• Herz · Jul 2008

    Clinical Trial

    Safety and effectiveness of levosimendan in patients with predominant right heart failure.

    • Gerhard Poelzl, Ralph H Zwick, Willhelm Grander, Bernhard Metzler, Patrycja Jonetzko, Mathias Frick, Hanno Ulmer, Otmar Pachinger, and Franz X Roithinger.
    • Clinical Division of Cardiology, Clinical Department of Internal Medicine, Innsbruck Medical University, Innsbruck, Austria. gerhard.poelzl@uki.at
    • Herz. 2008 Jul 1; 33 (5): 368-73.

    Background And PurposeLevosimendan is a new calcium sensitizer that enhances the contractile force of the myocardium and exhibits additional vasodilating properties. The present study describes the hemodynamic effects of levosimendan in patients with acute predominant right heart failure in need of inotropic therapy.Patients And Methods18 patients (15 male, age 60 +/- 17 years) with acute heart failure, predominant right ventricular dysfunction, left ventricular ejection fraction (LVEF) < or = 30%, cardiac index (CI) < or = 2.5 l/min/m(2), right atrial pressure (RAP) > or = 10 mmHg, and pulmonary capillary wedge pressure (PCWP) > or = 15 mmHg were investigated. Following a loading dose, levosimendan was administered intravenously for 24 h.ResultsAfter 24 h, CI and left ventricular stroke work index increased from 1.7 +/- 0.4 to 2.3 +/- 0.6 l/min/m(2) (p < 0.001) and 14 +/- 6 to 17.3 +/- 8 g-m/m(2)/beat (p < 0.05), respectively. PCWP and systemic vascular resistance decreased from 25 +/- 7 to 21 +/- 5 mmHg (p < 0.01) and 1,724 +/- 680 to 1,096 +/- 312 dyne * s * cm(-5) (p < 0.0001), respectively. RAP was reduced from 15 +/- 5 to 10 +/- 3 mmHg (p < 0.001), whereas decreases in mean pulmonary artery pressure and pulmonary vascular resistance were not significant. Right ventricular stroke work index (RVSWI) increased from 4.8 +/- 1.8 to 7.6 +/- 3.4 g-m/m(2)/beat (p < 0.01).ConclusionLevosimendan therapy is feasible and improves hemodynamics in patients with acute predominant right heart failure. Augmentation in RVSWI indicates an increase in right ventricular contractility rather than reduction in afterload as a possible pathophysiological mechanism.

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