title: Levosimendan in acute heart failure following primary percutaneous coronary intervention-treated acute ST-elevation myocardial infarction. Results from the LEAF trial: a randomized, placebo-controlled study.
abstract: OBJECTIVE
  The calcium sensitizer levosimendan may counteract stunning after reperfusion of ischaemic myocardium, but no randomized placebo-controlled trials exist regarding its use in PCI-treated ST-segment elevation infarction (STEMI). We evaluated the efficacy and safety of levosimendan in patients with a primary PCI-treated STEMI complicated by symptomatic heart failure (HF).
  
  
  RESULTS
  A total of 61 patients developing clinical signs of HF within 48 h after a primary PCI-treated STEMI (including cardiogenic shock) were randomized double-blind to a 25 h infusion of levosimendan or placebo. The primary endpoint was change in wall motion score index (WMSI) from baseline to day 5 measured by echocardiography. There was a significantly larger improvement in WMSI from baseline to day 5 in the levosimendan group compared with placebo (from 1.94 ± 0.20 to 1.66 ± 0.31 vs. 1.99 ± 0.22 to 1.83 ± 0.26, respectively, P = 0.031). There were significantly more episodes of hypotension during study drug infusion in the levosimendan group (67% vs. 36%, P = 0.029), but no significant difference in blood pressure at the end of infusion or in use of vasopressors. No significant between-group differences in changes in NT-proBNP levels, clinical composite score, frequency of atrial fibrillation or ventricular arrhythmia, infarct size at 6 weeks, or new clinical events up to 6 months were found. One and four patients died in the levosimendan and placebo group, respectively.
  
  
  CONCLUSIONS
  Levosimendan treatment improved contractility in post-ischaemic myocardium in patients with PCI-treated STEMI complicated by HF. The treatment was well tolerated, without any increase in arrhythmias.
authors.affiliation: Department of Cardiology, Oslo University Hospital Ullevål, Norway. tr-huse@online.no
authors.forename: Trygve
authors.initials: T
authors.lastname: Husebye
authors.forename: Jan
authors.initials: J
authors.lastname: Eritsland
authors.forename: Carl
authors.initials: C
authors.lastname: Müller
authors.forename: Leiv
authors.initials: L
authors.lastname: Sandvik
authors.forename: Harald
authors.initials: H
authors.lastname: Arnesen
authors.forename: Ingebjørg
authors.initials: I
authors.lastname: Seljeflot
authors.forename: Arild
authors.initials: A
authors.lastname: Mangschau
authors.forename: Reidar
authors.initials: R
authors.lastname: Bjørnerheim
authors.forename: Geir Øystein
authors.initials: GØ
authors.lastname: Andersen
mesh_terms: D000208:Acute Disease; D000368:Aged; D002316:Cardiotonic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D006835:Hydrazones / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy*; D009664:Norway; D062645:Percutaneous Coronary Intervention; D011724:Pyridazines / Q000009:adverse effects / Q000627:therapeutic use*; D000077464:Simendan; D016896:Treatment Outcome
chemical_list: D002316:Cardiotonic Agents; D006835:Hydrazones; D011724:Pyridazines; D000077464:Simendan