Key result
Consumptive coagulopathy phenotypes at ECPR initiation had lower survival than preserved coagulation (0% and 8.6% vs 33.1%; phenotype 2 vs 3 OR 0.25, 95% CI 0.12-0.55).
Why the study?
Coagulopathy is frequent in refractory out-of-hospital cardiac arrest patients treated with extracorporeal cardiopulmonary resuscitation, yet its prognostic significance and heterogeneity remain poorly characterised.
Are coagulation phenotypes identified at ECPR initiation associated with survival, neurological outcomes, and bleeding complications in patients with refractory out-of-hospital cardiac arrest?
Cohort (n=360)
Are coagulation phenotypes identified at ECPR initiation associated with survival, neurological outcomes, and bleeding complications in patients with refractory out-of-hospital cardiac arrest?
Unsupervised clustering at ECPR initiation identifies three distinct coagulation phenotypes in refractory OHCA patients that correlate with ischemic injury severity and strongly predict survival, neurological recovery, and bleeding risk.
Answers are grounded in this paper and cite their sources.
Coagulation phenotypes may stratify ECPR prognosis in refractory OHCA; leaves open clinical utility pending prospective validation.
INTRODUCTION: Coagulopathy is frequent in refractory out-of-hospital cardiac arrest (OHCA) patients treated with extracorporeal cardiopulmonary resuscitation (ECPR), yet its prognostic significance and heterogeneity remain poorly characterised. OBJECTIVES: To characterize coagulopathy at ECPR initiation, identify coagulation phenotypes, evaluate their association with outcomes, and describe their temporal evolution. METHODS: All consecutive refractory OHCAs treated with ECPR (2013-2024) were included. Phenotypes were identified by unsupervised K-means clustering on PT-INR, aPTT, platelets, antithrombin, fibrinogen, and D-dimer measured at ECPR initiation. Associations with survival, neurological outcomes, and complications were assessed by multivariable logistic regression. RESULTS: Of 406 ECPR patients, 360 had coagulation data for analysis (initial shockable rhythm 67%, low-flow 70 min [IQR 58-81]). Three phenotypes were identified: severe consumptive coagulopathy (phenotype 1, n=49, 13.6%), mild consumptive coagulopathy (phenotype 2, n=175, 48.6%), and preserved coagulation (phenotype 3, n=136, 37.8%). Phenotype 1 had no survivors, compared with survival of 8.6% and 33.1% in phenotypes 2 and 3, respectively; favourable neurological outcome was achieved in 0%, 5.1%, and 17.6%. Phenotype severity correlated with ischaemic burden (lactate, arterial pH, end-tidal CO2, and low-flow duration). On multivariable analysis, phenotype 2 was associated with lower survival (OR 0.25, 95% CI 0.12-0.55) and favourable neurological outcome (OR 0.31, 95% CI 0.12-0.81) versus phenotype 3. Bleeding incidence rates were 38, 12, and 2.5 events per 100 patient-days in phenotype 1, 2, and 3, respectively (all p < 0.001). CONCLUSIONS: Three distinct coagulation phenotypes at ECPR initiation were independently associated with survival and neurological outcome and appear to reflect ischaemic injury severity. These findings require validation in independent cohorts before clinical application.
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Scquizzato et al. (2026) conducted a cohort in Refractory out-of-hospital cardiac arrest (OHCA) treated with extracorporeal cardiopulmonary resuscitation (ECPR) (n=360). Mild consumptive coagulopathy (phenotype 2) and severe consumptive coagulopathy (phenotype 1) at ECPR initiation vs. Preserved coagulation (phenotype 3) at ECPR initiation was evaluated on Survival (OR 0.25, 95% CI 0.12-0.55). Consumptive coagulopathy phenotypes at ECPR initiation had lower survival than preserved coagulation (0% and 8.6% vs 33.1%; phenotype 2 vs 3 OR 0.25, 95% CI 0.12-0.55).
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