From the Departments of Cardiology, Endocrinology, and Nuclear Medicine,
Christchurch Hospital and Department of Medicine, Christchurch School of
Medicine, Christchurch, New Zealand.
Correspondence to Prof A.M. Richards, Department of Medicine, Christchurch School of Medicine, Riccarton Ave, PO Box 4345, Christchurch, New Zealand. E-mail bgriffin{at}chmeds.ac.nz
Methods and Results—The association between radionuclide left
ventricular ejection fraction (LVEF) and N-BNP at 2 to 4
days (r=-.63, P<.0001) and 3 to 5
months (r=-.58, P<.0001) after
infarction was comparable to that for C-terminal BNP and far stronger
than for ADM (r=-.26, P<.01),
N-terminal atrial natriuretic peptide (N-ANP), C-terminal
ANP, cGMP, or plasma catecholamine concentrations. For
prediction of death over 24 months of follow-up, an early
postinfarction N-BNP level
Conclusions—Plasma N-BNP measured 2 to 4 days after myocardial
infarction independently predicted left ventricular
function and 2-year survival. Stratification of patients into low- and
high-risk groups can be facilitated by plasma N-BNP or BNP
measurements, and one of these could reasonably be included in the
routine clinical workup of patients after myocardial infarction.
ADM is a newly discovered 52–amino acid peptide with structural
homology with calcitonin gene–related peptide.17
Originally isolated from human pheochromocytoma cells, immunoreactive
ADM has been detected in other tissues including adrenal medulla,
heart, brain, lung, kidney, and gastrointestinal
organs.17 18 The limited data available
concerning the biologic activity of ADM suggest that it has powerful
direct vasodilator effects and is able to increase cardiac output and
induce diuresis and natriuresis.19 20 21 22
Plasma ADM levels are typically in the lower picomolar range in normal
humans but are reported to be increased in hypertension, congestive
heart failure, and chronic renal failure in proportion to the severity
of disease.23 24 In heart failure, plasma ADM is
inversely related to LVEF and positively associated with
LVEDP.23 24 The potential value of plasma ADM
levels as indicators of cardiovascular prognosis is
unknown.
The current study was designed to test the following hypotheses: (1)
That after myocardial infarction, plasma N-BNP is equal or superior to
other cardiac peptides, the second messenger cGMP and plasma
catecholamines as an indicator of LV function both early
and late after myocardial infarction, and of
cardiovascular prognosis. (2) Plasma adrenomedullin is
related to LV function, cardiovascular prognosis, and
to other neurohormonal markers after myocardial infarction.
LV function was first assessed by radionuclide ventriculography within
24 hours of blood sampling and then repeated 3 to 5 months after
infarction. Each study was performed with a General Electric 400 AC
gamma camera interfaced to a General Electric 3000i computer system
after standard in vivo technetium-99m red blood cell
labeling. Clinical events including death, heart failure (defined by
the presence of new symptoms of dyspnea and/or edema, with one or more
concordant signs including ventricular gallop rhythm,
pulmonary crepitations, elevated venous pressure, and/or
radiologic evidence of left ventricular failure), unstable
angina, and recurrent myocardial infarction were recorded for 24
months of follow-up in all patients.
Statistical Analysis
Hormone-Hormone Associations
Hormones and LV Function
Optimal levels of N-BNP and BNP for indicating LVEF
Hormones and Clinical Events
Mean early postinfarction values of all neurohormones except ADM and
EPI were significantly higher for those dying during follow-up (Table 3
Cumulative (24-month) event rates for death (all causes) and LVF for
those with early postinfarction neurohormone levels or LV function
above the group median are compared with those with values below the
median in Table 4
Kaplan-Meier survival curves by median levels of candidate indicators
are shown in Figs 2
ROC analyses provided the optimal values of candidate
markers for prediction of death and LVF, as shown in Table 5
Multivariate analyses testing for independent
predictive information among candidate cardiac markers for death and
for heart failure are shown in Table 6
For the end point of LVF, serial substitution of cardiac peptides, and
then cGMP, gave more complex results. ANP (P<.001) gave
independent information together with NE (P=.047) and LVEF
(P=.015). BNP (P=.009) and a previous history of
heart failure (P=.038) were the independent variables
(but not NE or LVEF) when BNP was substituted in the model. Previous
heart failure (P=.048), NE (P=.033), and LVEF
(P=.009) but not N-ANP itself (P=.143) were
independently predictive when N-ANP was the cardiac peptide
incorporated in the model. Finally, cGMP (P=.003) and a
previous history of heart failure (P=.044) were the only
independent variables when cGMP was examined.
Plasma ADM levels have a statistically significant (but modest)
inverse relation with LV function, which is comparable to that of NE.
We report for the first time that plasma ADM is predictive of death in
the 2 years after myocardial infarction, but this relation is generally
far weaker than observed for N-BNP and does not retain independent
significance by multivariate analysis. Plasma
ADM levels in heart failure presumably reflect a systemic or
peripheral response to cardiac impairment and may be
mediated by a variety of mechanisms including induction of
endothelial production of ADM, elevated levels
of endothelin, or other humoral and neural mechanisms. There is little
knowledge of the possible effects of heart failure on ADM clearance.
Hence ADM appears an indirect reflector of LV function and has a weaker
association with LV size or contractile function or prognosis than BNP
or N-BNP. The latter two peptides are the true
"ventricular" hormones studied. Their release is
mediated by ventricular wall stress, and their synthesis is
increased with cardiac injury (especially in the periinfarct zone). The
superior performance of BNP and N-BNP as cardiac markers is
consistent with their site of synthesis and its regulation.
Hormones and LV Function
Hormones and Clinical Events
Univariate analyses (Tables 3
The two end points of death and heart failure contrasted with respect
to predictive factors in that age and history of previous myocardial
infarction remained powerful predictors of death in all
multivariate analyses. In contrast, for heart
failure, neurohormones (a cardiac peptide and/or NE), a history of
previous heart failure, and/or LVEF remained statistically independent.
This presumably reflects the importance of age and previous cardiac
injury in the overall likelihood of deaths that occurred evenly over
the 2 years of follow-up (Figs 2
Although mean levels were higher in those dying during follow-up, in
other analyses NE proved to be of little value in predicting
death. However, event rates above and below the group median level of
NE did differ for heart failure (Table 4
BNP has been previously reported to predict mortality in some
categories of cardiac injury.11 12 13 14 In contrast
to some reports in which BNP has been reported to correlate less well
to LVEF but better to mortality,11 or better to
mortality but less well to heart failure14 than
ANP, the current larger study indicated that BNP and now N-BNP were
consistently more closely related to each of LV dysfunction and
mortality than the other cardiac peptides and exhibited comparable
predictive power for heart failure.
In this first report of the potential postinfarction utility of
the plasma concentrations of the cardiac peptide second messenger,
plasma cGMP maintained obvious relations with concurrent plasma cardiac
peptide concentrations (most notably ANP and N-BNP), but it was clearly
a less powerful indicator of LVEF or of death than N-BNP or BNP. This
presumably reflects the fact that plasma cGMP is merely spillover
of a tiny proportion of that produced intracellularly and responds to a
number of stimuli, such as nitric oxide as well as cardiac peptide
levels. However, in multivariate analyses it
remained a powerful independent predictor of LVF.
N-ANP has previously been reported to reflect LVEF and
prognosis.5 6 7 8 N-ANP was consistently and
significantly related to the other cardiac peptides and to cGMP as well
as to LVEF and to adverse outcomes, at least in univariate
analyses. However, it clearly performed less well than N-BNP,
BNP, or ANP as an indicator of LVEF. This seems intuitively acceptable
because N-BNP and BNP released from the ventricle (the only truly
"ventricular" hormones measured in the study) in
response to LV wall stress might logically relate most closely to LV
status. The finding conflicts with other
studies8 11 reporting N-ANP equal or superior to
BNP in predicting LVEF
Notably, nonfatal ischemic events over follow-up were not
predicted by any of the hormones measured or by LV scan data.
Presumably this reflects the weakness of any possible association of
intracardiac distending pressures (the main regulator of cardiac
peptide release) and the risk of renewed coronary
atherosclerotic plaque rupture and subsequent thrombosis.
The strong relations of N-BNP to LV function and
cardiovascular prognosis have been observed despite the
heterogeneity of the group under study. Wide variation
in age, previous blood pressure, preinfarction LV function, or history
of previous ischemic events is present, together with some
variation in acute management (eg, use of thrombolytic
therapy, ß-blockers, and other vasoactive drugs). It will be of
interest to see whether any particular clinical or therapeutic
subgroups exhibit an altered relation between cardiac peptides and LV
function or prognosis. However, this task is beyond the current study;
the population described would not provide adequate statistical power
to appropriately examine these questions, which should be the subject
of later prospective studies in larger populations.
A shortcoming of the current study and all similar studies is the
necessary limit to the number of potential neurohumoral markers
assessed. Renin was not measured because many of the group received
converting enzyme inhibitors, thus distorting any relation
between renin and ventricular function or
cardiovascular prognosis. Endothelin has shown promise
despite its diffuse vascular (rather than specific cardiac) origin and
warrants further study.32 33 Similarly, further
consideration of cytokines including tumor necrosis factor is
also required.34 The list of circulating factors
with potential prognostic utility will inevitably expand with time.
Among plasma cardiac peptides, cGMP, ADM, and
catecholamine levels, the ventricular hormones
N-BNP and BNP best reflected LV function and gave prognostic
information (independent of age, sex, clinical history, and LVEF)
regarding the risk of death or heart failure in the 2 years after
myocardial infarction. Stratification of patients into low- and
high-risk groups can be facilitated by plasma N-BNP or BNP
measurements, and one of these could reasonably be included in the
routine clinical workup of patients after myocardial infarction.
Received October 31, 1997;
revision received January 8, 1998;
accepted January 12, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Plasma N-Terminal Pro–Brain Natriuretic Peptide and Adrenomedullin
New Neurohormonal Predictors of Left Ventricular Function and Prognosis After Myocardial Infarction
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Newly discovered
circulating peptides, N-terminal pro–brain natriuretic
peptide (N-BNP) and adrenomedullin (ADM), were examined for prediction
of cardiac function and prognosis and compared with previously reported
markers in 121 patients with myocardial infarction. 
160 pmol/L had sensitivity, specificity,
positive predictive value, and negative predictive values of 91%,
72%, 39%, and 97%, respectively, and was superior to any other
neurohormone measured and to LVEF. Only 1 of 21 deaths occurred in a
patient with an N-BNP level below the group median (Kaplan-Meier
survival analysis, P<.00001). For prediction of
heart failure (left ventricular failure), plasma N-BNP
145 pmol/L had sensitivity (85%) and negative predictive value
(91%) comparable to the other cardiac peptides and was superior to
ADM, plasma catecholamines, and LVEF. By
multivariate analysis, N-BNP but not ADM
provided predictive information for death and left
ventricular failure independent of patient age, sex, LVEF,
levels of other hormones, and previous history of heart failure,
myocardial infarction, hypertension, or diabetes.
Key Words: brain natriuretic peptide • atrial natriuretic factor • peptides • myocardial infarction • ventricles • prognosis
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
A number of
circulating factors reflect LV function and/or predict
cardiovascular prognosis in a spectrum of
cardiovascular disease ranging from severe heart
failure from different causes to well-defined asymptomatic
ischemic LV impairment.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Recently,
the cardiac peptides have received close attention as
cardiovascular markers.3 4 5 6 7 8 9 10 11 12 13 14 We
have recently reported that the 76–amino acid residue amino terminal
portion of pro-BNP (N-BNP) circulates in human
plasma15 and that levels are elevated in cardiac
impairment.15 16 In normal subjects, levels are
similar to those of BNP (10.8±1.3 versus 9.7±0.5 pmol/L,
respectively, NS), whereas in cardiac impairment, the proportional and
absolute increment above normal levels of the N-BNP peptide exceeds
that for BNP, which suggests that it may be the more discerning
marker.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
A consecutive series of 121 patients (Table 1
) admitted to the Christchurch Hospital
Coronary Care Unit with acute myocardial infarction between
November 1994 and June 1995 were studied. All patients gave written
informed consent for participation in the study. The protocol was
approved by the Southern Regional Health Authority Ethics Committee
(Canterbury). Acute myocardial infarction was defined by the presence
of typical cardiac ischemic symptoms, the presence of
ischemic changes on the ECG in two or more ECG leads, and peak
elevation of plasma creatine kinase to at least twice normal (400 U/L).
Inclusion criteria included age >80 years, absence of cardiogenic
shock, and survival for at least 24 hours after myocardial infarction.
Blood samples were taken between 24 and 96 hours after the onset of
symptoms, in the morning (7 AM to 1 PM),
through an indwelling intravenous cannula placed at least
30 minutes before sampling, with the patient resting quietly while
semirecumbent. Samples were taken into chilled EDTA Vacutainers, placed
immediately on ice, centrifuged within 20 minutes at -4°C,
and the plasma stored at -80°C before assay for N-BNP, BNP, N-ANP,
ANP, cGMP, ADM, and plasma catecholamines (NE and
EPI).16 25 26 27 28 29
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Table 1. Patients With Myocardial Infarction (n=121)
Values are expressed as mean±SD. For correlation
analysis (Pearson product moment), the log of neurohumoral
factors was used to normalize the distribution of data. Multiple
logistic regression was undertaken to test for independent prediction
of LVEF of <40% by one or more neurohumoral factors. The relative
abilities of neurohumoral factors to predict death or clinical LVF were
assessed by ROC analysis. Areas under the ROC curves for each
marker were compared by the method of Hanley and
McNeil.30 Optimal values for specificity and
sensitivity were estimated by finding the position on the ROC curves
with the minimum euclidian distance to the point of perfect specificity
and sensitivity (100%, 100%). Mean levels of neurohumoral factors and
ventricular scan variables for patients incurring or
spared specific adverse events were compared by use of independent
t tests. Cumulative adverse event rates were compared by use
of 
2 tests (with Yates correction for low
expected frequencies) with risk ratios (with 95% confidence intervals)
and Kaplan-Meier survival curves calculated for groups with admission
levels above and below the median of individual neurohumoral factors,
ejection fraction, and LVESV and LVEDV. Multiple logistic regression
analyses were conducted to test the independent predictive
power of neurohormones, ventricular scan data, sex, age,
and clinical history for two outcomes: death (all causes) and LVF
within 24 months of myocardial infarction. Demographic and clinical
variables forced into the model as standard predictors included
age, sex, history of previous myocardial infarction, hypertension,
diabetes, and previous heart failure. Concordant with the Kaplan-Meier
survival curve and 2 event rate
analyses, candidate predictors including LVEF, ADM, EPI, NE,
the cardiac peptides, and cGMP were entered in the multiple logistic
regression analyses as binary variables with values falling
above or below the group median. For all analyses, a value of
P<.05 was taken as statistically significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The clinical and demographic features, together with plasma
neurohumoral results and LV parameters, for the study group
are given in Table 1
. At discharge, the percentages of the group
receiving aspirin, ß-blockers, ACE inhibitors, and/or
diuretics were 95%, 86%, 43%, and 25%, respectively. Mean
plasma levels of both ANP and BNP were elevated (P<.001)
well above the upper limit of normal (Table 1). Mean N-BNP levels were
12-fold the upper limit of normal.15 16 In
contrast, mean plasma catecholamine levels were within the
normal range. Worldwide, normal ranges for plasma N-ANP, cGMP, and ADM
are yet to be formally established, but levels were all significantly
greater than those observed in our laboratory in a group of 35 normal
subjects (not matched for age with the current study group). Over the 4
months after infarction, LVEF rose marginally from 46±1% to 49±1%
(P<.05).
Strong positive relations were observed between plasma N-BNP
levels and concurrent levels of BNP, N-ANP, ANP, and cGMP (Table 2), but associations with the
catecholamines and ADM were weaker. The correlations
between N-BNP and other neurohormones were most powerful for BNP and
ANP (Table 2). The correlation of ADM to other neurohormones was
strongest with N-BNP (r=.40, P<.001, Table 2)
and fell in the range of r=.20 to .29 (P<.05 to
.01) for NE, ANP, N-ANP, BNP, and cGMP.
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Table 2. Correlations (r) of N-BNP and LVEF
With Each Other and Other Neurohumoral Factors at Admission and 4
Months After Myocardial Infarction
In the early postinfarction period, the relations between LVEF and
systolic volume with concomitant cardiac plasma peptide
concentrations were strongest for N-BNP (r=-.63 and
r=.61, respectively, both P<.0001) and BNP
(Table 2). Multiple logistic regression analysis incorporating
all the neurohormones except BNP indicated N-BNP alone remained
independently predictive of LVEF <40% (P<.001), and a
similar analysis that included BNP but not N-BNP indicated a
similar finding for BNP (P<.001). Both the slope and
strength of the relation between early postinfarction neurohormones and
LV scan data were similar whether plotted against early or late
(4-month) LVEF or LVESV measurements (Table 2; Fig 1).
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Figure 1. Individual early postinfarction plasma
concentrations of BNP (top plots) and N-BNP (bottom plots) plotted (log
scale) against corresponding early (left plots) and late (right plots)
postinfarction radionuclide scan LVEF (regression lines with 95%
confidence intervals) for 121 patients with myocardial infarction.
Vertical dotted lines are marked at 40% ejection fraction. N-BNP
levels <50 pmol/L (less than threefold the upper limit of normal)
correspond with both early and late ejection fractions >40% (bottom
plots). 
40% were 145
pmol/L and 30 pmol/L, respectively; yielding sensitivities of 71% and
68%, specificities of 69% and 69%, positive predictive values of
56% and 56%, and negative predictive values of 80% and 79%,
respectively. Notably, N-BNP levels fivefold (70 pmol/L) and BNP
twofold (20 pmol/L) the upper limit of normal retained both sensitivity
and negative predictive values of 90% for LVEF <40%.
During 24 months of follow-up (complete for all 121 patients), 21
deaths (18 cardiovascular), 33 episodes of clinical
heart failure, and 36 unstable ischemic syndrome events
(nonfatal myocardial infarction or unstable angina) occurred, giving
cumulative event rates of 17%, 27%, and 30%, respectively. ). Similarly, all but ADM were increased
in those later developing heart failure. Notably, the ratio of mean
neurohormone levels for those incurring over those spared both death
and heart failure was greatest for N-BNP (Table 3). In contrast,
baseline neurohormones did not differ between those destined to incur
or to be spared a new acute ischemic coronary
syndrome.
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Table 3. Adverse Events: Neurohormones and Left
Ventricular Function (Mean±SEM) . N-BNP yields the
clearest separation for death, with only 1 death in 21 occurring within
the half of the group with N-BNP values below the median. Median BNP
and N-ANP are the next-ranked discriminators, with ANP, ADM, and LVEF
somewhat weaker. For LVF, median N-BNP, BNP, ANP, and LVESV display
similar separation of events with 85% or more of 33 episodes of frank
clinical heart failure occurring in those with early postinfarction
levels of these indicators above the group median.
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Table 4. Cumulative Death and Heart Failure by Median Levels
of Neurohormones and Radionuclide Left Ventricular Size and
Ejection Fraction (Mean Follow-up, 2.0 Years) , 3, and 4. Clear
separation of curves, most clear-cut for N-BNP, was also demonstrated
for ANP, N-ANP, and BNP. Survival curves for cGMP (not shown) did not
separate significantly. ADM (Fig 3)
curves exhibited a separation similar to that of ANP (Fig 2). All the
cardiac peptides and ADM were superior to NE (Fig 3). Radionuclide data
curves separate widely about median LVEF and LVESV with less though
still significant distinction by LVEDV (Fig 4).
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Figure 2. Kaplan-Meier survival curves for subgroups with
early postinfarction plasma peptide (N-ANP, ANP, N-BNP, and BNP)
concentrations above (solid line) and below (dashed line) the group
median in 121 patients with myocardial infarction.
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Figure 3. Kaplan-Meier survival curves for subgroups with
early postinfarction plasma peptide (ADM and NE) concentrations above
(solid line) and below (dashed line) the group median in 121 patients
with myocardial infarction.
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Figure 4. Kaplan-Meier survival curves for subgroups with
radionuclide scan indicators of LV function (LVEF, LVESV, and LVEDV)
above (solid line) and below (dashed line) the group median in 121
patients with myocardial infarction. . For death, N-BNP had the strongest
sensitivity, specificity, positive predictive value, and negative
predictive value. An early postinfarction N-BNP value >160 pmol/L
included 91% of those later to die, and in this group nearly 40% did
die, whereas a value <160 pmol/L conferred a 97% probability of
survival over 24 months of follow-up. For prediction of LVF, BNP
performed marginally better than N-BNP, which, nevertheless, still
exhibited sensitivity >80% and negative predictive value >90% at a
cutoff of 145 pmol/L. Both N-BNP and BNP performed notably better than
LVEF, LVESV, and NE for both end points (P<.01 for ROC
curve comparisons). Values for ADM were comparable to those of NE
(Table 5).
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Table 5. Sensitivity, Specificity, Positive Predictive
Values, and Negative Predictive Values for Prediction of Death and LVF
by Optimal Values of Neurohormones and Radionuclide Ventriculography
Measurements .
Overall N-BNP was the top-ranking neurohormonal predictor for death
while also retaining independent predictive power for LVF. For both end
points, when either N-BNP or BNP were included in the
multivariate analysis, no additional
independent information was provided by LVEF or other hormones
including ADM, NE, or EPI. Age (P=.016), a history of
previous myocardial infarction (P=.044), and N-BNP
(P=.024) level were all predictive of death independent of
each other and of the other neurohormonal, LV scan, demographic, and
clinical history variables tabled. A previous history of heart
failure (P=.032) and N-BNP (P=.013) level were
predictive of heart failure independent of each other and the other
variables tabled. With serial substitution of the individual
cardiac peptides and then cGMP in this model, age and a previous
history of myocardial infarction retained their independent
significance for prediction of death in all analyses. Of the
other cardiac peptides, BNP (P=.041) but not ANP, N-ANP, or
cGMP (P=.139 to .847) gave independent information for
death.
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Table 6. Multiple Logistic Regression Analysis of
Cardiac Markers for Independent Prediction of Death or Heart Failure in
the 24 Months After Acute Myocardial Infarction
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
The current findings indicate that the plasma concentration of the
newly discovered circulating N-terminal portion of pro-BNP, N-BNP, is
equal or superior to the other cardiac peptides (ANP, N-ANP, and BNP),
their second messenger (cGMP), ADM, and the plasma
catecholamines as an indicator of LV function (both
systolic volume and ejection fraction), both early and late
after infarction. Similarly, the early postmyocardial infarction level
of N-BNP is a powerful independent predictor of death or heart failure
over the 2 years after myocardial infarction.
We have shown for the first time that the relations of N-BNP
with LVEF and LVESV were comparable with those observed for BNP and
clearly stronger than for any of the other neurohormones examined
(Table 2). Furthermore, the relation between early postinfarction N-BNP
and LVEF is as strong for late (3 to 5 months after infarction) LVEF as
for concurrent LVEF, and therefore early postinfarction N-BNP can aid
in prediction of LV function some months after acute infarction. The
current results concur with those reported by Davidson et
al,8 Yamamoto et al,9 and
Motwani et al14 and contrast with Omland et
al11 in showing that the inverse relation of LVEF
with BNP is stronger than with ANP or N-ANP (and now cGMP). However, in
contrast to the preliminary report on 16 patients from Motwani et
al,14 despite the superior strength of the
relation of BNP (and now N-BNP) with LVEF (compared with other
hormones), the positive predictive value for LVEF <40% is only fair
at 
40%.
By multiple forms of analysis, N-BNP emerged as the single
most powerful predictor of death. Only 1 of 21 deaths occurred in those
with early postinfarction N-BNP levels below the group median (and none
within the first 18 months of follow-up). and 4 and figures)
showed the expected association of many individual hormonal and LV scan
features with both death and heart failure.
Multivariate analyses demonstrated that N-BNP
and BNP both retained statistically significant power for prediction of
death and LVF independent of other demographic, clinical, hormonal, and
LV scan variables. , 3, and 4). Many heart failure events
were brief, and the majority occurred in the predischarge,
postinfarction period. In this setting it appears that neurohormonal
indicators are more powerful independent indicators of incipient or
imminent frank (though often transient) LVF than age, previous clinical
history, or LVEF. ), and NE added information
beyond that given by some individual cardiac peptides and/or LVEF for
prediction of LVF in most multivariate
analyses. Generally, our findings are in accord with the bulk
of reports that attest to the superiority of ANP over NE as a
cardiovascular marker.4 31 We
report for the first time that this is also true for N-BNP and BNP. 45% in smaller groups including LV impairment
of different causes.8 The current study indicates
that within days or months of myocardial infarction, N-ANP will be less
closely related to LV parameters and to later prognosis
than N-BNP or BNP.
Selected Abbreviations and Acronyms
ADM
=
adrenomedullin
ANP
=
atrial natriuretic peptide
BNP
=
brain natriuretic peptide
EPI
=
epinephrine
LV
=
left ventricular
LVEDV
=
LV end-diastolic volume
LVEF
=
LV ejection fraction
LVESV
=
LV end-systolic volume
LVF
=
LV failure
N-BNP
=
N-terminal pro-BNP
NE
=
norepinephrine
ROC
=
receiver operating characteristic
Acknowledgments
Funding was provided by grants from the National Heart
Foundation and the Health Research Council of New Zealand. The authors
gratefully acknowledge the assistance of Leanne Liggett and Rose
Richards (research assistants), Nuclear Medicine and Endocrine
Department technical and nursing staff, and Coronary Care
nursing staff. Secretarial assistance was provided by Barbara
Griffin.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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 R J Hillock, C M Frampton, T G Yandle, R W Troughton, J G Lainchbury, and A M Richards B-type natriuretic peptide infusions in acute myocardial infarction Heart, May 1, 2008; 94(5): 617 - 622. [Abstract] [Full Text] [PDF]
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 H. Nishida, T. Sato, M. Miyazaki, and H. Nakaya Infarct size limitation by adrenomedullin: protein kinase A but not PI3-kinase is linked to mitochondrial KCa channels Cardiovasc Res, January 15, 2008; 77(2): 398 - 405. [Abstract] [Full Text] [PDF]
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M G Nicholls, C M Frampton, and T G Yandle BNP: not just for heart failure Heart, January 1, 2008; 94(1): 6 - 7. [Full Text] [PDF]
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S Q Khan, P Quinn, J E Davies, and L L Ng N-terminal pro-B-type natriuretic peptide is better than TIMI risk score at predicting death after acute myocardial infarction Heart, January 1, 2008; 94(1): 40 - 43. [Abstract] [Full Text] [PDF]
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L. B. Daniels and A. S. Maisel Natriuretic Peptides J. Am. Coll. Cardiol., December 18, 2007; 50(25): 2357 - 2368. [Abstract] [Full Text] [PDF]
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 R. D. Mainwaring, C. Parise, S. B. Wright, A. L. Juris, R. A. Achtel, and H. Fallah Brain Natriuretic Peptide Levels Before and After Ventricular Septal Defect Repair Ann. Thorac. Surg., December 1, 2007; 84(6): 2066 - 2069. [Abstract] [Full Text] [PDF]
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T. Kempf, E. Bjorklund, S. Olofsson, B. Lindahl, T. Allhoff, T. Peter, J. Tongers, K. C. Wollert, and L. Wallentin Growth-differentiation factor-15 improves risk stratification in ST-segment elevation myocardial infarction Eur. Heart J., December 1, 2007; 28(23): 2858 - 2865. [Abstract] [Full Text] [PDF]
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 W.H. Wilson Tang, G. S. Francis, D. A. Morrow, L. K. Newby, C. P. Cannon, R. L. Jesse, A. B. Storrow, R. H. Christenson, COMMITTEE MEMBERS, R. H. Christenson, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Utilization of Cardiac Biomarker Testing in Heart Failure Circulation, July 31, 2007; 116(5): e99 - e109. [Full Text] [PDF]
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F. M. Fruhwald, A. Fahrleitner-Pammer, R. Berger, F. Leyva, N. Freemantle, E. Erdmann, D. Gras, L. Kappenberger, L. Tavazzi, J.-C. Daubert, et al. Early and sustained effects of cardiac resynchronization therapy on N-terminal pro-B-type natriuretic peptide in patients with moderate to severe heart failure and cardiac dyssynchrony Eur. Heart J., July 1, 2007; 28(13): 1592 - 1597. [Abstract] [Full Text] [PDF]
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S. Q Khan, D. Kelly, P. Quinn, J. E Davies, and L. L Ng Myeloperoxidase aids prognostication together with N-terminal pro-B-type natriuretic peptide in high-risk patients with acute ST elevation myocardial infarction Heart, July 1, 2007; 93(7): 826 - 831. [Abstract] [Full Text] [PDF]
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J. Bergler-Klein, G. Mundigler, P. Pibarot, I. G. Burwash, J. G. Dumesnil, C. Blais, C. Fuchs, D. Mohty, R. S. Beanlands, Z. Hachicha, et al. B-Type Natriuretic Peptide in Low-Flow, Low-Gradient Aortic Stenosis: Relationship to Hemodynamics and Clinical Outcome: Results From the Multicenter Truly or Pseudo-Severe Aortic Stenosis (TOPAS) Study Circulation, June 5, 2007; 115(22): 2848 - 2855. [Abstract] [Full Text] [PDF]
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T. J. Mocatta, A. P. Pilbrow, V. A. Cameron, R. Senthilmohan, C. M. Frampton, A. M. Richards, and C. C. Winterbourn Plasma Concentrations of Myeloperoxidase Predict Mortality After Myocardial Infarction J. Am. Coll. Cardiol., May 22, 2007; 49(20): 1993 - 2000. [Abstract] [Full Text] [PDF]
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 B. Assmus, U. Fischer-Rasokat, J. Honold, F. H. Seeger, S. Fichtlscherer, T. Tonn, E. Seifried, V. Schachinger, S. Dimmeler, and A. M. Zeiher Transcoronary Transplantation of Functionally Competent BMCs Is Associated With a Decrease in Natriuretic Peptide Serum Levels and Improved Survival of Patients With Chronic Postinfarction Heart Failure: Results of the TOPCARE-CHD Registry Circ. Res., April 27, 2007; 100(8): 1234 - 1241. [Abstract] [Full Text] [PDF]
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S. Q. Khan, O. S. Dhillon, R. J. O'Brien, J. Struck, P. A. Quinn, N. G. Morgenthaler, I. B. Squire, J. E. Davies, A. Bergmann, and L. L. Ng C-Terminal Provasopressin (Copeptin) as a Novel and Prognostic Marker in Acute Myocardial Infarction: Leicester Acute Myocardial Infarction Peptide (LAMP) Study Circulation, April 24, 2007; 115(16): 2103 - 2110. [Abstract] [Full Text] [PDF]
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