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ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Identification of Factors Causing Sudden Coagulation in Patients with Acute Myocardial Infarction

Arnaldo Pinelli1*, S. Trivulzio1, S. Brenna2, V. Rosato3, L. Rivoltini4 and G. Rossoni1
1Department of Medical Biotechnology and Translational Medicine, University of Milan, Italy
2Laboratory of Clinical Chemistry, Ospedale Niguarda Ca’ Granda, Milan, Italy
3Department of Clinical Science and Community, Milan, Italy
4IRCCS Foundation National Institute of Cancer, Milan, Italy
Corresponding Author : Professor Arnaldo Pinelli
Department of Medical Biotechnology and Translational Medicine
Via Vanvitelli 32, 20129 - Milan, Italy
Tel: +39 02 50317086
Fax: +39 02 50316949
E-mail: [email protected]
Received April 03, 2012; Accepted June 22, 2012; Published June 25, 2012
Citation: Pinelli A, Trivulzio S, Brenna S, Rosato V, Rivoltini L, et al. (2012) Identification of Factors Causing Sudden Coagulation in Patients with Acute Myocardial Infarction. J Clin Exp Cardiolog 3:202. doi:10.4172/2155-9880.1000202
Copyright: © 2013 Jung YG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Background: Coronary artery disease (CAD) evolving to acute myocardial infarction (AMI) is due to the thrombotic occlusion of coronary vessels in the presence of destabilized atheroma, rich in inflammatory cells secreting proteolytic enzymes that induce the development of thrombosis. The aim of this study was to analyse the plasma of AMI patients for the detection of proteases or factors that may cause fast coagulation. Methods: The patients were analysed for the presence in plasma of cardiac troponin T (c-TnT) or proteases as neutrophil gelatinase-associated lipocalin (NGAL) using ELISA method and matrix metalloproteinase-9 (MMP-9) utilising flow cytometry technique and interleukin-8 (IL-8) using flow cytometry methodology. Results: The presence of AMI was demonstrated by high levels of c-TnT; in comparison with controls the AMI patients displayed a significant increase in the values of MMP-9 and low levels of antithrombin III: these markers were negatively correlated: MMP-9 appeared to cause the coagulation activity documented by the consumption of antithrombin III. The same patients also showed high levels of NGAL, which is known to modulate MMP-9 activity and to be involved in coagulation process: patients also exhibited an increased amount of IL-8 which appears to be associated with high levels of NGAL: this cytokine seems to affect the values of NGAL which is linked to coagulation process. Conclusion: The high levels of MMP-9, NGAL and IL-8 in AMI patients seemed to be interrelated and connected with the process leading to rapid coagulation. These markers may be measured in absence of AMI, particularly in CAD patients, as their detection may reveal a risk of sudden coronary coagulation.

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