of acute heart failure (AHF).

    Basics regarding natriuretic peptides (NPs)

    B-type natriuretic peptide (BNP) is first synthesised in the myocytes as a 132 amino acid intracellular precursor known as preproBNP. During decompensation, volume overload and high pulmonary capillary wedge pressure cause the ventricle walls to stretch, triggering the cleavage and release of preproBNP as the biologically active 32 amino acid hormone BNP and its inactive N-terminal fragment (NT-proBNP). Once released, BNP has pronounced natriuretic, diuretic, and vasodilating properties, working to dramatically reduce volume overload and hypertension in patients. BNP is then believed to be removed quickly from circulation (half-life of 22 min) by both NP receptor endocytosis and endopeptidase enzymatic degradation.2 In contrast, NT-proBNP is suspected to be cleared from the plasma largely by renal excretion, and thus has slower fluctuations in circulating concentrations as well as a notably longer half-life of 60–120 min.2 In general, BNP and NT-proBNP values are reasonably correlated, and either can be used in patient care settings as long as their respective absolute values and cut points are not used interchangeably.

    Diagnostic utility of NPs

    In …

    View Full Text

    Footnotes

    • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The authors have no competing interests.

    • Provenance and peer review Commissioned; not externally peer reviewed.