Bolus-free low-dose levosimendan infusion for acute decompensated hypoperfused heart failure. (26th April 2021) - Baldetti, L
Abstract: Funding Acknowledgements: Type of funding sources: None. Aims and Methods Aim of this study was to assess the feasibility of a bolus-free, low-dose levosimendan infusion for acute decompensated heart failure (ADHF) with hypoperfusion. All consecutive patients who received levosimendan without intravenous bolus at our Department for ADHF in the last 6 months were included in this is a single-center retrospective study. To avoid abrupt drop in blood pressure, all patients started infusion at 0.01 mcg/kg/min, and gradual titration was achieved, up to 0.1 mcg/kg/min. Continuous variables are reported as medians (IQR), categorical as proportions. Paired measures were compared with the Wilcoxon signed-rank test. p-value was set at 5%. Analyses were performed using RStudio v1.3. Results: We included 26 patients [males 84.6%; age 72 (59-76) years]. Patients had severe LV dysfunction [LVEF of 20 (20-25)%] and moderate/severe RV dysfunction in 46.2%. Most patients were admitted for cardiogenic shock (26.9%) or low-output state (61.5%); baseline serum lactate was 1.6 (1.2-3.2) mmol/L. Etiology was ACS in 26.9% patients, worsening HF in 53.8%, and valvular disease in 26.9%. All patients required inotropes: 73.1% required adrenaline [max dose 0.10 (0.05-0.15) mcg/kg/min]; 50.0% required noradrenaline [max dose 0.10 (0.05-0.18) mcg/kg/min]; 26.9% received levosimendan alone [max dose 0.05 (0.03-0.10) mcg/kg/min]. Levosimendan was used in combination with adrenaline in 69.2%, after 3 (0-4) days of adrenaline initiation. Duration of levosimendan infusion was 3 (1-4) days. MCS was pursued in 69.2% [57.7% IABP, 15.4% Impella CP, and 3.8% VA-ECMO]. Oro-tracheal intubation was required in 50.0%, CVVHDF was required in 11.5% patients. No patient required levosimendan interruption for hypotension/arrhythmia. In-hospital mortality was 7.7%. One patients underwent successful LVAD implantation, and one patient was referred for HTx. Invasive hemodynamic data, before and during levosimendan, was available for 7 patients. Initiation of levosimendan led to a non-significant drop in SVR [14.8 (13.3-16.9) vs 19.5 (14.6-25.4) WU; p = 0.093], but SBP was unchanged (p = 0.470). Left ventricular systolic performance was improved: CI [2.6 (2.4-2.7) vs 2.2 (2.0-2.3) Lt/min/m²; p = 0.016]; CPO [0.9 (0.8-1.0) vs 0.8 (0.8-0.9) W; p = 0.031]. Mean PAP (p = 0.297), and PCWP (p = 0.149) remained unchanged. Notably, no significant adjustments in diuretic (p = 0.422) or adrenaline (p = 0.999) doses, IABP counterpulsation ratio (p = 0.999), or Impella flow (p = 0.999) were recorded between these longitudinal assessments. As a result of improved myocardial function, LVEF increased from admission to discharge [20 (20-25) vs 25 (20-32)%; p = 0.024]. Discussion: This preliminary study reports on a bolus-free, low-intensity levosimendan regimen for ADHF with hypoperfusion. Levosimendan improved indexes of myocardial performance. In this cohort, levosimendan often required concomitant inopressor and was started at a very low dose to avoid abrupt drop in blood pressure.