title: Increased pericardial fluid level of matrix metalloproteinase-9 activity in patients with acute myocardial infarction: possible role in the development of cardiac rupture.
abstract: BACKGROUND
  In an animal model of acute myocardial infarction (AMI), deletion of matrix metalloproteinase (MMP)-9 results in suppression of the development of cardiac rupture. The present study sought to clarify how myocardial MMP-9 activity is related to the pathophysiologies of AMI and cardiac rupture in humans.
  
  
  RESULTS
  Levels of interleukin-8 (IL-8), polymorphonuclear leukocyte (PMN) elastase, monocyte chemotactic protein-1 (MCP-1) and MMP activity were measured in the pericardial fluid obtained from 28 patients with angina pectoris (AP group) and 16 patients with AMI (AMI group) undergoing cardiac surgery. In the AMI group, 5 were complicated with ventricular septal perforation (VSP) and the remaining 11 were not (non-VSP). Levels of IL-8, PMN elastase, MMP-2 and MMP-9 activity were all higher in the AMI group than in the AP group. In the AMI group, all levels other than MMP-2 activity were further elevated in cases with VSP compared with those in the non-VSP group. There was no significant difference in MCP-1 among the groups
  
  
  CONCLUSIONS
  Markers of neutrophil activation in the infarcted cardiac tissue seem to be elevated in AMI. Highly elevated levels of MMP-9 activity, which may be derived from neutrophils, and PMN elastase may be related to the pathophysiology of VSP or cardiac rupture in AMI.
authors.affiliation: Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, Japan.
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Kameda
authors.forename: Toshiro
authors.initials: T
authors.lastname: Matsunaga
authors.forename: Naoki
authors.initials: N
authors.lastname: Abe
authors.forename: Takayuki
authors.initials: T
authors.lastname: Fujiwara
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hanada
authors.forename: Kozo
authors.initials: K
authors.lastname: Fukui
authors.forename: Ikuo
authors.initials: I
authors.lastname: Fukuda
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Osanai
authors.forename: Ken
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000208:Acute Disease; D000368:Aged; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D017353:Gene Deletion; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D019272:Leukocyte Elastase / Q000378:metabolism; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology / Q000601:surgery; D018375:Neutrophil Activation; D009504:Neutrophils / Q000201:enzymology; D010496:Pericardium / Q000201:enzymology* / Q000503:physiopathology / Q000601:surgery; D018658:Ventricular Septal Rupture / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology / Q000601:surgery
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; C508606:CXCL8 protein, human; D018932:Chemokine CCL2; D016209:Interleukin-8; D019272:Leukocyte Elastase; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9