• Cardiol J · Jan 2011

    Effects of levosimendan without loading dose on systolic and diastolic function in patients with end-stage heart failure.

    • Stefano Lunghetti, Elisabetta Palmerini, Rossella Urselli, Silvia Maffei, Elisa Guarino, Marta Focardi, Sergio Mondillo, and Roberto Favilli.
    • Department of Cardiology, University of Siena, Italy. stefano.lunghetti@libero.it
    • Cardiol J. 2011 Jan 1;18(5):532-7.

    BackgroundLevosimendan (L) is used in clinical practice for the treatment of severe heart failure (HF); it has inotropic and vasodilatory effects, without increasing myocardial oxygen consumption. In acute HF, levosimendan improves hemodynamic parameters; previous studies have demonstrated that it has favorable effects on left ventricular (LV) diastolic function. The aim of our study was to evaluate the effect of on LV long-axis function that represents the earlier marker of diastolic dysfunction.MethodsWe enrolled 41 patients (age 62 ± 12 years) admitted to our Department for acute HF, NYHA class IV and severe LV dysfunction. Twenty-six patients were treated with L (0.1 μg/kg/min ev for 24 h without loading dose) and 15 patients were treated with standard therapy (C). We evaluated clinical, blood exams and echocardiographic parameters at baseline and one week after L or C treatment.ResultsBaseline demographic, clinical and biochemical data were similar in both groups. After one week, the L group had shown a significant improvement in NYHA class and a reduction of pro-B-type natriuretic peptide (pro-BNP). In echocardiographic study, we observed an improvement in LV longitudinal function (p 〈 0.05) and LV ejection fraction (p 〈 0.05) with a reduction of E/E' (p 〈 0.05) in the L group. We divided the L group into ischemic and non- -ischemic patients and we demonstrated a significant increase in systolic function in the former. No differences were found between subgroups in diastolic function.ConclusionsL therapy, without loading dose, improves NYHA class and ventricular function in patients with acute HF; we believe that these prolonged hemodynamic effects are due to active metabolities of L.

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