The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury.

Abstract

Cardiac dysfunction is frequently observed after severe traumatic brain injury (sTBI); however, its significance is poorly understood. Our study sought to elucidate the association of cardiac troponin I (cTnI) elevation with all-cause in-hospital mortality following isolated sTBI (brain Abbreviated Injury Scale score ≥3 and admission Glasgow Coma Scale score ≤8, no Abbreviated Injury Scale score ≥3 to any other bodily regions). We retrospectively reviewed all adult patients (aged ≥18 years) with isolated sTBI admitted to a Level I trauma center between June 2007 and January 2014. Patients must have cTnI values within 24 hours of admission. Mortality risks were examined by Cox proportional hazard model. Of 580 patients identified, 30.9% had detectable cTnI in 24 hours of admission. The median survival time was 4.19 days (interquartile range, 1.27-11.69). When adjusted for potential confounders, patients in the highest cTnI category (≥0.21 ng/mL) had a significantly higher risk of in-hospital mortality (hazard ratio, 1.39; 95% confidence interval, 1.04-1.88) compared with patients with undetectable cTnI. Mortality risk increased with higher troponin levels (p < 0.0001). This association was more pronounced in patients aged 65 years or younger (hazard ratio, 2.28; 95% confidence interval, 1.53-3.40; p < 0.0001) while, interestingly, insignificant in those older than 65 years (p = 0.0826). Among patients with sTBI, cTnI elevation is associated with all-cause in-hospital mortality via a nonlinear positive trend. Age modified the effect of cTnI on mortality. Prognostic and epidemiologic study, level III.