WJCD  Vol.2 No.4 , October 2012
Mechanisms of C-reactive protein, interleukin-6 and soluble CD40L blood concentration changes after coronary stent implantation
ABSTRACT
Background: The pathway linking inflammation and thrombosis has been extensively studied. Experimental data support that arterial thrombosis also induces a detectable inflammatory response, which in turn, activates prothrombotic pathways closing a vicious circle that interconnects inflammation and thrombosis. Aim: We designed this study to investigate the causes of inflammatory markers increase after coronary angioplasty. Methods: We analyzed the interrelationship of thrombotic and inflammatory markers and the effect of blocking thrombus formation on the inflammatory response in 50 patients undergoing high thrombotic risk coronary angioplasty. The relationship of platelet number to soluble CD40 Ligand, Interleukin-6 and C-reactive protein blood levels was studied. Half of the study population was treated with standard antithrombotic drugs and the other half with the standard therapy plus platelet GP IIb-IIIa receptor inhibitor Eptifibatide. Results: There was a clear correlation between basal platelet count and sCD40L basal levels, post-angioplasty sCD40L increase and post-angioplasty IL-6 levels and post-angioplasty IL-6 levels with post-angioplasty CRP levels. Postangioplasty CRP, IL-6 and sCD40L blood levels were influenced by GP IIb-IIIa treatment in patients with angiographic thrombus. Conclusion: Platelet aggregation induces a proinflammatory response which is blocked by a GP IIb-IIIa inhibitor agent, particularly in patients with patent angiographic thrombus.

Cite this paper
Merino, A. , Calvo, J. , Gayá, A. , Segura, I. and Imízcoz, C. (2012) Mechanisms of C-reactive protein, interleukin-6 and soluble CD40L blood concentration changes after coronary stent implantation. World Journal of Cardiovascular Diseases, 2, 227-236. doi: 10.4236/wjcd.2012.24038.
References
[1]   Ross, R. (1999) Atherosclerosis—An inflammatory disease. The New England Journal of Medicine, 340, 115- 126. doi:10.1056/NEJM199901143400207

[2]   Libby, P., Ridker, P.M., and Maseri, A. (2002) Inflammation and atherosclerosis. Circulation, 105, 1135-1143. doi:10.1161/hc0902.104353

[3]   Liuzzo, G., Biasucci, L.M., Gallimore, R., et al. (1994) The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. The New England Journal of Medicine, 331, 417-424. doi:10.1056/NEJM199408183310701

[4]   Biasucci, L.M., Liuzzo, G., Grillo, R.L., et al. (1999) Elevated levels of C-reactive protein at discharge in patients with unstable angina predicts recurrent instability. Circulation, 99, 855-860. doi:10.1161/01.CIR.99.7.855

[5]   Liuzzo, G., Buffon, A., Biasucci, L.M., et al. (1998) Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina. Circulation, 98, 2370- 2376. doi:10.1161/01.CIR.98.22.2370

[6]   Levi, M., van der Poll, T. and Büller, H.R. (2004) Bidirectional relation between inflammation and coagulation. Circulation, 109, 2698-2704. doi:10.1161/01.CIR.0000131660.51520.9A

[7]   Furman, M.I., Krueger, L.A., Linden, M.D., Barnard, M.R., Frelinger III, A.R. and Michelson, A.D. (2004) Release of soluble CD40L from platelets is regulated by glycoprotein IIb/IIIa and actin polymerization. Journal of the American College of Cardiology, 43, 2319-2325. doi:10.1016/j.jacc.2003.12.055

[8]   Aukrust, P., Damas, J.K. and Solum, N.O. (2004) Soluble CD40L and platelets: Self-perpetuating pathogenic loop in thrombosis and inflammation. Journal of the American College of Cardiology, 43, 2326-2328. doi:10.1016/j.jacc.2004.03.023

[9]   Aukrust, P., Müller, F., Ueland, T., et al. (1999) Enhanced levels of soluble and membrane bound CD40 ligand in patients with unstable angina: Possible reflection of T lymphocyte and platelet involvement in the pathogenesis of acute coronary syndromes. Circulation, 100, 614-620. doi:10.1161/01.CIR.100.6.614

[10]   Henn, V., Steinbach, S., Büchner, K., Presek, P. and Kroc- zek, R. (2001) The inflammatory action of CD40 ligand (CD154) expressed on activated human platelets is temporally limited by coexpressed CD40. Blood, 98, 1047- 1054. doi:10.1182/blood.V98.4.1047

[11]   Henn, V., Slupsky, J.R. and Grafe, M. (1998) CD40 lig- and in activated platelets triggers an inflammatory reaction of endothelial cells. Nature, 391, 591-594. doi:10.1038/35393

[12]   Ambrose, J.A., Winters, S.L., Arora, R.R., et al. (1985) Coronary angiographic morphology in myocardial infarction: A link between the pathogenesis of unstable angina and myocardial infarction. Journal of the American College of Cardiology, 6, 1233-1238. doi:10.1016/S0735-1097(85)80207-2

[13]   Ambrose, J.A., Hjemdahl-Monsen, C.E., Borrico, S., Gor- lin, R. and Fuster, V. (1988) Angiographic demonstration of a common link between unstable angina pectoris and non-Q wave myocardial infarction. Journal of the American College of Cardiology, 61, 244-247. doi:10.1016/0002-9149(88)90924-1

[14]   Cohen, M., Merino, A., Hawkins, L., Greenberg, S. and Fuster, V. (1991) Clinical and angiographic characteristics and outcome of patients with restunstable angina occurring during regular aspirin use. Journal of the American College of Cardiology, 18, 1458-1462. doi:10.1016/0735-1097(91)90675-Y

[15]   Myers, G.L., Rifai, N., Tracy, R.P., et al. (2004) CDC; AHA. CDC/AHA workshop on markers of inflammation and cardiovascular disease: Application to clinical and public health practice: Report from the laboratory science discussion group. Circulation, 110, 545-549. doi:10.1161/01.CIR.0000148980.87579.5E

[16]   Bereczki, C., Nagy, E., Pal, A., Magyar, M.T. and Balla, J. (2003) Should soluble CD40 ligand be measured from serum or plasma samples? Letter. Arteriosclerosis, Throm-bosis, and Vascular Biology, 23, 1129-1131. doi:10.1161/01.ATV.0000072368.37740.8E

[17]   Ahn, E.R., Lander, G., Jy, W., Bidot, C.J., Jimenez, J.J., Horstman, L.L. and Ahn, Y.S. (2004) Differences of soluble CD40L in sera and plasma: Implications on CD40L assay as a marker of thrombotic risk. Thrombosis Research, 114, 143-148. doi:10.1016/j.thromres.2004.06.005

[18]   Calvo, J., Martínez, N., Etxagibel, A., et al. (2002) Allelic frequencies of polymorphic variants of cytokine genes (IL-1A, IL-1B, IL-1RN, IL-6, IL-10, IL-12P40, and IFNG ) in a Spanish population. Inmunología, 21, 76-86.

[19]   Lincoff, A.M., Kereiakes, D.J., Mascelli, M.A., et al. (2001) Abciximab suppresses the rise in levels of circulating inflammatory markers after percutaneous coronary revascularization. Circulation, 104, 163-167. doi:10.1161/01.CIR.104.2.163

[20]   Merino, A., Gayá, A., Segura, I., et al. (2004) Platelet aggregation inhibition blocks C-reactive protein and interleukin-6 (IL-6) elevation after the coronary angioplasty: Effect of the ?174 G/C IL-6 gene polymorphism. Journal of the American College of Cardiology, 94, 1300-1303. doi:10.1016/j.amjcard.2004.07.119

[21]   Merino, A., Artaiz, M., Bergadá, J., Riera, M., Vidal, B. and Rodriguez, A. (2002) El eptifibatide reduce los valores de Proteina C Reactiva tras angioplastia coronaria. Revista Espa?ola de Cardiología, 55, 186-189.

[22]   James, S.K., Siegbahn, A., Armstrong, P.A., et al. (2004) Activation of the inflammation, coagulation and fibrin-olysis Systems, without influence of abciximab infusión in patients with non-ST-elevation acute coronary síndromes treated with dalteparin: A GUSTO IV substudy. American Heart Journal, 147, 267-274. doi:10.1016/j.ahj.2003.09.014

[23]   Gawaz, M., Langer, H. and May, A.E. (2005) Platelets in inflammation and atherogenesis. The Journal of Clinical Investigation, 115, 3378-3384. doi:10.1172/JCI27196

[24]   Silber, S., Albertsson, P., Aviles, F.F., et al. (2005) Guidelines for percutaneous coronary interventions.The task force for percutaneous coronary interventions of the European Society of Cardiology. European Heart Journal, 26, 804-847. doi:10.1093/eurheartj/ehi138

[25]   Palmerini, T., Nedelman, M.A., Scudder, L.E., et al. (2002) Effects of abciximab on the acute pathology of blood vessels after arterial stenting in nonhuman primates. Journal of the American College of Cardiology, 40, 360- 366. doi:10.1016/S0735-1097(02)01951-4

[26]   Curran, M.P. and Keating, G.M. (2005) Eptifibatide: A review of its use in patients with acute coronary syndromes and/or undergoing percutaneous coronary intervention. Drugs, 65, 2009-2035. doi:10.2165/00003495-200565140-00007

[27]   Anand, S.X., Viles-Gonzalez, J.S., Badimon, J.J., Cavusoglu, E. and Marmur, J.D. (2003) Membrane-associated CD40L and sCD40L in atherothrombotic disease. Journal of Thrombosis and Haemostasis, 90, 377-384.

[28]   Aukrust, P., W?hre, T., Damas, J.K., Gullestad, L. and Solum, N.O. (2001) Inflammatory role of platelets in acute coronary syndromes. Heart, 86, 605-606. doi:10.1136/heart.86.6.605

[29]   Antoniades, C., Bakogiannis, C., Tousoulis, D., Antono-poulos, A.S. and Stefanadis, C. (2009) The CD40/CD40 ligand system. Journal of the American College of Cardiology, 54, 669-677. doi:10.1016/j.jacc.2009.03.076

[30]   Libby, P. and Simon, D.I. (2001) Inflammation and Thrombosis: The Clot Thickens. Circulation, 103, 1718-1720. doi:10.1161/01.CIR.103.13.1718

[31]   Libby, P., Ridker, P.M. and Hansson, G. (2009) Inflammation in atherosclerosis: From pathophysiology to practice. Journal of the American College of Cardiology, 54, 2129-2138. doi:10.1016/j.jacc.2009.09.009

[32]   Muhlestein, J.B. (2010) Effect of antiplatelet therapy on inflammatory markers in atherothrombotic patients. Jour- nal of Thrombosis and Haemostasis, 103, 71-82. doi:10.1160/TH09-03-0177

 
 
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