title: The role of intravenous immunoglobulin in the treatment of chronic heart failure.
abstract: Chronic heart failure (HF), including both ischemic and idiopathic dilated cardiomyopathies, is accompanied by a dysregulated cytokine network characterized not only by a rise in inflammatory cytokines, but also by an inadequate elevation of anti-inflammatory mediators. This dysregulation has been implicated in the development and progression of chronic HF, and in the last decade, attempts have been made to modulate this persistent inflammation. Failure of anti-tumor necrosis factor therapy in HF has led to further interest in a more general immunomodulatory approach, directed against the inflammatory imbalance rather than one particular cytokine. Treatment with intravenous immunoglobulin (IVIg) may represent such a broad-based approach trying to restore the dysregulated cytokine network through various mechanisms such as Fc receptor blockade, neutralization of microbial antigens and superantigens and more direct anti-inflammatory effects on the cytokine network. However, although one randomized placebo-controlled study in patients with chronic HF showed that IVIg improved left ventricular ejection fraction, accompanied by anti-inflammatory net effects, IVIg had no effect in another placebo-controlled study examining the effect of this medication in recent-onset cardiomyopathy. So far, few patients have been included in clinical trials, and there is clearly a need for larger placebo-controlled mortality studies involving a diverse group of patients with regard to cause and severity of HF.
authors.affiliation: Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, N-0027 Oslo, Norway. pal.aukrust@rikshospitalet.no
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
authors.forename: Arne
authors.initials: A
authors.lastname: Yndestad
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Jan Kristian
authors.initials: JK
authors.lastname: Damås
authors.forename: Stig S
authors.initials: SS
authors.lastname: Frøland
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
mesh_terms: D001323:Autoantibodies / Q000187:drug effects; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy; D002908:Chronic Disease; D003167:Complement Activation / Q000187:drug effects; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy* / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000494:pharmacology / Q000627:therapeutic use*; D007155:Immunologic Factors / Q000494:pharmacology / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000378:metabolism; D020782:Matrix Metalloproteinases / Q000187:drug effects / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy; D013318:Stroke Volume / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D016756:Immunoglobulins, Intravenous; D007155:Immunologic Factors; D018836:Inflammation Mediators; D020782:Matrix Metalloproteinases