Distinct Coagulation Phenotypes and Long-Term Neurological Outcomes in Post-Cardiac Arrest Syndrome: A Latent Class Analysis of a 9-Year Single-Center Cohort

<b>Background/Objectives:</b> Post-cardiac arrest syndrome (PCAS) induces systemic ischemia-reperfusion injury accompanied by sepsis-like coagulopathy. This coagulopathy presents heterogeneously, yet distinct coagulation phenotypes and their impact on hypoxic-ischemic brain injury (HIBI) remain poorly defined. We aimed to identify coagulation phenotypes using latent class analysis (LCA) and assess their association with 6-month neurological outcomes. <b>Methods:</b> We retrospectively analyzed adult out-of-hospital cardiac arrest (OHCA) patients treated with targeted temperature management (TTM) between 2011 and 2019 from a prospective registry at a tertiary academic center. LCA was performed using coagulation biomarkers measured at admission and 24 h post-return of spontaneous circulation: D-dimer, fibrinogen, antithrombin III (ATIII), platelet count, and PT-INR. The primary outcome was poor neurological outcome (Cerebral Performance Category 3-5) at 6 months. Secondary outcomes included in-hospital mortality and cerebral edema severity assessed by gray-to-white matter ratio (GWR) on brain CT. <b>Results:</b> Among 325 patients, LCA identified three phenotypes: Class 1 (Preserved Coagulation, 36.9%), Class 2 (Hypercoagulable State, 41.5%) characterized by elevated D-dimer with preserved fibrinogen and ATIII, and Class 3 (Consumptive Coagulopathy, 21.5%) marked by profound D-dimer elevation with fibrinogen <150 mg/dL and ATIII <60%. Class 3 exhibited the lowest GWR and highest neuron-specific enolase levels. In multivariable analysis adjusting for age, low-flow time, initial rhythm, and lactate, Class 3 independently predicted poor neurological outcome (adjusted OR 4.52; 95% CI 2.15-9.48), whereas Class 2 did not. <b>Conclusions:</b> PCAS-related coagulopathy is heterogeneous. A consumptive coagulopathy phenotype identifies a high-risk subgroup associated with severe brain injury and poor long-term neurological outcomes. Early identification of this phenotype may enable targeted prognostication and guide future phenotype-specific interventional strategies.