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  • 1.
    Orrem, Hilde L
    et al.
    Oslo University Hospital, Norway.
    Nilsson, Per H.
    Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences. University of Oslo, Norway;Oslo University Hospital, Rikshospitalet, Norway.
    Pischke, Søren E
    Oslo University Hospital, Rikshospitalet, Norway.
    Grindheim, Guro
    Oslo University Hospital, Rikshospitalet, Norway.
    Garred, Peter
    University of Copenhagen, Denmark.
    Seljeflot, Ingebjørg
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Husebye, Trygve
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Aukrust, Pål
    University of Oslo, Norway;Oslo University Hospital, Norway.
    Yndestad, Arne
    University of Oslo, Norway;Oslo University Hospital, Norway.
    Andersen, Geir Ø
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Barratt-Due, Andreas
    Oslo University Hospital, Rikshospitalet, Norway.
    Mollnes, Tom E
    Oslo University Hospital, Rikshospitalet, Norway;University of Oslo, Norway;University of Tromsø, Norway;Norwegian University of Science and Technology, Norway.
    Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.2018In: ESC Heart Failure, E-ISSN 2055-5822, Vol. 5, no 3, p. 292-301Article in journal (Refereed)
    Abstract [en]

    AIMS: Heart failure (HF) is an impending complication to myocardial infarction. We hypothesized that the degree of complement activation reflects severity of HF following acute myocardial infarction.

    METHODS AND RESULTS: The LEAF trial (LEvosimendan in Acute heart Failure following myocardial infarction) evaluating 61 patients developing HF within 48 h after percutaneous coronary intervention-treated ST-elevation myocardial infarction herein underwent a post hoc analysis. Blood samples were drawn from inclusion to Day 5 and at 42 day follow-up, and biomarkers were measured with enzyme immunoassays. Regional myocardial contractility was measured by echocardiography as wall motion score index (WMSI). The cardiogenic shock group (n = 9) was compared with the non-shock group (n = 52). Controls (n = 44) were age-matched and sex-matched healthy individuals. C4bc, C3bc, C3bBbP, and sC5b-9 were elevated in patients at inclusion compared with controls (P < 0.01). The shock group had higher levels compared with the non-shock group for all activation products except C3bBbP (P < 0.05). At Day 42, all products were higher in the shock group (P < 0.05). In the shock group, sC5b-9 correlated significantly with WMSI at baseline (r = 0.68; P = 0.045) and at Day 42 (r = 0.84; P = 0.036). Peak sC5b-9 level correlated strongly with WMSI at Day 42 (r = 0.98; P = 0.005). Circulating endothelial cell activation markers sICAM-1 and sVCAM-1 were higher in the shock group during the acute phase (P < 0.01), and their peak levels correlated with sC5b-9 peak level in the whole HF population (r = 0.32; P = 0.014 and r = 0.30; P = 0.022, respectively).

    CONCLUSIONS: Complement activation discriminated cardiogenic shock from non-shock in acute ST-elevation myocardial infarction complicated by HF and correlated with regional contractility and endothelial cell activation, suggesting a pathogenic role of complement in this condition.

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