Systemic inflammation 72 hours after cardiac arrest is associated with poor neurological outcome and long term all-cause mortality - the prospective Norwegian Cardio-Respiratory Arrest Study (NORCAST)

Abstract

Abstract Background Post-cardiac arrest (CA) anoxic brain injury seems to involve local and systemic inflammation. The interleukin (IL)-1/IL-6 pathway has gained increased interest both as prognostic markers and as possible targets for intervention. Purpose To evaluate the associations of the IL-1 receptor family, IL-6 and procalcitonin as a marker of systemic inflammation, with neurological outcome and long-term all-cause mortality in patients with out-of-hospital cardiac arrest (OHCA). Methods In this prospective observational study, we included 259 adult patients (> 18 years) hospitalized after OHCA. Blood sampling were performed on admission and 72 hours after cardiac arrest. IL-1 receptor antagonist (IL-1ra), ST2 (soluble interleukin 1 receptor-like 1), IL-6 and procalcitonin were analysed on admission and 72 hours after cardiac arrest. Neurological outcome was measured as cerebral performance category score (CPC score) assessed by two experienced neurologists six months after OHCA. CPC score was dichotomized into good (CPC score 1-2) or poor (CPC score 3-5) neurological outcome. All-cause mortality was registered after median 10.7-year follow-up. Results Patients with poor neurological outcome six months after CA (red bars) had significant higher levels of IL-6 (p = 0.002), IL-1Ra (p < 0.001), ST2 (p < 0.001) and procalcitonin (p < 0.001) 72 hours after CA (Fig. 1). High levels of IL-6, IL-1Ra, ST2 and procalcitonin measured 72 hours after cardiac arrest were significantly associated with long-term all-cause mortality (Fig. 2). Conclusions High levels of inflammatory biomarkers 72 hours after CA were significantly associated with poor neurological outcome and long-term all-cause mortality.Figure 1Figure 2