title: Levosimendan is superior to enoximone in refractory cardiogenic shock complicating acute myocardial infarction.
abstract: OBJECTIVE
  Cardiogenic shock is the leading cause of death in patients hospitalized for acute myocardial infarction. The objectives were to investigate the effects of levosimendan, a novel inodilator, compared with the phosphodiesterase-III inhibitor enoximone in refractory cardiogenic shock complicating acute myocardial infarction, on top of current therapy.
  
  
  METHODS
  Prospective, randomized, controlled single-center clinical trial.
  
  
  METHODS
  Medical and coronary intensive care unit in a university hospital.
  
  
  METHODS
  Thirty-two patients with refractory cardiogenic shock for at least 2 hrs requiring additional therapy.
  
  
  METHODS
  Infusion of either levosimendan (12 microg/kg over 10 min, followed by 0.1 microg/kg/min over 50 min, and of 0.2 microg/kg/min for the next 23 hrs) or enoximone (fractional loading dose of 0.5 mg/kg, followed by 2-10 microg/kg/min continuously) after initiation of current therapy, always including revascularization, intra-aortic balloon pump counterpulsation, and inotropes.
  
  
  RESULTS
  Survival rate at 30 days was significantly higher in the levosimendan-treated group (69%, 11 of 16) compared with the enoximone group (37%, 6 of 16, p = 0.023). Invasive hemodynamic parameters during the first 48 hrs were comparable in both groups. Levosimendan induced a trend toward higher cardiac index, cardiac power index, left ventricular stroke work index, and mixed venous oxygen saturation. In addition, lower cumulative values for catecholamines at 72 hrs and for clinical signs of inflammation were seen in the levosimendan-treated patients. Multiple organ failure leading to death occurred exclusively in the enoximone group (4 of 16 patients).
  
  
  CONCLUSIONS
  In severe and refractory cardiogenic shock complicating acute myocardial infarction, levosimendan, added to current therapy, may contribute to improved survival compared with enoximone.
authors.affiliation: Department of Internal Medicine and Cardiology, Heart Center Dresden-University Hospital, University of Technology, Dresden, Germany. joerg.fuhrmann@lycos.de
authors.forename: Joerg T
authors.initials: JT
authors.lastname: Fuhrmann
authors.forename: Alexander
authors.initials: A
authors.lastname: Schmeisser
authors.forename: Matthias R
authors.initials: MR
authors.lastname: Schulze
authors.forename: Carsten
authors.initials: C
authors.lastname: Wunderlich
authors.forename: Steffen P
authors.initials: SP
authors.lastname: Schoen
authors.forename: Thomas
authors.initials: T
authors.lastname: Rauwolf
authors.forename: Christof
authors.initials: C
authors.lastname: Weinbrenner
authors.forename: Ruth H
authors.initials: RH
authors.lastname: Strasser
mesh_terms: D000368:Aged; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D003325:Coronary Care Units; D017335:Enoximone / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics; D017052:Hospital Mortality; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use*; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000175:diagnosis; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D011724:Pyridazines / Q000627:therapeutic use*; D012770:Shock, Cardiogenic / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality; D000077464:Simendan
chemical_list: D002316:Cardiotonic Agents; D006835:Hydrazones; D010726:Phosphodiesterase Inhibitors; D011724:Pyridazines; D000077464:Simendan; D017335:Enoximone