Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 8  |  Issue : 5  |  Page : 614-618  

Correlation of high sensitive C-reactive protein with cardiac markers in the diagnosis of acute coronary artery disease: A study of 100 cases


Department of Pathology, C. U. Shah Medical College, Surendranagar, Gujarat, India

Date of Web Publication10-Sep-2015

Correspondence Address:
Atul Shrivastav
Department of Pathology, C. U. Shah Medical College, Surendranagar - 363 001, Gujarat
India
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Source of Support: Nil., Conflict of Interest: None declared.


DOI: 10.4103/0975-2870.164976

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  Abstract 

Introduction: High sensitive C-reactive protein (HS-CRP) is very sensitive acute phase reactant of inflammation. It is hypothesized that a relationship exists between HS-CRP and acute coronary artery disease (CAD). Materials and Methods: Consecutive sampling of 100 patients were done who presented with acute attack of CAD. In all these patients, Serum analysis for cardiac markers such as troponin-T and creatine phosphokinase-MB (CPK-MB) and serum analysis for quantitative estimation of HS-CRP were done along with few other parameters. Results: In our study, HS-CRP was raised in 90% of patients, along with CPK-MB and troponin-T and as an acute phase reactant, it showed parallel rise in total leukocyte count and absolute neutrophil count. The correlation scatter graphs were plotted, which were found to be statistically significant, (P < 0.05). Conclusion: HS-CRP as an acute phase reactant correlates with other acute phase reactants such as total leukocyte count and absolute neutrophil count and also the rise in HS-CRP value in patients of acute CAD correlates with CPK-MB and troponin-T, so that it can be used as a marker for diagnostic purpose in these patients.

Keywords: Acute coronary artery disease, creatine phosphokinase-MB, high sensitive C-reactive protein, troponin-T


How to cite this article:
Gurunani RH, Shrivastav A, Maru AM, Choksi TS, Agnihotri AS. Correlation of high sensitive C-reactive protein with cardiac markers in the diagnosis of acute coronary artery disease: A study of 100 cases. Med J DY Patil Univ 2015;8:614-8

How to cite this URL:
Gurunani RH, Shrivastav A, Maru AM, Choksi TS, Agnihotri AS. Correlation of high sensitive C-reactive protein with cardiac markers in the diagnosis of acute coronary artery disease: A study of 100 cases. Med J DY Patil Univ [serial online] 2015 [cited 2024 Mar 29];8:614-8. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2015/8/5/614/164976


  Introduction Top


Coronary artery disease (CAD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium. It typically occurs when there is an imbalance between myocardial oxygen supply and demand. The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial coronary artery or arteries sufficient to cause a regional reduction in myocardial blood flow and inadequate perfusion of the myocardium supplied by the involved coronary artery.[1]

The predilection of Indians to CAD has been confirmed beyond doubt.[2],[3] Indian population are more prone to develop CAD at a younger age.[2] By the year 2015, India will have the largest CAD burden in the world.[3],[4]

The diagnosis of acute coronary disease was based on clinical symptoms and cardiac marker levels. In an effort to better identify patients at high-risk for cardiovascular events, several markers of risk have been proposed for use in screening. Acute phase reactants are proteins in plasma whose levels increase during inflammatory states secondary to certain tissue damage.[5] With the recognition that atherosclerosis is an inflammatory process, several plasma markers of inflammation have also been evaluated as potential tools for prediction of the risk of coronary events.[6]

Several population-based studies have revealed that high sensitive C-reactive protein (HS-CRP) is an exquisitely sensitive systemic marker of inflammation and a powerful predictive marker of future cardiovascular risk.[7],[8],[9] HS-CRP levels increase after acute myocardial infarction. Therefore; it is interesting to discuss the value of follow-up measurements of HS-CRP in patients with CAD.

Aims

The aim is to study Serum levels of HS-CRP as acute phase reactant in comparison with total leukocyte count and absolute neutrophil count in patients of acute CAD and evaluate the correlation of HS-CRP with cardiac markers such as troponin-T and creatine phosphokinase-MB (CPK-MB) to test the hypothesis that a relationship exists between HS-CRP and acute CADs.


  Materials and Methods Top


This study was carried out at central clinical laboratory of Pathology Department of C. U. Shah Medical College Hospital, Surendranagar. In this observational study, patients were taken from emergency medicine and general medicine wards. Detailed history, general physical examination, and relevant investigations helped in the selection of cases in comparison to age and sex matched healthy controls. Prior approval from institutional ethical committee was taken.

We set following inclusion and exclusion criteria for our study.

Inclusion criteria

Acute CAD was classified as confirmed when symptoms met the criteria of the World Health Organization,[10] and the event was associated with abnormal levels of cardiac enzymes or diagnostic electrocardiographic changes.

Exclusion criteria

Patients who are not undergone complete investigations and/or having conditions known to be associated with raised acute phase proteins were excluded from the study.

The baseline investigations performed in each patient that was complete hemogram, total leukocyte count and absolute neutrophils count, electrocardiograph, cardiac markers (troponin-T and CPK-MB), and HS-CRP. Serum analysis for quantitative estimation of HS-CRP (cut-off values <5 ng/ml) and for cardiac markers; troponin-T (cut-off values <0.1 ng/ml) and CPK-MB (cut-off values <4.88 ng/ml) were done in each included cases. Estimation of HS-CRP was done by quantitative immunoassay using HS-CRP clinical chemistry system of SIEMENS.

After completion of the study, all data were divided according to age groups and mean for each parameter for individual age group, and then calculated and tabulated. Data were then plotted into selected scatter graph format, according to the parameter values. To statistically check our results, we had calculated P value by Pearson's correlation coefficient test on SPSS (software package for statistical analysis).


  Results Top


Of 100 patients, 68 were male and 32 were female as shown in [Figure 1]. The age range of this study was 30-100 years. We divided these 100 patients in 7 age groups of 10 years range. The data obtained for individual patients were arranged according to the age group of patient and mean value of each parameter that is HS-CRP, troponin-T, CPK-MB, total leukocyte count, neutrophil percentage, and absolute neutrophil count for each age group was calculated. Then, HS-CRP was correlated with the rest of the parameters in tabulated form [Table 1], [Table 2], [Table 3]. Figures are plotted [Figure 2], [Figure 3], [Figure 4], [Figure 5] and X axis shows mean values in seven groups and Y axis is having markings of values of comparables. In our study, HS-CRP was raised in 90% of patients, along with CPK-MB and troponin-T, and as an acute phase reactant, it showed approximate parallel rise in total leukocyte count, neutrophil percentage, and absolute neutrophils count.
Figure 1: Gender distribution of patients (n = 100)

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Figure 2: Correlation of C-reactive protein and creatine phosphokinase-MB

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Figure 3: Correlation of C-reactive protein with troponin-T

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Figure 4: Correlation of C-reactive protein and total leukocyte count

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Figure 5: Correlation of C-reactive protein with absolute neutrophil count

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Table 1: Correlation between HS-CRP with CPK-MB and troponin-T

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Table 2: Correlation of HS-CRP and TLC (mean value)

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Table 3: Correlation of HS-CRP with mean neutrophil percentage and absolute neutrophil count

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Results were found to be statistically significant (P < 0.05).


  Discussion Top


A large body of evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop into an acute clinical event by the induction of plaque rupture, leading to acute coronary syndromes (ACSs).[11] More than 20 large prospective trials have shown that the inflammatory biomarker HS-CRP is an independent predictor of future cardiovascular events, in addition to predicting the risk of incident hypertension and diabetes.[12]

In ACSs, plaque rupture is induced by the inflammatory process in the atherosclerotic tissue. The pathogenesis of atherosclerosis is influenced by inflammatory mechanisms and different plasmatic markers of inflammation have been studied. HS-CRP has been the most extensively studied. Initially, it was suggested that HS-CRP was a by-stander marker of inflammation,[13] but subsequent works demonstrated that it was a risk marker in both ACSs and in patients with myocardial ischemia.[14],[15]

The fact that there are reliable, widely available assays to determine the serum concentration of HS-CRP, and that this concentration is essentially entirely dependent on the rate of primary production, renders HS-CRP a particularly attractive candidate serum marker for this purpose. With a view toward widespread clinical applicability, the assay used for this protocol is a highly sensitive, fully automated, commercially available assay.[9],[16],[17]

Various studies have shown a rise in these acute phase reactants in unstable angina. A meta-analysis by Danesh et al.[18] showed that the baseline values for four acute phase reactants; HS-CRP, serum amyloid protein, leukocyte count, and albumin are associated with one another as well as with the future risk of coronary heart disease. These data support the idea that there are some underlying processes related to inflammation that are relevant to CAD. A study by Berk et al.[19] found HS-CRP level significantly elevated in unstable angina as compared to the control group with no ischemic illness. Another study by Abdelmouttaleb et al.[20] in 142 patients with coronary disease (Group 1), 37 patients with normal angiograms (Group 2), and 37 control healthy subjects (Group 3) found higher levels of HS-CRP in patients with unstable angina and previous myocardial infarction than in patients with stable symptoms and Groups 2 and 3.

Although not designed to answer pathophysiological questions, a study done by Ginnetti et al.[21] provides novel information on the link between inflammation and cardiovascular disease in a group of patients with preexisting atherosclerosis severe enough to require peripheral vascular intervention. In addition, the median concentration of HS-CRP in the overall population of this study was similar to that found by our group in patients with unstable angina and single-vessel coronary disease, which suggests that HS-CRP is not merely the reflection of the severity of the atherosclerotic process, but rather of a particular type of activity of the disease. Conversely, the majority of the events were represented by the development of MI, which seems related to the sudden occlusion of an artery without flow limit stenosis in 70% of the cases.

In our prospective observational study, marker of inflammation — HS-CRP was found to be significant predictor of acute cardiovascular event. The results of the current study have several important implications. First, the findings confirm that markers of inflammation are important predictors of acute cardiovascular events and support the hypothesis that atherosclerosis is, in part, an inflammatory disease. Second, because we used a commercially available assay to measure plasma HS-CRP,[22] our results provide clinically relevant confirmation findings. The commercial assay is inexpensive and can be used with standard hospital and outpatient laboratory equipment; thus, screening for this predictor of cardiovascular risk would be practical in many clinical settings. And third, we have correlated the HS-CRP values with cardiac markers troponin-t and CPK-MB which is statistically significant.[23],[24]

The limitation of our study is that we measured HS-CRP and other markers at study entry and thus could not evaluate the effects of changes in the levels of these markers over time.


  Conclusion Top


Finally, we concluded that HS-CRP is a risk marker of acute CAD as it is increased with the relation of other markers of disease. HS-CRP as an acute phase reactant and there is consistent rise in HS-CRP value in patients of acute CAD along with CPK-MB and troponin-T, so that it can be used as a marker for diagnostic purpose in these patients.

 
  References Top

1.
Clinical Management Guidelines for Coronary Artery Disease for National Programme for Prevention and Control of Diabetes, Cardiovascular Disease and Stroke. Developed Under the Government of India — WHO Collaborative Programme; 2008-2009. Available from: http://www.google.co.in/url/www.searo.who.int%2Findia%2Ftopics%2Fcardiovascular_diseases%2FNCD_Resources_CLINICAL_MANAGEMENT_GUIDELINES_FOR_CAD.pdf. [Last assessed on 2015 Feb 15].  Back to cited text no. 1
    
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Mohan V, Deepa R, Rani SS, Premalatha G, Chennai Urban Population Study (CUPS No.5). Prevalence of coronary artery disease and its relationship to lipids in a selected population in South India: The Chennai Urban Population Study (CUPS No. 5). J Am Coll Cardiol 2001;38:682-7.  Back to cited text no. 2
    
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Blake GJ, Ridker PM. Inflammatory bio-markers and cardiovascular risk prediction. J Intern Med 2002;252:283-94.  Back to cited text no. 13
    
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Zebrack JS, Anderson JL, Maycock CA, Horne BD, Bair TL, Muhlstein JB. Usefulness of high-sensitivity C-reactive protein in predicting long-term risk of death or acute myocardial infarction in patients with unstable or stable angina pectoris or acute myocardial infarction. Am J Cardiol 2002;89:145-9.  Back to cited text no. 14
    
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Topol EJ. A guide to therapeutic decision-making in patients with non-ST-segment elevation acute coronary syndromes. J Am Coll Cardiol 2003;41:S123-9.  Back to cited text no. 15
    
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Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL, Rebuzzi AG, Pepys MB, et al. The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med 1994;331:417-24.  Back to cited text no. 17
    
18.
Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, et al. Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. BMJ 2000;321:199-204.  Back to cited text no. 18
    
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Berk BC, Weintraub WS, Alexander RW. Elevation of C-reactive protein in "active" coronary artery disease. Am J Cardiol 1990;65:168-72.  Back to cited text no. 19
    
20.
Abdelmouttaleb I, Danchin N, Ilardo C, Aimone-Gastin I, Angioï M, Lozniewski A, et al. C-Reactive protein and coronary artery disease: Additional evidence of the implication of an inflammatory process in acute coronary syndromes. Am Heart J 1999;137:346-51.  Back to cited text no. 20
    
21.
Ginnetti F, Angiolillo DJ, Grieco G, Liuzzo G, Maseri A. Predictive role of C-reactive protein. Am Heart J 2002;105:800-3.  Back to cited text no. 21
    
22.
Pepys MB, Baltz ML. Acute phase proteins with special reference to C-reactive protein and related proteins (pentaxins) and serum amyloid A protein. Adv Immunol 1983;34:141-212.  Back to cited text no. 22
    
23.
Hutchinson WL, Koenig W, Fröhlich M, Sund M, Lowe GD, Pepys MB. Immunoradiometric assay of circulating C-reactive protein: Age-related values in the adult general population. Clin Chem 2000;46:934-8.  Back to cited text no. 23
    
24.
Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342:836-43.  Back to cited text no. 24
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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