title: Association between endogenous complement inhibitor and myocardial salvage in patients with myocardial infarction.
abstract: BACKGROUND
  Many pathogenic processes and diseases are the result of an erroneous activation of the complement cascade and a number of inhibitors of complement have thus been examined for anti-inflammatory actions. It was recently demonstrated that supraphysiological concentrations of the endogenous complement inhibitor MAp44 (also denoted MAP1) protect against myocardial reperfusion injury. In the present study, we examined the association between outcome after acute myocardial infarction (MI) and the plasma levels of MAp44 and its related proteins MASP-1 and MASP-3 in patients with first-time MI. In addition, we compared plasma levels of MAp44, MASP-1, and MASP-3 in MI patients to levels in a healthy control group.
  
  
  METHODS
  A total of 192 MI patients and 140 control persons were included. Plasma samples were obtained and analysed with time-resolved immunofluorometric assays determining the plasma levels of MAp44, MASP-1, and MASP-3. The myocardial outcomes (salvage index and final infarct size) were measured by gated single-photon emission CT.
  
  
  RESULTS
  MI patients had 18 % higher plasma levels of MAp44 (IQR 11-25%) as compared to the healthy control group (p<0.001. However, neither salvage index (Spearman rho -0.1, p=0.28) nor final infarct size (Spearman rho 0.02, p=0.83) correlated with plasma levels of MAp44. Likewise, MASP-1 and MASP-3 were elevated in MI patients (p=0.002 and p<0.001), but the levels were not correlated to outcome.
  
  
  CONCLUSIONS
  Plasma levels of MAp44, MASP-1, and MASP-3 are significantly higher in patients with MI compared to healthy control persons, but are not associated with short-term outcome measured as salvage index and final infarct.
authors.affiliation: Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Charlotte B
authors.initials: CB
authors.lastname: Holt
authors.forename: Steffen
authors.initials: S
authors.lastname: Thiel
authors.forename: Kim
authors.initials: K
authors.lastname: Munk
authors.forename: Jakob A
authors.initials: JA
authors.lastname: Østergaard
authors.forename: Hans E
authors.initials: HE
authors.lastname: Bøtker
authors.forename: Troels K
authors.initials: TK
authors.lastname: Hansen
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D003167:Complement Activation; D051056:Complement Inactivating Agents / Q000378:metabolism*; D005260:Female; D015200:Fluoroimmunoassay; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D050606:Mannose-Binding Protein-Associated Serine Proteases / Q000378:metabolism*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy; D009206:Myocardium / Q000378:metabolism*; D011379:Prognosis; D012189:Retrospective Studies; D016879:Salvage Therapy / Q000379:methods*
chemical_list: D015415:Biomarkers; D051056:Complement Inactivating Agents; C084067:MASP1 protein, human; D050606:Mannose-Binding Protein-Associated Serine Proteases
keywords: Complement system; immunology; myocardial infarction; reperfusion