Matthias Ebner1, Charlotta F Pagel2, Carmen Sentler2, Veli-Pekka Harjola3, Héctor Bueno4, Markus H Lerchbaumer5, Karl Stangl6, Burkert Pieske7, Gerd Hasenfuß8, Stavros V Konstantinides9, Mareike Lankeit10. 1. Department of Cardiology and Angiology, Campus Charité Mitte (CCM), Charité - University Medicine Berlin, Germany; German Center for Cardiovascular Research (DZHK), Partner site Berlin, Germany. 2. Clinic of Cardiology and Pneumology, University Medical Center Göttingen, Germany. 3. University of Helsinki, Emergency Medicine, Department of Emergency Medicine and Services, Helsinki University Hospital, Helsinki, Finland. 4. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Cardiology Department, Hospital Universitario 12 de Octubre and Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain; Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain. 5. Department of Radiology, Campus Charité Mitte (CCM), Charité - University Medicine Berlin, Germany. 6. Department of Cardiology and Angiology, Campus Charité Mitte (CCM), Charité - University Medicine Berlin, Germany. 7. German Center for Cardiovascular Research (DZHK), Partner site Berlin, Germany; Department of Internal Medicine and Cardiology, Campus Virchow Klinikum (CVK), Charité - University Medicine Berlin, Germany; Berlin Institute of Health, Berlin, Germany. 8. Clinic of Cardiology and Pneumology, University Medical Center Göttingen, Germany; German Center for Cardiovascular Research (DZHK), Partner site Göttingen, Germany. 9. Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Germany; Department of Cardiology, Democritus University of Thrace, Alexandroupolis, Greece. 10. German Center for Cardiovascular Research (DZHK), Partner site Berlin, Germany; Clinic of Cardiology and Pneumology, University Medical Center Göttingen, Germany; Department of Internal Medicine and Cardiology, Campus Virchow Klinikum (CVK), Charité - University Medicine Berlin, Germany; Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Germany. Electronic address: mareike.lankeit@charite.de.
Abstract
BACKGROUND: Arterial lactate is an established risk marker in patients with pulmonary embolism (PE). However, its clinical applicability is limited by the need of an arterial puncture. In contrast, venous lactate can easily be measured from blood samples obtained via routine peripheral venepuncture. METHODS: We investigated the prognostic value of venous lactate with regard to in-hospital adverse outcomes and mortality in 419 consecutive PE patients enrolled in a single-center registry between 09/2008 and 09/2017. RESULTS: An optimised venous lactate cut-off value of 3.3 mmol/l predicted both, in-hospital adverse outcome (OR 11.0 [95% CI 4.6-26.3]) and all-cause mortality (OR 3.8 [95%CI 1.3-11.3]). The established cut-off value for arterial lactate (2.0 mmol/l) and the upper limit of normal for venous lactate (2.3 mmol/l) had lower prognostic value for adverse outcomes (OR 3.6 [95% CI 1.5-8.7] and 5.7 [95% CI 2.4-13.6], respectively) and did not predict mortality. If added to the 2019 European Society of Cardiology (ESC) algorithm, venous lactate <2.3 mmol/l was associated with a high negative predictive value (0.99 [95% CI 0.97-1.00]) for adverse outcomes in intermediate-low-risk patients, whereas levels ≥3.3 mmol/l predicted adverse outcomes in the intermediate-high-risk group (OR 5.2 [95% CI 1.8-15.0]). CONCLUSION: Venous lactate above the upper limit of normal was associated with increased risk for adverse outcomes and an optimised cut-off value of 3.3 mmol/l predicted adverse outcome and mortality. Adding venous lactate to the 2019 ESC algorithm may improve risk stratification. Importantly, the established cut-off value for arterial lactate has limited specificity in venous samples and should not be used.
BACKGROUND: Arterial lactate is an established risk marker in patients with pulmonary embolism (PE). However, its clinical applicability is limited by the need of an arterial puncture. In contrast, venous lactate can easily be measured from blood samples obtained via routine peripheral venepuncture. METHODS: We investigated the prognostic value of venous lactate with regard to in-hospital adverse outcomes and mortality in 419 consecutive PE patients enrolled in a single-center registry between 09/2008 and 09/2017. RESULTS: An optimised venous lactate cut-off value of 3.3 mmol/l predicted both, in-hospital adverse outcome (OR 11.0 [95% CI 4.6-26.3]) and all-cause mortality (OR 3.8 [95%CI 1.3-11.3]). The established cut-off value for arterial lactate (2.0 mmol/l) and the upper limit of normal for venous lactate (2.3 mmol/l) had lower prognostic value for adverse outcomes (OR 3.6 [95% CI 1.5-8.7] and 5.7 [95% CI 2.4-13.6], respectively) and did not predict mortality. If added to the 2019 European Society of Cardiology (ESC) algorithm, venous lactate <2.3 mmol/l was associated with a high negative predictive value (0.99 [95% CI 0.97-1.00]) for adverse outcomes in intermediate-low-risk patients, whereas levels ≥3.3 mmol/l predicted adverse outcomes in the intermediate-high-risk group (OR 5.2 [95% CI 1.8-15.0]). CONCLUSION: Venous lactate above the upper limit of normal was associated with increased risk for adverse outcomes and an optimised cut-off value of 3.3 mmol/l predicted adverse outcome and mortality. Adding venous lactate to the 2019 ESC algorithm may improve risk stratification. Importantly, the established cut-off value for arterial lactate has limited specificity in venous samples and should not be used.