Prognostic Value of N-Terminal Pro-Brain Natriuretic Peptide in Acute Pulmonary Embolism

doi:10.4236/ojemd.2012.24009

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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

Email: *[email protected]

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.

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.

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.