General cardiology

ROLE OF B-TYPE NATRIURETIC PEPTIDE

(BNP) AND NT-PROBNP IN CLINICAL
ROUTINE
Michael Weber, Christian Hamm
Heart 2006; 92:843849. doi: 10.1136/hrt.2005.071233
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n recent years biomarkers have emerged as important tools for diagnosis, risk stratification and
therapeutic decision making in cardiovascular diseases. Cardiac troponins in particular have
become the cornerstone for diagnostic work up of patients with acute coronary syndromes.
Currently, several promising new biomarkers are under scientific investigation. Most of these new
biomarkers, however, are not yet suitable for clinical application, with the exception of B-type
natriuretic peptide (BNP) and its N-terminal fragment (NT-proBNP). Both markers have proven
their diagnostic usefulness in a great number of studies and thus have progressed from bench to
clinical application. This article aims to summarise existing data concerning BNP and NT-proBNP
measurement in cardiovascular disorders and to outline how these markers can be integrated into
clinical routine. Furthermore, future perspectives of these markers will be discussed.

PHYSIOLOGY
B-type natriuretic peptide, which is also called brain-type natriuretic peptide (BNP), was first
described in 1988 after isolation from porcine brain. However, it was soon found to originate
mainly from the heart, representing a cardiac hormone.
BNP belongs to the natriuretic peptide family together with other structurally similar peptides,
namely atrial natriuretic peptide (ANP), C-type natriuretic peptide (CNP), and urodilatin. The
natriuretic peptides have in common a characteristic biochemical structure which consists of a 17
amino-acid ring and a disulfide bridge between two cysteine molecules. The major source of BNP
synthesis and secretion is the ventricular myocardium. Whereas ANP is stored in granules and
can be released immediately after stimulation, only small amounts of BNP are stored in granules
and rapid gene expression with de novo synthesis of the peptide is the underlying mechanism for
the regulation of BNP secretion. BNP is synthesised as a prehormone (proBNP) comprising 108
amino acids. Upon release into the circulation it is cleaved in equal proportions into the
biologically active 32 amino acid BNP, which represents the C-terminal fragment, and the
biologically inactive 76 amino acid N-terminal fragment (NT-proBNP).
Both molecules are constantly released and can be detected in the blood. The main stimulus for
increased BNP and NT-proBNP synthesis and secretion is myocardial wall stress. Furthermore,
factors such as myocardial ischaemia and endocrine (paracrine) modulation by other
neurohormones and cytokines are also of importance.
In the systemic circulation BNP mediates a variety of biological effects by interaction with the
natriuretic peptide receptor type A (NPR-A) causing intracellular cGMP production. The
physiological effects of BNP are manifold and comprise natriuresis/diuresis, peripheral
vasodilatation, and inhibition of the reninangiotensinaldosterone system (RAAS) and the
sympathetic nervous system (SNS). BNP is cleared from plasma by binding to the natriuretic
peptide receptor type C (NPR-C) and through proteolysis by neutral endopeptidases. In contrast,
NT-proBNP is mainly cleared by renal excretion. However, recent studies suggest that there might
also be other important clearing mechanisms for NT-proBNP. The half-life of BNP is 20 mins
whereas NT-proBNP has a half-life of 120 mins, which explains why NT-proBNP serum values are
approximately six times higher than BNP values, even though both molecules are released in
equimolar proportions (figs 1 and 2).1

See end of article for authors

affiliations
_________________________
Correspondence to:
Michael Weber, MD,
Kerckhoff Heart Center,
Department of Cardiology,
Benekestrae 28, 61231 Bad
Nauheim, Germany; M.
Weber@kerckhoff-klinik.de
_________________________

ANALYTIC CONSIDERATIONS
Both BNP and NT-proBNP can be measured by fully automated and commercially available assays
(AxSYM BNP, Abbot; ADVIA centaur BNP, Bayer; Elecsys NT-proBNP, Roche Diagnostics), which
have proven excellent test precision. Reliable point of care tests are also available for both markers
(Triage BNP, Biosite; Cardiac Reader NT-proBNP, Roche Diagnostics). BNP and NT-proBNP
plasma concentrations are expressed in pg/ml or pmol/l. The conversion factor for BNP is
1 pg/ml = 0.289 pmol/l, and for NT-proBNP it is 1 pg/ml = 0.118 pmol/l. BNP values obtained
with various assays are not comparable and there is no conversion factor for the comparison of
BNP and NT-proBNP values.

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Figure 1 Schematic illustration of B-type natriuretic peptide (BNP) and NT-proBNP synthesis, release and receptor interaction. BNP is synthesised as
prohormone in the cardiomyocytes. Upon release into the circulation proBNP is cleaved into BNP and the N-terminal fragment (NT-proBNP) in
equimolar proportions. Interaction of BNP and the natriuretic peptide receptor type A (NPR-A) mediates the biological effects via intracellular cGMP
increase. Reproduced with permission from E Spannuth.

BNP is stable in whole blood at room temperature with the

addition of EDTA for at least 24 h, whereas NT-proBNP is
stable for at least 72 h in whole blood at room temperature
and requires no additives. Both BNP and NT-proBNP are
stable during freeze and thaw processes.
There are several determinants for BNP and NT-proBNP
concentrations. It has been shown consistently in several
studies that BNP and NT-proBNP are related to sex, with
higher values in females, and to age, with higher values in
older individuals. The sex relation is thought to be caused by
differences in metabolism, whereas the association with age
might reflect preclinical structural and functional myocardial
alterations not detectable by current techniques.2
In patients with reduced renal function, BNP and NTproBNP values are increased with a negative correlation to
creatinine clearance. NT-proBNP seems to be affected more
by worsening renal function than BNP. Besides diminished
renal clearance, higher prevalence of concomitant left
ventricular alterations such as left ventricular hypertrophy,
diastolic and systolic dysfunction as well as fluid overload
might contribute to elevated BNP and NT-proBNP concentrations. However, recent results of a head to head comparison
of both markers in patients with renal disease indicate
similar diagnostic performance of both markers.3

CLINICAL APPLICATIONS
Heart failure
The diagnostic value of BNP and NT-proBNP is best
investigated in patients with heart failure. In a large number
of studies it has been consistently found that BNP and NTproBNP are elevated in patients with heart failure, and values

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were found to be related to disease severity as assessed by

New York Heart Association (NYHA) functional class (fig 3),
left ventricular systolic ejection fraction, and left ventricular
diastolic function.1
Emergency room setting
In the Breath Not Properly (BNP) trial 1586 patients
presenting to the emergency department with shortness of
breath were investigated. The main finding of this study was
that BNP testing provided high test accuracy for the detection
of heart failure, being superior to clinical judgement. At a
cut-off value of 100 pg/ml BNP had a very high negative
predictive value, thus making it especially applicable as a
rule-out test for heart failure in this setting.4 Similar results
were obtained in the N-terminal proBNP Investigation of
Dyspnoea in the Emergency department (PRIDE)5 study and
in the International Collaboration of NT-proBNP (ICON), in
which the diagnostic role of NT-proBNP in patients presenting with the cardinal symptom of shortness of breath has
been established. In these studies, a cut-off value for NTproBNP of 300 pg/ml to exclude heart failure has been
determined. Several further studies which evaluated the
diagnostic performance of BNP and NT-proBNP demonstrated similar results of a high negative predictive value at
the respective thresholds (table 1).6 Thus, the particular
strength of these markers is their ability to rule out the
diagnosis of heart failure. In general, heart failure is unlikely
at BNP values , 100 pg/ml and is very likely at BNP
values . 500 pg/ml and, similarly, unlikely at NT-proBNP
values , 300 pg/ml and very likely at NT-proBNP values

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Figure 2 Physiological effects of B-type natriuretic peptide (BNP). Volume or pressure overload leads to ventricular wall stress and BNP release. The
systemic biological effects of BNP are peripheral vasodilatation, increase in natriuresis and diuresis, and inhibition of the sympathetic nervous system
(SNS) and the reninangiotensinaldosterone system (RAAS).

. 450 pg/ml (. 900 pg/ml in patients above 50 years of age)

(table 2).
In the B-Type Natriuretic Peptide for Acute Shortness of
Breath Evaluation (BASEL) study 452 patients presenting to
the emergency department with acute dyspnoea were
included. They were randomised for a clinically guided
diagnostic strategy or for a strategy which integrated rapid
BNP measurement. If BNP was below 100 mg/ml, clinicians
were advised that heart failure was unlikely, and if BNP was
above 500 mg/ml they were advised that heart failure was
likely to be the origin of the dyspnoea. As demonstrated in
this trial, measurement of BNP applying the above mentioned threshold in conjunction with other clinical information reduced hospitalisation rate, the need for intensive care,
and total treatment time, and significantly reduced total

Figure 3 Median B-type natriuretic peptide (BNP) in patients with

heart failure according to New York Heart Association (NYHA)
functional status. Adapted from Wieczorek et al.6

treatment cost. However, clinical outcome over 30 days was

equal in both study arms (table 3).7
Prognostic value of BNP and NT-proBNP
Independent of their diagnostic value, several large scale
studies have convincingly shown that BNP and NT-proBNP
provide strong prognostic information for an unfavourable
outcome (death, cardiovascular death, readmission or cardiac
events) in patients with heart failure or asymptomatic left
ventricular dysfunction.8 In multivariable models BNP and
NT-proBNP proved to be superior to other prognostic
parameters and in some studies even to be the only
independent prognostic factor. Head to head studies comparing the diagnostic performance of BNP and NT-proBNP
testing have been performed in patients with heart failure
and in patients with asymptomatic left ventricular dysfunction. They revealed that both markers performed equally well
with almost identical areas under the curve (AUC) of the
receiver operating characteristic (ROC) curves.9 Thus, it can
be concluded from those studies that there is no meaningful
difference for risk stratification in clinical routine between
the two markers.
Guiding and monitoring heart failure treatment
Even though there is a large body of evidence demonstrating
the association of elevated BNP or NT-proBNP values with
disease severity and prognosis in heart failure patients, there
are limited data available which focus on the therapeutic
implications derived from BNP and NT-proBNP assessment.
It has been reported that BNP and NT-proBNP can be
attenuated by treatment with drugs such as angiotensin
receptor blockers or b blockers. Furthermore, several studies

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EDUCATION IN HEART

Table 1 Trials evaluating the diagnostic performance of B-type natriuretic peptide (BNP) and NT-proBNP

846

Studies

Diagnosis of HF

Analyse

Cut-off

Sens
(%)

Spec
(%)

PPV
(%)

NPV
(%)

McCullough 2002 BNP

Wieczorek 2002
Januzzi 2005 PRIDE
Januzzi 2005 ICON
Bay 2003

1538
1050
599
1256
2193

Clinical
Clinical
Clinical
Clinical
EF ,40%

BNP
BNP
NT-proBNP
NT-proBNP
NT-BNP

100
100
300
300
357

90
82
99
99
73

73
97
68
60
82

75

90

62
77
24

99
98
98

pg/ml
pg/ml
pg/ml
pg/ml
pmol/l

AUC
0.90
0.93
0.94
0.830.99
0.85

EF, ejection fraction; HF, heart failure; NPV, negative predictive value; PPV, positive predictive value; Sens, sensitivity; Spec, specificity.

have been able to demonstrate changes of BNP and NTproBNP values during recompensation therapy in acute heart
failure related to an improvement in invasively measured
haemodynamic parameters.10 Subsequently, it was also
shown that a decrease in BNP during the initial hospital
stay was associated with a favourable clinical outcome,
whereas no change or an increase in BNP values was
associated with an unfavourable outcome.11 In a small pilot
study by Troughton et al involving 79 patients with clinically
overt heart failure and an ejection fraction below 40%,
patients were randomly assigned either to clinically guided
therapy or a combination of clinical parameters and BNP
measurement to guide therapy. The event-free survival rate
over 180 days was significantly lower in the BNP guided
group.12 In another study, a substudy of the Australia-New
Zealand heart failure trial, 297 patients with ischaemic heart
disease and an ejection fraction below 45% were randomised
to placebo or carvedilol treatment. Patients with NT-proBNP
values on admission above the median had a significant risk
reduction if they were treated with carvedilol, whereas in the
group of patients with BNP values below the median, the
clinical outcome was identical for both the carvedilol and
placebo treatment groups. This suggests that NT-proBNP
might help to identify those heart failure patients who derive
benefit from active treatment with carvedilol (fig 4).13 These
results are in contrast to the COPERNICUS trial, which
enrolled 2289 patients with severe chronic heart failure
(NYHA class III or IV) and an ejection fraction below 25%.
The overall one year mortality of 14.9% in this study was
extremely high and it was found that patients receiving active
treatment with carvedilol had a better outcome than placebo
treated patients. In a substudy of this trial including 1011
European patients, NT-proBNP values were obtained at study
entry. Even though NT-proBNP was highly predictive for an
unfavourable outcome in those patients, the treatment effect
of carvedilol did not differ between patients with high NTproBNP values (above the median) and those with low NTproBNP values.14 Therefore, the data from these studies are
promising and suggest that BNP and NT-proBNP might be
Table 2 Cut-off values for BNP (derived from the BNP
study4) and for NT-proBNP (derived from the PRIDE and
ICON study5) for the diagnosis of heart failure of patients
presenting with dyspnoea

BNP (pg/ml)
NT-proBNP (pg/ml),
age ,50 years
NT-proBNP (pg/ml),
age .50 years

Rule-out
HF unlikely

Rule-in
HF likely

100
300

500
450

300

900

clinically useful for determining the optimal treatment for

patients with heart failure and for monitoring treatment
effects. The results of ongoing larger prospective trials,
however, are awaited before definite conclusions can be
reached.

Coronary artery disease

Originally BNP and NT-proBNP were considered biomarkers
for heart failure only. More recently, however, there has been
a growing body of data on the relevance of both markers in
coronary artery disease. It is widely believed that the
underlying pathophysiological process for an increase in

Figure 4 KaplanMeier curves for event-free survival of patients with

ischaemic left ventricular dysfunction treated with carvedilol (blue line)
or placebo (red line), with NT-proBNP below the median (circles) and
NT-proBNP above the median (squares). ns, not significant;
*p , 0.001. Modified from Richards et al.13

Table 3 Results of the BASEL (B-Type Natriuretic Peptide

for Acute Shortness of Breath Evaluation) study
BNP group
n = 225
Time to treatment (mins)
63 (16153)
Time to discharge (days)
8 (116)
Hospitalisation rate (%)
75
Admission to intensive care (%) 15
Total treatment costs (US$)
5410
In-hospital mortality (%)
6
30-day mortality (%)
10
30-day readmission rate (%) 12

Control group
n = 227

p Value

90 (20205)
11 (518)
85
24
7264
9
12
10

0.03
0.001
0.008
0.01
0.006
0.21
0.45
0.63

Values are expressed as median and interquartile range in parenthesis,

or as percentage.

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EDUCATION IN HEART

BNP and NT-proBNP values is left ventricular systolic or

diastolic dysfunction caused by myocardial ischaemia leading
to an increased wall stress. Nevertheless, data derived from
experimental studies suggest a direct release of BNP and NTproBNP from cardiomyocytes in response to myocardial
ischaemia independent of ventricular wall stress. It has also
been demonstrated that BNP even rises after temporary
myocardial ischaemia induced by balloon inflation during
coronary intervention.
Acute coronary syndromes (ACS)
Substudies of large scaled clinical trials (OPUS-TIMI 16,
TACTICS-TIMI 18, FRISC II, GUSTO IV, PRISM)15 16 have
evaluated the prognostic value of BNP and NT-proBNP in
patients presenting with non-ST elevation acute coronary
syndromes (NSTE-ACS). In all studies elevated values of BNP
and NT-proBNP have consistently been found. Furthermore,
both markers were highly predictive for an adverse outcome
independently of other biomarkers, especially troponins and
C reactive protein (CRP). However, it must be emphasised
that BNP and NT-proBNP were predictive for mortality and
heart failure after an ACS but not for recurrent ischaemic
events. Similar results were reported for the predictive value
of BNP and NT-proBNP after ST elevation myocardial
infarction (STEMI).17 Different studies evaluated whether
serial assessment of NT-proBNP is superior to a one time
point assessment at admission. Jernberg et al studied 755
patients with an ACS and observed no difference in the
predictive value as indicated by the AUC of the ROC curve for
NT-proBNP on admission and after 6 h.15 In a substudy of the
PRISM trial Heeschen et al demonstrated an incremental
prognostic value of serial NT-proBNP assessment on admission and a second measurement 72 h later. In the FRISC-II
trial serial NT-proBNP analyses were evaluated during the
acute and the chronic phase of ACS and disclosed that the
predictive value of NT-proBNP value measured three and six
months after the index event is a better predictor for two year
mortality than early NT-proBNP determination at admission
or at 48 h after the acute event. However, the best time to
take a sample for BNP or NT-proBNP assessment still
remains to be fully established.
In addition, the therapeutic benefits that can be derived
from BNP and NT-proBNP assessment in ACS are not clear.
The only published study to date which investigated the
usefulness of NT-proBNP for identifying patients who might
benefit from an early invasive strategy is a substudy of the
FRISC-II trial. In this study a trend towards a better outcome
of patients with NT-proBNP values in the highest tertile was
observed. However, in combination with elevated interleukin
(IL)-6 concentrations, NT-proBNP values in the third tertile
indicated a significant treatment benefit from early invasive
therapy.18 In the substudy of the PRISM trial, Heeschen et al
analysed the effect of glycoprotein IIb/IIIa inhibition with
tirofiban with respect to NT-proBNP values.16 Even though
they found that patients with high NT-proBNP values had a
lower event rate with tirofiban treatment compared to
placebo at 48 h, they found no significant interaction
between NT-proBNP values and the clinical benefit of
tirofiban treatment at 30 days.
Several matters need to be addressed before BNP and NTproBNP can be recommended for application in clinical
routine in patients with ACS. Different cut-off values have
been applied in the various studies, but to date no clearly
defined cut-off value has been established. Moreover, further

studies are needed to assess the therapeutic benefits that can

be derived from BNP and NT-proBNP assessment.
Stable coronary artery disease
Recent studies have evaluated the relevance of BNP and NTproBNP in patients with stable angina pectoris. It could be
demonstrated that NT-proBNP serum concentrations show a
close relation to the extent of coronary artery disease and
inducible myocardial ischaemia.19 20 Furthermore, three independent studies have indicated that BNP and NT-proBNP
provide prognostic information on long term mortality and
adverse cardiovascular events superior to that provided by
traditional risk factors.21 However, no cut-off values are
clearly defined and therapeutic consequences remain open.
Valvular heart disease
Valvular heart diseases lead to either volume or pressure
overload of the left ventricle. Thus it is reasonable to expect
that BNP and NT-proBNP could be useful in evaluating the
severity and prognosis of valve diseases. However, data are
sparse. For patients with valvular aortic stenosis it has been
shown in several small studies that both BNP and NTproBNP are related to disease severity, functional status and
disease progression, with a decline of elevated values after
successful valve replacement. Furthermore, the values
provide prognostic information for an unfavourable postoperative outcome.2224 The therapeutic implications of these
findings are uncertain, but it can be speculated that BNP or
NT-proBNP assessment might help to decide upon the
optimal timing for valve surgery. Data on the diagnostic
utility of BNP and NT-proBNP in patients with aortic
regurgitation and mitral regurgitation are very limited,
demonstrating that both markers are elevated in relation to
disease severity. However, there are no data available
concerning the prognostic value. Generally, there is good
evidence that BNP and NT-proBNP assessment might play a
role in the future diagnostic work up of patients with valvular
heart diseases, but the clinical benefits that can be derived
have not yet been established. Thus, further studies are
warranted.
Future perspectives
Several large studies which aimed to evaluate the usefulness
of BNP or NT-proBNP for population screening demonstrated
a predictive value of both markers for death or the existence
of cardiovascular diseases. However, BNP and NT-proBNP
population screening is generally not advised. Nevertheless, it
seems reasonable to use BNP and NT-proBNP for screening
and risk assessment of well defined risk groupsfor
example, cardiovascular patients scheduled to undergo noncardiac surgery, patients to be treated with COX-2 inhibitors,

Table 4 Clinical information that can be obtained from

BNP or NT-proBNP assessment

Heart failure
Stable CAD
ACS
Aortic stenosis

Diagnosis

Severity

Prognosis

Decision

++
0
0
0

++
+
0
+

++
++
++
+

+
0
0
0

++, strong evidence; +, evidence derived from smaller studies; 0, no data

available.
ACS, acute coronary syndrome; CAD, coronary artery disease.

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848

or patients with malignant disease being treated with

cardiotoxic chemotherapeutic agents. Studies are in progress
for these indications.
In a variety of small studies it has been found that BNP
and NT-proBNP values are elevated in patients with atrial
fibrillation, even in the absence of structural heart disease,
and that they are predictive of successful cardioversion. To
date no threshold values are defined and further studies are
necessary. In the future, however, BNP and NT-proBNP
assessment could prove useful for deciding on the best
treatment of patients with atrial fibrillation and to monitor
patients after successful cardioversion.
Resynchronisation therapy has become an accepted therapeutic option for patients with severe heart failure. The
optimal stimulation mode needs to be adapted using
different diagnostic tools such as echocardiography, ergospirometry or the six minute walk test. Recently, some
smaller studies have suggested that BNP or NT-proBNP
assessment can be used to optimise biventricular stimulation.
Implementation of BNP and NT-proBNP assessment
into current ESC guidelines
The role of BNP and NT-proBNP testing is included in the
guidelines for the diagnosis and treatment of chronic heart
failure of the task force of the European Society of
Cardiology, first published in 2000 and most recently updated
in 2005. Assessment of both markers is considered to be a
reliable rule-out test of heart failure in primary care and in
the emergency room. However, it is clearly stated that the
role for treatment monitoring needs to be determined.
Assessment of BNP for risk stratification is also mentioned
in the current task force report on the management of acute
coronary syndromes in patients presenting without persistent
ST segment elevation, but without any recommendations for
the application of BNP and NT-proBNP in clinical routine.

CONCLUSIONS
BNP and NT-proBNP have emerged as powerful biomarkers
in various cardiovascular diseases. Both markers can be
detected in serum plasma using commercially available
assays. The diagnostic performance of BNP and NT-proBNP
is comparable and there is no meaningful difference between
them. They reflect haemodynamic myocardial stress independent of the underlying pathology, thus they are not

specific for a distinct pathology such as heart failure but for

cardiovascular diseases in general. Their particular strength is
to rule out heart failure in patients presenting to the
emergency department with shortness of breath. They
provide strong and independent prognostic information in
patients with heart failure, stable coronary artery disease,
acute coronary syndromes, and valvular aortic stenosis. There
are some data available to suggest that BNP and NT-proBNP
values might assist in deciding upon the optimal treatment of
patients with heart failure, but to date there are no data to
support the use of these markers for reaching therapeutic
decisions in patients with coronary artery disease or valvular
heart disease (table 4).
Additional references appear on the Heart websitehttp://
www.heartjnl.com/supplemental

..................
Authors affiliations

M Weber, C Hamm, Kerckhoff Heart Center, Department of Cardiology,

Bad Nauheim, Germany
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

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c This review summarises present knowledge on the physiology of BNP

and provides comprehensive data on the diagnostic and therapeutic

potential of BNP in patients with heart failure.

2 Redfield MM, Rodeheffer RJ, Jacobsen SJ, et al. Plasma brain natriuretic
peptide concentration: impact of age and gender. J Am Coll Cardiol
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3 Luchner A, Hengstenberg C, Lowel H, et al. Effect of compensated renal
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c The BASEL study demonstrated that BNP measurement in the

Role of BNP and NT-proBNP in clinical routine:

key points
c

B-type natriuretic peptide (BNP) and NT-proBNP are

reliable biomarkers, reflecting myocardial stress caused
by various cardiovascular diseases
Both markers are stable in whole blood and can be
measured in clinical routine using fully automated
commercially available assays
The diagnostic performance of BNP and NT-proBNP is
comparable and there is no meaningful difference
between the two
The particular strength of BNP and NT-proBNP is to rule
out heart failure in patients with shortness of breath in the
emergency department
Both markers provide prognostic information in patients
with heart failure, coronary artery disease, and valvular
heart disease

www.heartjnl.com

emergency department reduces hospitalisation rate and total

treatment costs with comparable clinical outcome.

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and norepinephrine over time and mortality and morbidity in the valsartan
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BNP measurement and follow-up data of 4305 patients with heart

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concentrations. Lancet 2000;355:112630.
c This small study demonstrated for the first time that NT-proBNP guided

treatment results in better clinical outcome compared to clinically

guided therapy without NT-proBNP assessment.

13 Richards AM, Doughty R, Nicholls MG, et al. Plasma N-terminal pro-brain

natriuretic peptide and adrenomedullin: prognostic utility and prediction of

EDUCATION IN HEART
benefit from carvedilol in chronic ischemic left ventricular dysfunction.
Australia-New Zealand heart failure group. J Am Coll Cardiol
2001;37:17817.

c This study showed that NT-proBNP is able to discern heart failure

patients who derive a benefit from carvedilol treatment. Thus this study
demonstrates that therapeutic implications can be derived from BNP
and NT-proBNP assessment.

14 Hartmann F, Packer M, Coats AJ, et al. Prognostic impact of plasma Nterminal pro-brain natriuretic peptide in severe chronic congestive heart
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16 Heeschen C, Hamm CW, Mitrovic V, et al. N-terminal pro-B-type natriuretic
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c Among the large multicentre studies, the data from the PRISM trial

emphasises the importance of serial NT-proBNP measurement for

assessing dynamic risk stratification.

17 Richards AM, Nicholls MG, Espiner EA, et al. B-type natriuretic peptides and
ejection fraction for prognosis after myocardial infarction. Circulation
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18 Jernberg T, Lindahl B, Siegbahn A, et al. N-terminal pro-brain natriuretic
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19 Weber M, Dill T, Arnold R, et al. N-terminal B-type natriuretic peptide predicts
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20 Bibbins-Domingo K, Ansari M, Schiller NB, et al. B-type natriuretic peptide

and ischemia in patients with stable coronary disease: data from the Heart
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21 Kragelund C, Gronning B, Kober L, et al. N-terminal pro-B-type natriuretic
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c This study examines the prognostic information which can be derived

from measurement of NT-proBNP in patients with stable coronary

artery disease.

22 Gerber IL, Stewart RA, Legget ME, et al. Increased plasma natriuretic peptide
levels reflect symptom onset in aortic stenosis. Circulation
2003;107:188490.
23 Weber M, Arnold R, Rau M, et al. Relation of N-terminal pro B-type natriuretic
peptide to progression of aortic valve disease. Eur Heart J 2005;26:102330.
24 Bergler-Klein J, Klaar U, Heger M, et al. Natriuretic peptides predict
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c The presented data demonstrate that elevated BNP values in patients

with aortic stenosis provide prognostic information for an unfavourable

clinical course.

Additional references appear on the Heart

websithttp://www.heartjnl.com/supplemental

www.heartjnl.com

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