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Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction

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Author: Borne, S.W.M. van den · Cleutjens, J.P.M. · Hanemaaijer, R. · Creemers, E.E. · Smits, J.F.M. · Daemen, M.J.A.P. · Blankesteijn, W.M.
Type:article
Date:2009
Institution: TNO Kwaliteit van Leven
Source:Cardiovascular Pathology, 1, 18, 37-43
Identifier: 241315
doi: doi:10.1016/j.carpath.2007.12.012
Keywords: Biology · Biomedical Research · Infarct rupture · Inflammation · Matrix metalloproteinases · MMP activity assay · MMP immunohistochemistry · Myocardial infarction · gelatinase A · gelatinase B · neutrophil collagenase · tissue inhibitor of metalloproteinase 1 · adult · aged · article · clinical article · controlled study · enzyme activity · female · heart · heart disease · heart infarction · human · human tissue · immunohistochemistry · infarct rupture · inflammatory cell · male · priority journal · zymography · Aged · Aged, 80 and over · Cell Count · Female · Heart Rupture, Post-Infarction · Humans · Immunohistochemistry · Male · Matrix Metalloproteinase 2 · Matrix Metalloproteinase 8 · Matrix Metalloproteinase 9 · Middle Aged · Myocardial Infarction · Myocarditis

Abstract

Background: Infarct rupture is a usually fatal complication of myocardial infarction (MI), for which no molecular mechanism has been described in humans. Experimental evidence in mouse models suggests that the degradation of the extracellular matrix by matrix metalloproteinases (MMPs) plays an important role in infarct rupture. The present study was designed to study the role of MMP-2, MMP-8, and MMP-9 in human infarct rupture. Methods: Heart samples were obtained from patients who died from infarct rupture and control MI patients. The MMP activity was determined by zymography and quantitative immunocapture activity assay. TIMP-1 levels were measured and immunohistochemistry for MMP-2 and MMP-9 was performed. Results: The amounts of both total and active MMP-8 and MMP-9 were significantly higher in ruptured infarct tissue than in control MI tissue, but no differences in MMP-2 activity were observed. Furthermore, the number of inflammatory cells was significantly higher in the ruptured infarcts than in control infarcts. Conclusions: These data suggest that increased MMP-8 and MMP-9 activity in the infarct area, caused by a more prominent infiltration of inflammatory cells, contribute to infarct rupture in humans. © 2009 Elsevier Inc. All rights reserved.