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Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock *

Russ, Martin A. MD; Prondzinsky, Roland MD; Christoph, Arnd MD; Schlitt, Axel MD; Buerke, Ute MD; Söffker, Gerold MD; Lemm, Henning; Swyter, Michael; Wegener, Nikolas; Winkler, Matthias MD; Carter, Justin M. MRCP; Reith, Sebastian MD; Werdan, Karl MD; Buerke, Michael MD

Clinical Investigations
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Objectives: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with acute exacerbation of congestive heart failure. We wanted to determine the hemodynamic effects of levosimendan following ineffective conventional therapy (with catecholamines) in patients with cardiogenic shock following myocardial infarction.

Design: Observational hemodynamic study.

Setting: Tertiary care center university hospital.

Patients: Fifty-six patients with cardiogenic shock secondary to myocardial infarction were treated with percutaneous revascularization (intra-aortic balloon pump where appropriate) and commenced on conventional inotropic therapy.

Interventions: Patients with persisting cardiogenic shock 24 hrs after revascularization were additionally treated with levosimendan (rapid bolus of 12 μg/kg for 10 mins, then 0.05–0.2 μg/kg/min for 24 hrs) (n = 25).

Measurements and Main Results: With conventional catecholamine therapy (norepinephrine and dobutamine), we observed only marginal improvement in mean arterial pressure or cardiac index. In contrast, the addition of levosimendan produced a significant increase in cardiac index (2.1 ± 0.56 to 3.0 ± 1.11 L/min/m2,p< .01) and cardiac power index (0.32 ± 0.08 to 0.44 ± 0.18 W,p< .01), whereas systemic vascular resistance decreased significantly (1208 ± 333 to 858 ± 299 dyne·sec·cm-5,p< .01). There was no significant change in blood pressure during levosimendan treatment. Hemodynamic improvement was sustained after levosimendan infusion was stopped.

Conclusions: Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.

From the Department of Internal Medicine III, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany.

Supported, in part, by grant DFG Bu 819/5 from the Deutsche Forschungsgesellschaft (MB) and grant FK12–28 from the Wilhelm-Roux-Programm of the Medical Faculty of the Martin-Luther-University Halle-Wittenberg (MR). Dr. Prondzinsky has received honoraria from Datascope.

For information regarding this article, E-mail: michael.buerke@medizin.uni-halle.de

*See also p. 2862.

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