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European Journal of Heart Failure 2006 8(8):804-809; doi:10.1016/j.ejheart.2006.03.003
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© 2006 European Society of Cardiology

Long-term effects of levosimendan infusion on inflammatory processes and sFas in patients with severe heart failure

Athanasios Trikas*, Charalambos Antoniades, Giorgos Latsios, Karmen Vasiliadou, Ioannis Karamitros, Dimitris Tousoulis, Costantinos Tentolouris and Christodoulos Stefanadis

Athens University Medical School, A' Cardiology Department Athens, Greece

* Corresponding author. 52, Bizaniou Street, Panorama Voulas - 16673, Athens, Greece. Tel.: +30 210 7782446; fax: +30 210 7485039. E-mail address: atrikas{at}otenet.gr


  Abstract

Background: The calcium sensitizer levosimendan improves myocardial contractility in patients with heart failure, although its effects on inflammation and apoptosis are unknown.

Aim: To examine the effects of levosimendan on markers of inflammation and apoptosis, over a period of 30 d following a 24 h infusion, in patients with heart failure.

Methods: Thirty four patients with severe heart failure were randomised to receive a 24 h infusion of levosimendan or placebo, in a double-blind trial. Haemodynamic evaluation and blood sampling were performed at baseline, 24 h, 30 h, 48 h, 7 d and 30 d after the end of the infusion.

Results: Seven patients (1 levosimendan, 6 placebo), were excluded during follow-up. In the remaining 27 patients, levosimendan decreased serum IL-6 and sFAS, 24 h after the infusion (p<0.01 and p<0.05 vs baseline), an effect sustained for 7–30 d. Serum TNF-{alpha} and sTNF-R1 were decreased between 48 h (p<0.01 vs baseline for both) and 7 d (p<0.05 vs baseline for sTNF-R1) after infusion. Serum sTNF-R2 was decreased at 24 h (p<0.05 vs baseline) and remained lower than baseline for at least 7 d (p<0.05).

Conclusions: These findings indicate that levosimendan decreases the expression of proinflammatory cytokines, TNF-{alpha} receptors and sFAS, immediately after infusion, an effect which persists for 7–30 d.

Key Words: Levosimendan • Inflammatory process • Apoptosis • Heart failure

Received August 25, 2005; Revised February 2, 2006; Accepted March 8, 2006


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