Abstract
BackgroundLow-cardiac output syndrome (LCOS) after cardiac surgery secondary to systemic hypoperfusion is associated with a higher incidence of renal and neurological damage. A range of effective therapies are available for LCOS. The beneficial systemic effects of levosimendan persist even after cardiac output is restored, which suggests an independent cardioprotective effect.MethodsA double-blind clinical trial was conducted in patients with a confirmed diagnosis of LCOS randomized into two treatment groups (levosimendan vs. dobutamine). Monitoring of hemodynamic (cardiac index, systolic volume index, heart rate, mean arterial pressure, central venous pressure, central venous saturation); biochemical (e.g. creatinine, S100B protein, NT-proBNP, troponin I); and renal parameters was performed using acute kidney injury scale (AKI scale) and renal and brain ultrasound measurements [vascular resistance index (VRI)] at diagnosis and during the first 48 h.ResultsSignificant differences were observed between groups in terms of cardiac index, systolic volume index, NT-proBNP, and kidney injury stage at diagnosis. In the levosimendan group, there were significant variations in AKI stage after 24 and 48 h. No significant differences were observed in the other parameters studied.ConclusionLevosimendan showed a beneficial effect on renal function in LCOS patients after cardiac surgery that was independent from cardiac output and vascular tone. This effect is probably achieved by pharmacological postconditioning.Clinical Trial RegistrationEUDRA CT, identifier 2014-001461-27. https://www.clinicaltrialsregister.eu/ctr-search/search?query=2014-001461-27
Highlights
The incidence of low cardiac output syndrome (LCOS) after cardiac surgery is 10–20%
When LCOS is treated with levosimendan, renal function improves at 24 and 48 h of treatment, as compared to dobutamine
We evaluated the central nervous system (CNS) using a specific biochemical marker of cell damage (S100B protein)
Summary
The incidence of low cardiac output syndrome (LCOS) after cardiac surgery is 10–20%. The effects of this syndrome on cardiac function are induced by splanchnic hypoperfusion, which requires treatment with inotropic drugs to restore organ perfusion (Lomivorotov et al, 2017).LCOS is treated with inotropics, which improve cardiovascular function after volume optimization. The incidence of low cardiac output syndrome (LCOS) after cardiac surgery is 10–20%. The effects of this syndrome on cardiac function are induced by splanchnic hypoperfusion, which requires treatment with inotropic drugs to restore organ perfusion (Lomivorotov et al, 2017). Inotropics restore cardiac function and an adequate blood flow in central and peripheral organs. The selection of the inotropic agent for the treatment of LCOS is based on the hemodynamic status of the patient. Low-cardiac output syndrome (LCOS) after cardiac surgery secondary to systemic hypoperfusion is associated with a higher incidence of renal and neurological damage. The beneficial systemic effects of levosimendan persist even after cardiac output is restored, which suggests an independent cardioprotective effect
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