title: Effects of levosimendan without loading dose on systolic and diastolic function in patients with end-stage heart failure.
abstract: BACKGROUND
  Levosimendan (L) is used in clinical practice for the treatment of severe heart failure (HF); it has inotropic and vasodilatory effects, without increasing myocardial oxygen consumption. In acute HF, levosimendan improves hemodynamic parameters; previous studies have demonstrated that it has favorable effects on left ventricular (LV) diastolic function. The aim of our study was to evaluate the effect of on LV long-axis function that represents the earlier marker of diastolic dysfunction.
  
  
  METHODS
  We enrolled 41 patients (age 62 ± 12 years) admitted to our Department for acute HF, NYHA class IV and severe LV dysfunction. Twenty-six patients were treated with L (0.1 μg/kg/min ev for 24 h without loading dose) and 15 patients were treated with standard therapy (C). We evaluated clinical, blood exams and echocardiographic parameters at baseline and one week after L or C treatment.
  
  
  RESULTS
  Baseline demographic, clinical and biochemical data were similar in both groups. After one week, the L group had shown a significant improvement in NYHA class and a reduction of pro-B-type natriuretic peptide (pro-BNP). In echocardiographic study, we observed an improvement in LV longitudinal function (p 〈 0.05) and LV ejection fraction (p 〈 0.05) with a reduction of E/E' (p 〈 0.05) in the L group. We divided the L group into ischemic and non- -ischemic patients and we demonstrated a significant increase in systolic function in the former. No differences were found between subgroups in diastolic function.
  
  
  CONCLUSIONS
  L therapy, without loading dose, improves NYHA class and ventricular function in patients with acute HF; we believe that these prolonged hemodynamic effects are due to active metabolities of L.
authors.affiliation: Department of Cardiology, University of Siena, Italy. stefano.lunghetti@libero.it
authors.forename: Stefano
authors.initials: S
authors.lastname: Lunghetti
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Palmerini
authors.forename: Rossella
authors.initials: R
authors.lastname: Urselli
authors.forename: Silvia
authors.initials: S
authors.lastname: Maffei
authors.forename: Elisa
authors.initials: E
authors.lastname: Guarino
authors.forename: Marta
authors.initials: M
authors.lastname: Focardi
authors.forename: Sergio
authors.initials: S
authors.lastname: Mondillo
authors.forename: Roberto
authors.initials: R
authors.lastname: Favilli
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002316:Cardiotonic Agents / Q000378:metabolism / Q000627:therapeutic use*; D016009:Chi-Square Distribution; D003971:Diastole / Q000187:drug effects; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006835:Hydrazones / Q000378:metabolism / Q000627:therapeutic use*; D007558:Italy; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011724:Pyridazines / Q000378:metabolism / Q000627:therapeutic use*; D012720:Severity of Illness Index; D000077464:Simendan; D013599:Systole / Q000187:drug effects; D016896:Treatment Outcome; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D006835:Hydrazones; D011724:Pyridazines; D020097:Natriuretic Peptide, Brain; D000077464:Simendan