Coenzyme Q10 levels are low and associated with increased mortality in post-cardiac arrest patients.

Abstract

Survival after cardiac arrest (CA) is limited by the profound neurologic insult from ischemia-reperfusion injury. Therapeutic options are limited. Previous data suggest a benefit of coenzyme Q(10) (CoQ(10)) in post-arrest patients. We hypothesized that plasma CoQ(10) levels would be low after CA and associated with poorer outcomes. Prospective observational study of post-arrest patients presenting to a tertiary care center. CoQ(10) levels were drawn 24h after return of spontaneous circulation (ROSC) and compared to healthy controls. Levels of inflammatory cytokines and biomarkers were analyzed. Primary endpoints were survival to discharge and neurologic status at time of discharge. 23 CA subjects and 16 healthy controls were enrolled. CoQ(10) levels in CA patients (0.28 μmol L(-1), inter-quartile range (IQR): 0.22-0.39) were significantly lower than in controls (0.75 μmol L(-1), IQR: 0.61-1.08, p<0.0001). The mean CoQ(10) level in CA patients who died was significantly lower than in those who survived (0.27 vs 0.47 μmol L(-1), p = 0.007). There was a significant difference in median CoQ(10) level between patients with a good vs poor neurological outcome (0.49 μmol L(-1), IQR: 0.30-0.67 vs 0.27 μmol L(-1), IQR: 0.21-0.30, p = 0.02). CoQ(10) was a statistically significant predictor of poor neurologic outcome (adjusted p = 0.02) and in-hospital mortality (adjusted p = 0.026). CoQ(10) levels are low in human subjects with ROSC after cardiac arrest as compared to healthy controls. CoQ(10) levels were lower in those who died, as well as in those with a poor neurologic outcome.