Mechanisms and Clinical Impact of Myocardial Injury Following Traumatic Brain Injury

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PROJECT SUMMARY/ABSTRACT Traumatic brain injury (TBI) is a major public health concern, affecting more than 1.7 million individuals annually in the United States. Hypotension after severe TBI results in cerebral hypoperfusion and poor clinical outcomes. Approximately 50% of severe TBI patients are treated for hypotension and maintenance of cerebral perfusion; this may be due to unrecognized myocardial injury and cardiac dysfunction. My prior research has demonstrated that: 22% of patients with moderate-severe TBI have early cardiac dysfunction, patients with TBI and cardiac dysfunction exhibit signs of sympathetic activation, and patients with TBI and cardiac dysfunction experience hypotension and cerebral hypoperfusion. Sympathetic activation is implicated in cardiac dysfunction and hypotension after TBI, but mechanistic data is limited. The central hypothesis of the current proposal is that severe TBI causes myocardial injury through activation of the sympathetic nervous system, and this results in systolic cardiac dysfunction, reduced cardiac output, hypotension, decreased cerebral perfusion, and poor neurologic outcomes. We propose 3 Specific Aims in patients with severe TBI: 1) Determine the effect of severe TBI on autonomic nervous system function, 2) Determine if autonomic dysfunction contributes to myocardial injury after severe TBI, and 3) Examine the impact of myocardial injury on echocardiographic, hemodynamic, and clinical outcomes after severe TBI. Results of this study, as well as completion of a rigorous career development plan, will lead to a larger trial that examines the impact of reduction of sympathetic nervous system activation on myocardial injury and neurologic outcomes after severe TBI. The long-term goal of my work is to personalize hemodynamic management and improve clinical outcomes after severe TBI.