title: Levosimendan use reduces matrix metalloproteinase-2 in patients with decompensated heart failure.
abstract: BACKGROUND
  Extracellular matrix metabolism (ECM) has an important role in left ventricular (LV) remodeling in chronic heart failure (CHF). Matrix metalloproteinases (MMPs) are involved in the regulation of extracellular matrix (ECM) metabolism. We investigated the effect of levosimendan, a novel calcium sensitizer, on serum levels of MMP-2.
  
  
  METHODS
  Our study population consisted of 60 consecutive patients with advanced heart failure who were admitted to hospital with an acute decompensation of their CHF. Patients were randomized to levosimendan (n = 30; 18 men, aged 65 +/- 3 years) or placebo (n = 30; 15 men, aged 67 +/- 4 years). Serum MMP-2 levels were assessed before and after treatment with levosimendan or placebo, using a commercially available ELISA.
  
  
  RESULTS
  Serum levels of MMP-2 were reduced from 427 ng/ml 95%CI 372-484 to 371 ng/ml 95%CI 329-413 in the levosimendan treated group and from 433 ng/ml 95%CI 422-444 to 425 ng/ml 95%CI 414-436 in the placebo group. Repeated measurements ANOVA showed that treatment with levosimendan significantly affected levels of MMP-2 (p = 0.019).
  
  
  CONCLUSIONS
  The present study showed that levosimendan may beneficially affect ECM remodeling in patients with acutely decompensated CHF. Whether these effects translate into added clinical benefits, as suggested by an improved ejection fraction in the levosimendan group, deserves further investigation.
authors.affiliation: Cardiology Department, Democritus University of Thrace, Alexandroupolis, Greece. dtziakas@med.duth.gr
authors.forename: Dimitrios N
authors.initials: DN
authors.lastname: Tziakas
authors.forename: Georgios K
authors.initials: GK
authors.lastname: Chalikias
authors.forename: Helen I
authors.initials: HI
authors.lastname: Hatzinikolaou
authors.forename: Dimitrios A
authors.initials: DA
authors.lastname: Stakos
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Papanas
authors.forename: Ioannis K
authors.initials: IK
authors.lastname: Tentes
authors.forename: Alexandros X
authors.initials: AX
authors.lastname: Kortsaris
authors.forename: Efstratios
authors.initials: E
authors.lastname: Maltezos
authors.forename: Dimitrios I
authors.initials: DI
authors.lastname: Hatseras
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Kaski
mesh_terms: D000368:Aged; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D018450:Disease Progression; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000473:pathology; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use*; D007275:Injections, Intravenous; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000097:blood* / Q000187:drug effects; D010919:Placebos; D011724:Pyridazines / Q000627:therapeutic use*; D000077464:Simendan; D016896:Treatment Outcome
chemical_list: D002316:Cardiotonic Agents; D006835:Hydrazones; D010919:Placebos; D011724:Pyridazines; D000077464:Simendan; D020778:Matrix Metalloproteinase 2