Key result
Levosimendan significantly increased the cardiac index from 1.96 to 3.19 L/min/m2 and mean arterial pressure from 63 to 76 mmHg at 48 hours in patients with cardiogenic shock refractory to catecholamines.
Why the study?
Does levosimendan improve hemodynamic parameters in patients with cardiogenic shock refractory to catecholamines?
Observational (n=26)
No
Does levosimendan improve hemodynamic parameters in patients with cardiogenic shock refractory to catecholamines?
Absolute Event Rate: 3.19% vs 1.96%
p-value: p=<0.0001
Levosimendan effectively stabilizes hemodynamic parameters and reduces the need for catecholamines in patients with cardiogenic shock refractory to standard inotropes.
May support levosimendan in refractory cardiogenic shock; hypothesis-generating and requires randomized confirmation before practice change.
Cardiogenic shock (CS) is acute inadequate tissue perfusion caused by the heart's inability to pump an adequate amount of blood. Due to the failure of classic inotrope agents, a sensitizer agent, levosimendan, has been used as a rescue therapy in such situations. In order to assess the effectiveness of levosimendan to treat CS, we studied its hemodynamic effects on patients with CS. A retrospective study was conducted at the ICU of the Military Hospital of Tunis between January 2004 and December 2009, and between January 2011 and December 2013. Twenty-six patients with CS refractory to catecholamines were included in our study. When catecholamines failed to improve the hemodynamic condition, levosimendan was introduced. This treatment was administered in two steps: a loading dose of 12 µg/kg/min was infused for 30 min; and then continuous infusion was given for 24 h at a dose of 0.1 µg/kg/min. Levosimendan significantly increased mean arterial pressure to 76 ± 7 mmHg at 48 h and cardiac index to 3.19 ± 0.68 L/min/m2 and decreased pulmonary wedge pressure to 17 ± 3 mmHg at 48 h. Pulmonary arterial systolic pressure, pulmonary arterial diastolic pressure, and mean pulmonary arterial pressure were significantly reduced at 24 h. A significant decrease in lactate from 3.77 ± 2.93 to 1.60 ± 1.32 mmol/L, by 72 h, was also noted. Levosimendan significantly reduced systemic vascular resistance and pulmonary vascular resistances. Administration of levosimendan also reduced the need for catecholamines. Our study confirms the efficacy of levosimendan to stabilize hemodynamic parameters in patients with CS.
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Janen et al. (2014) conducted an observational in Cardiogenic shock (n=26). Levosimendan vs. Baseline was evaluated on Cardiac index at 48 hours (p=<0.0001). Levosimendan significantly increased the cardiac index from 1.96 to 3.19 L/min/m2 and mean arterial pressure from 63 to 76 mmHg at 48 hours in patients with cardiogenic shock refractory to catecholamines.
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