824 HEMODYNAMIC EFFECTS OF LEVOSIMENDAN IN PATIENTS WITH ACUTE HEART FAILURE AND SEVERE RENAL FAILURE. (15th December 2022)

• Record Type: Journal Article
• Authors: Baldetti, Luca; Romagnolo, Davide; Peveri, Beatrice; Frias, André; Calvo, Francesco; Gramegna, Mario; Pazzanese, Vittorio; Sacchi, Stefania; Ajello, Silvia; Scandroglio, Anna Mara
• Is Part Of: European heart journal supplements. Volume 24(2022)Supplement K
• Publication Date: 2022-12-15
• Subjects: Cardiology -- Periodicals; Cardiology -- Europe -- Periodicals; 616.12005
• DOI: 10.1093/eurheartjsupp/suac121.001
• Languages: English
• ISSNs: 1520-765X

Abstract

Abstract: Background: The inodilator levosimendan has shown improved outcomes in acute heart failure (AHF) and cardiac surgery. Its hemodynamic effect is persistent, owing to a long (70-80 hours) elimination half-life of its active metabolites. No robust data is available of the use of levosimendan in patients with severe renal failure (SRF), thus its use is contraindicated in patients with estimated glomerular filtration rate (eGFR≤30 mL/min). Hypothesis: Different pharmacokinetics due to renal failure may alter levosimendan active metabolites elimination, causing more pronounced hemodynamic effects. We aimed to characterize the hemodynamic effect of levosimendan in a real-world cohort of SRF patients. Methods: We reviewed patients who received levosimendan (12.5 mg) for AHF or cardiogenic shock in our CICU (N=132), excluding those without invasive hemodynamics (n=85), and those without data before and during levosimendan infusion (n=11), a total of 36 patients were finally included in this analysis. We compared hemodynamics before and during levosimendan infusion in the study cohort with CKD-EPI eGFR≤30 mL/min/1.73 m 2 or CRRT and those without. Results: Patients with low eGFR (n=11) were older, they had similar LVEF and invasive hemodynamics before levosimendan infusion to the higher eGFR cohort. Visual inspection of the LOESS regression plots (Figure ) revealed an higher drop in mean arterial pressure (MAP) and diastolic arterial pressure (DAP) in the low eGFR cohort. The maximum drop was observed at day 4 from levosimendan initiation, invasive hemodynamics at this timepoint revealed a lower DAP (44.6±8.8 vs 62.6±11.9 mmHg; p =0.014) and a tendentially lower MAP (73.6±5.5 vs 84.4±11.5 mmHg; p =0.079) while systolic arterial pressure (125.0±24.6 vs 121.3±21.8 mmHg; p =0.779), cardiac index (2.1±0.5 vs 2.5±0.7 L/m 2 ; p =0.211), and mean pulmonary arterial pressure (25.8±8.3 vs 24.8±9.6 mmHg; p =0.844) did not differ between groups. In-hospital death was not different in the two cohorts (27.3 vs 16.0%; p =0.650). Conclusions: Patient with eGFR≤30 mL/min/1.73 m 2 demonstrated a higher drop in DAP and MAP four days after levosimendan infusion start, without impact on hospital mortality. These findings may suggest a more pronounced hemodynamic effect of levosimendan in patients with SRF, possibly due to altered pharmacokinetics of its active metabolites.