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Updated: May 29, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
Effects of levosimendan without loading dose on systolic and diastolic function in patients with end-stage heart
Stefano Lunghetti1, Elisabetta Palmerini, Rossella Urselli
1Department of Cardiology, University of Siena, Italy. stefano.lunghetti@libero.it
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.
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