Unknown

Dataset Information

0

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


ABSTRACT: 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.

SUBMITTER: Orrem HL 

PROVIDER: S-EPMC5933968 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

altmetric image

Publications

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

Orrem Hilde L HL   Nilsson Per H PH   Pischke Søren E SE   Grindheim Guro G   Garred Peter P   Seljeflot Ingebjørg I   Husebye Trygve T   Aukrust Pål P   Yndestad Arne A   Andersen Geir Ø GØ   Barratt-Due Andreas A   Mollnes Tom E TE  

ESC heart failure 20180209 3


<h4>Aims</h4>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.<h4>Methods and results</h4>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 samp  ...[more]

Similar Datasets

| S-EPMC9286066 | biostudies-literature
| S-EPMC5955398 | biostudies-literature
| S-EPMC10051785 | biostudies-literature
| S-EPMC10532159 | biostudies-literature
| S-EPMC7261549 | biostudies-literature
| S-EPMC6712338 | biostudies-literature
| S-EPMC7141492 | biostudies-literature
| S-EPMC8751815 | biostudies-literature
| S-EPMC7261623 | biostudies-literature
| S-EPMC6713772 | biostudies-literature