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  • Poster presentation
  • Open Access

Hemodynamic effects of levosimendan in patients with low-output heart failure

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Critical Care200812 (Suppl 2) :P264

  • Published:


  • Cardiomyopathy
  • Left Ventricular Ejection Fraction
  • Cardiac Index
  • Dobutamine
  • Cardiogenic Shock


Levosimendan is a positive inotropic drug agent that increases the sensibility of contractile proteins to calcium [1]. The drug is used in patients with decompensated low-output heart failure [2]. The aim of our study is to analyze the hemodynamic effects of levosimendan in patients with refractory cardiogenic shock.


After approval by our institutional ethics committee, 16 patients who had a refractory cardiogenic shock after myocardial infarction (n = 10), peripartum cardiomyopathy (n = 3) and cardiomyopathy (n = 3) were prospectively included in our study. Levosimendan was added to conventional inotropic agents (dobutamine) with a bolus dose of 12 μg/kg for 30 minutes followed by a continuous infusion at a rate of 0.1 μg/kg/min for 24 hours. Hemodynamic data (continuous cardiac output and venous oxygen saturation) were obtained by a Swan–Ganz catheter at T0, 30 minutes, 90 minutes, 2 hours, 4 hours, 8 hours, 12 hours, 24 hours and 48 hours. A transoesophageal echocardiography was performed at T0, day 1, day 2, day 7 and day 15. SPSS version 10 was used for all statistical analyses.


After levosimendan administration, a significant reduction of pulmonary and vascular resistances values was followed by a significant increase of the cardiac index and venous oxygen saturation. Changes in heart rates and mean arterial blood pressure were not significant. The left ventricular ejection fraction was increased from 24% (T0) to 40% (day 2).


This study showed that levosimendan improves hemodynamic parameters and left ventricular ejection fraction in patients with cardiogenic shock. Controlled trials of sufficient size are needed, however, to confirm these results.

Authors’ Affiliations

Military Hospital of Tunis, Tunisia


  1. Figgitt DP, Gillies PS, Goa KL: Drugs. 2001, 61: 613-627. 10.2165/00003495-200161050-00006PubMedView ArticleGoogle Scholar
  2. Follath F, Cleland JGF, Just H, et al.: Lancet. 2002, 360: 196-202. 10.1016/S0140-6736(02)09455-2PubMedView ArticleGoogle Scholar


© BioMed Central Ltd 2008

This article is published under license to BioMed Central Ltd.