Key result
Sodium lactate increases cardiac output by ~1.5 L/min IV versus placebo in chronic HFrEF.
Why the study?
Although emerging evidence identifies lactate as an important metabolic substrate and signaling molecule, the acute hemodynamic effects of intravenous and oral lactate in patients with chronic heart failure remained unknown.
Does acute intravenous and oral sodium lactate administration improve cardiac output and hemodynamics compared with placebo in patients with chronic HFrEF?
RCT (n=12)
Double-blind
Randomized crossover
No
Does acute intravenous and oral sodium lactate administration improve cardiac output and hemodynamics compared with placebo in patients with chronic HFrEF?
In patients with chronic HFrEF on contemporary medical therapy, both intravenous and oral sodium lactate administration acutely improve cardiac output, systolic and diastolic function, and reduce afterload and cardiac filling pressures.
Answers are grounded in this paper and cite their sources.
Both IV and oral sodium lactate acutely raise cardiac output in chronic HFrEF; extends lactate's role as myocardial substrate to randomized data.
Lactate has traditionally been regarded as a harmful by-product of anaerobic metabolism, and elevated blood lactate concentrations are associated with adverse outcomes in acute heart failure and critical illness. However, emerging evidence identifies lactate as an important metabolic substrate and signaling molecule. The hemodynamic effects of lactate in patients with chronic heart failure remain unknown. To determine the acute hemodynamic effects of intravenous and oral lactate treatment in patients with heart failure. In a randomized, double-blind, crossover study, 12 patients with chronic heart failure with reduced ejection fraction underwent intravenous sodium lactate and isovolumic saline placebo infusion on one study day and oral sodium lactate and isocaloric placebo on a separate day. Hemodynamics were assessed hourly using pulmonary artery catheterization and echocardiography. The trial was registered at Clinicaltrials.gov (NCT06121323) released September 20th 2023. Intravenous and oral lactate administration increased blood lactate concentrations compared with placebo by 2.3 mmol/L ( P < 0.001) and 0.9 mmol/L ( P < 0.001), respectively. Intravenous lactate increased cardiac output by 1.5 L/min ( P < 0.001), and oral lactate by 0.4 L/min ( P = 0.01). Stroke volume and heart rate increased during intravenous administration (both P < 0.001), and heart rate increased during oral administration ( P < 0.001). Systemic vascular resistance decreased during intravenous lactate infusion ( P < 0.001), whereas pulmonary capillary wedge pressure ( P = 0.02) and central venous pressure ( P = 0.004) decreased during oral administration. LVOT velocity–time integral increased during both routes of administration and global longitudinal strain improved following intravenous lactate. Indices of diastolic function improved during lactate administration. In patients with chronic heart failure, lactate administration improved systolic and diastolic function and reduced afterload and cardiac filling pressures.
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Jespersen et al. (2026) conducted an RCT in Chronic heart failure with reduced ejection fraction (HFrEF) (n=12). Sodium lactate (intravenous and oral) vs. Isovolumic isotonic sodium chloride placebo (IV) and isocaloric, isovolumic maltodextrin placebo (oral) was evaluated on Cardiac output (CO) presented as the model-adjusted mean value of the three-hour infusion periods (MD 1.5 L/min (IV) and MD 0.4 L/min (oral), 95% CI 1.2-1.8, p=<0.001). Intravenous and oral sodium lactate increased cardiac output by 1.5 L/min (P<0.001) and 0.4 L/min (P=0.01), respectively, compared with placebo in chronic HFrEF patients.
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