title: Early measurements of plasma matrix metalloproteinase-2 predict infarct size and ventricular dysfunction in ST-elevation myocardial infarction.
abstract: BACKGROUND
  Immediate reopening of the acutely occluded infarct-related artery via primary PCI is the preferred treatment in ST-elevation myocardial infarction (STEMI). However, the sudden reinitiation of blood flow can lead to a local acute inflammatory response with further endothelial and myocardial damage, so-called reperfusion injury. The activation of matrix metalloproteinases (MMPs) is suggested to be a key event in this process.
  
  
  OBJECTIVE
  To investigate circulating MMPs, tissue inhibitors of metalloproteinases (TIMPs) and myeloperoxidase (MPO) in relation to infarct size, left ventricular dysfunction and remodelling in a STEMI population undergoing PCI.
  
  
  METHODS
  58 Patients with STEMI undergoing primary PCI were included. Blood samples were collected at baseline before PCI and at 12, 24 and 48 h for later analysis of MMPs, TIMPs and MPO by ELISA. Infarct size, left ventricular (LV) dysfunction and remodelling were assessed by cardiac MRI at 5 days and 4 month after STEMI.
  
  
  RESULTS
  Plasma MMP-2 at 0 and 12 h showed a consistent and significant correlation with infarct size and LV dysfunction measured both at 5 days and at 4 months and correlated well with troponin I measurements. For TIMP-1 and TIMP-2 some support was found for associations with infarct size and LV dysfunction, but these were not as consistent as for MMP-2. MMP-8, MMP-9 and MPO did not overall correlate with measures of infarct size, LV dysfunction or remodelling.
  
  
  CONCLUSIONS
  In patients with STEMI, circulating levels of MMP-2, measured early and even before reperfusion therapy, are strongly associated with infarct size and LV dysfunction. This provides further evidence for the role of MMP-2 in ischaemia-reperfusion injury.
authors: Department of Cardiology, University Hospital, Linköping S-58185, Sweden. lennart.nilsson@liu.se
authors: Lennart
authors: L
authors: Nilsson
authors: Jonas
authors: J
authors: Hallén
authors: Dan
authors: D
authors: Atar
authors: Lena
authors: L
authors: Jonasson
authors: Eva
authors: E
authors: Swahn
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D004311:Double-Blind Method; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000627:therapeutic use; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D018810:Magnetic Resonance Angiography; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000473:pathology; D010446:Peptide Fragments / Q000627:therapeutic use; D009195:Peroxidase / Q000378:metabolism; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000473:pathology; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D010446:Peptide Fragments; D019715:Tissue Inhibitor of Metalloproteinase-1; C033786:fibrinogen Bbeta (15-42); D019716:Tissue Inhibitor of Metalloproteinase-2; D009195:Peroxidase; D020778:Matrix Metalloproteinase 2