Vol 18, No 5 (2011)
Original articles
Published online: 2011-09-21

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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, Roberto Favilli
Cardiol J 2011;18(5):532-537.


Background: Levosimendan (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.
Methods: We 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.
Results: Baseline 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.
Conclusions: L 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.
(Cardiol J 2011; 18, 5: 532–537)

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