title: Immunoadsorption in dilated cardiomyopathy: long-term reduction of cardiodepressant antibodies.
abstract: BACKGROUND
  Disturbances of humoral immunity have been described in dilated cardiomyopathy (DCM), and a number of antibodies against cardiac cell proteins have been identified. Previous studies showed that immunoadsorption therapy with subsequent IgG substitution (IA/IgG) enhances cardiac function, and that removal of cardiodepressant antibodies may represent one essential mechanism of this therapy. The long-term effect of IA/IgG on the level of cardiodepressant antibodies remains to be elucidated.
  
  
  METHODS
  A total of 17 patients with DCM were observed up to 12 months after IA/IgG. Echocardiographic measurements were performed at baseline, 3, 6 and 12 months after therapy. Cardiodepressant antibodies were detected by incubation of rat cardiomyocytes with purified patients' IgG and recording of contractility and Ca(2+) ratio.
  
  
  RESULTS
  In contrast to patients without cardiodepressant antibodies before IA/IgG, patients with negative inotropic antibodies showed an improvement of left ventricular ejection fraction (LVEF) from 33.8 +/- 1.7% to 44.7 +/- 2.7%; 44.5 +/- 2.3% and 51.8 +/- 1.7% after 3, 6 and 12 months (P < 0.001 vs. baseline, P < 0.05 vs. LVEF of non-cardiodepressant group). Immediately after IA/IgG therapy, no cardiodepressant effects of patients' IgG on isolated cardiomyocytes were detectable, and this effect remained diminished until 6 months after IA/IgG (P < 0.001 for contractility and Ca(2+) ratio). Compared with the levels after 3 and 6 months, cardiodepressant antibodies reoccured after 12 months (P = 0.067 for contractility, P < 0.05 for Ca(2+) ratio vs. 6 months after IA/IgG). However, the negative inotropic reaction is still diminished compared with the reaction before IA/IgG.
  
  
  CONCLUSIONS
  IA/IgG therapy induces long-term reduction of negative inotropic antibodies. After 12 months, however, re-increase of negative inotropic antibodies cannot be excluded.
authors.affiliation: University Hospital Greifswald, Department of Internal Medicine B, Greifswald, Germany.
authors.forename: Christiane
authors.initials: C
authors.lastname: Trimpert
authors.forename: Lars R
authors.initials: LR
authors.lastname: Herda
authors.forename: Lars G
authors.initials: LG
authors.lastname: Eckerle
authors.forename: Susanne
authors.initials: S
authors.lastname: Pohle
authors.forename: Carina
authors.initials: C
authors.lastname: Müller
authors.forename: Martin
authors.initials: M
authors.lastname: Landsberger
authors.forename: Stephan B
authors.initials: SB
authors.lastname: Felix
authors.forename: Alexander
authors.initials: A
authors.lastname: Staudt
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000097:blood*; D002118:Calcium / Q000378:metabolism; D002311:Cardiomyopathy, Dilated / Q000097:blood* / Q000503:physiopathology / Q000628:therapy*; D004452:Echocardiography; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007163:Immunosorbent Techniques; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D051381:Rats; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy
chemical_list: D001323:Autoantibodies; D007074:Immunoglobulin G; D002118:Calcium