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Published on: May 26, 2023
Comparative analysis of inflammatory response on post resuscitation syndrome in extracorporeal cardiopulmonary
Kostiantyn Kozakov1, Zdenek Provaznik1, Maik Foltan1
1Department of Cardiothoracic Surgery, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg 93053, Germany.
Background:
Extracorporeal life support (ECLS) is increasingly employed for severe respiratory or cardiac failure, alongside a rising adoption of extracorporeal cardiopulmonary resuscitation (eCPR). Despite increased adoption, limited evidence underscores possible cytokines' pivotal role in the inflammatory response during ECLS.
Methods:
The study involved 546 eCPR patients using veno-arterial extracorporeal membrane oxygenation from 2013 to 2023. Categorized into in-hospital eCPR (IHCA, 358 patients) and out-of-hospital eCPR (OHCA, 188 patients) groups, a retrospective analysis explored associations among interleukin 6 (IL6), interleukin 8 (IL8), tumor necrosis factor-alpha (TNF-alpha), soluble interleukin-2 receptor (sIL2R), and pivotal post-resuscitation syndrome (PRS) components. Cytokine dynamics were assessed before and after ECLS initiation.
Results:
CPR-to-ECLS time was significantly longer in the OHCA group (p = 0.009), correlating with elevated IL6 and IL8 levels. The IHCA group showed more favorable neurological outcomes (p < 0.001), but presented with a higher incidence of multiple organ failure (p < 0.001) compared to the OHCA group. The IHCA group exhibited pronounced IL6 and IL8 levels prior to ECLS initiation significantly decreasing post-ECLS initiation (p = 0.01 and p = 0.008), whereas OHCA patients showed peak levels of IL6 and IL8 during the course of ECLS (p < 0.001).
Conclusion:
IL6 and IL8 are associated with key elements of the post-resuscitation syndrome (neurological outcome, organ dysfunction and hemodynamic status) in patients undergoing eCPR for refractory cardiac arrest, possibly providing a predictive ability of organ dysfunction in OHCA patients without a preceding pro-inflammatory burden.

