Natriuretic peptide measurement in non-heart failure settings

Natriuretic peptide measurement in non-heart failure settings

Authors
Horng H Chen, MD
Wilson S Colucci, MD
Section Editors
Stephen S Gottlieb, MD
Allan S Jaffe, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2012. | This topic last updated: Apr 20, 2012.
INTRODUCTION The natriuretic peptide system impacts salt and water handling and
pressure regulation and may influence myocardial structure and function.
Brain natriuretic peptide (BNP) is a natriuretic hormone initially identified in the brain but
released primarily from the heart, particularly the ventricles. Cleavage of the prohormone
proBNP produces biologically active 32 amino acid BNP as well as biologically inert 76 amino
acid N-terminal pro-BNP (NT-proBNP).
Atrial natriuretic peptide (ANP) is a hormone that is released from myocardial cells in the atria
and in some cases the ventricles in response to volume expansion and possibly increased wall
stress [1]. ANP circulates primarily as a 28 amino acid polypeptide, consisting of amino acids 99
to 126 from the C-terminal end of its prohormone, pro-ANP.
The release of both ANP and BNP is increased in heart failure (HF), as ventricular cells are
recruited to secrete both ANP and BNP in response to the high ventricular filling pressures [2].
The plasma concentrations of both hormones are increased in patients with asymptomatic and
symptomatic left ventricular dysfunction, permitting their use in diagnosis (figure 1).
Natriuretic peptide levels are elevated in some patients with coronary heart disease, valvular
heart disease, constrictive pericarditis, pulmonary hypertension, and sepsis. The diagnostic and
prognostic value of measuring plasma BNP and N-terminal pro-BNP (NT-proBNP) in
asymptomatic individuals and patients with such non-heart failure conditions is discussed here.
While the discussion here will focus on patients without overt heart failure, BNP or NT-proBNP
elevations in some of these settings may be a sign of undiagnosed heart failure.
The diagnostic and prognostic value of measuring plasma BNP, NT-proBNP, and mid-regional
pro-atrial natriuretic peptide (MR-proANP) in patients with heart failure and the possible
therapeutic role of nesiritide (recombinant human BNP) in the management of patients with

decompensated HF is discussed separately. (See "Natriuretic peptide measurement in heart

failure" and "Nesiritide in the treatment of acute decompensated heart failure".)
ASSAY INTERPRETATION A number of variables affect plasma BNP and NT-proBNP
levels including the assay used, age (higher normal values with age), sex (higher values in
women), and body mass index (lower levels with higher body mass index), and genetic factors.
In addition, there is intraindivual and analytic assay variation. These issues are discussed in
greater detail separately. (See "Natriuretic peptide measurement in heart failure", section on
'Assay interpretation' and "Natriuretic peptide measurement in heart failure", section on
'Obesity'.)
CONDITIONS
Renal failure Plasma BNP and NT-proBNP concentrations are elevated in patients with renal
failure. In patients with chronic kidney disease, decreased estimated GFR is associated with
increased plasma BNP and even greater elevation in NT-proBNP concentrations. This issue is
discussed in detail separately. (See "Natriuretic peptide measurement in heart failure", section on
'Renal failure'.)
Predictor of cardiovascular events Plasma BNP and the N-terminal fragment of pro-ANP (NproANP) levels are predictors of the development of HF, as well as other cardiovascular events,
in asymptomatic patients without HF. This was demonstrated in a prospective evaluation of 3346
participants (mean age 59 years) in the Framingham Heart Study [3]. At five years, 119 patients
died (3.6 percent) and 79 had a first cardiovascular event (MI, coronary insufficiency, death from
coronary heart disease, HF, or stroke; 2.4 percent). Baseline plasma BNP and N-proANP levels
above the 80th percentile were both associated with a significant increase in the subsequent
development of HF (adjusted hazard ratio [HR] 3.07 and 5.02), as well as less marked increases
in all-cause mortality, atrial fibrillation, and stroke or transient ischemic attack.