{"id":"63b18afa48c0","type":"article","url":"https://hartvaat.nl/2018/06/01/complementactivatie-bij-acuut-hartfalen-na-mi-correlatie-met-ernst/","title":"Complementactivatie bij acuut hartfalen na MI: correlatie met ernst","title_en":"Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.","category":"hartfalen","category_label":"Hartfalen","professions":["cardioloog"],"tags":[],"journal":"ESC heart failure","doi":"10.1002/ehf2.12266","source_url":"https://doi.org/10.1002/ehf2.12266","authors":["Hilde 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"],"significance":5,"published":"2018-06-01","source_date":"2018-06-01","image":"","kennis":[],"congress":"","summary_en":"This study showed that complement activation correlates with heart failure severity following acute MI, providing immunological insights into the pathogenesis of post-infarction cardiac dysfunction.","created":"2026-07-03T10:27:18Z","updated":"2026-07-03T13:26:33Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie die aantoont dat complementactivatie correleert met de ernst van hartfalen bij patiënten met acuut MI. Immunologische mechanismen bij acuut HF.","abstract_original":"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."}