Levosimendan reduces pulmonary vascular resistance: clinical echocardiographic study

Introduction

The calcium sensitizer levosimendan is a novel inotrope used for the treatment of cardiac failure. Animal data suggest pulmonary vasodilating properties and levosimendan has been suggested for the treatment of right ventricular (RV) failure despite scarce data in patients [1].

Settings

An ICU and echo-laboratory in a tertiary teaching hospital.

Methods

We reviewed prospectively recorded transthoracic echocardiograms of seven cardiac failure patients and six critically ill patients before and after 24 hours of levosimendan infusion (bolus 12 μg/kg + 0.1 μg/kg/min) in whom continuous wave Doppler signal (CW) of peak tricuspid regurgitant (TR) flow velocity recordings before and after levosimendan infusion were available. The left ventricular ejection fraction (LVEF) was measured by the Simpson's method. RV contractility was assessed by the maximal tricuspid annulus displacement during the cardiac cycle by M-mode (six patients only) and/or by a blinded observer. The maximal RV–right atrium gradient (TRmax) calculated from the CW recording (by the modified Bernoulli equation) of peak TR flow velocity in parasternal short axis or apical four-chamber views is regarded as a preload independent estimate of pulmonary artery vascular resistance (PVR) [2].

Values are expressed as the mean ± SD. The Wilcoxon Signed-Rank test was used to calculate the difference before and after levosimendan infusion.

Results

The patients were 10 males and three females with mean age 66 ± 14 years. The mean TRmax was 38.0 ± 9.2 mmHg prior to levosimendan infusion. After 24 hours of levosimendan infusion TRmax decreased to 30.9 ± 6.7 mmHg (P = 0.0015). In patients with markedly elevated baseline TRmax (> 35 mmHg), the median drop in TRmax was more pronounced then in patients with mild elevation of baseline TRmax (7.8 mmHg vs 2.4 mmHg). Although LVEF increased in all patients (from 18 ± 6% to 25 ± 7%) and RV contractility assessed by M-mode was better (from 1.48 ± 0.2 cm to 1.61 ± 0.2 cm), the blinded observer was not able to confirm improvement in RV contractility.

Conclusion

Levosimendan reduced the TRmax of peak TR flow velocity in cardiac failure and critically ill patients, implying a reduction in PVR. The degree of PVR reduction is greater in patients with baseline pulmonary hypertension.

Figure 1

Effect of levosimendan on TRmax.