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Hemodynamic and echographic effects of levosimendan in patients with cardiogenic shock refractory to catecholamines

Background

Levosimendan is a novel inodilator that has proved effective in treating advanced congestive heart failure but has been poorly evaluated in cardiogenic shock.

Objective

To characterize the hemodynamic and echographic effects of levosimendan in patients with cardiogenic shock refractory to catecholamines.

Methods

Nine patients (53.3 ± 19 years, five male/four female) with persisting cardiogenic shock following acute myocardial infarction (five cases), peripartum cardiomyopathy (two cases) or dilated cardiomyopathy (two cases) were candidates for levosimendan infusion. In all patients, a high dose of inotropic treatment failed to improve hemodynamic parameters. Levosimendan was introduced at a loading dose of 12 μg/kg followed by a continuous infusion of 0.1 μg/kg/min for 24 hours. Hemodynamic measurements were performed using a Swan–Ganz thermodilution catheter (744HF75; Edwards Life Sciences, Carolina, USA) at baseline and at 30 and 90 min, 6, 12, 24 and 48 hours after the start of levosimendan. Transoesophageal echocardiography was performed at baseline, 12 and 24 hours and then after 7 and 15 days in survivors.

Results

Levosimendan induced a significant decline of pulmonary capillary wedge pressure and systemic vascular resistances, followed by a significant increase in the cardiac index and mixed venous oxygen saturation. Changes in the heart rate and mean arterial blood pressure were not significant. The left ventricular ejection fraction was improved from 24% to 40% within 48 hours.

Conclusion

This study showed that the use of levosimendan in cardiogenic shock improved hemodynamics and left ventricular performance. Additional clinical trials on hemodynamics and mortality are needed to safely broaden its indications in cardiogenic shock.

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Labbene, I., Amor, M.B.h., Dhahri, S. et al. Hemodynamic and echographic effects of levosimendan in patients with cardiogenic shock refractory to catecholamines. Crit Care 10 (Suppl 1), P358 (2006). https://doi.org/10.1186/cc4705

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  • DOI: https://doi.org/10.1186/cc4705

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