Cardiovascular effects of lactate infusion in cardiogenic shock complicating acute myocardial infarction

TY - ABST

T1 - Cardiovascular effects of lactate infusion in cardiogenic shock complicating acute myocardial infarction

AU - Hørsdal, Oskar Kjærgaard

AU - Ellegaard, Mark Stoltenberg

AU - Larsen, Alexander Møller

AU - Guldbrandsen, Halvor Østerby

AU - Moeslund, Niels

AU - Wiggers, Henrik

AU - Nielsen, Bent Roni Ranghøj

AU - Gopalasingam, Nigopan

AU - Berg-Hansen, Kristoffer

PY - 2025

Y1 - 2025

N2 - Background Cardiogenic shock complicating myocardial infarction (AMI-CS) is charactirized by reduced cardiac output (CO), poor end-organ perfusion, and high mortality. Current medical therapies have not significantly improved survival rates. Lactate, though often considered a toxic byproduct of anaerobic metabolism, serves as an oxygen efficient alternative, readily oxidizable substrate for the myocardium. Lactate infusion has been shown to improve CO and left ventricular ejection fraction (LVEF) in acute heart failure patients and in experimental septic shock models while the effects of treatment with lactate in AMI-CS remains unexplored. This study aimed to elucidate the cardiovascular effects of lactate infusion in a porcine model of AMI-CS. Methods In a randomized, assessor-blinded design, we studied 20 female Danish Landrace pigs (60 kg). AMI-CS was induced by left main coronary artery microsphere injections. Predefined criteria for AMI-CS were a 30% reduction in CO or mixed venous saturation (SvO2). Pigs were randomized to receive either intravenous lactate infusion or a matched control saline for 180 minutes (n=10 per group). Hemodynamic measurements were obtained by right and left heart catheterisation. The primary endpoint was CO through 180 minutes of lactate infusion compared with control. Results Compared with control, lactate infusion increased arterial lactate levels increased by 5.1 mmol/L (95% CI 4.4 to 5.8; P<0.001) (Fig. 1). CO increased by 0.7 L/min (95% CI 0.4 to 1.0; P<0.001), driven by increased stroke volume of 7 mL (95% CI 3 to 11; P=0.003), while heart rate was unchanged (P=0.71) (Fig. 2). SvO2 increased by 7 %-points (95% CI 2 to 12; P=0.018) while the venous-to-arterial CO2 gap (P(v-a)CO2 decreased (P=0.004), indicating improved tissue perfusion. Pulmonary vascular resistance was reduced (P=0.031), while systemic vascular resistance remained unaltered (P=0.275). Systemic and pulmonary blood pressures and rate-pressure-product showed no significant differences between the two treatments. LV end-systolic elastance (contractility), was higher during lactate infusion (P=0.048), along with dP/dt(max) (P=0.041) and LVEF (P=0.009). While arterial elastance (afterload) was not significantly reduced (P=0.121), ventriculo-arterial coupling improved significantly by -0.67 (95% CI -1.13 to -0.21; P=0.012). Cardiac mechano-energetics were significantly improved with increased cardiac efficiency (P=0.003) while pressure-volume area was unchanged. Finally, lactate infusion resulted in increased diuresis (P=0.016) and alkalosis (P<0.001). Conclusions Lactate infusion significantly enhanced CO and peripheral tissue perfusion in a porcine model of AMI-CS. This was driven by increased stroke volume and enhanced LV contractility, without changes in heart rate or systemic blood pressure. Further studies are warranted to explore the long-term effects of lactate infusion and its potential integration with existing therapies for AMI-CS.

AB - Background Cardiogenic shock complicating myocardial infarction (AMI-CS) is charactirized by reduced cardiac output (CO), poor end-organ perfusion, and high mortality. Current medical therapies have not significantly improved survival rates. Lactate, though often considered a toxic byproduct of anaerobic metabolism, serves as an oxygen efficient alternative, readily oxidizable substrate for the myocardium. Lactate infusion has been shown to improve CO and left ventricular ejection fraction (LVEF) in acute heart failure patients and in experimental septic shock models while the effects of treatment with lactate in AMI-CS remains unexplored. This study aimed to elucidate the cardiovascular effects of lactate infusion in a porcine model of AMI-CS. Methods In a randomized, assessor-blinded design, we studied 20 female Danish Landrace pigs (60 kg). AMI-CS was induced by left main coronary artery microsphere injections. Predefined criteria for AMI-CS were a 30% reduction in CO or mixed venous saturation (SvO2). Pigs were randomized to receive either intravenous lactate infusion or a matched control saline for 180 minutes (n=10 per group). Hemodynamic measurements were obtained by right and left heart catheterisation. The primary endpoint was CO through 180 minutes of lactate infusion compared with control. Results Compared with control, lactate infusion increased arterial lactate levels increased by 5.1 mmol/L (95% CI 4.4 to 5.8; P<0.001) (Fig. 1). CO increased by 0.7 L/min (95% CI 0.4 to 1.0; P<0.001), driven by increased stroke volume of 7 mL (95% CI 3 to 11; P=0.003), while heart rate was unchanged (P=0.71) (Fig. 2). SvO2 increased by 7 %-points (95% CI 2 to 12; P=0.018) while the venous-to-arterial CO2 gap (P(v-a)CO2 decreased (P=0.004), indicating improved tissue perfusion. Pulmonary vascular resistance was reduced (P=0.031), while systemic vascular resistance remained unaltered (P=0.275). Systemic and pulmonary blood pressures and rate-pressure-product showed no significant differences between the two treatments. LV end-systolic elastance (contractility), was higher during lactate infusion (P=0.048), along with dP/dt(max) (P=0.041) and LVEF (P=0.009). While arterial elastance (afterload) was not significantly reduced (P=0.121), ventriculo-arterial coupling improved significantly by -0.67 (95% CI -1.13 to -0.21; P=0.012). Cardiac mechano-energetics were significantly improved with increased cardiac efficiency (P=0.003) while pressure-volume area was unchanged. Finally, lactate infusion resulted in increased diuresis (P=0.016) and alkalosis (P<0.001). Conclusions Lactate infusion significantly enhanced CO and peripheral tissue perfusion in a porcine model of AMI-CS. This was driven by increased stroke volume and enhanced LV contractility, without changes in heart rate or systemic blood pressure. Further studies are warranted to explore the long-term effects of lactate infusion and its potential integration with existing therapies for AMI-CS.

U2 - 10.1093/ehjacc/zuaf044.160

DO - 10.1093/ehjacc/zuaf044.160

M3 - Conference abstract in journal

SN - 2048-8726

VL - 14

JO - European Heart Journal: Acute Cardiovascular Care

JF - European Heart Journal: Acute Cardiovascular Care

IS - Supplement 1

T2 - European Society of Cardiology: Acute CardioVascular Care Congress 2025

Y2 - 14 March 2025 through 15 March 2025

ER -