Magnitude of blood pressure reduction in response to levosimendan infusion independently predicts in-hospital mortality in patients with acute heart failure

Abstract

The impact of blood pressure (BP) reduction induced by levosimendan infusion on in-hospital mortality in patients with acute heart failure (AHF) and systolic ventricular dysfunction still needs to be clarified. We conducted a retrospective cohort study involving 161 patients hospitalized for AHF and treated with a 24-hour infusion of levosimendan between 2017 and 2024, following a standard protocol. During hospitalization, biometric, clinical, laboratory, and echocardiographic parameters were assessed. The results revealed that the difference in systolic and mean BP before and after levosimendan infusion (delta-SBP and delta-MAP) were significantly associated with higher in-hospital mortality (delta-SBP in survivors: 10.1±19.1 mmHg vs. in non-survivors: 21.4±23.6 mmHg, p=0.023; delta-MAP in survivors: 8.8±15.8 mmHg vs. in non-survivors: 17.8±23.3 mmHg, p=0.034), regardless of baseline BP values and despite the fact that the majority of patients had absolute values of SBP after levosimendan infusion >90 mmHg. Multivariable analysis confirmed that a larger reduction in SBP was an independent predictor of in-hospital mortality (OR: 1.053, 95% CI: 1.015-1.092, p=0.006). Absolute values of SBP after levosimendan infusion (post-SBP) were also independently associated with mortality (OR: 0.942, 95% CI: 0.896-0.990, p=0.019). However, when the analysis was repeated in a subgroup of subjects with SBP after infusion >90 mmHg, only delta-SBP remained independently associated with mortality (OR 1.051, 95% CI 1.009-1.095, p=0.017). In patients with AHF treated with levosimendan, larger reductions in SBP after therapy are independently associated with in-hospital mortality. Monitoring SBP changes after levosimendan infusion may improve risk stratification and guide clinical decisions.

Keywords: Prognosis; hypotension; inotropic agents; outcomes; shock; systolic dysfunction.