Systemic and coronary levels of CRP, MPO, sCD40L and PlGF in patients with coronary artery disease

Siew Wai Fong, Ling Ling Few, Wei Cun See Too, Boon Yin Khoo, Nik Nor Izah Nik Ibrahim, Shaiful Azmi Yahaya, Zurkurnai Yusof, Rosli Mohd Ali, Abdul Rashid Abdul Rahman, Get Bee Yvonne-Tee, Siew Wai Fong, Ling Ling Few, Wei Cun See Too, Boon Yin Khoo, Nik Nor Izah Nik Ibrahim, Shaiful Azmi Yahaya, Zurkurnai Yusof, Rosli Mohd Ali, Abdul Rashid Abdul Rahman, Get Bee Yvonne-Tee

Abstract

Background: Biomarkers play a pivotal role in the diagnosis and management of patients with acute coronary syndrome. This study aimed to investigate the differences in level of several biomarkers, i.e. C-reactive protein, myeloperoxidase, soluble CD40 ligand and placental growth factor, between acute coronary syndrome and chronic stable angina patients. The relationship between these biomarkers in the coronary circulation and systemic circulation was also investigated.

Methods: A total of 79 patients were recruited in this study. The coronary blood was sampled from occluded coronary artery, while the peripheral venous blood was withdrawn from antecubital fossa. The serum concentrations of C-reactive protein, soluble CD40 ligand and placental growth factor and plasma concentration of myeloperoxidase were measured using ELISA method.

Results: The systemic level of the markers measured in the peripheral venous blood was significantly increased in acute coronary syndrome compared to chronic stable angina patients. The concentrations of the C-reactive protein, myeloperoxidase and soluble CD40 ligand taken from peripheral vein were closely similar to the concentration found in coronary blood of ACS patients. The level of placental growth factor was significantly higher in coronary circulation than its systemic level.

Conclusion: The concentration of these C-reactive protein, myeloperoxidase, soluble CD40 ligand and placental growth factor were significantly increased in acute coronary syndrome patients. The concentration of the markers measured in the systemic circulation directly reflected those in the local coronary circulation. Thus, these markers have potential to become a useful tool in predicting plaque vulnerability in the future.

References

    1. Apple FS, Wu AH, Mair J, Ravkilde J, Panteghini M, Tate J, Pagani F, Christenson RH, Mockel M, Danne O, Jaffe AS. Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome. Clin Chem. 2005;51:810–824. doi: 10.1373/clinchem.2004.046292.
    1. Fu X, Kassim SY, Parks WC, Heinecke JW. Hypochlorous acid oxygenates the cysteine switch domain of pro-matrilysin (MMP-7). A mechanism for matrix metalloproteinase activation and atherosclerotic plaque rupture by myeloperoxidase. J Biol Chem. 2001;276:41279–41287. doi: 10.1074/jbc.M106958200.
    1. Shabani F, McNeil J, Tippett L. The oxidative inactivation of tissue inhibitor of metalloproteinase-1 (TIMP-1) by hypochlorous acid (HOCI) is suppressed by anti-rheumatic drugs. Free Radic Res. 1998;28:115–123. doi: 10.3109/10715769809065797.
    1. Andre P, Nannizzi-Alaimo L, Prasad SK, Phillips DR. Platelet-derived CD40L: the switch-hitting player of cardiovascular disease. Circulation. 2002;106:896–899. doi: 10.1161/01.CIR.0000028962.04520.01.
    1. Schonbeck U, Libby P. CD40 signaling and plaque instability. Circ Res. 2001;89:1092–1103. doi: 10.1161/hh2401.101272.
    1. Maglione D, Guerriero V, Viglietto G, Delli-Bovi P, Persico MG. Isolation of a human placenta cDNA coding for a protein related to the vascular permeability factor. Proc Natl Acad Sci. 1991;88:9267–9271. doi: 10.1073/pnas.88.20.9267.
    1. Iyer S, Acharya KR. Role of placenta growth factor in cardiovascular health. Trends Cardiovasc Med. 2002;12:128–134. doi: 10.1016/S1050-1738(01)00164-5.
    1. Heeschen C, Dimmeler S, Hamm CW, van den Brand MJ, Boersma E, Zeiher AM, Simoons ML. Soluble CD40 ligand in acute coronary syndromes. N Engl J Med. 2003;348:1104–1111. doi: 10.1056/NEJMoa022600.
    1. Heeschen C, Dimmeler S, Fichtlscherer S, Hamm CW, Berger J, Simoons ML, Zeiher AM. Prognostic value of placental growth factor in patients with acute chest pain. JAMA. 2004;291:435–441. doi: 10.1001/jama.291.4.435.
    1. Ndrepepa G, Braun S, Mehilli J, von Beckerath N, Schomig A, Kastrati A. Myeloperoxidase level in patients with stable coronary artery disease and acute coronary syndromes. Eur J Clin Invest. 2008;38:90–96. doi: 10.1111/j.1365-2362.2007.01908.x.
    1. Chang PY, Wu TL, Hung CC, Tsao KC, Sun CF, Wu LL, Wu JT. Development of an ELISA for myeloperoxidase on microplate: normal reference values and effect of temperature on specimen preparation. Clin Chim Acta. 2006;373:158–163. doi: 10.1016/j.cca.2006.05.030.
    1. Rifai N. C-reactive protein and coronary heart disease: diagnostic and therapeutic implications for primary prevention. Cardiovasc Toxicol. 2001;1:153–157. doi: 10.1385/CT:1:2:153.
    1. Rifai N, Tracy RP, Ridker PM. Clinical efficacy of an automated high-sensitivity C-reactive protein assay. Clin Chem. 1999;45:2136–2141.
    1. Calabro P, Willerson JT, Yeh ET. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation. 2003;108:1930–1932. doi: 10.1161/01.CIR.0000096055.62724.C5.
    1. Wagner DD, Burger PC. Platelets in inflammation and thrombosis. Arterioscler Thromb Vasc Biol. 2003;23:2131–2137. doi: 10.1161/.
    1. Ruggeri ZM. Platelets in atherothrombosis. Nat Med. 2002;8:1227–1234. doi: 10.1038/nm1102-1227.
    1. Lee Y, Lee WH, Lee SC, Ahn KJ, Choi YH, Park SW, Seo JD, Park JE. CD40L activation in circulating platelets in patients with acute coronary syndrome. Cardiology. 1999;92:11–16. doi: 10.1159/000006940.
    1. Henn V, Steinbach S, Buchner K, Presek P, Kroczek RA. The inflammatory action of CD40 ligand (CD154) expressed on activated human platelets is temporally limited by coexpressed CD40. Blood. 2001;98:1047–1054. doi: 10.1182/blood.V98.4.1047.
    1. Buffon A, Biasucci LM, Liuzzo G, D’Onofrio G, Crea F, Maseri A. Widespread coronary inflammation in unstable angina. N Engl J Med. 2002;347:5–12. doi: 10.1056/NEJMoa012295.
    1. Jaremo P, Hansson G, Nilsson O. Elevated inflammatory parameters are associated with lower platelet density in acute myocardial infarctions with ST-elevation. Thromb Res. 2000;100:471–478. doi: 10.1016/S0049-3848(00)00366-2.
    1. Iwama H, Uemura S, Naya N, Imagawa K, Takemoto Y, Asai O, Onoue K, Okayama S, Somekawa S, Kida Y, et al. Cardiac expression of placental growth factor predicts the improvement of chronic phase left ventricular function in patients with acute myocardial infarction. J Am Coll Cardiol. 2006;47:1559–1567. doi: 10.1016/j.jacc.2005.11.064.
    1. Torzewski J, Torzewski M, Bowyer DE, Frohlich M, Koenig W, Waltenberger J, Fitzsimmons C, Hombach V. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol. 1998;18:1386–1392. doi: 10.1161/01.ATV.18.9.1386.
    1. Torzewski M, Rist C, Mortensen RF, Zwaka TP, Bienek M, Waltenberger J, Koenig W, Schmitz G, Hombach V, Torzewski J. C-reactive protein in the arterial intima: role of C-reactive protein receptor-dependent monocyte recruitment in atherogenesis. Arterioscler Thromb Vasc Biol. 2000;20:2094–2099. doi: 10.1161/01.ATV.20.9.2094.
    1. Yasojima K, Schwab C, McGeer EG, McGeer PL. Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Pathol. 2001;158:1039–1051. doi: 10.1016/S0002-9440(10)64051-5.
    1. Ishikawa T, Hatakeyama K, Imamura T, Date H, Shibata Y, Hikichi Y, Asada Y, Eto T. Involvement of C-reactive protein obtained by directional coronary atherectomy in plaque instability and developing restenosis in patients with stable or unstable angina pectoris. Am J Cardiol. 2003;91:287–292. doi: 10.1016/S0002-9149(02)03156-9.
    1. Maier W, Altwegg LA, Corti R, Gay S, Hersberger M, Maly FE, Sutsch G, Roffi M, Neidhart M, Eberli FR, et al. Inflammatory markers at the site of ruptured plaque in acute myocardial infarction: locally increased interleukin-6 and serum amyloid A but decreased C-reactive protein. Circulation. 2005;111:1355–1361. doi: 10.1161/01.CIR.0000158479.58589.0A.

Source: PubMed

3
S'abonner