title: Immunoglobulin adsorption in patients with idiopathic dilated cardiomyopathy.
abstract: BACKGROUND
  Idiopathic dilated cardiomyopathy (IDC) frequently is a progressive disease without causative therapy options. Following the hypothesis that in certain patients autoantibodies against cardiac structures may induce, maintain, or promote the progression of the disease, we investigated whether the elimination of these autoantibodies through immunoadsorption would improve cardiac function.
  
  
  RESULTS
  This prospective case-control study included 34 patients with IDC. Each patient presented with moderate to severe heart failure and evidence of autoantibodies directed against beta(1)-adrenoceptors (beta(1)-AABs). Seventeen patients received standard medical therapy (control group), whereas 17 were also treated with immunoadsorption (treatment group) to eliminate beta(1)-AABs. A 1-year follow-up included echocardiographic assessment of left ventricular ejection fraction and internal diameters, beta(1)-AAB levels, and clinical status every 3 months. Within 1 year, the mean+/-SD left ventricular ejection fraction rose from 22.3+/-3.3% to 37.9+/-7.9% (P=0.0001) in the treatment group, with a relative increase of 69.9%. However, in the control group, no overall increase was seen (from 23.8+/-3.0% to 25.2+/-5.9%, P=0. 3154). Left ventricular diameter in diastole decreased by 14.5% from 74.5+/-7.1 to 63.7+/-6.0 mm in the treatment group (P=0.0001) and by 3.8% (P=0.2342) in the control group. In the treatment group, the NYHA functional rating improved after immunoadsorption (P=0.0001). beta(1)-AABs did not increase anew.
  
  
  CONCLUSIONS
  In IDC, the use of immunoadsorption is superior to the use of standard medical therapy. It significantly improves cardiac performance and clinical status.
authors.affiliation: German Heart Institute Berlin, Germany. jmueller@dhzb.de
authors.forename: J
authors.initials: J
authors.lastname: Müller
authors.forename: G
authors.initials: G
authors.lastname: Wallukat
authors.forename: M
authors.initials: M
authors.lastname: Dandel
authors.forename: H
authors.initials: H
authors.lastname: Bieda
authors.forename: K
authors.initials: K
authors.lastname: Brandes
authors.forename: S
authors.initials: S
authors.lastname: Spiegelsberger
authors.forename: E
authors.initials: E
authors.lastname: Nissen
authors.forename: R
authors.initials: R
authors.lastname: Kunze
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
mesh_terms: D001323:Autoantibodies / Q000097:blood* / Q000302:isolation & purification; D002311:Cardiomyopathy, Dilated / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy*; D016022:Case-Control Studies; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood* / Q000302:isolation & purification; D007075:Immunoglobulin M / Q000097:blood; D007163:Immunosorbent Techniques; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018342:Receptors, Adrenergic, beta-1 / Q000276:immunology*; D016277:Ventricular Function, Left
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D018342:Receptors, Adrenergic, beta-1; D007073:Immunoglobulin E