Open Journal of Endocrine and Metabolic Diseases, 2012, 2, 58-62
http://dx.doi.org/10.4236/ojemd.2012.24009 Published Online November 2012 (http://www.SciRP.org/journal/ojemd)
Prognostic Value of N-Terminal Pro-Brain Natriuretic
Peptide in Acute Pulmonary Embolism
Abdelhakem Selem*, Hanan Radwan, Abdelaziz M. Gomaa
Cardiology Department, Ibn Sina Faculty of Medicine, Zagazig University, Zagazig, Egypt
Received August 3, 2012; revised September 5, 2012; accepted October 6, 2012
ABSTRACT
Patients with pulmonary embolism (PE) have a high risk of death and it is important to recognize factors associated
with high mortality. N-Terminal pro-Brain Natriuretic Peptide (NT-pro BNP) has recently emerged as a promising
biomarker for risk assessment in acute pulmonary embolism (PE). The aim of this study is to detect the in hospital
prognostic value of NT-pro BNP in patients with acute (PE). Methods: This study included 64 patients diagnosed as
(PE) with the mean age of 59.1 ± 16.5 years, 40 patients of them (62.5%) were male. All patients were subjected to 12
leads ECG. X-ray chest, laboratory tests including D-Dimer, troponin I, NT-pro BNP, Doppler ultrasound for the ve-
nous system of both lower limbs, Echocardiograhy and 64 multislices CT pulmonary angiography. Results: According
to the admission level of NT-pro BNP our patients were divided into two groups: group I included 22 patients with nor-
mal NT-pro BNP (less than 300 pg/ml), and group II included 42 patients with elevated NT-pro BNP (more than or
equal 300 pg/ml). Patients in group II were found to have a significantly higher incidence of heart failure (28.6% vs
4.6%, p = 0.025), impaired kidney function (serum creatinine was 1.7 ± 0.6 vs 1.1 ± 0.2, p = 0.018), tachypnea (85.7%
vs 54.5%, p = 0.006) and cardiogenic shock (26.2% vs 0%, p = 0.014) but a significantly lower incidence of chest pain
(21.4% vs 45.5%, p = 0.04) and lower left ventricular ejection fraction (51.3% ± 16.9% vs 67.3% ± 12.8%, p = 0.043)
compared to group I. There were a significantly higher treatment with thrombolytic therapy (35.7% vs 9.1%, p =0.021)
and positive inotropics (35.71% vs 4.55%, p = 0.006) in group II compared to group I. Also group II had a higher need
for mechanical ventilation (26.12% vs 4.55%, p = 0.04) and a longer in hospital stay (19.5 ± 10.3 vs 5.3 ± 4.5, p = 0.001)
than group I. The in hospital mortality was significantly higher in group II compared to group I (19.05% vs 0.0%, p =
0.042). Conclusion: Elevated NT-pro BNP levels in patients with (PE) are associated with worse short term prognosis
in terms of higher morbidity and mortality and it could be used as a valuable prognostic parameter and good indicator
for the need of more aggressive therapy.
Keywords: Pulmonary Embolism; N-Terminal Pro-Brain Natriuretic Peptide
1. Introduction
Pulmonary embolism is a common and serious disease
with an incidence rate in hospitalized patients above 5%
[1]. It has a high morbidity and mortality both early and
late, the overall mortality is 7% to 11% while late mor-
tality is 15% at three months and reaches 50% in patients
presenting with cardiogenic shock on admission [2].
Patients with hemodynamic instability at presentation
have a high mortality rate [3]. Hemodynamically stable
patients with RV dysfunction have high mortality. How-
ever; those patients are more difficult to recognize [4].
PE is caused by either inherited or acquired risk fac-
tors. Combination of thrombophilia and acquired risk
factors often precipitate overt thrombosis. The two most
common genetic causes of thrombophilia are factor V
Leiden and prothrombin gene mutation while the most
common acquired thrombophilia is anti-phospholipid
syndrome. The common acquired causes of PE include:
advanced age, personal or family history, recent surgery,
trauma, or immobility, congestive heart failure, acute
infection, pregnancy, oral contraceptive pills and COPD
[5].
Dyspnea is the most common symptom of PE. Other
symptoms include chest pain, cough, hemoptysis and
syncope. Tachycardia is the most frequent sign of PE.
Other signs include tachypnea, left parasternal upleft,
tricuspid regurgitation murmer, accentuated pulmonary
second sound, and evidence of DVT [5].
Right ventricular dysfunction from PE results from a
combination of increased wall stress and cardiac ische-
mia [6]. Myocradial wall stress is a potent stimulus for
increased synthesis and secretion of BNP, which gives
*Corresponding author.
C
opyright © 2012 SciRes. OJEMD

A. SELEM ET AL. 59
the plausibility of elevation of BNP and NT-pro BNP in
the setting of acute PE and right ventricular strain [7].
Accurate risk stratification is of paramount importance
in selecting the optimal management of pulmonary em-
bolism. BNP and pro BNP has recently emerged as pro-
mising parameters for risk stratification of acute pul-
monary embolism [8].
The aim of this study is to detect the prognostic value
of N terminal pro BNP in patient with acute pulmonary
embolism during the hospital stay.
2. Methodology
This study included 64 patients admitted to the hospital
during the period from November 2008 to December
2011 with diagnosis of pulmonary embolism with the
mean age of 59.1 ± 16.5 years, 40 patients of them
(62.5%) were male. The local ethics committee approved
the study protocol and written informed consent was ob-
tained from all stable patients and from the first degree
relatives of the unstable patients.
Diagnosis of PE in our study depended primarily upon
the presence of high clinical suspicion of PE with either:
1) positive CT pulmonary angiography; or 2) the pre-
sence of pulmonary hypertension and right ventricular
dilatation by echocardiography plus positive Doppler for
DVT.
All patients were subjected to full history taking and
clinical examination, standard 12 leads ECG, X-ray chest,
laboratory tests including D-Dimer, complete blood
count, troponin I, NT-pro BNP, kidney and liver function
tests. Doppler ultrasound for the venous system of both
lower limbs to detect venous thrombosis, echocardio-
grahy to assess pulmonary artery pressure, right ven-
tricular diameter, right ventricular free wall motion, tri-
cuspid regurgitation, presence of right ventricular or a
trial thrombus and left ventricular ejection fraction were
done. Also 64 multislices CT pulmonary angiography
was done for all patients during the first 24 hours of ad-
mission and was considered as the gold standard for dia-
gnosis of pulmonary embolism.
Exclusion criteria included patients with history of
preexisting left ventricular dysfunction and chronic renal
impairment, acute coronary syndrome, chronic lung di-
sease with cor-pulmonale and patients with negative D-
dimer.
According to the admission levels of NT-pro BNP, our
patients were divided into two groups: group I included
22 patients with normal NT-pro BNP (less than 300
pg/ml), and group II included 42 patients with elevated
NT-pro BNP (≥300 pg/ml). This cutoff value was pre-
viously reported by Vuilleumier et al., 2007 [9].
Both groups were compared in terms of demographic
data, clinical presentation, laboratory data, ECG, echo-
cardiography, CT pulmonary angiography and hospital
course including right sided heart failure, hypotension,
cardiogenic shock, needs for thrombolytic therapy or
positive inotropic support, needs for mechanical ventila-
tion, duration of hospital stay and number of deaths. Sta-
tistical analyses were done using SPSS for windows ver-
sion 17. Continuous variables were expressed as means
and standard deviation and compared by student T test
while categorical variables were expressed as percent-
ages and compared by chi square test, and results were
considered significant if the p-value is <0.05.
3. Results
According to the admission level of NT-pro BNP, our
patients were divided into two groups: group I included
22 patients with NT-pro BNP less than 300 pg/ml, and
group II included 42 patients with elevated NT-pro BNP
(≥300 pg/ml).
We found that there were no significant differences
regarding the base line characteristics of the studied
population including demographic variables, risk factors
for cardiovascular diseases and risk factors for venous
thromboembolism except the incidence of heart failure
which was found to be statistically significantly higher in
group II compared to group I (28.6% vs 4.55%, p = 0.025)
(Table 1).
Patients in group II were found to have a significantly
higher incidence of impaired kidney function (serum
creatinine was 1.7 ± 0.6 vs 1.1 ± 0.2, p = 0.018), tachyp-
Table 1. Patients’ characteristics.
Variable Group I
22 Group II 42 p-value
Age, years (mean ±
SD) 58.7 ± 12 59.3 ± 15 0.87
Sex male n (%) (14) 63.6% (26) 61.9%0.89
Body mass index
(mean ± SD) 31.6 ± 5 32.3 ± 6 0.64
Diabetes mellitus n
(%) 5 (22.7%) 10 (23.8%)0.92
Hypertension n (%)13 (59.1%) 26 (61.9%)0.82
Dyslipidemia n (%)9 (40.9%) 19 (45.2%)0.74
Stable coronary
artery disease n (%)3 (13.6%) 6 (14.3%) 0.75
Atrial fibrillation n
(%) 5 (22.7%) 12 (28.6%)0.61
Heart failure n (%) 1 (4.55%) 12 (28.6%)0.025
Trauma n (%) 1 (4.55%) 3 (7.14%) 0.89
Post operative n (%)3 (13.63%) 6 (14.28%)0.75
Bed ridden n (%) 1 (4.55%) 4 (9.52%) 0.83
Oral contraceptives
n (%) 2 (9.09%) 3 (7.14%) 0.83

A. SELEM ET AL.
60
nea (85.7% vs 54.5%, p = 0.006) and cardiogenic shock
(26.2% vs 0%, p = 0.014) but a significantly lower inci-
dence of chest pain (21.4% vs 45.5%, p = 0.04) and
lower left ventricular ejection fraction (51.3% ± 16.9%
vs 67.3% ± 12.8%, p = 0.043) compared to group I (Ta-
ble 2).
There were no significant difference between the two
groups regarding the electrocardiographic signs of pul-
monary embolism but there was a significantly higher
incidence of dilatation of the right ventricular diameter
(more than 30 mm) assessed by echocardiography in
group II compared to group I (88.1% vs 45.45%, p =
0.001) (Table 3).
There were a significantly higher treatment with
thrombolytic therapy (35.7% vs 9.1%, p = 0.021) and
positive inotropics (35.71% vs 4.55%, p = 0.006) in
group II compared to group I. Also group II had a higher
need for mechanical ventilation (26.12% vs 4.55%, p =
0.04) and a longer in hospital stay (19.5 ± 10.3 vs 5.3 ±
4.5, p = 0.001) than group I. The in hospital mortality
was significantly higher in group II compared to group I
(19.05% vs 0.0%, p = 0.042) (Table 4).
Table 2. Clinical and laboratory data of the studied pop ula-
tion.
Variable Group I
22 Group II 42 p-value
Dyspea n (%) 19 (86.36%) 40 (95.2%) 0.44
Chest pain n (%) 10 (45.45%) 9 (21.4%) 0.04
Hemoptysis n (%) 3 (13.63%) 5 (11.9%) 0.84
Syncope n (%) 2 (9.09%) 7 (16.67%) 0.65
Cough n (%) 2 (9.09%) 4 (9.25%) 0.69
DVT n (%) 4 (18.18%) 7 (16.6%) 0.84
Tachypnea n (%) 12 (54.54%) 36 (85.7%) 0.006
Heart rate (mean ±
SD) 99.5 ± 21.4 105.3 ± 35.2 0.36
Systolic blood
pressure (mean ±
SD)
130 ± 22.5 120.5 ± 32.6 0.19
Cardiogenic shock
(Systolic blood
pressure <90
mmHg) n (%)
0 (0%) 11 (26.2%) 0.014
D-dimer (mean ±
SD)
1936.6 ±
415.7
2317.9 ±
678.4 0.06
Troponin I (mean ±
SD) 0.31 ± 0.5 1.1 ± 0.9 0.03
NT-pro BNP (mean
± SD) 179 ± 68 1843 ± 538 0.0001
Serum creatinine
(mean ± SD) 1.1 ± 0.2 1.7 ± 0.6 0.018
Table 3. ECG, Echocardiography and CT pulmonary an-
giography data.
Variable Group I
22 Group II 42 p-value
Sinus tachycardia n
(%) 10 (45.5%) 31 (73.81%) 0.024
Atrial fibrillation n
(%) 0 (0%) 2 (4.76%) 0.77
Right bundle branch
block n (%) 2 (9.09%) 7 (16.67%) 0.65
S1Q3T3 n (%) 4 (18.18%) 4 (9.52%) 0.55
T wave inversion in
V1-4 n (%) 7 (31.82%) 13 (30.95%) 0.94
RV >30 mm n (%) 10 (45.45%) 37 (88.1%) 0.001
Pulmonary artery
pressure (mmHg)
(mean ± SD)
52.1 ± 24 59.3 ± 18.2 0.65
Right ventricular
and right atrial
thrombus n (%)
1 (4.55%) 2 (4.76%) 0.55
Ejection fraction%
(mean ± SD) 67.3 ± 12.8% 51.3 ± 16.9%0.043
CT pulmonary
angiography n (%) 19 (86.36%) 40 (95.23%) 0.44
Doppler evidence of
DVT n (%) 14 (62.64%) 24 (57.14%) 0.61
Table 4. Treatment and prognosis.
Variable Group I 22 Group II 42 p-value
Positive inotropics n
(%) 1 (4.55%) 15 (35.71%) 0.006
Low molecular
weight heparin n (%)22 (100%) 42 (100%) 1.0
Pharmacological
thrombolysis n (%) 2 (9.09%) 15 (35.7%) 0.021
Duration of
hospital stay (mean ±
SD)
5.3 ± 4.5 19.5 + 10.3 0.001
Mechanical
ventilation n (%) 1 (4.55%) 11 (26.19%) 0.04
Hospital mortality n
(%) 0 (0%) 8 (19.05%) 0.042
4. Discussion
Plasma NT-pro BNP elevation in acute pulmonary em-
bolism is probably caused by increased myocardial sheer
stress mainly in the right ventricle and depends on the
degree and dynamics of embolus events [10].
Patients presented with overt heart failure and hemo-
dynamic instability are known to have high mortality rate
in acute phase of the disease [11] and there is consensus
that emergency thrombolytics, interventional or surgical
therapies is warranted to save their lives [12].

A. SELEM ET AL. 61
We found that the most common clinical presentation
in our study was dyspnea which was 86.4% in group I
and 95% in group II, this was comparable to the result of
Dores et al., 2011 who found that dyspnea was 83.3% in
patients with less than median pro BNP and it was 87.1%
among those with more than median pro BNP.
The incidence of chest pain was significantly higher in
group I compared to group II (45.5% vs 21.4%) while the
incidence of tachypnea was higher in group II than group
I (85.7% vs 54.5%) and this was comparable to the result
obtained by Dorese et al., 2011 [13].
In our study we found elevated NT-pro BNP at ad-
mission in patients with pulmonary embolism correlated
significantly with worse in-hospital complications in-
cluding the need for positive inotropics, the need for
thrombolysis, the need for mechanical ventilation and
duration of hospital stay as well as in-hospital mortality.
The overall mortality rate in our patients was found to
be 12.5% (0% within group I and 19.05% in group II,
p-value 0.042) this result was consistent with keron [2]
2003 who reported that in-hospital mortality was 7% -
11%. Dores et al., 2011 [13] reported that the overall
three months mortality was 15% while it was 50% for
patients presented with cardiogenic shock.
Recent meta analyses of 32 studies including 1172 pa-
tients with pulmonary embolism demonstrated the abi-
lity of NT-pro BNP to predict adverse effect and also
concluded that in patient with higher NT-pro BNP, the
concomitant elevation of Troponin I added a prognostic
value [14].
N terminal pro BNP or troponin I combined with Echo-
cardiography reliably identify patients with high risk of
pulmonary embolism [8].
Agterof et al., 2010 [15] suggested that patients with
PE who are hemodynamically stable and with low NT-
pro BNP levels (less than 500 pg/ml) can be treated as
outpatients, with no increase in complication or adverse
events which if confirmed would bring considerable
benefits in both clinical and economic terms.
Cavallazi et al., 2008 [7] meta-analyzed 16 studies and
concluded that BNP and NT-pro BNP are associated with
right ventricular dysfunction in patients with acute PE
and are significant predictor of all cause in hospital or
short term mortality in these patients.
If both troponin I and BNP levels were normal a low
risk population free of adverse clinical outcome likely
exists and right ventricular function in echocardiography
will almost be normal and these patients may be suitable
for short hospital stay [16] or even for outpatient ma-
nagement [17].
In contrast patient with elevated cardiac markers may
require immediate triage for ICU, urgent thrombolysis
[18] and catheter embolectomy [19] or open surgical em-
bolectomy [20].
Kostrubiec et al., 2007 [21] found that persistent ele-
vation of NT-pro BNP 24 hours after diagnosis (reduc-
tion of less than 50% from initial values) predicts higher
mortality at thirty days. Serial measurements of NT-pro
BNP may provide additional prognostic information com-
pared to a single measurement at admission as well as
being an indicator of therapeutic efficacy.
Despite its proven relevance for prognostic assessment
routine NT-pro BNP measurement is not universally ac-
cepted strategy for patients with pulmonary embolism [13].
5. Limitations of the Study
1) We studied a small number of patients because we are
working in a low capacity general hospital and not a
specified big cardiac center; 2) The cutoff value of NT
pro BNP which we used in our analysis was relatively
low, 300 pg/ml [9]. However, other authors used a higher
different cutoff values of 500 pg/ml [10] 600 [21] and
1000 pg/ml [8].
6. Conclusion
Elevated NT-pro BNP levels in patients with pulmonary
embolism are associated with worse short term prognosis
in terms of higher morbidity and mortality and it could
be used as a valuable prognostic parameter and good
indicator for the need of more aggressive therapy.
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Abbreviations
PE = pulmonary embolism; DVT = deep venous throm-
bosis; RV = right ventricle; BNP = brain natriuretic pep-
tide; NT-pro BNP = N terminal pro brain natriuretic pep-
tide.