Original Article

Clinical and Applied

Thrombosis/Hemostasis
Relation of Neutrophil-to-Lymphocyte 2015, Vol. 21(4) 383-388
ª The Author(s) 2013

Ratio With GRACE Risk Score to Reprints and permission:

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DOI: 10.1177/1076029613505763
In-Hospital Cardiac Events in Patients With cat.sagepub.com

ST-Segment Elevated Myocardial Infarction

Ramazan Can Oncel, MD1, Mustafa Ucar, MD1,

Mustafa Serkan Karakas, MD2, Baris Akdemir, MD3,
Atakan Yanikoglu, MD1, Ali Riza Gulcan, MD4,
Refik Emre Altekin, MD1, and Ibrahim Demir, MD1

Abstract
In this study, we aimed to investigate the association of the neutrophil-to-lymphocyte ratio (NLR) with Global Registry of Acute
Coronary Events (GRACE) risk score in patients with ST-segment elevated myocardial infarction (STEMI). We analyzed 101 con-
secutive patients with STEMI. Patients were divided into 3 groups by use of GRACE risk score. The association between NLR and
GRACE risk score was assessed. The NLR showed a proportional increase correlated with GRACE risk score (P < .001). The
occurrence of in-hospital cardiac death, reinfarction, or new-onset heart failure was significantly related to NLR at admission
(P < .001). Likewise, NLR and GRACE risk score showed a significant positive correlation (r ¼ .803, P < .001). In multivariate
analysis, NLR resulted as a predictor of worse in-hospital outcomes independent of GRACE risk score. Our study suggests that
the NLR is significantly associated with adverse in-hospital outcomes, independent of GRACE risk score in patients with STEMI.

Keywords
GRACE risk score, inflammation, neutrophil-to-lymphocyte ratio, acute myocardial infarction

Introduction that current European Acute Coronary Syndrome guidelines

Atherosclerosis is the major cause of cardiovascular disease that
still accounts for most of the mortality worldwide.1 The role of
inflammation in the development and progression of athero-
sclerosis has been clarified.2 Inflammation characterizes all
phases of atherothrombosis, and the presence of inflammation
at the site of the atherosclerotic lesion has a critical pathophysio-
logical role in plaque formation and acute rupture.2,3 The rupture
of a vulnerable atherosclerotic plaque and consecutive thrombus
formation leads to occlusion of the affected coronary artery
followed by necrosis of the subtended myocardial tissue. These
events are clinically referred to as acute coronary syndrome
(ACS), which includes ST-segment elevated myocardial infarc-
tion (STEMI), non-STEMI, and unstable angina pectoris.3,4
The ACSs are a heterogeneous population with varying risks
of death and recurrent cardiac events, in long-term as well as
short-term follow-up. In these patients, early risk stratification
plays a central role, as the benefit of more aggressive treatment
strategies seems to be proportional to the risk of adverse
outcomes. The Global Registry of Acute Coronary Events
(GRACE) risk scores has a high diagnostic performance for
adverse outcomes in ACS and are the preferred scoring system
recommend to apply on admission and at discharge in daily
clinical practice.5
White blood cell (WBC) count and its subtypes are also
known as classic markers of inflammation in cardiovascular
diseases.6 In recent years, neutrophilia and relative lymphope-
nia were shown to be an independent predictor of mortality in
patients with acute heart failure.7,8 Moreover, neutrophil-to-
lymphocyte ratio (NLR) was introduced as a potential marker
to determine inflammation in cardiac and noncardiac disorders
and shown as a predictor of long-term mortality in patients who
1
Department of Cardiology, Akdeniz University Medical Faculty, Dumlupinar
Bouleward, Konyaaltı, Antalya, Turkey
2
Department of Cardiology, Nigde State Hospital, Nigde, Turkey
3
Department of Cardiology, Burdur State Hospital, Burdur, Turkey
4
Department of Cardiology, Sanliurfa Research and Education Hospital,
Sanliurfa, Turkey
Corresponding Author:
Mustafa Serkan Karakas, Department of Cardiology, Nigde State Hospital,
Nigde, Turkey.
Email: mserkan19@hotmail.com
384
underwent percutaneous coronary intervention (PCI).9-14 Addi-
tionally, the NLR has been associated with long-term mortality
in patients with STEMI.10,15,16 As neutrophil and lymphocyte
values are readily available in routine blood count analysis,
NLR may be used as a cost-effective predictor of inflammation
and cardiovascular complications.
The relationship between NLR and STEMI has been shown
in several studies, but there are no data available about the
association of NLR levels with GRACE risk score. In this
study, we aimed to investigate the association of the NLR with
GRACE risk score and in-hospital major advanced cardiac
events in patients with STEMI undergoing primary PCI.
Methods
Study Design, Definitions, and End Points
In this retrospective observational study, between May 2010 and
December 2010, 101 consecutive patients with STEMI treated
with PCI within 6 hours from symptoms onset were investigated.
The STEMI was defined based on the criteria formulated by the
American College of Cardiology and the European Society of
Cardiology.17 Briefly, typical chest pain >30 minutes with a new
ST-segment elevation measured from the J point in 2 consec-
utive leads with at least 0.2 mV in leads V1, V2, and V3 or at
least 0.1 mV in the remaining leads on the electrocardiogram
or new on set left bundle branch block. Demographic data and
variables that determine the in-hospital death or myocardial
infarction (MI) GRACE risk score points (that include age, crea-
tinine, heart rate, systolic blood pressure, Killip class, cardiac
arrest at admission, elevated cardiac markers, and ST-segment
deviation) were recorded.18 The GRACE risk scores were strati-
fied as low (<108 points), intermediate (108-140 points), and
high (>140 points). For each patient, we estimated the risk of
in-hospital mortality and coronary events according to Grace
risk score. Diabetes mellitus was defined as a fasting blood glu-
cose level >126 mg/dL or current use of a diet or medication to
lower blood glucose and/or hemoglobin A1c >6.5%. Hyperten-
sion was considered to be present if the systolic pressure was
>140 mm Hg and/or diastolic pressure was >90 mm Hg as well
as patients receiving antihypertensive treatment were accepted
as hypertensive. Hyperlipidemia was defined as low-density
lipoprotein cholesterol >130 mg/dL, total cholesterol >200 mg/
dL, triglyceride >200 mg/dL, or current use of any antihyperlipi-
demic medication. We considered depressed left ventricle
ejection fraction as values <50%. Smoking was defined as active
smoking in the last 6 months.
Patients with clinical evidence of active infection, cancer,
hematological disease, systemic inflammatory conditions,
autoimmune disease, end-stage liver disease, and renal failure
were excluded from the study.
The primary end point was the combination of death of any
cause, acute MI, and onset of heart failure in-hospital period.
Reinfarction was defined as the appearance of new ischemic
symptoms or electrocardiographic ischemic changes accompa-
nied by reelevation of cardiac biomarkers.
Clinical and Applied Thrombosis/Hemostasis 21(4)
Laboratory Analysis
On admission, venous blood was obtained from all the patients.
Neutrophils, lymphocytes, and WBC were measured as part of
the automated complete blood count before starting any medi-
cation. The NLR was calculated as the ratio of the neutrophils
and lymphocytes, both obtained from the same automated
blood sample at admission. All measurements were performed
30 minutes after blood collection by an automatic blood
counter.
Statistical Analysis
Statistical analyses were performed using the SPSS software
version 17.0 (SPSS Inc, Illinois). Categorical variables were
summarized as percentages and compared with Pearson chi-
square test. Continuous variables were presented as mean +
standard deviation and tested for normal distribution by the
Kolmogorov-Smirnov test. Comparison analyses between
groups were made using Kruskal-Wallis test and one-way
analysis of variance test followed by Mann-Whitney U test and
Tukey test where appropriate. Spearman test was used for
correlation analysis between NLR and GRACE risk score. A
multivariable logistic regression model was used to evaluate
the independent contribution of NLR to the risk of new cardiac
events. Age, NLR, GRACE risk score, MPV, and troponin T
levels were selected for multivariable logistic regression anal-
yses. The adjusted odd ratios and 95% confidence intervals
(CIs) are presented. A P value lower than .05 was considered
significant.
Results
Baseline Characteristics
The study population consisted of 101 consecutive patients
with STEMI. In all, 80.2% of the patients were male, and mean
age of patients was 57.97 + 12.24 years. In all, 42 (41.6%)
patients were hypertensive, 23 (22.8%) patients were diabetic,
34 (33.7%) patients were hyperlipidemic, and 57 (56.4%)
patients were smokers.
According to the GRACE risk score, 21 (20.8%) patients
had low GRACE risk scores, 48 (47.5%) patients had inter-
mediate GRACE risk scores, and 32 (31.7%) patients had high
GRACE risk scores. Demographic and biochemical character-
istics of patients in GRACE risk score groups are shown in
Table 1. The NLR showed a proportional increase correlated
with GRACE risk score (P < .001; Table 1; Figure 1).
Correlation With In-Hospital Events
During the in-hospital period, 11 (10.9%) patients presented
cardiac events (3 cardiac death, 2 reinfarction, and 6 new-
onset heart failure). These patients had more advanced Killip
functional class and higher GRACE risk score (all of these
patients are in the GRACE > 140 points group). Demographic
and biochemical characteristics of patients with and without
Oncel et al 385

Table 1. Demographic and Biochemical Characteristics of Patients in GRACE Risk Score Groups.

Variables GRACE <108 Points GRACE 108-140 Points GRACE >140 Points P

Age, years 48.33 + 8.77a 55.52 + 8.87a,b 67.97 + 11.7c,d < .001
Men, n (%) 16 (76.2) 43 (89.6) 22 (68.8) .063
BMI, kg/m2 28.06 + 3.70 27.27 + 4.09 26.40 + 3.20 .449
HT, n (%) 9 (42.9) 13 (21.7) 20 (62.5) .007
DM, n (%) 3 (14.3) 11 (22.9) 9 (28.1) .501
HPL, n (%) 11 (52.4) 13 (27.1) 10 (31.3) .116
Smoker, n (%) 15 (71.4) 28 (58.3) 14 (43.8) .130
Glucose, mg/dL 162.8 + 64.0 151.4 + 52.1 192.2 + 131.4 .745
WBC, cells/mL 12 459 + 3041 12 269 + 3643 11 787 + 4113 .492
Neutrophil, % 54.64 + 12.15a,d 65.59 + 5.82a,c 79.2 + 5.25c,d < .001
Lymphocyte, % 37.42 + 6.42a,d 25.70 + 4.47a,c 13.44 + 4.32c,d < .001
NLR 1.52 + 0.50a,d 2.65 + 0.65a,c 6.48 + 1.99c,d < .001
Troponin T, ng/dL 0.18 + 0.64a 0.63 + 1.86a,e 1.06 + 1.57c,d < .001
MPV, fL 8.18 + 0.81f 8.26 + 0.95g 9.04 + 0.98h .002
Abbreviations: BMI, body mass index; HT, hypertension; DM, diabetes mellitus; HPL, hyperlipidemia; WBC, white blood cell; NLR, neutrophil-to-lymphocyte ratio;
MPV, mean platelet volume; GRACE, Global Registry of Acute Coronary Events.
a
P < .001 compared with GRACE > 140 points.
b
P ¼ .01 compared with GRACE < 108 points.
c
P < .001 compared with GRACE < 108 points.
d
P < .001 compared with GRACE 108 to 140 points.
e
P ¼ .007 compared with GRACE < 108 points.
f
P ¼ .995 compared with GRACE 108 to 140 points.
g
P ¼ .001 compared with GRACE > 140 points.
h
P ¼ .008 compared with GRACE < 108 points.

Multivariate Analysis
For in-hospital cardiac events, NLR, mean platelet volume at
admission, troponin level at admission, in-hospital GRACE
death or MI point, and age were analyzed using a multivariate
logistic regression model. The NLR was the only independent
predictor of in-hospital cardiac events (odds ratio 3.63, 95% CI:
1.23-10.67, P ¼ .019; Table 3).

Figure 1. Comparison of Global Registry of Acute Coronary Events
(GRACE) risk score groups in terms of neutrophil-to-lymphocyte
ratio (NLR).
in-hospital cardiac events are shown in Table 2. The occur-
rence of in-hospital cardiac death, reinfarction, or new-onset
heart failure was significantly related to NLR at admission
(8.18 + 1.16 vs 3.07 + 1.77, P < .001). In the correlation
analysis, NLR showed a significant positive correlation with
the following; GRACE risk score (r ¼ .803, P < .001, Fig-
ure 2), age (r ¼ .516, P < .001), and troponin T levels (r ¼
.507, P < .001).
Discussion
Neutrophil-to-lymphocyte ratio has recently emerged as a
potential new biomarker, which singles out individuals at risk
of future cardiovascular events in patients with STEMI. In our
study, we showed that NLR was significantly associated with
adverse in-hospital outcomes, independent of GRACE risk
score. It is also the first study to correlate the levels of NLR
with the GRACE risk score. Our results were in accordance
with several previous studies that NLR was a predictor of neg-
ative outcome.10,19,20 In contrast with the results of our study,
theirs did not demonstrate a relation with GRACE risk score,
which is the most useful tool proposed by clinical guidelines
for stratification of patients with acute MI.
Coronary atherosclerosis is the main cause of STEMI. Mul-
tiple pathophysiological factors influence this atherosclerotic
process, and one of the most important factor is inflamma-
tion.2,21 Inflammatory process that underlines atherosclerosis
has a critical role in plaque destabilization and appearence of
a thrombus superimposed on the erosion of an atherosclerotic
plaque is the mechanism that cause MI.22
386 Clinical and Applied Thrombosis/Hemostasis 21(4)

Table 2. Demographic and Biochemical Characteristics of Patients With and Without In-Hospital Cardiac Events.

Patients Without Cardiac Patients With Cardiac

Variables Events (n ¼ 90) Events (n ¼ 11) P

Age, years 56.47 + 11.64 70.27 + 10.24 .001

Men, n (%) 72 (80.0) 9 (81.8) .99
BMI, kg/m2 27.25 + 3.80 26.39 + 3.48 .67
HT, n (%) 34 (37.8) 8 (72.7) .04
DM, n (%) 20 (22.2) 3 (27.3) .71
HPL, n (%) 31 (34.4) 3 (27.3) .74
Smoker, n (%) 50 (55.6) 7 (63.6) .75
Glucose, mg/dL 155.80 + 60.71 256.45 + 187.15 .10
WBC, cells/mL 11 956 + 3457 13 789 + 4935 .35
Neutrophil, % 65.95 + 11.11 81.40 + 3.38 <.001
Lymphocyte, % 25.99 + 9.08 10.09 + 1.18 <.001
NLR 3.07 + 1.77 8.18 + 1.16 <.001
Troponin T, ng/dL 0.64 + 1.63 0.88 + 1.41 .024
MPV, fL 8.38 + 0.96 9.40 + 0.77 .001
GRACE risk score points 127.38 + 30.20 208.36 + 50.95 <.001
Abbreviations: BMI, body mass index; HT, hypertension; DM, diabetes mellitus; HPL, hyperlipidemia; WBC, white blood cell; NLR, neutrophil-to-lymphocyte ratio;
MPV, mean platelet volume; GRACE, Global Registry of Acute Coronary Events.

Table 3. Multivariate Logistic Regression Analyses In-Hospital Cardiac

Events.

Variables Odds Ratio 95% CI P

Age 1.01 0.92-1.11 .755

_In hospital GRACE death or MI point 1.02 0.99-1.06 .157
MPV 1.24 0.35-4.41 .733
Troponin T 0.971 0.49-1.89 .932
NLR 3.63 1.23-10.67 .019
Abbreviations: CI, confidence interval; GRACE, Global Registry of Acute
Coronary Events; MI, myocardial infarction; MPV, mean platelet volume; NLR,
neutrophil–lymphocyte ratio.

have important microcirculatory effects and regulate the inflam-

Figure 2. Correlation between neutrophil-to-lymphocyte ratio
(NLR) and Global Registry of Acute Coronary Events (GRACE) risk
score.
Previous studies showed that WBC count and its subtypes are
indicator of systemic inflammation and have an important role in
modulating the inflammatory response in the atherosclerotic pro-
cess.6,23 In the acute period, leukocyctosis usually accompanies
STEMI in proportion to the magnitude of the necrotic process,
elevated glucocorticoid levels, and possibly inflammation in the
coronary arteries. The magnitude of elevation in the leukocyte
count associates with in-hospital mortality after STEMI, and
leukocyte subtypes modulate the inflammatory response in this
process.16,20 In particular, neutrophils are the first leukocytes
to be found in the dameged myocardial area. Activation of neu-
trophils produce large amount of inflammatory mediators that
matory response to tissue injury.16 Furthermore, in the previous
studies, increased neutrophil count has been independently
related to large infarct size, mechanical complication, and mor-
tality in patients with acute MI.24,25 In an animal study, neutro-
phil invasion to atherosclerotic plaque has been visualized
directly in vivo.26 It was previously suggested that neutrophils
might be associated with the formation of aggregates between
platelets and leukocytes in the intravascular lumen, hence even
play a pivotal role in determining the infarct extension areas and
might facilitate plaque rupture through the release of proteolytic
enzymes, arachidonic acid derivatives, and superoxide radicals.
Therefore, increased neutrophil count may not only reflect the
aggravated inflammation but also play a pathogenic role in the
atherosclerotic plaque instability.27,28 In the acute setting of
coronary events, lymphocytopenia is a common finding during
the stress response secondary to increased corticosteroids lev-
els.29 Furthermore, lymphopenia and decreased CD4 counts with
inverted CD4–CD8 ratio are correlated with low ejection
fraction, high degree of myocardial necrosis, and mortality in
patients with acute MI.30
Oncel et al
The NLR is a combination of 2 independent markers of
inflammation, neutrophils as a marker of the ongoing nonspe-
cific inflammation and lymphocytes as a marker of the regula-
tory pathway.10,31 Unlike many other inflammatory markers
and bioassays, NLR is an inexpensive and readily available
marker that provides an additional level of risk scores in
predicting in-hospital and long-term outcomes.16
Due to understanding of the important relationship between
inflammatory status and adverse outcomes in patients with sta-
ble coronary artery disease; several studies focused on NLR
and its association with adverse outcomes in patients with
ACSs.9,31,32 Akpek et al demonstrated that preprocedural NLR
is an independent predictor of no reflow in patients with
STEMI. Neutrophilia can aggravate myocardial ischemia by
neutrophil-mediated microvascular plugging and can extend
the infarct area.20 Nunez et al followed patients with STEMI
for 4.2 years and evaluated the predictive value of NLR in
long-term mortality and found that an increased NLR is associ-
ated with an increased risk of long-term mortality.10 Moreover,
Shen et al concluded that NLR is independently associated with
long-term mortality in STEMI.16 In both of these single-center
studies; the NLR was measured at admission and following
days up to 3 or 4 days. We measured the NLR at admission
before starting any medication because leukocyte count and its
subytpes (neutrophils and lymphocytes) could be affected by
infectious disorders, anxiety, and medication.
The GRACE risk score is a more accurate risk score than
other risk scores in stratfying patients according to the prob-
ability of adverse outcomes during ACSs. The GRACE risk
scores include variables such as hemodynamic status, killip
class, cardiac markers, and ST-segment deviation but not
inflammatory markers. Correia et al demonstrated that
assessment of inflammation improves risk prediction and
provides additional prognostic information to the GRACE
risk score.33
Similar to previous studies, our current study has confirmed
the relationship between NLR and STEMI. However, there have
been no reports on association between NLR and GRACE risk
score. In the present study, we showed that NLR was signifi-
cantly associated with in-hospital adverse cardiac events
independent of GRACE risk score. Also, we demonstrated that
NLR and GRACE risk score showed a significant positive
correlation. Based on our knowlodge, this is the first study to
correlate NLR with GRACE risk score.
Study Limitations
The limitations of the present study are as follows. (1) This was
a retrospective and single-center study that included a
relatively small number of patients. Further studies with a
larger sample size may be needed. (2) Only 1 measurement
of admission full blood count and calculation of NLR were
included in the analysis. (3) We could not compare NLR with
other inflammatory markers, such as C-reactive protein, fibri-
nogen, or myeloperoxidase, because they were not routinely
obtained in our study population.
387
Conclusion
The GRACE risk score is routinely used for stratification of
patients with ACS. Our study showed that NLR may provide
additional prognostic value in patients with STEMI and
increased NLR is associated with in-hospital cardiac events.
The determination of NLR for risk stratification of patients
with STEMI during hospitalization period may be useful. We
think that these significant findings of our analysis can guide
for the further clinical practice. However, these findings must
be confirmed on a study with larger number of patients.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
References
1. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ.
Global and regional burden of disease and risk factors, 2001: sys-
tematic analysis of population health data. Lancet. 2006;
367(9524):1747-1757.
2. Libby P. Inflammation in atherosclerosis. Nature. 2002;
420(6917):868-874.
3. Fiechter M, Ghadri JR, Jaguszewski M, Siddique A, Vogt S,
Haller RB. Impact of inflammation on adverse cardiovascular
events in patients with acute coronary syndromes [published
online April 6, 2013]. J Cardiovasc Med (Hagerstown). 2013.
4. Corti R, Hutter R, Badimon JJ, Fuster V. Evolving concepts in the
triad of atherosclerosis, inflammation and thrombosis. J Thromb
Thrombolysis. 2004;17(1):35-44.
5. de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R.
TIMI, PURSUIT, and GRACE risk scores: sustained prognostic
value and interaction with revascularization in NSTE-ACS. Eur
Heart J. 2005;26(9):865-872.
6. Horne BD, Anderson JL, John JM, et al; Intermountain Heart
Collaborative Study Group. Which white blood cell subtypes pre-
dict increased cardiovascular risk? J Am Coll Cardiol. 2005;
45(10):1638-1643.
7. Arruda-Olson AM, Reeder GS, Bell MR, Weston SA, Roger VL.
Neutrophilia predicts death and heart failure after myocardial
infarction: a community-based study. Circ Cardiovasc Qual
Outcomes. 2009;2(6):656-662.
8. Rudiger A, Burckhardt OA, Harpes P, Muller SA, Follath F. The
relative lymphocyte count on hospital admission is a risk factor
for long-term mortality in patients with acute heart failure. Am
J Emerg Med. 2006;24(4):451-454.
9. Tamhane UU, Aneja S, Montgomery D, Rogers EK, Eagle KA,
Gurm HS. Association between admission neutrophil to lympho-
cyte ratio and outcomes in patients with acute coronary syndrome.
Am J Cardiol. 2008;102(6):653-657.
388
10. Nunez J, Nunez E, Bodi V, et al. Usefulness of the neutrophil to
lymphocyte ratio in predicting long-term mortality in ST segment ele-
vation myocardial infarction. Am J Cardiol. 2008;101(6):747-752.
11. Walsh SR, Cook EJ, Goulder F, Justin TA, Keeling NJ.
Neutrophil-lymphocyte ratio as a prognostic factor in colorectal
cancer. J Surg Oncol. 2005;91(3):181-184.
12. Duffy BK, Gurm HS, Rajagopal V, Gupta R, Ellis SG, Bhatt DL.
Usefulness of an elevated neutrophil to lymphocyte ratio in
predicting long-term mortality after percutaneous coronary inter-
vention. Am J Cardiol. 2006;97(7):993-996.
13. Cingoz F, Iyisoy A, Demirkol S, et al. Carotid intima-media thick-
ness in patients with slow coronary flow and its association with
neutrophil-to-lymphocyte ratio: a preliminary report [published
online April 23, 2013]. Clin Appl Thromb Hemost. 2013.
14. Demirkol S, Balta S, Unlu M, et al. Neutrophils/lymphocytes ratio
in patients with cardiac syndrome X and its association with car-
otid intima-media thickness [published online November 26,
2012]. Clin Appl Thromb Hemost. 2012.
15. Park JJ, Jang HJ, Oh IY, et al. Prognostic value of neutrophil to
lymphocyte ratio in patients presenting with ST-elevation myo-
cardial infarction undergoing primary percutaneous coronary
intervention. Am J Cardiol. 2013;111(5):636-642.
16. Shen XH, Chen Q, Shi Y, Li HW. Association of neutrophil/lym-
phocyte ratio with long-term mortality after ST elevation myocar-
dial infarction treated with primary percutaneous coronary
intervention. Chin Med J. 2010;123(23):3438-3443.
17. No authors listed. Myocardial infarction redefined: a consensus
document of the joint European society of cardiology/American
college of cardiology committee for the redefinition of myocar-
dial infarction. Eur Heart J. 2000;21(18):1502-1513.
18. Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital
mortality in the global registry of acute coronary events. Arch
Intern Med. 2003;163(5):2345-2353.
19. Arbel Y, Finkelstein A, Halkin A, et al. Neutrophil/lymphocyte
ratio is related to the severity of coronary artery disease and
clinical outcome in patients undergoing angiography. Athero-
sclerosis. 2012;225(2):456-460.
20. Akpek M, Kaya MG, Lam YY, et al. Relation of neutrophil/lym-
phocyte ratio to coronary flow to in-hospital major adverse
cardiac events in patients with ST-elevated myocardial infarction
undergoing primary coronary intervention. Am J Cardiol. 2012;
110(5):621-627.
21. Pearson TA, Mensah GA, Alexander RW, et al. Markers of
inflammation and cardiovascular disease: application to clinical
and public health practice. Circulation. 2003;107(3):499-511.
22. Zairis MN, Lyras AG, Bibis GP, et al. Association of inflamma-
tory biomarkers and cardiac troponin I with multifocal activation
Clinical and Applied Thrombosis/Hemostasis 21(4)
of coronary artery tree in the setting of non-ST-elevation acute
myocardial infarction. Atherosclerosis. 2005;182(1):161-167.
23. Gurm HS, Bhatt DL, Lincoff AM, et al. Impact of preprocedural
white blood cell count on long term mortality after percutaneous
coronary intervention: insights from the EPIC, EPILOG, and
EPISTENT trials. Heart. 2003;89(10):1200-1204.
24. O’Donoghue M, Morrow DA, Cannon CP, et al. Association
between baseline neutrophil count, clopidogrel therapy, and
clinical and angiographic outcomes in patients with ST-
elevation myocardial infarction receiving fibrinolytic therapy.
Eur Heart J. 2008;29(8):984-991.
25. Kirtane AJ, Bui A, Murphy SA, Barron HV, Gibson CM.
Association of peripheral neutrophilia with adverse angiographic
outcomes in ST elevation myocardial infarction. Am J Cardiol.
2004;93(5):532-536.
26. Eriksson EE, Xie X, Werr J, Thoren P, Lindbom L. Direct view-
ing of atherosclerosis in vivo: plaque invasion by leukocytes is
initiated by the endothelial selectins. FASEB J. 2001;15(7):
1149-1157.
27. Roy D, Quiles J, Avanzas P, Arroyo-Espliguero R, Sinha M,
Kaski JC. A comparative study of markers of inflammation for the
assessment of cardiovascular risk in patients presenting to the
emergency department with acute chest pain suggestive of acute
coronary syndrome. Int J Cardiol 2006;109(3):317-321.
28. Muhammed Suliman MA, Bahnacy Juma AA, Ali Almadhani
AA, Pathare AV, Alkindi SS, Uwe Werner F. Predictive value
of neutrophil to lymphocyte ratio in outcomes of patients with
acute coronary syndrome. Arch Med Res. 2010;41(8):618-622.
29. Onsrud M, Thorsby E. Influence of in vivo hydrocortisone on
some human blood lymphocyte subpopulations. I. effect on natu-
ral killer cell activity. Scand J Immunol. 1981;13(6):573-579.
30. Blum A, Sclarovsky S, Rehavia E, Shohat B. Levels of T-
lymphocyte subpopulations, interleukin-1 beta, and soluble
interleukin-2 receptor in acute myocardial infarction. Am Heart
J. 1994;127(5):1226-1230.
31. Azab B, Zaher M, Weiserbs KF, et al. Usefulness of neutrophil to
lymphocyte ratio in predicting short- and long-term mortality
after non-ST-elevation myocardial infarction. Am J Cardiol.
2010;106(4):470-476.
32. Papa A, Emdin M, Passino C, Michelassi C, Battaglia D, Cocci F.
Predictive value of elevated neutrophil-lymphocyte ratio on
cardiac mortality in patients with stable coronary artery disease.
Clin Chim Acta. 2008;395(1-2):27-31.
33. Correia LC, Andrade BB, Borges VM, et al. Prognostic value of
cytokines and chemokines in addition to the GRACE Score in
non-ST-elevation acute coronary syndromes. Clin Chim Acta.
2010;411(7-8):540-545.