Intravenous immunoglobulin does not reduce left ventricular remodeling in patients with myocardial dysfunction during hospitalization after acute myocardial infarction |
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Authors: | Lars Gullestad,Stein Ø rn,Kenneth Dickstein,Christian Eek,Thor Edvardsen,Svend Aakhus,Erik T. Askevold,Annika Michelsen,Bjø rn Bendz,Rita Skå rdal,Hans-Jø rgen Smith,Arne Yndestad,Thor Ueland,På l Aukrust |
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Affiliation: | 1. Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway;2. Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway;3. Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Oslo, Norway;4. Department of Radiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway;5. Faculty of Medicine and K.G. Jebsen Cardiac Research Centre, University of Oslo, Norway;6. Center for Heart Failure Research, Faculty of Medicine, University of Oslo, Norway;g Department of Cardiology, Stavanger University Hospital, Stavanger, Norway;h Institute of Internal Medicine, University of Bergen, Norway;i Faculty of Medicine, University of Oslo, Oslo, Norway |
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Abstract: | BackgroundLeft 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.MethodsSixty-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.ResultsOur 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.ConclusionsIVIg 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. |
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Keywords: | Myocardial infarction Heart failure Inflammation |
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