International Journal of Clinical Medicine, 2011, 2, 218-223
doi:10.4236/ijcm.2011.23036 Published Online July 2011 (http://www.SciRP.org/journal/ijcm)
N-Terminal Pro-BNP in Acute Coronary
Syndrome Patients with ST Elevation versus
Non ST Elevation Myocardial Infarction
Ragaa H. M. Salama1*, Alaa E. A. El-Moniem2, Nour El-Hefney2, Tarek Samor3
Department of 1Biochemistry; 2Medicine, College of Medicine, Qassim University, Qassim, Kingdom of Saudi Arabia; 3Consultant
of Coronary Care Unite, King Fahed Specialist Hospital, Kingdom of Saudi Arabia.
Received August 25th, 2010; revised January 11th, 2011; accepted January 28th, 2011.
ABSTRACT
The study aimed to evaluate the differences in secretion of NT-proBNP and conventional cardiac markers in patients
with STE-ACS vs NSTE-ACS as a trial to solve the dilemma of the early detection of myocardial ischemia in NSTE-ACS.
Sixty two patients with acute coronary syndrome (ACS) divided into 2 groups according to ECG: group 1 with elevated
ST segment in ECG (STE-ACS) and group 2 with non elevated ST segment (NSTE-ACS). Twenty healthy subjects with
matched age and sex were enrolled as control group in this study. In the sera of all subjects, levels of NT-proBNP,
CK-MB and troponin-T were measured by different kits. CK-MB and TnT were both significantly higher in STE-ACS
patients compared to NSTE-ACS patients. Conversely , NT-proBNP was significantly higher in NSTE-ACS patients than
STE-ACS especially within 4 hours from onset of chest pain. Comparison between NT-proBNP, TnT and CK-MB levels
by ROC curves revealed area under the curves = 0.68, 0.31, 0.17 respectively. NT-proBNP at cutoff 415 pg/mL in
NSTE-ACS patients had higher sensitivity and specificity (92%, 39%; respectively) than other markers that will help in
early diagnosis of NSTE-ACS.
Keywords: NT-proPNB, Acute Coronary Syndrome, ST Segment, Cardiac Markers
1. Introduction
The serum level of N-terminal B-type natriuretic peptide
(NT-proBNP) was elevated in patients with left ven-
tricular (LV) dysfunction and showed a close correlation
with the BNP level. Many reports declared that the ab-
solute increment of NT-proBNP exceeded that of BNP,
and that NT-proBNP would be a more discerning marker
for the detection and evaluation of cardiac dysfunction
than BNP [1]. B-type natriuretic peptide (BNP) and
NT-proBNP can help to identify and accurately dis-
criminated CHF from respiratory disease and non-car-
diac causes of acute dyspnea [2,3]. NT-proBNP meas-
urement act as a guide to current treatment strategies, as
well as novel strategies, in patients with acute myocar-
dial infarction and as markers for the severity of heart
failure [4,5]. NT-proBNP provided information that may
be superior to clinical judgment for the diagnostic
evaluation of the patient with possible HF. It was a sur-
rogate biomarker for prognosis of myocardial damage as
assessed by contrast-enhanced Cardiac MRI [6]. It was
an independent predictor of survival in patients with
hypertension and increased left ventricular mass [7].
CK-MB was a marker of cytosolic damage that reflected
the area at risk and the resultant size of the infarction.
Whereas Tn-T was a marker of myofibril damage and
elevated in proportion to infarct size per se. The clinical
spectrum of ACS consists of ST elevated (STE) myo-
cardial infarction (MI) (STEMI) and non-STE (NSTE)
MI (NSTEMI)/or unstable angina (UA), which are clas-
sified from the acute phase electrocardiography (ECG)
changes and the development of myocardial necrosis.
STEMI caused by acute total coronary occlusion,
whereas NSTEMI associated with vulnerable plaque and
subocclusive thrombosis [8].
This study aimed to evaluate the clinical utility
NT-proBNP in Saudi patients and early detection of
myocardial ischemia in NSTE-ACS and the best time for
treatment of the disease by synthetic peptide molecule.
2. Materials and Methods
This is a prospective case control hospital based study

N-Terminal Pro-BNP in Acute Coronary Syndrome Patients with ST Elevation versus Non ST 219
Elevation Myocardial Infarction
included 62 selected patients with acute chest pain or
dyspnea. The informed consent was obtained from every
patient. Those patients diagnosed as ACS according to
Braunwald’s classification [9], or acute MI (AMI) ac-
cording to the redefined ESC/ACC Committee criteria
were admitted to Coronary Care Unit (CCU), King
Fahed Spealist Hospital in the duration from January to
June 2009. Fifty four of them were males and 8 were
females with ages ranged 27 - 65 years. All patients pre-
sented to CCU within 10 hours from onset of chest pain.
Also, 20 healthy subjects served as control group with
matched age and sex. The patients had cardiopulmonary
resuscitation before admission, serum creatinine level >
2.0 mg/dl, overt pump failure (≥NYHA class II) or hy-
pertension were excluded, in order to focus on the effect
of myocardial ischemia per se on the release of
NT-pro-BNP. All patients subjected to standard 12-lead
ECG immediately after admission. The patients were
classified into STE and NSTE groups based on the ECG
findings on admission. Patients with ST segment eleva-
tion at the J point in 2 or more consecutive leads (with
the cut-off point being >0.2 mV in leads V1, V2, or V3,
and >0.1 mV in the other leads) were defined as having
STE-ACS while patients with ST segment depression, T
wave inversion, or no ECG abnormalities were defined
as having NSTE-ACS, 17 of them diagnosed as unstable
angina. Transthoracic 2-dimensional echocardiography
was performed within 24 h of admission. The LV
end-diastolic (LVEDD) and left ventricular end-systolic
diameters (LVESD) were measured according to the
guidelines of the American Society of Echocardiography
[10]. The LV ejection fraction (LVEF) was calculated
by the modified Simpson’s method. Coronary angiogra-
phy was done for determination of the affected vessel.
The study was approved by the ethical committee of
Kingdom of Saudi Arabia, Qassium province, Ministry
of Health.
Blood samples were taken from every patient imme-
diately after admission, centrifuged for 20 min at 2000
xg on 4˚C, and sera were separated divided into aliquots,
kept at –70˚C for biochemical measurements of CK-MB,
TnT and NT-proBNP.
Serum CK-MB levels measured kinetically by UV
method (Stein and Bohner, 1985). Serum level of Tn-T
measured by an electrochemiluminescence assay (Elec-
sys 2010, Roche Diagnostics Germany). NT-proBNP
was measured by using sandwich enzyme immunoassay
kit for the quantitative determination of N-terminal
proBNP human in serum from Alpco diagnostics™ USA.
Catalog # (SK-1204 BNP fragment EIA).
3. Statistical Analysis
SPSS version 16 was used in analysis of the data. The
cardiac markers expressed as mean ± standard error. The
NSTE-ACS and STE-ACS groups compared by the
Mann-Whitney U test. While ANOVA test used to
compare between different cardiac markers. Correlation
coefficient calculated to asses the relation between
NT-proBNP and CK-MB, TnT. Differences of percent-
ages were compared by the chi-square test. ROC curves
done and area under the curves determined. The cardiac
markers and NT-proBNP levels on admission were
grouped according to the time from onset of chest pain
to admission of hospital, and the values compared be-
tween NSTE-ACS and STE-ACS patients by independ-
ent T-test at cut point 4 hours, 6 hours and 8 hours to
detect the peck point of secretion of NT-proBNP. A
p-value equal or less than 0.05 was considered statisti-
cally significant.
4. Results
The data of all patients (62) with acute coronary syn-
drome (ACS) were shown in Table 1. The number of
STE-ACS was 36 while NSTE-ACS was 26 patients.
There was no statistical significant difference in age,
DM, smokers, previous MI, hyperlipidemia, EF% or
angiography between STE-ACS and NSTE-ACS. How-
ever, the female was significantly increased in STE-ACS
while smokers are higher in STE-ACS but, didn’t reach
significant level. NT-proBNP level on admission was
significantly higher in the NSTE-ACS compared to
STE-ACS as shown in Figure 1. However, the conven-
tional cardiac markers (CK-MB and Tn-T) levels on
admission were significantly higher in STE-ACS pa-
tients than NSTE-ACS as shown in Figures 2, 3 respec-
tively and Table 2.
Table 1. Baseline characteristics of the patients with acute
coronary syndrome (ACS).
STE-ACS, ST elevation acute coronary syndrome; NSTE-ACS, non-ST
elevation acute coronary syndrome; EF%, ejection fraction; MI, myocardial
infarction. *statistically significance, p < 0.05 by chi square test.
STE-ACS
(n = 36)
NSTE-ACS
(n = 26)
Age, years 60.72 ± 0.9 62.38 ± 0.8
Male/female 28/8 26/0*
Smoking n (%) 20 (55.5%) 10 (38%)
DM, n (%) 20 (55.5%) 12 (46.1%)
Hyperlipidemia, n (%) 28 (77.7%) 18 (69.2%)
Previous MI, n (%) 12 (33.3%) 12 (46.15)
EF% (57.1% ± 9.8%) (56.6% ± 10.9%)
Coronary angiography:
One vessels disease
Two vessels disease
Three vessels disease
24 (66.7%)
8 (22.2%)
4 (11.1%)
16 (61.5%)
8 (30.7%)
2 (7.8%)

N-Terminal Pro-BNP in Acute Coronary Syndrome Patients with ST Elevation versus Non ST
Elevation Myocardial Infarction
220
In Figure 4, ROC curves of STE-ACS patients
showed that CK-MB had higher sensitivity and specific-
ity, followed by Tn-T then NT-proBNP (cut-off = 415
pg/mL, 61%, 8%, respectively). The area under the curve
was 0.82, 0.69, 0.32, respectively. On the other hand, in
Figure 5, ROC curves of NSTE-ACS patients showed
that NT-proBNP had higher sensitivity and specificity
(cut-off = 415 pg/mL, 92%, 39%, respectively), fol-
lowed by Tn-T (cut-off = 0.045 ng/mL) and CK-MB,
(cut-off = 5.7 IU/L ), for both (84%, 6%, respectively)
as shown in Table 3 . The area under the curves was 0.68,
0.31, 0.17, for NT-proBNP, Tn-T, CK-MB, respectively.
In Figure 5, NT-proBNP had clinical significance, p =
0.02, at 95% confidence interval, the lower bound = 0.52
and the upper bound = 0.82). There was a correlation
between Tn-T and CK-MB (r = 0.3, p = 0.01) and in-
verse correlation between NT-BNP and CK-MB (r =
–0.2, p = 0.03), positive correlation between smoking
and dyslipidymia (r = 0.4, p = 0.01), inverse correlation
between number of vessels affected and smoking (r =
–0.34, p = 0.01). There was no significant difference in
the LVEF determined by echocardiography between
NSTE-ACS patients (57.1% ± 9.8%) and STE-ACS pa-
tients (56.6% ± 10.9%) because we excluded patients
with pump failure (≥Killip class II). NT-proBNP in-
creased in NSTE-ACS patients in the early phase of ACS
Figure 1. NT-proBNP in STE-ACS and NST-ACS.
Figure 2. CK-MB in STE-ACS and NST-ACS.
Figure 4. ROC Curve in STE-ACS.
Figure 3. Tn-T in STE-ACS and NST-ACS.
Table 2. Comparison of cardiac markers in all patients (62) with ACS by ANOVA test.
percentiles
Mean ± SE p Minimum Maximum Mode
(frequency) 25th 50th (median) 75th
NT-proBNP (pg/mL) 1124.35 ± 103.9 0.001 200 2800 2400
(10) 380 680 2000
CK-MB (IU/L) 10.75 ± 0.6 0.000 5.60 19.20 5.6, 18
(6) 6.1 9.2 15
Tn-T (ng/mL) 0.41 ± 0.02 0.002 0.01 0.80 0.6
(6) 0.32 0.45 0.6

N-Terminal Pro-BNP in Acute Coronary Syndrome Patients with ST Elevation versus Non ST 221
Elevation Myocardial Infarction
Table 3. Sensitivity and specificity of cardiac markers.
STE-ACS
Sensitivity specificity
NT-proBNP
cut-off = 415 pg/mL
61% 8%
CK-MB
cut-off = 5.7 IU/L
94% 6%
Tn-T
cut-off = 0.045 ng/mL
94% 6%
NSTE-ACS
NT-proBNP
cut-off = 415 pg/mL
92% 39%
CK-MB
cut-off = 5.7 IU/L
84% 6%
Tn-T
cut-off = 0.045 ng/mL
84% 6%
and it was inversely proportional to the duration of chest
pain. It was more significant increased when the dura-
tion of chest pain was ≤4 hours than ≤6 or ≤8 hours as
shown Figures 6-8 respectively.
5. Discussion
Cardiac markers, such as troponin T (TnT), and creatine
kinase (CK)-MB isozyme, detect the development of
minor myocardial necrosis, and have emerged as pow-
erful predictors of risk in patients with ACS [11,12].
Pro-BNP was synthesized as a pro-hormone by cardiac
myocytes then cleaved by enzyme to N-teminal proBNP
(NT-proBNP) and BNP. NT-proBNP levels predicted
long term survival in patients. The highest NT pro-BNP
quartile was twice as likely to die when compared to
patients with left ventricular hypertrophy in the lowest
NT-ptoBNP quartile [7].
In this study, Nt-proBNP was significantly higher in
NSTE-ACS patients than in STE-ACS patients despite
lower values of the conventional cardiac markers
CK-MB and Tn-T in NSTE-ACS patients. The incre-
ment of NT-proBNP in NSTE-ACS patients was in-
versely proportional to the duration of chest pain. It was
more significant increased when the duration of chest
pain was ≤4 hours than ≤6 or ≤8 hours. It increased dur-
ing the hyperacute phase in NSTE-ACS patients, and
wasn’t raised by the process of myocardial necrosis but
the ischemic insult per se. This may be explained on the
basis that the release kinetics of cardiac markers, espe-
cially NT-proBNP, in patients with NSTE-ACS differed
from those in STE-ACS patients. The ischemic area or
area at risk showed different spectrum in these 2 groups.
The massive elevations of NT-pro-BNP observed in the
early phase of coronary syndrome seemed to be inde-
pendent of ventricular performance. Also, STEMI was
caused by acute total coronary occlusion, whereas
NSTEMI was associated with vulnerable plaque and
Figure 5. ROC Curve in NSTE-ACS.
Figure 6. NT-proBNP in all patients with ACS.
Figure 7. CK-MB in in all patients with ACS.

N-Terminal Pro-BNP in Acute Coronary Syndrome Patients with ST Elevation versus Non ST
222
Elevation Myocardial Infarction
Figure 8. Tn-T in all patients with ACS.
subocclusive thrombosis [8]. The myocardial ischemia
was also a stimulus for the release of BNP and
NT-proBNP [13,14]. The underlying pathomechanism
was not fully understood, but a direct release of BNP
from ischemic cardiomyocytes in addition to ischemia
induced by increase in ventricular wall stress was postu-
lated and, moreover, there was evidence suggested a
protective role of BNP on the myocardium. BNP and
other natriuretic peptides limit the extent of tissue in-
farction during ischaemia and reperfusion. The mecha-
nism of cytoprotection is related to cGMP accumulation
and opening of ATP-sensitive K(+) channels [15,16].
The early activation of the natriuretic peptide recep-
tor/cGMP signalling system may be an important auto-
crine/paracrine response in cardiac ischaemia. This in-
cludes inotropic effects, acute regulation of coronary
vascular tone and attenuation of the susceptibility of
myocardium to ischaemic injury, suppression of growth
and proliferative responses in a variety of myocardial
and vascular cells. In ischaemic myocardium, acute
treatment with BNP prior to and during coronary artery
occlusion exerts a markedly protective, concentration-
dependent infarct-limiting action. This cytoprotective
effect of the natriuretic peptide signalling pathway might
conceivably represent an alternative endogenous salvage
pathway in myocardium which is potentially exploitable
therapeutically. Taken together, the acute actions of na-
triuretic peptides on the coronary vasculature and in
myocardial ischaemia suggest a profile of activity that
may be therapeutically beneficial in the management of
patients with acute coronary syndromes [17]. Thus may
be according to our data, treatment with BNP or
NT-BNP peptide within 4 hours from onset of chest pain
will give best results of protection. Age stratification of
NT-proBNP using cut points of 450, 900, and 1,800
ng/L (for age groups of <50, 50 - 75, and >75 years)
reduced false-negative findings in younger patients, re-
duced false-positive findings in older patients, and im-
proved the overall positive predictive value of the
marker without a change in overall sensitivity or speci-
ficity [18]. In this study, the elevation of NT-proBNP
was much higher in the NSTE-ACS patients than STE-
ACS patients (506 pg/mL vs 201 pg/ml). NT-pro- BNP
was higher in NSTE-ACS patients than STE-ACS pa-
tients (758 pg/mL vs 258 pg/mL). Such early increased
would reflect the amount of ischemic insult to the myo-
cardium rather than the actual extent of myocardial
damage or degree of heart failure [19]. A correlation
between LVEF and plasma levels of BNP (r = –0.44, p =
0.002) was detected [6]. However, in this study, this
correlation couldn’t detect because we exclude the heart
failure. The use of NT-proBNP for the evaluation of the
patient with suspected acute HF is useful, cost-effective,
and may reduce adverse outcomes compared with stan-
dard clinical evaluation without natriuretic peptide test-
ing [20].
In a multivariate Cox regression model, N-BNP added
prognostic information above and beyond Killip class,
patient age, and left ventricular ejection fraction. Ad-
justment for peak troponin T levels did not markedly
alter the relation between N-BNP and mortality. In pa-
tients with no evidence of clinical heart failure, N-BNP
remained a significant predictor of mortality after ad-
justment for age and ejection fraction. N-BNP is a pow-
erful indicator of long-term mortality in patients with
ACS and provided prognostic information above and
beyond conventional risk markers [21,22].
6. Conclusions
NT-proBNP is an early sensitive marker of ACS as it
increased significantly in the early phase of ACS (less
than 8 hours), with much increment when the chest pain
duration less than 4 hours. It is very sensitive and spe-
cific than other traditional cardiac markers (CK-MB and
TnT) in the early diagnosis of NSTE-ACS which caused
very big problem in the early diagnosis than STE-ACS.
REFERENCES
[1] Y. Seino, A. Ogawa, T .Yamashita, M. Fukushima, K.
Ogata, H. Fukumoto and T. Takano, “Application of Nt-
Probnp and Bnp Measurements in Cardiac Care: A More
Discerning Marker for the Detection and Evaluation of
Heart Failure,” European Journal of Heart Failure, Vol.
6, No. 3, 2004, pp. 295-300.
doi:10.1016/j.ejheart.2003.12.009
[2] N. Van Der Burg-de Graauw, C. M Cobbaert, C. J. Mid-
delhoff, T. A. Bantje and C. Van Guldener, “The Additive
Value of N-Terminal Pro-B-Type Natriuretic Peptide
Testing at the Emergency Department in Patients with
Acute Dyspnea,” European Journal of Internal Medicine,
Vol. 20, No. 3, 2009, pp. 301-306.
doi:10.1016/j.ejim.2008.09.022
[3] P. R. Fox, M. A. Oyama, C. Reynolds, J. E. Rush, T. C.
Defrancesco, B. W. Keene, C. E. Atkins, K. A. Mac-
donald, K. ESchober, J. D. Bonagura, R. L. Stepien, H. B.
Kellihan, T. P. Nguyenba, L. B. Lehmkuhl, B. K. Lefbom,

N-Terminal Pro-BNP in Acute Coronary Syndrome Patients with ST Elevation versus Non ST
Elevation Myocardial Infarction
223
N. S. Moise and D. F. Hogan, “Utility of Plasma
N-Terminal Pro-brain Natriuretic Peptide (NT-proBNP)
to Distinguish between Congestive Heart Failure and
Non- Cardiac Causes of Acute Dyspnea in Cats,” Journal
of Veterinary Cardiology, Vol. 11, Supplement 1, 2009,
pp. S51-61.
doi:10.1016/j.jvc.2008.12.001
[4] L. Lorgis, M. Zeller, G. Dentan, P. Sicard, P. Buffet , I.
L’Huillier, J. C. Beer, M. Vincent-Martin, H. Makki,
P .Gambert and Y. Cottin, “RICO Survey Working Group:
Prognostic Value of N-Terminal Pro-brain Natriuretic
Peptide in Elderly People with Acute Myocardial Infarc-
tion: Prospective Observational Study,” British Medical
Journal, Vol. 6, No. 338, 2009, p. b1605.
[5] M. Heringlake, T. Kox, J. Poeling, S. Klaus, T. Hanke, N.
Franz, F. Eberhardt, H. Heinze, F. P. Armbruster and L.
Bahlmann, “The Effects of Physical Exercise on Plasma
Levels of Relaxin, NT-proANP, and NT-proBNP in Pa-
tients with Ischemic Heart Disease,” European Journal of
Medical Research, Vol. 14, No. 3, 2009, pp. 106-112.
[6] O. Bruder, C. Jensen, M. Jochims, M. Farazandeh, J.
Barkhausen, T. Schlosser, G. V. Sabin and P. Hunold,
“Relation of B-Type Natriuretic Peptide (BNP) and Infarct
Size as Assessed by Contrast-Enhanced MRI,” Internal
Journal of Cardiology, Vol. 144, No. 1, 2009, pp. 53-58.
[7] S. Garcia, M. S. Akbar, S. SAli, F. Kamdar, M. Y. Tsai
and D. A. Duprez, “N-Terminal Pro-B-type Natriuretic
Peptide Predicts Mortality in Patients with Left Ventricu-
lar Hypertrophy,” Internal Journal of Cardiology, Vol.
143, No. 3, 2009, pp. 349-352.
doi:10.1016/j.ijcard.2009.03.070
[8] J. Alpert, K. Thygesen, E. Antman and J. P. Bassand,
“Myocardial Infarction Redefined: A Consensus Docu-
ment of the Joint European Society of Cardiology
/American College of Cardiology Committee for the Re-
definition of Myocardial Infarction,” Journal of the
American College of Cardiology, Vol. 36, No. 3, 2000, pp.
959-969.
[9] E. Braunwald, E. Antman, J. Beasley, R. M. Califf, M. D.
Cheitlin, J. S. Hochman, R. H. Jones, D. Kereiakes, et al.,
“ACC/AHA Guidelines for the Management of Patients
with Unstable Angina and Non-ST-Segment Elevation
Myocardial Infarction: A Report of the American College
of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on the Management of
Patients with Unstable Angina),” Journal of the American
College of Cardiology, Vol. 36, No. 3, 2000, pp. 970-
1062.
[10] D. Sahn, A. DeMaria, J. Kisslo, et al., “Recommenda-
tions Regarding Quantitation in M-Mode Echocardiogra-
phy: Results of a Survey of Echocardiographic Measure-
ments,” Circulation, Vol. 58, No. 6, 1978, pp. 1072-1083.
[11] B. Haastrup, S. Gill, S. Kristensen, et al., “Biochemical
Markers of Ischemia for the Early Identification of Acute
Myocardial Infarction without St Segment Elevation,”
Cardiology, Vol. 94, No. 4, 2000, pp. 254-261.
[12] Y. Seino, K. Ogata, T. Takano, et al., “Use of a Whole
Blood Rapid Panel Test for Heart-Type Fatty Acid-
Binding Protein in Patients with Acute Chest Pain: Com-
parison with Rapid Troponin T and Myoglobin Tests,”
The American Journal of Medicine, Vol. 115, No. 3, 2003,
pp. 185-190. doi:10.1016/S0002-9343(03)00325-5
[13] K. Bibbins-Domingo, M. Ansari, N. B. Schiller, B.
Massie and M. A. Whooley, “B-Type Natriuretic Peptide
and Ischemia in Patients with Stable Coronary Disease:
Data from the Heart and Soul Study,” Circulation, Vol.
108, No. 24, 2003, pp. 2987-2992.
doi:10.1161/01.CIR.0000103681.04726.9C
[14] M. Weber, T. Dill, R. Arnold, M. Rau, O. Ekinci, K. D.
Müller, A. Berkovitsch, V. Mitrovic and C. Hamm,
“N-Terminal B-Type Natriuretic Peptide Predicts Extent
of Coronary Artery Disease and Ischemia in Patients with
Stable Angina Pectoris,” American Heart Journal, Vol.
148, No. 4, 2004, pp. 612-620.
doi:10.1016/j.ahj.2004.04.021
[15] J. Goetze, C. Christoffersen, M. Perko, H. Arendrup, J. F.
Rehfeld, J. Kastrup and L. B. Nielsen, “Increased Cardiac
BNP Expression Associated with Myocardial Ischemia,”
The Journal of the Federation of American Societies for
Experimental Biology, Vol. 17, No. 9, 2003, pp. 1105-1107.
[16] G. F. Baxter, “Natriuretic Peptides and Myocardial Is-
chaemia,” Basic Research in Cardiology, Vol. 99, No. 2,
2004, pp. 90-93. doi:10.1007/s00395-004-0458-7
[17] Y. Rautureau and G. F. Baxter, “Acute Actions of Natri-
uretic Peptides in Coronary Vasculature and Ischaemic
Myocardium,” Current Pharmaceutical Design, Vol. 10,
No. 20, 2004, pp. 2477-2482.
doi:10.2174/1381612043383854
[18] J. Januzzi, A. Chen-Tournoux and G. Moe, “Amino-Ter-
minal Pro-B-Type Natriuretic Peptide Testing for the Di-
agnosis or Exclusion of Heart Failure in Patients with
Acute Symptoms,” The American Journal of Cardiology,
Vol. 101, No. 3, 2008, pp. 29A-38A.
doi:10.1016/j.amjcard.2007.11.017
[19] A. Ogawa, Y. Seino, T. Yamashita, K. Ogata and T. Ta-
kano, “Difference in Elevation of N-Terminal Pro-BNP
and Conventional Cardiac Markers between Patients with
ST Elevation vs. Non-ST Elevation Acute Coronary Syn-
drome,” Circulation Journal, Vol. 70, No. 11, 2006, pp.
1372-1378. doi:10.1253/circj.70.1372
[20] A. Tuğcu, O. Yıldırımtürk and S. Aytekin, “The Diagnos-
tic Value of N-Terminal B-Type Natriuretic Peptide in
Diastolic Heart Failure: Comparison with Echocardio-
Graphic Findings,” Turk Kardiyoloji Dernegi Arsivi, Vol.
37, No. 2, 2009, pp. 112-121.
[21] T. Omland, J. De Lemos, D. Morrow, et al., “Prognostic
Value of N-Terminal Pro-atrial and Pro-brain Natriuretic
Peptide in Patients with Acute Coronary Syndromes,”
American Journal of Cardiology, Vol. 89, No. 4, 2002, pp.
463-465. doi:10.1016/S0002-9149(01)02271-8
[22] T. Omland, A. Persson, L. Ng, et al., “N-Terminal
Pro-B-Type Natriuretic Peptide and Long-Term Mortality
in Acute Coronary Syndromes,” Circulation, Vol. 106,
2002, pp. 2913-2918.