Comparative analysis for the implication of serum cardiac troponin measurements by conventional versus high-sensitivity assays in patients with traumatic brain injury.
Academic Article
Overview
abstract
BACKGROUND: Stress-induced myocardial injury is not well-studied in patients with head injury. We aimed to assess the prognostic implication of positive (+ve) Troponins (Tn) measurements by conventional (cTnT) versus High-Sensitivity (HsTnT) assay in patients with traumatic brain injury (TBI). METHODS: A retrospective analysis was conducted for patients who were admitted with TBI. Patient demographics, clinical presentation, troponin assay results, TBI lesions, and hospital outcomes were analyzed and compared based on troponin assay (cTnT versus HsTnT). RESULTS: Across the study period, 654 patients with TBI had troponin levels measured within 24 h postinjury (cTnT=252 and HsTnT=402). The mean age was 31 years and 46% had positive troponins. There were 147 deaths (22.5%); of them 54% had +ve HsTnT, 23% had +ve cTnT, 16% had -ve cTnT and 7% had -ve HsTnT). When the troponins were tested ≤4 h postinjury, the mortality was 10.2% in patients with -ve cTnT and 4% in patients with -ve HsTnT. There was no documented obvious direct trauma to the heart. Overall, patients with positive troponins had lower Glasgow Coma Scale (GCS), higher Injury Severity Scores and higher rates of brain edema (P=0.001), pneumonia and sepsis (P=0.001) than those with negative troponin results. In two different models, multivariate regression analysis showed that +ve cTnT and +ve HsTnT were independent predictors of mortality (OR 4.02, 95% CI: 1.72-9.39) and (OR 4.31; 95% CI: 1.76-10.57); respectively, after adjusting for age, injury severity scores, GCS at ED, head AIS, pneumonia, ARDS, surgical interventions, and chest injury. CONCLUSIONS: Although the positivity of any troponin assay is associated with high mortality post-TBI, the use of HsTnT relatively outperforms the conventional troponin assay for early risk stratification and detection of stress-induced myocyte injury in patients with TBI.
