Abstract
The aim was to investigate blood concentrations of copeptin and the prognostication in 24 versus 48 hours of targeted temperature management (TTM) in patients resuscitated after out-of-hospital cardiac arrest. This is an exploratory biomarker substudy of the trial entitled; “Targeted temperature management for 48 vs 24 hours and neurologic outcome after out-of-hospital-cardiac-arrest: A randomized clinical trial.” Patients were randomized to target temperature of 33°C ± 1°C for 24 (TTM24) or 48 (TTM48) hours. The primary outcome was copeptin concentrations compared with TTM at admission, 24, 48, and 72 hours (t24, t48, and t72) after reaching target temperature. Secondary outcomes were the association between copeptin and cerebral performance category (CPC) score after 6 months, and copeptin level between cerebral or noncerebral causes of death. Blood samples from 117 patients were analyzed from two Scandinavian sites. No significant differences in copeptin concentrations were found between TTM24 versus TTM48 at admission 211.3 μg/L (148–276.6) versus 179.8 μg/L (127–232.6) (p = 0.45), t24: 23.3 μg/L (16.5–30.2) versus 18.6 μg/L (13.3–23.9) (p = 0.25), t48: 28.8 μg/L (20.6–36.9) versus 19.7 μg/L (14.3–25.1) (p = 0.06), and t72: 23.3 μg/L (13.8–26.8) versus 31.6 μg/L (22–41.2) (p = 0.05). Copeptin concentrations were significantly higher in poor neurological outcome group at t24, t48, and t72 (p < 0.01), but not at admission (p = 0.19). The prognostic ability of copeptin (area under the receiver operating characteristic curve) was at admission: 0.59 (95% confidence intervals: 0.46–0.72), t24: 0.74 (0.63–0.86), t48: 0.8 (0.7–0.9), and t72: 0.76 (0.65–0.87). Copeptin levels were not significantly different in noncerebral compared with cerebral causes at admission: p = 0.41, t24: p = 0.52, t48: p = 0.15, and t72: p = 0.38. There were no differences in the level of copeptin in TTM24 versus TTM48. Blood concentrations of copeptin were associated with CPC at 6 months, and no association between levels of copeptin and cerebral versus noncerebral causes of death was observed.
Get full access to this article
View all access options for this article.
