The availability of circulating biomarkers that helps to identify early out-of-hospital cardiac arrest survivors who are at increased risk of long-term mortality remains challenging. Our aim was to prospectively study the association between copeptin and 1-year mortality in patients with out-of-hospital cardiac arrest admitted in a tertiary cardiac arrest center.
Retrospective monocenter study.
Tertiary cardiac arrest center in Paris, France.
Copeptin was assessed at admission and day 3. Pre- and intrahospital factors associated with 1-year mortality were analyzed by multivariate Cox proportional analysis.
Two hundred ninety-eight consecutive out-of-hospital cardiac arrest patients (70.3% male; median age, 60.2 yr [49.9–71.4]) were admitted in a tertiary cardiac arrest center in Paris (France). After multivariate analysis, higher admission copeptin was associated with 1-year mortality with a threshold effect (hazard ratio5th vs 1st quintile = 1.64; 95% CI, 1.05–2.58; p = 0.03). Day 3 copeptin was associated with 1-year mortality in a dose-dependent manner (hazard ratio2nd vs 1st quintile = 1.87; 95% CI, 1.00–3.49; p = 0.05; hazard ratio3rd vs 1st quintile = 1.92; 95% CI, 1.02–3.64; p = 0.04; hazard ratio4th vs 1st quintile = 2.12; 95% CI, 1.14–3.93; p = 0.02; and hazard ratio5th vs 1st quintile = 2.75; 95% CI, 1.47–5.15; p < 0.01; p for trend < 0.01). For both admission and day 3 copeptin, association with 1-year mortality existed for out-of-hospital cardiac arrest of cardiac origin only (p for interaction = 0.05 and < 0.01, respectively). When admission and day 3 copeptin were mutually adjusted, only day 3 copeptin remained associated with 1-year mortality in a dose-dependent manner (p for trend = 0.01).
High levels of copeptin were associated with 1-year mortality independently from prehospital and intrahospital risk factors, especially in out-of-hospital cardiac arrest of cardiac origin. Day 3 copeptin was superior to admission copeptin: this could permit identification of out-of-hospital cardiac arrest survivors at increased risk of mortality and allow for close observation of such patients.
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1Medical Intensive Care Unit, Cochin Hospital, APHP, Paris, France.
2Paris Descartes University, Sorbonne Paris Cité, Paris, France.
3Sudden Death Expertise Centre, INSERM U970, Paris Cardiovascular Research Center, Paris, France.
4Emergency Department, Cochin Hospital, APHP, Paris, France.
5Department of Automated Biological Diagnosis, Cochin Hospital, APHP, Paris, France.
* See also p. 503.
Drs. Empana and Cariou are co-last authors of this article.
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Dr. Geri received support for the development of educational presentations from the Bristol Myers Squibb. His institution received support for travel from the Astellas. Dr. Chenevier-Gobeaux lectured for Biomerieux. Dr. Jouven’s institution received grant support from the Institut National de la Santé et de la Recherche Médicale. Dr. Mira served as a board member for Merck Sharp & Dohme-Chibret (MSD) (board of AMARCAND study) and Laboratoire français du fractionnement et des biotechnologies (LFB) (scientific committee); consulted for Astellas and Gilead; lectured for Astellas, LFB, Eli Lilly, and Brahms; and received support for the development of educational presentations from MSD. Dr. Pène lectured for the Roche. His institution received grant support from the Société de Réanimation de Langue Française and European Society of Intensive Care Medicine. Dr. Empana consulted for the Lundbeck factory. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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