Effects of levosimendan on TNF-alpha, BNP and MMP-1 in patients with heart failure with anemia
Özet
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. Objectives: 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). Conclusion: 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.
Anahtar Kelimeler
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.contributor.author | Büyüklü, Mutlu | |
| dc.contributor.author | Kürüm, Akif Turhan | |
| dc.contributor.author | Tatlís, Ersan | |
| dc.contributor.author | Set, Turan | |
| dc.date.accessioned | 2026-10-18T20:30:38.658739684Z | |
| dc.date.available | 2026-10-18T20:30:38.658739684Z | |
| dc.date.issued | 2012 | |
| dc.description.abstract | 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. Objectives: 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). Conclusion: 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. | |
| dc.identifier.doi | 10.1590/s0066-782x2012005000055 | |
| dc.identifier.endpage | 664 | |
| dc.identifier.issn | 1678-4170 | |
| dc.identifier.issue | 1 | |
| dc.identifier.pmid | 22735864 | |
| dc.identifier.scopus | 2-s2.0-84866052068 | |
| dc.identifier.startpage | 659 | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/15795 | |
| dc.identifier.volume | 99 | |
| dc.identifier.wos | WOS:000308332500014 | |
| dc.language.iso | en | |
| dc.publisher | ARQUIVOS BRASILEIROS CARDIOLOGIA | |
| dc.relation.ispartof | Arquivos Brasileiros de Cardiologia | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | Anemia | |
| dc.subject | Brain | |
| dc.subject | Factor-alpha | |
| dc.subject | Heart failure/drug therapy | |
| dc.subject | Matrix metalloproteinase 1 | |
| dc.subject | Natriuretic peptide | |
| dc.subject | Tumor necrosis | |
| dc.subject | Aged | |
| dc.subject | Cardiotonic Agents | |
| dc.subject | Chi-Square Distribution | |
| dc.subject | Female | |
| dc.subject | Heart Failure | |
| dc.subject | Humans | |
| dc.subject | Hydrazones | |
| dc.subject | Infusions, Intravenous | |
| dc.subject | Male | |
| dc.subject | Middle Aged | |
| dc.subject | Natriuretic Peptide, Brain | |
| dc.subject | Pyridazines | |
| dc.subject | Statistics, Nonparametric | |
| dc.subject | Treatment Outcome | |
| dc.subject | Tumor Necrosis Factor-alpha | |
| dc.subject | amino terminal pro brain natriuretic peptide | |
| dc.subject | beta adrenergic receptor blocking agent | |
| dc.subject | furosemide | |
| dc.subject | interstitial collagenase | |
| dc.subject | levosimendan | |
| dc.subject | spironolactone | |
| dc.subject | tumor necrosis factor alpha | |
| dc.subject | article | |
| dc.title | Effects of levosimendan on TNF-alpha, BNP and MMP-1 in patients with heart failure with anemia | |
| dc.type | Article | |
| dspace.entity.type | Publication | |
| rdl.citation.scopus | 3 | |
| rdl.citation.wos | 3 | |
| rdl.oa.status | gold | |
| rdl.source.index | SCOPUS | |
| rdl.source.index | WOS | |
| rdl.wos.index | Science Citation Index Expanded (SCI-EXPANDED) |
