Association of Early Myocardial Workload and Mortality Following Moderate to Severe Traumatic Brain Injury

Background: Cardiovascular dysfunction is increasingly recognized following traumatic brain injury (TBI), yet the association between early myocardial workload and mortality remains inadequately defined. Rate pressure product (RPP), a surrogate of myocardial oxygen demand, may serve as a simple bedside marker of cardiac stress after TBI. Objective: To determine the association between admission myocardial workload and in-hospital mortality in patients with isolated moderate to severe TBI. Methods: In this prospective observational study, 200 patients aged 18–65 years with isolated TBI (GCS <12) were enrolled. Admission RPP was calculated and categorized into five groups: <5000, 5000–9999, 10000–14999, 15000 19999, and >20000. Cardiac biomarkers, and transthoracic echocardiography were performed within 24–48 hours. LVEF <40% and regional wall motion abnormalities (RWMA) were recorded. The primary endpoint was in-hospital mortality. Logistic regression and ROC analyses were performed. Results: Overall mortality was 35%. Mortality was highest in the lowest RPP group (53.8%; OR 3.68, p=0.039) compared with the reference group (10000–14999). Elevated RPP was also associated with increased mortality. Reduced LVEF (OR 11.6), RWMA (OR 8.6), elevated troponin (OR 3.91), and elevated CPK-MB (OR 1.05) were independent predictors of mortality. ROC analysis demonstrated modest predictive performance of troponin (AUC 0.615) and CPK-MB (AUC 0.643). Conclusion: Both reduced and elevated myocardial workload at admission are associated with increased in-hospital mortality following moderate to severe TBI. Early cardiac dysfunction and biomarker elevation independently predict adverse outcomes.