Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock
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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; Nilsson, Per H; Pischke, Søren E; Grindheim, Guro; Garred, Peter; Seljeflot, Ingebjørg; Husebye, Trygve; Aukrust, Pål; Yndestad, Arne; Andersen, Geir Ø; Barratt-Due, Andreas; Mollnes, Tom E.
In: E S C Heart Failure, Vol. 5, No. 3, 2018, p. 292-301.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Acute heart failure following myocardial infarction
T2 - complement activation correlates with the severity of heart failure in patients developing cardiogenic shock
AU - Orrem, Hilde L
AU - Nilsson, Per H
AU - Pischke, Søren E
AU - Grindheim, Guro
AU - Garred, Peter
AU - Seljeflot, Ingebjørg
AU - Husebye, Trygve
AU - Aukrust, Pål
AU - Yndestad, Arne
AU - Andersen, Geir Ø
AU - Barratt-Due, Andreas
AU - Mollnes, Tom E
N1 - © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.
PY - 2018
Y1 - 2018
N2 - 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.
AB - 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.
KW - Acute Disease
KW - Aged
KW - Anterior Wall Myocardial Infarction/complications
KW - Complement Activation/physiology
KW - Echocardiography
KW - Female
KW - Heart Failure/blood
KW - Humans
KW - Male
KW - Middle Aged
KW - Percutaneous Coronary Intervention
KW - Severity of Illness Index
KW - Shock, Cardiogenic/complications
U2 - 10.1002/ehf2.12266
DO - 10.1002/ehf2.12266
M3 - Journal article
C2 - 29424484
VL - 5
SP - 292
EP - 301
JO - E S C Heart Failure
JF - E S C Heart Failure
SN - 2055-5822
IS - 3
ER -
ID: 217660296