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We analyzed the inodilator properties of levosimendan in patients with chronic heart failure and severe functional mitral regurgitation.We studied 20 patients under optimal treatment and in stable clinical condition (New York Heart Association 3.19 ± 0.66; 70 ± 7 years). Levosimendan was infused as a bolus (12 μg/kg in 10 min) followed by a 24-h infusion (0.1–0.2 μg/kg per min). Before and after infusion, Doppler echocardiography, brain natriuretic peptide determination and noninvasive hemodynamic monitoring with bioimpedance cardiography were performed.Levosimendan improved left ventricular ejection fraction (ejection fraction 31 ± 4 from 27 ± 4, P < 0.05), decreased brain natriuretic peptide (333 ± 139 from 629 ± 63 pg/ml, P < 0.01), reduced mitral valve effective regurgitant orifice area to 27 ± 5 from 36 ± 7 mm2 (P < 0.01) and the velocity of displacement of mitral annulus [ratio between E and E′ waves on Doppler and tissue Doppler (E/E′) from 22.7 ± 1.6 to 13.1 ± 0.6, P < 0.01]. Noninvasive hemodynamic monitoring showed increased acceleration index (a marker of inotropism), and reduced peripheral resistances and thoracic fluid content (P < 0.01). After 4 weeks of washout, some of these effects were still evident.In patients with chronic heart failure and functional mitral regurgitation, levosimendan acutely improved systolic and diastolic function, reduced mitral regurgitation and modulated neurohormonal activation, with a tendency for these changes to persist over a short-term follow-up.