Georg Fuernau1, Steffen Desch2, Suzanne de Waha-Thiele3, Ingo Eitel3, Franz-Josef Neumann4, Marcus Hennersdorf5, Stephan B Felix6, Andreas Fach7, Michael Böhm8, Janine Pöss9, Christian Jung10, Taoufik Ouarrak11, Steffen Schneider11, Karl Werdan12, Uwe Zeymer13, Holger Thiele9. 1. Medical Clinic II (Cardiology, Angiology, Intensive Care Medicine), University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany. Electronic address: georg.fuernau@uksh.de. 2. German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany; Department of Internal Medicine/Cardiology, Heart Center Leipzig at University of Leipzig, Leipzig and Leipzig Heart Institute, Leipzig, Germany. 3. Medical Clinic II (Cardiology, Angiology, Intensive Care Medicine), University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany. 4. Department of Cardiology, Bad Krozingen Heart Center, University of Freiburg, Bad Krozingen, Germany. 5. Department of Internal Medicine I, SLK Kiniken Heilbronn, Heilbronn, Germany. 6. Department of Internal Medicine B, University of Greifswald, Greifswald, Germany. 7. Department of Cardiology/Angiology, Klinikum Links der Weser, Bremen, Germany. 8. Department of Internal Medicine III, University of Homburg, Homburg/Saar, Germany. 9. Department of Internal Medicine/Cardiology, Heart Center Leipzig at University of Leipzig, Leipzig and Leipzig Heart Institute, Leipzig, Germany. 10. Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Düsseldorf, Düsseldorf, Germany. 11. Institut für Herzinfarktforschung, Ludwigshafen, Germany. 12. Department of Internal Medicine III, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany. 13. Institut für Herzinfarktforschung, Ludwigshafen, Germany; Medizinische Klinik B, Klinikum Ludwigshafen, Ludwigshafen, Germany.
Abstract
OBJECTIVES: This study sought to compare single lactate values at admission (L1) and after 8 h (L2) with lactate clearance (LC) for mortality prediction in cardiogenic shock (CS). BACKGROUND: Early estimation of prognosis in CS complicating acute myocardial infarction is crucial for tailored treatment selection. Arterial lactate is the most widely used point-of-care parameter in CS. In septic shock, lactate reduction over time-LC-has been extensively investigated. However, in CS, only limited data exist, and the prognostic value of LC is unknown. METHODS: This study is a subanalysis of the IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trial and the corresponding registry. Lactate levels were prospectively collected. All-cause mortality at 30 days was assessed as primary endpoint. RESULTS: For 671 of 783 (85.7%) patients, L1 and L2 values were available. The area under the receiver-operating characteristic curve (L1: 0.69; L2: 0.76; LC: 0.59) showed no difference between L1 and LC (p = 0.20). In contrast, L2 was a significantly better predictive parameter than L1 or LC (p < 0.001 for both). In multivariable stepwise Cox regression analysis, L2 ≥3.1 mmol/l (best cutoff value by Youden index) and LC <-3.45%/h remained independently predictive for time to death (p < 0.001 for both), with L2 showing the highest chi-square test score (42.1) and hazard ratio (2.89; 95% confidence interval: 2.10 to 3.97). CONCLUSIONS: Arterial lactate after 8 h is superior in mortality prediction in comparison with baseline lactate and LC. A cutoff value of 3.1 mmol/l for lactate after 8 h showed the best discrimination for assessing early prognosis in CS and may serve as new treatment goal. (Intraaortic Balloon Pump in Cardiogenic Shock II [IABP-SHOCK II]; NCT00491036).
OBJECTIVES: This study sought to compare single lactate values at admission (L1) and after 8 h (L2) with lactate clearance (LC) for mortality prediction in cardiogenic shock (CS). BACKGROUND: Early estimation of prognosis in CS complicating acute myocardial infarction is crucial for tailored treatment selection. Arterial lactate is the most widely used point-of-care parameter in CS. In septic shock, lactate reduction over time-LC-has been extensively investigated. However, in CS, only limited data exist, and the prognostic value of LC is unknown. METHODS: This study is a subanalysis of the IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trial and the corresponding registry. Lactate levels were prospectively collected. All-cause mortality at 30 days was assessed as primary endpoint. RESULTS: For 671 of 783 (85.7%) patients, L1 and L2 values were available. The area under the receiver-operating characteristic curve (L1: 0.69; L2: 0.76; LC: 0.59) showed no difference between L1 and LC (p = 0.20). In contrast, L2 was a significantly better predictive parameter than L1 or LC (p < 0.001 for both). In multivariable stepwise Cox regression analysis, L2 ≥3.1 mmol/l (best cutoff value by Youden index) and LC <-3.45%/h remained independently predictive for time to death (p < 0.001 for both), with L2 showing the highest chi-square test score (42.1) and hazard ratio (2.89; 95% confidence interval: 2.10 to 3.97). CONCLUSIONS: Arterial lactate after 8 h is superior in mortality prediction in comparison with baseline lactate and LC. A cutoff value of 3.1 mmol/l for lactate after 8 h showed the best discrimination for assessing early prognosis in CS and may serve as new treatment goal. (Intraaortic Balloon Pump in Cardiogenic Shock II [IABP-SHOCK II]; NCT00491036).
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