title: Intravenous immunoglobulin does not reduce left ventricular remodeling in patients with myocardial dysfunction during hospitalization after acute myocardial infarction.
abstract: BACKGROUND
  Left ventricular (LV) remodeling takes place after acute myocardial infarction (MI), potentially leading to overt heart failure (HF). Enhanced inflammation may contribute to LV remodeling. Our hypothesis was that the immunomodulating effects of intravenous immunoglobulin (IVIg) would be beneficial in patients with impaired myocardial function after MI by reducing myocardial remodeling and improving myocardial function.
  
  
  METHODS
  Sixty-two patients with acute MI treated by percutaneous coronary intervention, with depressed LV ejection fraction (LVEF) were randomized in a double-blinded fashion to IVIg as induction therapy and thereafter as monthly infusions or placebo for 26 weeks. The primary end point was changes in LVEF from baseline to 6 months as assessed by MRI.
  
  
  RESULTS
  Our main findings were: (i) LVEF increased significantly from 38 ± 10 (mean ± SD) to 45 ± 13% after IVIg and from 42 ± 9 to 49 ± 12% after placebo with no difference between the groups. (ii) The scar area decreased significantly by 3% and 5% in the IVIg and placebo group, respectively, with no difference between the groups. (iii) During the induction therapy (baseline to day 5), IVIg induced both inflammatory (e.g., increase in tumor necrosis factor α and monocyte chemoattractant protein-1) and anti-inflammatory (e.g., increase in interleukin-10 and decrease in leukocyte counts) variables, but during maintenance therapy there were no differences in changes of inflammatory mediators between IVIg and placebo.
  
  
  CONCLUSIONS
  IVIg therapy after ST elevation MI managed by primary PCI does not affect LV remodeling or function. This illustrates the challenges of therapeutic intervention directed against the cytokine network, to prevent post-MI remodeling.
authors.affiliation: Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. lars.gullestad@medisin.uio.no
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
authors.forename: Stein
authors.initials: S
authors.lastname: Orn
authors.forename: Kenneth
authors.initials: K
authors.lastname: Dickstein
authors.forename: Christian
authors.initials: C
authors.lastname: Eek
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
authors.forename: Svend
authors.initials: S
authors.lastname: Aakhus
authors.forename: Erik T
authors.initials: ET
authors.lastname: Askevold
authors.forename: Annika
authors.initials: A
authors.lastname: Michelsen
authors.forename: Bjørn
authors.initials: B
authors.lastname: Bendz
authors.forename: Rita
authors.initials: R
authors.lastname: Skårdal
authors.forename: Hans-Jørgen
authors.initials: HJ
authors.lastname: Smith
authors.forename: Arne
authors.initials: A
authors.lastname: Yndestad
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
mesh_terms: D004311:Double-Blind Method; D005260:Female; D006760:Hospitalization / Q000639:trends*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000502:physiology
chemical_list: D016756:Immunoglobulins, Intravenous