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Editorial
January 28, 2009

BNP-Guided Therapy for Heart Failure

Author Affiliations

Author Affiliations: School of Medicine, Case Western Reserve University, Cleveland, Ohio (Dr Piña); Louis Stokes VA Medical Center, Cleveland, Ohio (Dr Piña); and Department of Medicine, Duke University, Durham, North Carolina (Dr O’Connor).

JAMA. 2009;301(4):432-434. doi:10.1001/jama.2009.3

Clinicians continue to search for that one test, the one biomarker that will help them diagnose, prognosticate, and treat specific syndromes. Heart failure is undoubtedly one of those syndromes. All physicians who treat patients with heart failure seek a robust marker for this syndrome, and some may wonder, with the mounting evidence on brain natriuretic peptide (BNP), is such a biomarker finally here?

The current status of BNP in heart failure has been the result of an important historic journey. In 1981, de Bold et al1 injected myocardial homogenates into nondiuretic rats. The atrial muscle extract increased sodium and chloride excretion 30-fold, along with an impressive increase in urine volume. By 1985, this same group had identified specific granules that secreted the peptide, now known as atrial natriuretic factor (ANF), and noted that the substance also had a hypotensive effect and an inhibitory action on renin and aldosterone secretion.2 Thus, the heart was behaving as an endocrine organ. The investigators noted that the inability of the kidney to excrete sodium in chronic heart failure could be related to ANF and that the peptide might hold promise in the therapy for both hypertension and heart failure. Francis et al3 subsequently described the elevation of ANF early in heart failure and surprisingly in patients with asymptomatic left ventricular dysfunction. Several years later in 1988, Sudoh et al,4 from Japan, isolated an ANF-like peptide from mammalian brain tissue that had similar properties to ANF but was distinct in its amino acid sequence, hence the name brain natriuretic peptide. These investigators suggested that in human disease, both ANF and BNP might perhaps have a dual mechanistic action in sodium and volume homeostasis.

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