520 DOI

Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14,Number:
No. 1 10.37506/v14/i1/2020/ijfmt/192952

Leukocytosis as Prediction for Early and Late Complications

in Patient with St Segment Elevation Myocardial Infarction

Radhi Farhod Shlash1, Ahmed Diab Raheem2

1
Professor and Physician / Department of Internal Medicine / College of Medicine/ University of Al-Qadisiyah/
Iraq, 2M.B.Ch.B. / Department of Internal Medicine/ Al-Dewaniyah Teaching Hospital /Iraq

Abstract
Background: AMI ( acute myocardial infarction ) is one of the most common cause of death . In this study
the prognostic value of WBC count in patient with AMI was assessed in 24 hrs after admission.STEMI (ST
segment elevation myocardial infarction) is frequently associated with leukocytosis, it is that the peripheral
leukocyte count have important prognostic implication in AMI .

Aim of The Study: This study conducted to evaluate and measure level of WBC count in patient with
STEMI and their effect on cardiovascular outcome.

Patients and Method: we have 100 patients (male and female) with mean age (40-80) years admitted to
the AL-diwaniyha teaching hospital CCU ( coronary care unit )department and peripheral blood sampling
taken after 24 hrs of admission and another sample after 1 week and we record the main early and delay
squally occurred. Patient that admitted to CCU were confirmed with AMI by clinical features ,examination
and investigations (ECG with ST segment elevation, positive cardiac troponin) .

Results: The mean WBC count in all patients was 11.260 ± 3.600 X103/ CC. There is no significant difference
in mean WBC count among patients with inferior, lateral and posterior wall MI (P > 0.05); however, mean
WBC count was significantly highest in patients with extensive anterolateral MI (P<0.001); followed by
patients with anterior MI. Early complications were observed in 52 patients (52.0 %), these complications
were in the form of arrhythmias such as VF, VT, AF, heart block and bradycardia and acute heart failure. The
most common early complication was VF ( 32.0 %.)

Late complications were observed in 28 patients (28.0 %), these complications were in the form of chronic
heart failure or unfortunately death of patients. we noted that patient with high WBC after admission have
close relation to more damage and necrotic myocyte an liable for early complications like arrhythmia (VT
,VF) and acute HF.

Conclusion: WBC count remained a significant predictor of complication after admission for patients with
STEMI.

Keywords: late complications ; patient ; Leukocytosis; and myocardial infarction

Introduction and hypercholesterolemia). The pathogenesis of

AMI the most common form where patient atherosclerosis is multifactorial. Broadly, endothelial
presented acutely in previously asymptomatic patient. injury and dysfunction result in the adhesion and
STEMI occurs when coronary blood flow decrease transmigration of leukocytes from the circulation into
abruptly, often thrombotic occlusion of coronary arteries the arterial intimae as well as the migration of smooth
previously affected by atherosclerosis, this injury muscle cells from the media into the intimae, thus
produces or stimulate by risk factors (age, hypertension, initiating the formation of atheroma or atherosclerosis.
(1,2 )
DM, smoking, obesity, sedentary life style, alcohol
 Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14, No. 1 521
All myocardium that supplied by the offender artery There is significant correlations between the
become ischemic. Resulting in chest pain and ECG ischemic severity and consequence of acute phase
evidence of transmural (full thickness) ischemia (ST response (leukocytosis). ( 10,11,12 )
segment elevation) in the leads reflective of that region
of the heart. Aim of the Study: this study conducted to evaluate
level of WBC count in patients with STEMI and
Subsequently necrosis begins within minutes and
progress during several hours in a wave front fashion record their effect on outcome that occur in patients
from the endocardial surface to the epicardia surface. with leukocytosis .
(3,4, 5 )
If ischemia persists for several hours, transmural Patients and Methods : This study was done in
infarction result. In contrast if blood flow is restored CCU at Al-diwaniyah teaching hospital from (January
during the period of progressive necrosis, the ischemic 2018 –December 2018) including patients with STEMI.
myocardium is salvaged and size of infarction is reduced. patients with acute coronary syndrome and ST-segment
More than half of patient with AMI died before elevation in the ECG more than (1) mm in limbs leads
reaching the hospital. and 2mm in the chest leads or new onset LBBB.

To confirm the diagnosis of AMI in addition to ECG with elevated cardiac biomarkers especially cardiac
changes, positive cardiac biomarkers (troponin I, E ― troponin I, (patient with ACS without ST- segment
CK, MB‖ myoglobin) may be needed. ( 6 ) . elevation was excluded). which confirm the diagnosis
by supervisor .
This study focusing on leukocytosis as dependent
predictor for mortality or adverse cardiovascular A (100) patients with STEMI were included.
outcome in patients with STEMI. exclusion criteria:
In this setting elevated WBC count play a central Patient with any recent infection ,those with
role in the reparative process that takes place to replace hematological disorders , any chronic disease ,drugs,
the necrotic tissues. ( 7 ) that causes leukocytosis. Those with non STEMI
Traditionally an elevated WBC count is an indicator &females during menses were excluded. .
of systemic inflammation has been acceptable as part of Complete history & physical examination was done
healing response following AMI. for every patient. venous blood sample into the plain
It has frequently been shown to be a predictor of tube for CBC was taken immediately after admission.
adverse cardiovascular events in addition to part of Another sample was taken after 7-8 days .Early
systemic inflammatory response that mention. complications that occur during the hospitalization
Elevated WBC count to be a proxy for the intensity time or late complications that occurs any time after
of the peri-infarction inflammatory response( 8 ). discharge: VT, VF, HF, ventricular aneurism, dead , was
closely recorded .
The corner stone of this study shown an elevated
WBC count measured during acute phase of MI (24 hrs. Results
after admission) associated with adverse out come. In this study there is significant increase in WBC
This relation ship strongly associated with extension count in patient with STEMI The WBC count mean in
of infarcted area. ( 9 ) Leukocytosis in STEMI affect all patients was 11.260 ± 3.600 X103/ CC, as shown
on sequally through multiple pathogenic mechanisms in table 1. There was no significant difference in mean
that mediate inflammation cause proteolytic and WBC count among patients with inferior, lateral and
oxidative damage to the endothelial cells ,plug the posterior wall MI (P > 0.05); however, mean WBC
microvasculature ,induce hypercoagulability and count was significantly highest in patients with extensive
promote infarct expansion ,so leukocytosis is a risk anterolateral MI (P<0.001); followed by patients with
factor for early and future cardiovascular events. anterior MI, as shown in table 1.
522 Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14, No. 1
Table 1: WBC count according to location and extent of myocardial infarction

P Mean ± SD n Location
<0.001 15.903 ±0.936 18 Extensive
HS
8.257 ±2.204 36 Inferior
13.053 ±2.058 34 Anterior
8.266 ±1.691 10 Lateral
8.010 ±1.010 2 Posterior
11.260 ±3.600 100 Total

Early complications were observed in 52 patients (52.0 %), these complications were in the form of arrhythmias
such as VF, VT, AF, heart block and bradycardia and acute heart failure, as shown in table 2.

Table 2: Prevalence rate of early complications in patients with acute MI

% n Early

32.0 32 VF

20.0 20 VT

4.0 4 AF

13.0 13 Acute HF

6.0 6 Heart block

4.0 4 Bradycardia

11.0 11 Cardiogenic shock

The most common early complication was VF ( 32.0 %.) . Late complications were observed in 28 patients (28.0
%), these complications were in the form of chronic heart failure or unfortunately death of patients, as shown in table
3.

Table 3: Prevalence rate of late complications in patients with acute MI

% n Late

10.0 10 Chronic HF

8.0 8 Death

1.0 1 Ventricular aneurysm

10.0 10 Arrhythmia

WBC count Mean were significantly higher in ± 1.61 X 103 /CC versus 8.47 ± 2.15 X 103 /CC, P <
patients with complications, whether early or late . 0.001. Moreover, mean WBC count was significantly
Those with early complications in comparison with higher in patients with late complications in comparison
patients who were free of early complications, 13.84 with patients who were free of late complications, 13.85
 Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14, No. 1 523
± 3.41 X 103 /CC versus 10.85 ± 3.41 X 103 /CC, P < Furman et al( 15 ).
examined the association between
0.001, as shown in figure 1. WBC count and mortality..

Consistent with the findings from the present study.

More recently, Barron et al( 16 ) examined the

association between WBC count and angiographic
findings in the thrombolysis state in high TIMI score
AMI. They found that patients with a closed infarct-
related artery at 60 and 90 minute had a higher WBC
count than patients with patent artery. ( 17 )

Figure 1: mean WBC count in patient with early, late Many epidemiological studies state that the baseline
complication versus those without WBC is associated with increased incidence of AMI
The cutoff value that predicts any type of and mortality and there is current scientific interest in
complication was WBC count of > 10.5 X 103 / CC with the prognostic value of the WBC determined during the
a sensitivity of 88.9 % and specificity of 82.6 %. The acute phase of AMI to predict mortality. (18 )
cutoff value that predicts early complication was WBC These findings are in agreement not only with this
count of > 10.5 X 103 / CC with a sensitivity of 92.3 % study, but also with other studies of other inflammatory
and specificity of 83.3 %. The cutoff value that predicts markers as CRP and IL-6 elevations of which appear to
late complication was WBC count of > 13.5 X 103 / CC primarily predict death rather than recurrent ischemic
with a sensitivity of 71.4 % and specificity of 83.3 %, as events(19 ).The basis for this till now unknown, but the
shown in table 4. early divergence of the cumulative mortality curves
Table 4: Characteristics of ROC curve suggests that patients with an elevated WBC count have
a higher risk of death from the index event(20).
Late Early Complications Characteristic many explanations have been proposed to state this
association: resistance to thrombolytic therapy due to
>13.5 >10.5 >10.5 Cutoff alterations in the microcirculation, hypercoagulable
state, a no-reflow phenomenon caused by leukocytes,
0.789 0.929 0.919 AUC indirect cardiotoxicity mediated by proinflammatory
0.696 to 0.860 to cytokines, promoters of ischemia-reperfusion injury, and
0.847 to 0.964 95 % CI lastly expansion of the AMI. Regarding this final point,
0.864 0.971
it is important to bear in our mind that the leukocyte
<0.001 <0.001 <0.001 P response that occurs following AMI is a central part
of the inflammatory cascad which initiated to replace
71.4 92.3 88.9 Sensitivity
the necrotic tissue with fibrosis and scaring. This fact
may suggest that the greater the amount of necrosis,
83.3 83.3 82.6 Specificity
the larger the leukocyte response, an assertion based
on experimental studies that show a direct relationship
Discussion between the extent of necrosis and the level of both the
local and the systemic leukocyte response. ( 21 )
In 1974, Friedman et al( 13 ). first who described
the association between WBC count and ACS . they find In clinical settings, the extent of AMI is usually
that an increased WBC count associated with increased estimated using indirect parameters. Thus, various
risk of developing first AMI. Other studies Later on studies have related the WBC to various association
confirmed this observation . Schlant et al. were the first with the size of the AMI: the development of heart
to document an elevation in WBC count as a predictor of failure, significant correlations with the peak level of
morbidity and mortality in patients who survived AMI. isoenzyme MB of creatine kinase (CK-MB),or with left
( 14 )
ventricular ejection fraction. ( 22 )
524 Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14, No. 1
In this study, WBC acted as an independent predictor between neutrophil/lymphocyte ratio and
of early and late complications. This finding provides infarctrelate infarctrelated artery patency before
indirect evidence in favor of an independent role for mechanical reperfusion in patients with ST-
WBC in the pathogenesis of post-AMI complications. elevation myocardial infarction. Coron Artery Dis.
2014;25(2):159-66
Suggest that WBC is a useful and valid biochemical
3. Andreoli TE, Carpenter CJ, Griggs Benjamin IJ.
tool for risk prediction of patients with AMI. The
Cecil Essentials of Medicine. 7th edition. W.B.
neutrophils rule in animal models of ischemia-
Saunders. 2007.
reperfusion( 23 )
4. Núñez J, Fácila L, Llàcer A, Sanchís J, Bodí V,
the findings of this study and finding of Barron et al Bertomeu V, et al. [Prognostic value of white blood
are consistent with the fact that WBCs may in some way cell count in acute myocardial infarction: long-term
be linked to the cause of the increased. In animal models mortality]. Rev Esp Cardiol. 2005;58(6):631-9.
of ischemia-reperfusion, neutrophils appear to lead to 5. Furman MI, Gore JM, Anderson FA, Budaj A,
infarct expansion. In a canine model of AMI, neutrophil Goodman SG, Avezum A, et al. Elevated leukocyte
depletion was associated with a marked reduction in count and adverse hospital events in patients with
infarct size. The mechanism by which neutrophils cause acute coronary syndromes: findings from the Global
this damage is unclear. Engler et al. and others state that Registry of Acute Coronary Events (GRACE). Am
reperfusion after prolonged ischemia leads to progressive Heart J. Jan; 2004; 147(1):42-8.
leukocyte capillary plugging and the ―no reflow‖
6. Dharma S, Hapsari R, Siswanto BB, van der
phenomenon. This plugging seem to be results in part
Laarse A, Jukema JW. Blood Leukocyte Count
from neutrophils binding to the ischemic endothelium via
on Admission Predicts Cardiovascular Events
the leukocyte integrin CD11b/CD18 (Mac-1) receptor
in Patients with Acute ST Elevation Myocardial
.Three animal studies have demonstrated that treatment
Infarction. Int J Angiol. 2015;24(2):127-32.
with an antibody to the CD18 receptor on neutrophils
reduces infarct size ( 24) 7. Gardini E, Caravita L, Ottani F, Ferrini D, Galvani
M. Coronary care units: who to admit and how long.
Conclusions G Ital Cardiol (Rome). 2007;8(5 Suppl 1):5S-11S.

The finding of the current study showed that 8. Jones I, Flather M, Johnson M, Barrow S,
leukocytosis in patient with STEMI was significantly Thompson D. A description of the characteristics
associated with high rates of mortality in short term of patients with non-ST elevation acute coronary
follow up also more over the risk of in-hospital death . syndromes admitted to different settings in the
1990s. Intensive Crit Care Nurs. 2008;24(5):286-
Ethical Clearance: The Research Ethical 94.
Committee at scientific research by ethical approval of 9. Djurdjevic PM, Arsenijevic NN, Baskic DD, Djukic
both environmental and health and higher education and AL, Popovic S, Samardzic G. Systemic response of
scientific research ministries in Iraq peripheral blood leukocytes and their phagocytic
activity during acute myocardial infarction. Exp
Conflict of Interest: The authors declare that they
Clin Cardiol. 2001;6(3):159-66.
have no conflict of interest.
10. Saitto C, Ancona C, Fusco D, Arcà M, Perucci CA.
Funding: Self-funding Outcome of patients with cardiac diseases admitted
to coronary care units: a report from Lazio, Italy.
References Med Care. 2004;42(2):147-54
1. Bae MH, Lee JH, Yang DH, Park HS, Cho Y, Chae 11. Biasucci LM, Liuzzo G, Angiolillo DJ, Sperti
SC. White blood cell, hemoglobin and platelet G, Maseri A. Inflammation and acute coronary
distribution width as short-term prognostic markers syndromes. Herz. 2000;25(2):108-12.
in patients with acute myocardial infarction. J 12. Al-Ahmad RS, Mahafzah AM, Al-Mousa EN.
Korean Med Sci. 2014;29(4):519-26. Immunological changes in acute myocardial
2. Kurtul A, Murat SN, Yarlioglues M, Duran M, infarction. Saudi Med J. 2004;25(7):923-8.
Karadeniz M, Ergun G, et al. The relationship 13. Barron HV, Harr SD, Radford MJ, Wang Y,
 Indian Journal of Forensic Medicine & Toxicology, January-March 2020, Vol. 14, No. 1 525
Krumholz HM. The association between white 20. Mueller, C., Neumann, F.J., Perruchoud , A.P. and
blood cell count and acute myocardial infarction Buett-ner, H.J. White blood cell count and long term
mortality in patients > or =65 years of age: findings mortality after ST elevation acute coronary syn-
from the cooperative cardiovascular project. J Am drome treated with very early revascularisation.
Coll Cardiol. 2001;38(6):1654-61. Heart, (2003) ; 89: 389-392.
14. Furman MI, Gore JM, Anderson FA, Budaj A, 21. Cannon, C.P., McCabe, C.H., Wilcox, R.G.,
Goodman SG, Avezum A, et al. Elevated leukocyte Bentley, J.H. and Braunwald, E. Association of
count and adverse hospital events in patients with white blood cell count with increased mortality in
aute coronary syndromes : findings from the Global acute myocardial infarction and unstable angina
Registry of Acute Coronary Events (GRACE). Am pectoris. OPUS-TIMI 16 Investigators. American
Heart J 2004 ; 147 : 42-8. Journal of Cardiology, (2001) ; 87: 636- 639.
15. Dimitrijevic M, Vasiljevic Z, Vuckovic-Dekic L, 22. Hajj-Ali, R., Zareba, W., Ezzeddine, R. and
Spasic S. The involvement of immune reactions Moss, A.J. Relation of the leukocyte count to
in cardiac damage during acute myocardial recurrent cardiac events in stable patients after
infarction:role of cell-mediated immune response. acute myocardial in- farction. American Journal of
Panminerva Med. 1997;39(2):85-94. Cardiology, (2001) ; 88: 1221-1224.
16. Bhatt, D.L. and Topol, E.J. Need to test the arterial 23. Hoffman M, Blum A, Baruch R, Kaplan E,
inflammation hypothesis. Circulation, (2002) ; Benjamin M. Leukocytes and coronary heart
106:136-140. disease. Atherosclerosis. 2004;172:1–6.
17. Alexander, R.W. Inflammation and coronary artery 24. Pellizzon, G.G., Dixon, S.R., Stone, G.W., Cox,
disease. New England Journal of Medicine, (1994) D.A., Mattos, L., Boura, J.A., Grines, L.L.,
; 331: 468-469. Addala, S., O’Neill, W.W. and Grines, C.L. Stent
18. Libby, P., Ridker, P.M. and Maseri, A. Inflamma- PAMI Investigators. Relation of admission white
tion and atherosclerosis. Circulation, (2002) ; blood Cell count to long-term outcomes after
105:1135-1143. primary coronary angioplasty for acute myocardial
infarction (The Stent PAMI Trial). American
19. Kelly RA, Smith TW. Cytokines and Cardiac
Journal of Cardiology, (2003) ; 91: 729-731.
Contractile dysfunction. Circulation (1997); 95:
77-81.