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

AbstractAIMS:
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.
AuthorsHilde L Orrem, Per H Nilsson, Søren E Pischke, Guro Grindheim, Peter Garred, Ingebjørg Seljeflot, Trygve Husebye, Pål Aukrust, Arne Yndestad, Geir Ø Andersen, Andreas Barratt-Due, Tom E Mollnes
JournalESC heart failure (ESC Heart Fail) Vol. 5 Issue 3 Pg. 292-301 (06 2018) ISSN: 2055-5822 [Electronic] England
PMID29424484 (Publication Type: Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't)
Copyright© 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.
Topics
  • Acute Disease
  • Aged
  • Anterior Wall Myocardial Infarction (complications, diagnosis, surgery)
  • Complement Activation (physiology)
  • Echocardiography
  • Female
  • Heart Failure (blood, diagnosis, etiology)
  • Humans
  • Male
  • Middle Aged
  • Percutaneous Coronary Intervention
  • Severity of Illness Index
  • Shock, Cardiogenic (complications, diagnosis, physiopathology)

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