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10.1002/ehf2.12266 http://scihub22266oqcxt.onion/10.1002/ehf2.12266 C5933968!5933968!29424484     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29424484&cmd=llinks): Failed to open stream: HTTP request failed! 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Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock |pdf=|usr=}}{{29424484}} gab.com Text Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock JO: ESC Heart Fail http://www.kidney.de/pget.php?&tw=1&pmid=29424484 #FOAvip 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. Twit Text FOAVip Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock ????ESC Heart Fail http://www.kidney.de/pget.php?&tw=1&pmid=29424484 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29424484 #FOAvip English Wikipedia <ref>{{Cite pmid|29424484}}</ref> Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock #MMPMID29424484 Orrem HL; Nilsson PH; Pischke SE; Grindheim G; Garred P; Seljeflot I; Husebye T; Aukrust P; Yndestad A; Andersen GØ; Barratt?Due A; Mollnes TE ESC Heart Fail 2018[Jun]; 5 (3): 292-301 PMID29424484show ga 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. äAcute heart failure following myocardial infarction: complement activa(epmc).pdf DeepDyve Pubget Overpricing