• Nina Loretz, Christoph Becker, Seraina Hochstrasser, Kerstin Metzger, Katharina Beck, Jonas Mueller, Sebastian Gross, Alessia Vincent, Simon A Amacher, Raoul Sutter, Kai Tisljar, Philipp Schuetz, Luca Bernasconi, Peter Neyer, Hans Pargger, Stephan Marsch, and Sabina Hunziker.
• Department of Medical Communication and Psychosomatic Medicine, University Hospital Basel, Klingelbergstrasse 23, 4056 Basel, Switzerland. Electronic address: ninachiara.loretz@usb.ch.
• J Crit Care. 2022 Feb 1; 67: 57-65.

PurposeActivation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort.MethodsWe measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.Results120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p < 0.001) and a higher median kynurenine/tryptophan ratio (0.10 μmol/l [IQR 0.07 to 0.17] vs 0.07 μmol/l [IQR 0.05 to 0.1]; p < 0.001). In a model adjusted for age, gender and comorbidities, kynurenine (OR 1.16, 95% CI 1.05 to 1.27; p = 0.001) and kynurenine/tryptophan ratio (OR 1.19, 95% CI 1.08 to 1.31; p = 0.003) were significantly associated with mortality. Results were similar for neurological outcome.ConclusionsOur findings validate a previous study and show associations of the activation of the KP with unfavorable outcomes after CA. Future studies should evaluate whether therapeutic modulation of the KP may impact clinical outcomes after CA.Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

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