doi: 10.1161/01.CIR.0000042763.07757.C0
(Circulation. 2002;106:2868.)
© 2002 American Heart Association, Inc.
Brain Natriuretic Peptide Measurement in Acute Coronary Syndromes
Ready for Clinical Application?
From the Donald W. Reynolds Cardiovascular Clinical Research Center, UT Southwestern Medical School, Dallas, Tex (J.d.L.); and the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass (D.A.M.).
Correspondence to James de Lemos, MD, UT Southwestern Medical Center, 5323 Harry Hines Blvd, CS 7.102, Dallas, TX 75390-9047. E-mail james.delemos@utsouthwestern.edu
Key Words: Editorials • natriuretic peptides • coronary disease
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Brain (B-type) natriuretic peptide (BNP) is a 32 amino acid peptide that is synthesized and released predominantly from ventricular myocardium in response to myocyte stretch. Like atrial natriuretic peptide (ANP), BNP seems to have almost exclusively beneficial physiological properties, including balanced vasodilation, natriuresis, and inhibition of both the sympathetic nervous system and the renin-angiotensin-aldosterone axis. Attempts to exploit these properties for therapeutic benefit has led to the development of recombinant human BNP (nesiritide) for the acute treatment of decompensated heart failure, and also of novel compounds that inhibit neutral endopeptidase, an enzyme that is partially responsible for BNP degradation.
See p 2913
Measurement of BNP in Patients With Suspected Heart Failure
In patients with heart failure, the cardiac neurohormonal system is activated, and circulating plasma levels of ANP, BNP, and the N-terminal fragments of their prohormones (N-proANP and N-proBNP) are elevated. Compared with ANP and N-proANP, BNP and N-proBNP undergo a greater proportional rise in disease states (ie, higher "signal-to-noise" ratio), and thus have emerged as the preferred biomarkers for clinical development. With commercially available assays now available, measurement of BNP or N-proBNP can be integrated readily into the care of patients with suspected heart failure. Although data are limited, BNP and N-proBNP seem to provide qualitatively similar information, and for purposes of this editorial, will be referred to interchangeably.
Incorporation of BNP measurement into the clinical evaluation facilitates the diagnosis of heart failure due to either left ventricular (LV) systolic or diastolic dysfunction; a normal BNP level virtually rules out the diagnosis of decompensated heart failure, whereas a
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