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ORIGINAL ARTICLE  
Year : 2012  |  Volume : 55  |  Issue : 4  |  Page : 474-477
Significant increases in monocyte counts and serum creatine kinase in acute myocardial infarction versus general infections


1 Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia
2 Department of Pathology, Division of Clinical Biochemistry, Armed Forces Hospital, Riyadh, Saudi Arabia
3 Department of Adult Cardiology, Prince Sultan Cardiac Center, Riyadh, Saudi Arabia

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Date of Web Publication4-Mar-2013
 

   Abstract 

Background: Biomarkers specificity is an important factor for their reliable utilization. Known markers for acute myocardial infarction (AMI), including creatine kinase (CK), C-reactive protein (CRP), and blood cell counts are thought to be altered in other pathologic conditions, such as infections. Aim: To compare the level of these biomarkers in AMI patients and infected controls with respect to normal subjects. Materials and Methods: We recruited 15 AMI patients, 15 patients with bacterial infections (infected control group) and 35 normal subjects. Peripheral blood samples were obtained for blood cell counts and biochemical analyses. Results: Only monocytes were significantly increased in AMI patients (0.793 × 10 9 /L) than normal controls (0.497 × 10 9 /L). Infected controls showed a significant increase in total white blood cell (11.50 × 10 9 /L versus 6.149 × 10 9 /L) and neutrophil (9.360 versus 3.223 × 10 9 /L) counts and a significant decrease in red blood cell (3.750 versus 5.105 × 10 12 /L) counts as compared with normal controls. Serum CK was significantly increased in AMI patients (313.20 ± 94.84 U/L) and decreased in infected controls (48.40 ± 10.35 U/L) as compared with normal controls (100.82 ± 8.86 U/L). The levels of CRP were significantly higher in infected controls (136.93 ± 34.83 mg/L) and nonsignificantly higher in AMI patients (38.53 ± 12.76 mg/L) than normal controls (3.48 ± 0.59 mg/L). Monocytes were significantly correlated with both CK and CRP; however, there was no correlation between CK and CRP. Conclusion: Differential trends of monocytes and CK in AMI and infective controls point toward their possible application in prognosis of AMI patients.

Keywords: Acute myocardial infarction, biomarker, blood cells, C-reactive protein, creatine kinase, inflammation, infection

How to cite this article:
Khan HA, Alhomida AS, Sobki SH, Al Moghairi A. Significant increases in monocyte counts and serum creatine kinase in acute myocardial infarction versus general infections. Indian J Pathol Microbiol 2012;55:474-7

How to cite this URL:
Khan HA, Alhomida AS, Sobki SH, Al Moghairi A. Significant increases in monocyte counts and serum creatine kinase in acute myocardial infarction versus general infections. Indian J Pathol Microbiol [serial online] 2012 [cited 2017 Jul 22];55:474-7. Available from: http://www.ijpmonline.org/text.asp?2012/55/4/474/107783



   Introduction Top


Acute myocardial infarction (AMI) is a serious cardiovascular event with significant morbidity and mortality. Total white blood cell (WBC) count has been regarded as an independent predictor of death or myocardial infarction in patients with coronary artery disease. [1] A higher WBC count may be associated with progression of myocardial damage after recanalization in patients with early recanalization of an anterior AMI. [2] Dogan et al. [3] have shown that basal leukocyte and neutrophil counts on admission and first day are positively correlated with peak creatine kinase-myocardial band, peak cardiac troponin, and infarct size in AMI patients. Afiune Neto et al. [4] have observed a higher prevalence of leukocytosis in AMI patients than the stable coronary artery disease; monocytosis being an independent variable for AMI. Leukocyte thrombogenic profile is a relevant player in patients with a high risk of thromboembolic events and may represent a suitable target for molecular intervention. [5] Elevated leukocyte and neutrophil counts after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarctions are directly related to myocardial infarct size and the left ventricular ejection fraction and are independent predictors of cardiovascular outcomes. [6] A higher baseline platelet count in patients with AMI is a powerful independent predictor of death and reinfarction within the first year after primary percutaneous coronary intervention. [7] Goncalves et al. [8] have shown that an elevated mean platelet volume is a strong independent predictor of long-term outcomes after percutaneous coronary intervention and possesses a prognostic value similar to that of troponin in patients with AMI.

The above literature clearly indicates that cardiovascular pathology is associated with altered blood cell counts. However, such alterations are not specific to cardiovascular disease only but also observed in other clinical conditions, such as infections. [9],[10],[11],[12] Two other commonly used biomarkers for AMI, including creatine kinase (CK, a marker of tissue damage) and C-reactive protein (CRP, a marker of inflammation) are also known to change during infections. [11],[12],[13],[14],[15] In this study, we compared the differential blood cell counts and serum levels of CK and CRP in AMI patients, infected patients, and normal controls. We also studied the correlations between blood cell counts and CK and CRP.


   Materials and Methods Top


We selectively (serum troponin >0.100 ng/mL) recruited 15 AMI patients (10 males, 5 females; age 56.33 ± 13.34 years), admitted to our hospital. We also included 35 normal subjects (25 males, 10 females) for comparative evaluation of various parameters. In addition, a third group of 15 patients (9 males, 6 females) with bacterial infections (infected control group) was also included, primarily to compare the pattern of biomarkers alteration due to bacterial infections and hence evaluating the specificity of these biomarkers for AMI. Peripheral blood samples were obtained for blood cell counts (K 2 EDTA tubes), CK, CRP and troponin T analysis (serum separator tubes). All the blood cell counts were performed using an automated hematology analyzer, XE-2100 (Sysmex, UK). Serum CK was analyzed spectrophotometrically using COBAS Integra-800 system (Roche Diagnostics, Germany). Troponin T hs was analyzed using commercially available sandwich ELISA kit (Roche Diagnostics, Germany). Serum CRP was determined immunoturbidimetrically on COBAS system using the principle of human CRP agglutination with latex particles coated with monoclonal anti-CRP antibodies.

The data were evaluated by one-way analysis of variance (ANOVA) followed by Dunnett's multiple comparison test using SPSS statistical package version 17. Pearson's test was used for correlation analysis. P values <0.05 were considered as statistically significant.


   Results Top


The level of serum troponin in AMI patients was 0.822 ± 0.183 ng/ mL, whereas all the controls had troponin values of less than 0.003 ng/mL. Of all the blood cell types, only monocyte counts were significantly increased in AMI patients (0.793 × 10 9 /L) as compared with normal controls (0.497 × 10 9 /L) (ANOVA F = 4.39, P = 0.016) [Table 1]. There was about 3-fold and significant increase in neutrophil counts in infected patients (9.360 × 10 9 /L) than normal controls (3.223 × 10 9 /L) (ANOVA F = 9.72, P = 0.000). Total WBC counts were also significantly higher in infected patients (11.50 × 10 9 /L) as compared with normal controls (6.149 × 10 9 /L) (ANOVA F = 6.71, P = 0.002). There was a significant decrease in RBC counts in infected patients (3.750 × 10 12 /L) than in normal subjects (5.105 × 10 12 /L) (ANOVA F = 23.20, P = 0.000) [Table 1]. Although AMI patients showed increasing trends for neutrophils and total WBC counts and decreasing trend for RBC counts, they did not reach the level of significance when compared with normal control group. There were no significant differences for basophils, eosinophils, lymphocytes, and platelets among the 3 groups [Table 1].
Table 1: Blood cell counts in normal controls, infected controls, and AMI patients

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Serum CK was about 3-fold and significantly higher in AMI patients (313.20 ± 94.84 U/L) and about 0.5-fold lower in infected patients (48.40 ± 10.35 U/L) than normal controls (100.82 ± 8.86 U/L) (ANOVA F = 8.323, P = 0.001) [Figure 1]. The level of serum CRP was 3.48 ± 0.597 mg/L in normal controls, whereas it was several folds higher in infected controls 136.93 ± 34.83 mg/L) and AMI patients (38.53 ± 12.74 mg/L) (ANOVA F = 19.096, P = 0.000) [Figure 2].
Figure 1: Serum creatine kinase (CK) levels in normal controls, infected controls, and acute myocardial infarction (AMI) patients. Box plot values are median 25%-75% interquartile; outliers are shown as filled circles

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Figure 2: Serum C-reactive protein (CRP) levels in normal controls, infected controls, and acute myocardial infarction (AMI) patients. Box plot values are median 25%-75% interquartile; outlier is shown as filled circles

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There was a significant correlation between monocyte counts and serum CK (R = 0.401, P = 0.001) as well as CRP (R = 0.413, P = 0.001) [Figure 3]. Age was neither correlated with monocytes (R = 0.224, P = 0.073) nor CK (R = 0.018, P = 0.891), but it was significantly correlated with CRP (R = 0.268, P = 0.037). There was no significant correlation between CK and CRP (R = –0.089, P = 0.487).
Figure 3: Correlation between monocytes counts and serum creatine kinase (CK) (upper panel) and C-reactive protein (CRP) (lower panel) in all subjects

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   Discussion Top


Both AMI patients and the patients with bacterial infection (infected control group) showed increasing trends in total WBC, neutrophil, and monocyte counts as compared with normal subjects. However, statistically, the increases in WBC and neutrophils were significant only in the infected control group, whereas the increases in monocytes were significant in AMI patients [Table 1]. An elevated WBC count has been significantly associated with higher risk of in-hospital mortality; patients in the highest quartile of WBC count are about 3 times more likely to have a poor prognosis after AMI than those in the lowest quartile. [16] Monocytes are the cells of the immune system that give rise to macrophages that participate in a maladaptive and nonresolving inflammatory response triggering acute thrombotic vascular disease, including AMI. [17] Nozawa et al. [18] have suggested that circulating monocytes play an important role in the progression of coronary plaque in AMI, while the peak monocyte count during might be a predictor of plaque progression. Peripheral monocytosis is associated with left ventricular dysfunction, suggesting a possible role of monocytes in the development of left ventricular remodeling after reperfused AMI. [19]

Serum CK showed opposite trends in AMI (increased) and bacterial infections (decreased) [Figure 1]. Serum CRP was significantly higher in infected patients but only insignificantly higher in AMI patients [Figure 2]. Elevated serum CK and CRP have been reported earlier in AMI patients. [20],[21],[22],[23] We also observed significant correlations between monocyte counts and CK as well as CRP [Figure 3] suggesting that monocyte counts may reflect the extent of tissue damage (CK) and inflammation (CRP) in AMI patients. Hong et al. [24] have suggested an important role of monocytes in the expansion of the infarct and the development of chronic ischemic heart failure after reperfusion therapy. The peak monocyte count recorded during the immediate postinfarction period provides a bedside marker of the extent of myocardial damage. [25] Although neutrophils and monocytes counts on the first days after AMI treated with primary coronary angioplasty are related to markers of effective myocardial reperfusion, only monocytes are significantly associated with contractile recovery of the infarct area at 6 months. [26] Activated monocytes and neutrophils could be a significant source of free radicals, which are involved in lipid peroxidation and cause tissue damage in early postinfarction period. [27]

In conclusion, this study clearly showed a significant increase in monocyte counts in AMI patients but not in infection. Infected patients showed significant increases in total WBC and neutrophil counts and significant decrease in RBC counts. Serum CK was significantly increased in AMI patients but decreased in the infected group. Serum CRP was significantly higher in the infected group but only insignificantly higher in AMI patients. Thus, massive increases in WBC counts, neutrophils, and CRP due to infections might limit their prognostic value for AMI unless optimal cutoffs have been established. Nevertheless, differential trends of monocytes and CK in AMI and infective controls point toward their possible application in prognosis of AMI patients.


   Acknowledgments Top


This study was supported by National Plan for Science and Technology (NPST) Program by King Saud University Project Number 08-BIO571-02. The authors thank Dr. Hatim El Koronki for clinical diagnosis and Mr. Adnan Ali Khan for patients' data management. The technical assistance from the nursing staff of Prince Sultan Cardiac Center and Armed Forces Hospital, Riyadh, for blood collection is gratefully acknowledged.

 
   References Top

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Correspondence Address:
Haseeb A Khan
Department of Biochemistry, College of Science, Bldg 5, King Saud University, P.O. Box 2455, Riyadh
Saudi Arabia
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Source of Support: National Plan for Science and Technology (NPST) Program by King Saud University Project Number 08-BIO571-02, Conflict of Interest: None


DOI: 10.4103/0377-4929.107783

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