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Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.
Oslo University Hospital, Norway.
Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). University of Oslo, Norway;Oslo University Hospital, Rikshospitalet, Norway. (Linnaeus Ctr Biomat Chem, BMC;Host Response to Biomaterials)ORCID-id: 0000-0002-7192-5794
Oslo University Hospital, Rikshospitalet, Norway.
Oslo University Hospital, Rikshospitalet, Norway.
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2018 (Engelska)Ingår i: ESC Heart Failure, E-ISSN 2055-5822, Vol. 5, nr 3, s. 292-301Artikel i tidskrift (Refereegranskat) Published
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.

Ort, förlag, år, upplaga, sidor
John Wiley & Sons, 2018. Vol. 5, nr 3, s. 292-301
Nyckelord [en]
Acute heart failure, Cardiogenic shock, Complement activation, Inflammation, Myocardial infarction, Wall motion score index
Nationell ämneskategori
Kardiologi
Forskningsämne
Naturvetenskap, Medicin
Identifikatorer
URN: urn:nbn:se:lnu:diva-73333DOI: 10.1002/ehf2.12266ISI: 000431494800011PubMedID: 29424484Scopus ID: 2-s2.0-85052907722OAI: oai:DiVA.org:lnu-73333DiVA, id: diva2:1200086
Tillgänglig från: 2018-04-23 Skapad: 2018-04-23 Senast uppdaterad: 2019-08-29Bibliografiskt granskad

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Nilsson, Per H.
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Institutionen för kemi och biomedicin (KOB)
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ESC Heart Failure
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