title: Level of complement activity predicts cardiac dysfunction after acute myocardial infarction treated with primary percutaneous coronary intervention.
abstract: BACKGROUND
  The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human myocardial I/R injury. We evaluated the potential association between MBL and sC5b-9 in plasma and subsequent cardiac dysfunction in patients with STEMI treated with primary percutaneous coronary intervention (pPCI).
  
  
  METHODS
  The study included 74 STEMI-patients with acute occlusion of the left anterior descending coronary artery who were successfully treated with pPCI. Cardiac dysfunction was defined as left ventricular ejection fraction LVEF < 35%.
  
  
  RESULTS
  Patients with subsequent LVEF < 35% had significantly higher median MBL and lower sC5b-9 compared to patients with LVEF > or = 35%. After adjustment of the multivariate logistic regression analysis, the odds for reduced LVEF was 5.5 (95% CI:1.5-19.3; p = 0.01) for patients with MBL > or = 800 mcg/L, and 5.0 (95% CI 1.4-18.4; p = 0.01) for patients with sC5b-9 < or = 160 mcg/L.
  
  
  CONCLUSIONS
  High plasma MBL and low plasma sC5b-9 are independently associated with increased risk of cardiac dysfunction in STEMI patients treated with pPCI, probably due to increased complement activity during the ischemic and reperfusion process. The predictive value of low peripheral plasma sC5b-9 may be explained by an accumulation and activation of sC5b-9 in the infarcted myocardium.
authors.affiliation: Department of Cardiology P, Gentofte University Hospital, Niels Andersens Vej 65, Copenhagen, Denmark. sunped01@geh.regionh.dk
authors.forename: Sune
authors.initials: S
authors.lastname: Haahr-Pedersen
authors.forename: Mette
authors.initials: M
authors.lastname: Bjerre
authors.forename: Allan
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: Rasmus
authors.initials: R
authors.lastname: Mogelvang
authors.forename: Helena
authors.initials: H
authors.lastname: Dominquez
authors.forename: Troels Krarup
authors.initials: TK
authors.lastname: Hansen
authors.forename: Søren
authors.initials: S
authors.lastname: Galatius
authors.forename: Jan
authors.initials: J
authors.lastname: Bech
authors.forename: Jan Kyst
authors.initials: JK
authors.lastname: Madsen
authors.forename: Peter
authors.initials: P
authors.lastname: Søgaard
authors.forename: Jan Skov
authors.initials: JS
authors.lastname: Jensen
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015938:Complement Membrane Attack Complex / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000628:therapy*; D011237:Predictive Value of Tests; D012044:Regression Analysis; D015427:Reperfusion Injury / Q000097:blood; D012189:Retrospective Studies; D012307:Risk Factors; D015398:Signal Transduction; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000453:epidemiology* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D015938:Complement Membrane Attack Complex; D037601:Mannose-Binding Lectin