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Myeloperoxidase levels predicts angiographic severity of coronary artery disease in patients with chronic stable angina.
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PMID:  25161986     Owner:  NLM     Status:  PubMed-not-MEDLINE    
BACKGROUND: Myeloperoxidase (MPO) has an important role in the both processes of inflammation and oxidative stress. It plays proatherogenic role via low-density lipoprotein oxidation, functional inactivation of the high-density lipoprotein and endothelial dysfunction, and seems to be involved in the atherogenesis of coronary arteries. This study designed to evaluate the association between the plasma MPO levels and angiographic severity of coronary artery disease (CAD) in patients with the stable CAD.
MATERIALS AND METHODS: Sixty-eight patients who had documented CAD with angiography and 66 subjects who had normal angiography were selected as case and the control groups for this study, respectively. Gensini scoring system was used for evaluation of severity of coronary artery stenosis. Plasma MPO and C-reactiveprotein (CRP) levels of both case and control groups were determined.
RESULTS: Plasma MPO levels and CRP levels were significantly higher in CAD patients (P < 0.001), and plasma levels of MPO and CRP were correlated with Genssini scores.
CONCLUSIONS: Our findings indicated that the plasma MPO levels increase in patients with stable CAD and hence that, it can be used as adiagnostic factor to predict the coronary artery atherosclerosis severity in stable CAD patients; However, it needs further widespread investigations to achieve an accurate cut point.
Mehdi Baseri; Ramin Heidari; Behzad Mahaki; Yaghoub Hajizadeh; Amir Momenizadeh; Masoumeh Sadeghi
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Publication Detail:
Type:  Journal Article     Date:  2014-06-25
Journal Detail:
Title:  Advanced biomedical research     Volume:  3     ISSN:  2277-9175     ISO Abbreviation:  Adv Biomed Res     Publication Date:  2014  
Date Detail:
Created Date:  2014-08-27     Completed Date:  2014-08-27     Revised Date:  2014-08-29    
Medline Journal Info:
Nlm Unique ID:  101586897     Medline TA:  Adv Biomed Res     Country:  India    
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Languages:  eng     Pagination:  139     Citation Subset:  -    
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Journal Information
Journal ID (nlm-ta): Adv Biomed Res
Journal ID (iso-abbrev): Adv Biomed Res
Journal ID (publisher-id): ABR
ISSN: 2277-9175
ISSN: 2277-9175
Publisher: Medknow Publications & Media Pvt Ltd, India
Article Information
Copyright: © 2014 Baseri.
Received Day: 04 Month: 2 Year: 2013
Accepted Day: 12 Month: 3 Year: 2013
collection publication date: Year: 2014
Electronic publication date: Day: 25 Month: 6 Year: 2014
Volume: 3E-location ID: 139
PubMed Id: 25161986
ID: 4139978
Publisher Id: ABR-3-139
DOI: 10.4103/2277-9175.135155

Myeloperoxidase levels predicts angiographic severity of coronary artery disease in patients with chronic stable angina
Mehdi Baseriaff1
Ramin Heidariaff1
Behzad Mahaki1
Yaghoub Hajizadeh2
Amir Momenizadehaff1
Masoumeh Sadeghi3
Isfahan Cardiovascular Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
1Department of Biostatistics, Isfahan University of Medical Sciences, Isfahan, Iran
2Environment Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
3Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
Correspondence: Address for correspondence: Prof. Massoumeh Sadeghi, Cardiac Rehabililitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail:


In the way of atherosclerotic plaque formation, inflammation and inflammatory biomarkers and process have been involved at all stages, from the initial development of endothelial dysfunction, through to the formation of the established atheroma and its subsequent rupture.[1]

Myeloperoxidase (MPO) is secreted by activated neutrophils and macrophages, and has been known as inflammatory biomarker.[2] MPO has been associated as a noticeable contributor to the process of progress, propagation and complication of atherosclerosis.[3, 4] The enzyme and products of MPO catalyzed oxidation reactions (tyrosylation, nitration, and halogenation) have been recognized in human atherosclerotic lesions, further proposing that MPO may show a pathophysiological part in atherogenesis.[5] Several mechanisms may describe the proatherogenic role of the MPO, such as low-densitylipoprote in (LDL) oxidation and creation of foam cells, functional inactivation oft he high-densitylipoprotein (HDL), endothelial dysfunction due to reduction of nitricoxide bioavailability, activation of metalloproteinase 7, and rise in the vascular cell apoptosis, which result in endothelial erosion and plaque vulnerability.[5, 6, 7, 8, 9, 10]

Inflammation and oxidative stress are linked with atherosclerosis. MPO is linked to both processes inflammation and oxidative stress via its release by leukocytes and its character in catalyzing the creation of oxidizing agents. Recent studies have underlined the importance of the MPO for cardiovascular disease.[11, 12] MPO levels are higher in patients with the coronary artery disease[12], and it has been found to predict cardiovascular disease progress.[12, 13] Serum MPO levels help as a powerful and independent interpreter of endothelial dysfunction in human subjects. MPO mediated endothelia ldysfunction may be a significant mechanistic relation between inflammation, oxidation, and cardiovascular disease.[9] Furthermore, MPO has been stated to play a role in plaque vulnerability.[7] Oxidative stress biomarkers that recognize in stability in the coronary artery plaque (such as MPO) may be valuable for screening patients with the stable CAD who are under extreme risk and may need more aggressive treatment.

This study is designed to assess a likely relation between the plasma levels of MPO and the severity and extent of CAD documented byangiography.

Study design and population

The study protocol was accepted by the department of cardiology of Isfahan University of Medical Science. The ethical acceptance for the study was provided by the institutional ethics committee.

The population study were those had the clinical features of stable CAD, and stable angina diagnosis considered for them by a cardiologist and they were enrolled for elective diagnostic coronary angiography at Noor Hospital and Shahid Chamran Hospital (Isfahan University of Medical Science, Iran) between April 2011 and September 2011.

A total of 68 patients who had CAD documented by angiography were selected randomly among populations tudy as a case group and 66 subjects who had normal angiography were selected as a control group. The age, sex, and smoking variables were matched within the case and control groups.

Exclusion criteria for this study was: 1-Acutecorona rysyndrome 2-Prior Coronary artery bypass grapht (CABG) 3-Prior angioplasty 4-Chronic renal failure 5-Inflammatory and infective disease 6-History of malignancy, radiotherapy and chemotherapy 6-Sever valvular disease 7-diabetes mellitus.

The patients’ clinical data were recorded including acknowledged coronary risk-factors such as age, weight, height, waist, smoking and Hypertension (HTN).


Systemic hypertension was defined in-patients who take antihypertensive medication or patients with a systolic blood pressure of > 140 mmHg and/or diastolic blood pressure of > 90 mmHg on at least 2 separate times. Diabetes mellitus was defined in patients who take insulin or oral hypoglycemic medication. For other patients screening by fasting blood glucose test was performed.

Biochemical methods

All patients have gone under diagnostic coronary angiography. After femoral sheath inserted and before catheterization 10ml of bloods amples were drawn and transferred into EDTA-tube, centrifuged immediately at 4,000 rpmfor 10 min in a cold centrifuge, and plasma aliquots were stored at −80°C until analyses were performed. Plasma MPO level was determined with an ELISA assay kit (Immunology Consultants Laboratory, Inc., Newberg, OR, USA). Plasma total lipoproteinprofile (total cholesterol, triglycerides, LDLcholesterol, and HDL cholesterol) were determined using the standard enzymatickits (Parsazmun, Tehran, Iran). Plasma levels of hsC-reactive protein (CRP) were measured with a latex-enhanced immune turbidometric assay (Roche Diagnostics, Germany).

Angiographice valuation

All the patients’angiograms reviewed by two interventional cardiologists who were unaware of the scheduled patients’data and their MPO plasma levels.

Quantitative coronary angiography was performed using an automated edge detection system (SIEMENS). Genssini scoring system was applied for determining the extent and severity of coronary artery stenosis and to reveal the extent of coronary atherosclerosis. The genssini scores points were from 0 to 400.


Continuous variables were expressed as mean ± standard deviation. Furthermore, for categorical variables, frequencies and percent were reported.

According to the results achieved by the Kolmogrov Smirnov test, Mann–Whitney u test, and Chi-squared test were used to assess the variables between the case and the control groups. Multiple regression analysis was applied to assess the relationship between the genssini scores and CRP, HDL, MPO variables in case (CAD) group. All analyses performed using the SPSS 16.0 P < 0.05 were considered as significant.


The demographic and baseline characteristics of the populations studied are described in Table 1. In addition, to compare the continuous and discrete variables in two groups, Mann–Whitney u test and Chi-squared test were carried out respectively, which are also shown in Table 1.

These statistical tests clearly show that the sex, age and smoking habits of both study groups are well matched with P values of 0.36, 0.47 and 0.59, respectively as mentioned in the study methods.

Plasma levels of HDL were significantly higher in the control group than who had CAD (P < 0.001); however, according to the results from multiple regression in Table 2, nosignificant correlation was seen between HDL and genssini scores (P = 0.57).

Plasma concentrations of MPO were significantly higher in the CAD (stenosis showed angiographically) than the control group [median 44.00(24-93) and median 34.74(15-54) respectively; P < 0.001] [Figure 1] and also significant association was observed between MPO levels and genssini scores (P < 0.001) [Table 2].

Plasma levels of CRP were significantly lower in the control group than CAD group (4.07 ± 0.617; 5.15 ± 1.48 respectively; P < 0.001), and also there was a significant correlation between the CRP and genssini scores (P = 0.022) [Table 2].


MPO has been involved in atherosclerosis through mechanisms related to its role in inflammation.[5, 14] Inflammatory events have been involved at all stages in the progress of atherosclerotic plaque, from the initial development of endothelial dysfunction, through to the formation of the established atheroma, and its subsequent rupture.[1] Macrophages have a key role in lesion creation and evolution, raising the possibility that these inflammatory cells might be a main source of oxidants that damage HDL in the artery wall. One potential way includes reactive intermediates made by MPO, a heme enzyme produced at high levels by macrophages in the arterywall.[15] Human atherosclerotic lesions is enhanced by multiple oxidation products of LDL formed specifically by MPO, such as chlorotyrosine[16] and Schiff base adducts of p-hydroxyphenyl-acetaldehyde (atyrosineoxidation).[17] Oxidation of apolipoproteinA-I (apoA-I) by MPO has been proposed to deprive HDL of its cardioprotective effects. Tyrosine 192 is the main site of chlorination in apoA-I in both plasma and lesion HDL isolated from humans. Chlorination of apoA-I by MPO creates a dysfunctional form of HDL.[18] MPO also may has a role through enhancing endothelial dysfunctionin CAD patient.[19] It diminishes nitric oxide related smooth muscle relaxation[20] and MPO decreases nitricoxide mediated vasorelaxant replies.[19] Recent evidence suggests that MPO activeity precipitates atherogenesis. Several studies support potential links between the MPO and the development of CAD.

In our study, patients with the CAD had upper plasma MPO levels than control groups, and there were significant differences in MPO levels between two groups.

In a previous study, a correlation between systemic MPO levels and the level of stenosis in major coronary arteries has been shown.[12] MPO levels are associated with the presence of angiographically proven coronary atherosclerosis.[12, 21]

This association was studied by Düzgünçinar et al.[22] A relation was observed for MPO plasma levels and extension of CAD by Wainstein et al.[21]

Baldus et al. observed that MPO plasma levels were higher in patients with the CAD compared to a control group, although, the difference between two groups was not significant.[23]

In a study by A daStefanescu et al. on 382 patients elevated plasma MPO concentration was associated with a more advanced cardiovascular risk profile.[24] however, In a study on 557 patients by Kubala et al.the authors have found that MPO levels did not differ significantly between patients with and without CAD.[25]

Furthermore, in our study, MPO level showed a significant correlation with genssini scores either, this evidence can implicate a significant role of MPO in the pathogenesis of coronary atherosclerosis. Hence that MPO can be considered as independent risk-factor for CAD.

HDL normally defends against atherosclerosis by eliminating excess cholesterol from macrophages in the vascularwall, a process named reverse cholesterol transport.[26] Strong reverse relationship between HDL cholesterol and the coronary heart disease.[27] Ametaanalysis off our prospective studies (theFraminghamHeartStudy, the Multiple Risk-Factor InterventionTrial, the Lipid Research Clinics Prevalence Mortality Follow up Study and the Coronary Primary Prevention Trial) revealed that every 1 mg/dl (0.026 mmol/l) rise in HDL cholesterol is associated with a significant coronary disease risk reduction of 2% in men and 3% in women.[28] Patients with angiographically proven CAD more often have low levels of HDL.[29] The process of reverse cholesterol transport may explain protective role of HDL against coronary disease. HDL can also carry antioxidant enzymes that may reduce the levels of oxidizd phospholipids in atheromatous lesions, which could enhance atherogenesis.[27, 28, 29] In the present study, patients with CAD had lower HDL plasma levels than the control group; however, no relationship between HDL and genssiniscores was observed. Furthermore, total cholesterol/HDL ratio was lower in the control group. Inflammation and infection can deprive HDL of its cardioprotective effects and HDL becomes prooxidant.[30, 31] Several inflammatory markers were related with an increased Coronary artery disease (CHD) risk, independent of traditional CHD risk factors.[32] In our study, CRP plasma concentration was higher in the case group and significant relationship was found between CRP levels and genssini scores. These relationships between inflammatory biomarkers MPO, CRP, and CAD patients in this study can implicate the importance and the role of inflammation in development of atherosclerosis and CAD. Brennan et al. reported that a single determination of plasma MPO independently predicts the risk of myocardial infarction, in addition to the risk of major adverse cardiac events in the 1month and 6-monthperiods[11] and elevated level of MPO were independently related with increased risk of CHDevents.[33] Plasma MPO level can use as independent prognostic predictor for long term incident major adverse cardiovascular event in stable CAD patients followed medically.[34] Heslop et al. stated that MPO accurately predicts cardiovascular mortality risk in the CAD patients documented by angiography and considering MPO and CRP together may improve long term risk assessment of CAD patients outcomes.[35] MPO deficiency (a genetic disease) is related with a decreased prevalence of cardiovascular events.[36] A mutation in the MPO gene, which results in reduced enzyme expression was reported to be associated with the diminished risk of CAD.[37] When several biomarkers compared to each other, elevated MPO concentration were found to be highly sensitive predictors of future cardiovascular events.[38, 39]


The results of the presents tudy show significantly higher levels of plasma MPO in angiographically documented CAD than healthy individuals, and MPO can reflect the extent and burden of coronary artery atherosclerosis in stable CAD patients. As regards, other articles that state association between MPO levels and future cardiovascular events in CAD,[32, 33, 34, 35] MPO can beused as diagnostic and prognostic factors, and measurement of MPO may be used as an independent factor for risk stratificationin CAD patients. However, this aim entails future studies with a larger participants in order to determine accurate cut point value in CAD patients and healthy population.


Source of Support: Nil

Conflict of Interest: None declared.

1. Ross R. Atherosclerosis as an inflammatory diseaseNew Engl J MedYear: 1999340115269887164
2. Nicholls SJ,Hazen sl. Myeloperoxidase and cardiovascular diseaseArterioscl Throm Vas BiolYear: 200525110211
3. Ikitimur B,Karadag B. Role of myeloperoxidase in cardiologyFuture CardiolYear: 2010669370220932115
4. Lau D,Baldus S. Myeloperoxidase and its contributory role in inflammatory vascular diseasePharmacol TherapeutYear: 20061111626
5. Sugiyama S,Okada Y,Sukhova GK,Virmani R,Heinecke JW,Libby P. Macrophage myeloperoxidase regulation by granulocyte macrophage colony-stimulating factor in human atherosclerosis and implications in acute coronary syndromesAm J Clin PatholYear: 200115887991
6. Eiserich JP,Baldus S,Brennan ML,Ma W,Zhang C,Tousson A,et al. Myeloperoxidase a leukocyte-derived vascular No oxidaseScienceYear: 2002296239112089442
7. Hazen SL. Myeloperoxidase and plaque vulnerabilityArterioscl Throm Vas BiolYear: 20042411436
8. Podrez EA,Schmitt D,Hoff HF,Hazen SL. Myeloperoxidase-generated reactive nitrogen species convert LDL into an atherogenic form in vitroJ Clin InvestYear: 199910315476010359564
9. Vita JA,Brennan ML,Gokce N,Mann SA,Goormastic M,Shishehbor MH,et al. Serum Myeloperoxidase Levels Independently Predict Endothelial Dysfunction in HumansCirculationYear: 20041101349
10. Zheng L,Nukuna B,Brennan ML,Sun M,Goormastic M,Settle M,et al. Apolipoprotein AI is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular diseaseJ Clin InvestYear: 20041145294115314690
11. Brennan ML,Penn MS,VanLente F,Nambi V,Shishehbor MH,Aviles RJ,et al. Prognostic value of myeloperoxidase in patients with chest painNew Engl J MedYear: 2003349159560414573731
12. Zhang R,Brennan ML,Fu X,Aviles RJ,Pearce GL,Penn MS,et al. Association between myeloperoxidase levels and risk of coronary artery diseaseJAMAYear: 200128621364211694155
13. Meuwese MC,Stroes ES,Hazen SL,vanMiert JN,Kuivenhoven JA,Schaub RG,et al. Serum Myeloperoxidase Levels Are Associated With the Future Risk of Coronary Artery Disease in Apparently Healthy Individuals: The EPIC-Norfolk Prospective Population StudyJ Am Coll CardiolYear: 2007501596517616301
14. Podrez EA,Abu-Soud HM,Hazen SL. Myeloperoxidase-generated oxidants and atherosclerosisFree Radic Biol MedYear: 20002817172510946213
15. Daugherty A,Dunn JL,Rateri DL,Heinecke JW. Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesionsJ Clin InvestYear: 1994944378040285
16. Hazen SL,Heinecke JW. 3-Chlorotyrosine, a specific marker of myeloperoxidase-catalyzed oxidation, is markedly elevated in low density lipoprotein isolated from human atherosclerotic intimaJ Clin InvestYear: 19979920759151778
17. Hazen SL,Hsu FF,Heinecke JW. p-Hydroxyphenylacetaldehyde Is the Major Product of L-Tyrosine Oxidation by Activated Human Phagocytes A chloride-dependent mechanism for the conversion of free amino acids into reactive aldehydes by myeloperoxidaseJ Biol ChemYear: 1996271186178567631
18. Shao B,Pennathur S,Heinecke JW. Myeloperoxidase targets apolipoprotein AI, the major high density lipoprotein protein, for Site-Specific Oxidation in Human Atherosclerotic LesionsJ Biol ChemYear: 201228763758622219194
19. Soud HM,Hazen SL. Nitric oxide is a physiological substrate for mammalian peroxidasesJ Biol ChemYear: 2000275375243211090610
20. Soud HM,Khassawneh MY,Sohn JT,Murray P,Haxhiu MA,Hazen SL. Peroxidases inhibit nitric oxide (NO) dependent bronchodilation: development of a model describing NO-peroxidase interactionsBiochemistryYear: 200140118667511570887
21. Wainstein RV,Wainstein MV,Ribeiro JP,Dornelles LV,Tozzati P,Ashton-Prolla P,et al. Association between myeloperoxidase polymorphisms and its plasma levels with severity of coronary artery diseaseClin BiochemYear: 201043576219651119
22. Düzgünçinar O,Yavuz B,Hazirolan T,Deniz A,Tokgözoğlu SL,Akata D,et al. Plasma myeloperoxidase is related to the severity of coronary artery diseaseActa CardiolYear: 2008631475218468192
23. Baldus S,Rudolph V,Roiss M,Ito WD,Rudolph TK,Eiserich JP,et al. Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidaseCirculationYear: 20061131871816606792
24. Stefanescu A,Braun S,Ndrepepa G,Koppara T,Pavaci H,Mehilli J,et al. Prognostic value of plasma myeloperoxidase concentration in patients with stable coronary artery diseaseAm Heart JYear: 20081553566018215608
25. Kubala L,Lu G,Baldus S,Berglund L,Eiserich JP. Plasma levels of myeloperoxidase are not elevated in patients with stable coronary artery diseaseClin Chim ActaYear: 2008394596218440308
26. Lee CH,Tai BC,Lim GH,Chan MY,Low AF,Tan KC,et al. Correlation between high density lipoprotein-cholesterol and remodeling index in patients with coronary artery disease: IDEAS (IVUS diagnostic evaluation of atherosclerosis in Singapore)-HDL studyInt J Cardiovas Imag (formerly Cardiac Imaging)Year: 2012283341
27. Maron DJ. The epidemiology of low levels of high-density lipoprotein cholesterol in patients with and without coronary artery diseaseAm J cardiolYear: 20008611L14L
28. Gordon DJ,Probstfield JL,Garrison RJ,Neaton JD,Castelli WP,Knoke JD,et al. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studiesCirculationYear: 1989798152642759
29. Naito HK,Greenstreet RL,David JA,Sheldon WL,Shirey EK,Lewis RC,et al. HDL-cholesterol concentration and severity of coronary atherosclerosis determined by cine-angiographyArteryYear: 19808101127458675
30. Van Lenten BJ,Hama SY,deBeer FC,Stafforini DM,McIntyre TM,Prescott SM,et al. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell coculturesJ Clin InvestYear: 19959627588675645
31. VanLenten BJ,Wagner AC,Nayak DP,Hama S,Navab M,Fogelman AM. High-density lipoprotein loses its anti-inflammatory properties during acute influenza A infectionCirculationYear: 20011032283811342478
32. Mehta NM,Bechard LJ,Leavitt K,Duggan C,et al. Inflammatory biomarkers, physical activity, waist circumference, and risk of future coronary heart disease in healthy men and womenEur Heart JYear: 2011323364419224930
33. Karakas M,Koenig W,Zierer A,Herder C,Rottbauer W,Baumert J,et al. Myeloperoxidase is associated with incident coronary heart disease independently of traditional risk factors: results from the MONICA/KORA Augsburg studyJ Intern MedYear: 2012271435021535251
34. Tang WH,Wu Y,Nicholls SJ,Hazen SL. Plasma myeloperoxidase predicts incident cardiovascular risks in stable patients undergoing medical management for coronary artery diseaseClin BiochemYear: 201157339
35. Heslop CL,Frohlich JJ,Hill JS. Myeloperoxidase and C-reactive protein have combined utility for long-term prediction of cardiovascular mortality after coronary angiographyJ Am Coll CardiolYear: 2010551102920223364
36. Kutter D,Devaquet P,Vanderstocken G,Paulus JM,Marchal V,Gothot A. Consequences of total and subtotal myeloperoxidase deficiency: Risk or benefit?Acta HaematolYear: 200010410511111115
37. Nikpoor B,Turecki G,Fournier C,Théroux P,Rouleau GA. A functional myeloperoxidase polymorphic variant is associated with coronary artery disease in French-CanadiansAm Heart JYear: 2001142336911479475
38. Mocatta TJ,Pilbrow AP,Cameron VA,Senthilmohan R,Frampton CM,Richards AM,et al. Plasma concentrations of myeloperoxidase predict mortality after myocardial infarctionJ Am Coll CardiolYear: 2007491993200017512353
39. Morrow DA,Sabatine MS,Brennan ML,deLemos JA,Murphy SA,Ruff CT,et al. Concurrent evaluation of novel cardiac biomarkers in acute coronary syndrome: Myeloperoxidase and soluble CD40 ligand and the risk of recurrent ischaemic events in TACTICS-TIMI 18Eur Heart JYear: 200829109618339606

[TableWrap ID: T1] Table 1 

Baseline demographic, clinical and biochemical characteristics of subjects with and without CAD

[TableWrap ID: T2] Table 2 

Results of multiple regression analysis to test the relationship between genssini scores and MPO, CRP, HDL variables in coronary artery disease patients

Article Categories:
  • Original Article

Keywords: Angiography, coronary artery disease, C-reactiveproteine, myeloperoxidase.

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