Intravenous immunoglobulin does not reduce left ventricular remodeling in patients with myocardial dysfunction during hospitalization after acute myocardial infarction

被引:24
作者
Gullestad, Lars [1 ,5 ,6 ,7 ]
Orn, Stein [8 ]
Dickstein, Kenneth [8 ,9 ]
Eek, Christian [1 ]
Edvardsen, Thor [1 ,5 ,6 ]
Aakhus, Svend [1 ]
Askevold, Erik T. [1 ,2 ]
Michelsen, Annika [2 ]
Bendz, Bjorn [1 ]
Skardal, Rita [1 ]
Smith, Hans-Jorgen [4 ,5 ,6 ]
Yndestad, Arne [2 ]
Ueland, Thor [2 ]
Aukrust, Pal [2 ,3 ,10 ]
机构
[1] Oslo Univ Hosp, Rikshosp, Dept Cardiol, N-0027 Oslo, Norway
[2] Oslo Univ Hosp, Rikshosp, Internal Med Res Inst, N-0027 Oslo, Norway
[3] Oslo Univ Hosp, Rikshosp, Sect Clin Immunol & Infect Dis, N-0027 Oslo, Norway
[4] Oslo Univ Hosp, Rikshosp, Dept Radiol, N-0027 Oslo, Norway
[5] Univ Oslo, Fac Med, N-0316 Oslo, Norway
[6] Univ Oslo, KG Jebsen Cardiac Res Ctr, N-0316 Oslo, Norway
[7] Univ Oslo, Fac Med, Ctr Heart Failure Res, N-0316 Oslo, Norway
[8] Stavanger Univ Hosp, Dept Cardiol, Stavanger, Norway
[9] Univ Bergen, Inst Internal Med, N-5020 Bergen, Norway
[10] Univ Oslo, Fac Med, Oslo, Norway
关键词
Myocardial infarction; Heart failure; Inflammation; CHRONIC HEART-FAILURE; GENE-EXPRESSION; IMMUNE GLOBULIN; THERAPY; CARDIOMYOPATHY; AUTOIMMUNE; CELLS;
D O I
10.1016/j.ijcard.2012.09.092
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Left ventricular (LV) remodeling takes place after acutemyocardial 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 alpha 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. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:212 / 218
页数:7
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