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Acute heart failure following myocardial infarction : complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.

Orrem, Hilde L (author)
Oslo University Hospital, Norway
Nilsson, Per H., 1980- (author)
Linnéuniversitetet,Institutionen för kemi och biomedicin (KOB),University of Oslo, Norway;Oslo University Hospital, Norway,Linnaeus Ctr Biomat Chem, BMC;HoRB
Pischke, Søren E (author)
Oslo University Hospital, Norway
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Grindheim, Guro (author)
Oslo University Hospital, Norway
Garred, Peter (author)
University of Copenhagen, Denmark
Seljeflot, Ingebjørg (author)
Oslo University Hospital, Norway;University of Oslo, Norway
Husebye, Trygve (author)
Oslo University Hospital, Norway;University of Oslo, Norway
Aukrust, Pål (author)
University of Oslo, Norway;Oslo University Hospital, Norway
Yndestad, Arne (author)
University of Oslo, Norway;Oslo University Hospital, Norway
Andersen, Geir Ø (author)
Oslo University Hospital, Norway;University of Oslo, Norway
Barratt-Due, Andreas (author)
Oslo University Hospital, Norway
Mollnes, Tom E (author)
Oslo University Hospital, Norway;University of Oslo, Norway;University of Tromsø, Norway;Norwegian University of Science and Technology, Norway
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 (creator_code:org_t)
2018-02-09
2018
English.
In: ESC Heart Failure. - : John Wiley & Sons. - 2055-5822. ; 5:3, s. 292-301
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)

Keyword

Acute heart failure
Cardiogenic shock
Complement activation
Inflammation
Myocardial infarction
Wall motion score index
Medicin
Medicine

Publication and Content Type

ref (subject category)
art (subject category)

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