Effects of levosimendan on TNF-alpha, BNP and MMP-1 in patients with heart failure with anemia.
BACKGROUND
Levosimendan is known with its two-sided effects of strengthening myofibril contraction without increasing myocardial oxygen demand. Anemia is a deteriorating situation that causes increase of drug dosing in patients with heart failure.


OBJECTIVE
In this study, we compared the effectiveness of levosimendan treatment in decompensated heart failure patients with or without anemia.


METHODS
Twenty-three anemic patients having class 3 or 4 heart failure according to New York Heart Association (NYHA) and an ejection fraction of below 35% were included to the study. Another 23 patients with the same cardiac diagnosis but without anemia served as control group. Twenty-four hours levosimendan treatment was added to the traditional heart failure treatment of these patients. Samples were taken to measure serum tumor necrotizing factor alpha (TNF-alpha), aminoterminal pro-brain natriuretic peptide (NT-proBNP) and matrix metalloproteinase-1 (MMP-1) levels before and after the administration.


RESULTS
There was no significant difference between serum TNF-alpha and MMP-1 levels before and after the treatment (p>0.05). Although NT-proBNP level decreased in both groups after the treatment this was not statistically significant (p=0.531 and p=0.913 for anemia and control groups respectively). Significant restoration of functional capacity was seen in both groups assessed according to NYHA (p<0.001 and p=0.001 for anemia and control groups respectively).


CONCLUSIONS
Levosimendan treatment shows similar effects in heart failure patients with anemia to that of patients without anemia. However, the early effect of this treatment on TNF-alpha, NT-proBNP and MMP-1 levels is not evident. It provides significant improvement in functional capacity without influence from anemia.
Departamento de Cardiologia, Hospital Estadual de Erzincan, Erzincan. mutlubuyuklu@gmail.com
Mutlu
M
Büyüklü
Akif Turhan
AT
Kürüm
Ersan
E
Tatlý
Turan
T
Set
D000368:Aged; D000740:Anemia / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use; D016009:Chi-Square Distribution; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D006835:Hydrazones / Q000494:pharmacology / Q000627:therapeutic use*; D007262:Infusions, Intravenous; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000097:blood*; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D011724:Pyridazines / Q000494:pharmacology / Q000627:therapeutic use*; D000077464:Simendan; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
D002316:Cardiotonic Agents; D006835:Hydrazones; D011724:Pyridazines; D014409:Tumor Necrosis Factor-alpha; D020097:Natriuretic Peptide, Brain; D000077464:Simendan; D020781:Matrix Metalloproteinase 1