Early beta-blocker exposure and association with brain injury biomarkers following moderate to severe traumatic brain injury: A TRACK-TBI study.
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2025-06
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Abstract
Background
Beta-blockers have been studied for potential benefits in traumatic brain injury (TBI). This study aimed to investigate the association between early beta-blocker exposure and brain injury biomarkers following moderate-severe TBI.Methods
We conducted a retrospective cohort study using data from the Transforming Clinical Research and Knowledge in TBI (TRACK-TBI) study. Patients ⩾ 17 years with moderate-severe TBI (Glasgow Coma Scale 3-12) admitted to an intensive care unit (ICU) were included. Early beta-blocker exposure was defined as administration within the first 72 h of admission. The primary outcome was blood-based brain injury biomarker levels on day 3 post-injury. Biomarkers included glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B), and the inflammatory biomarker C-reactive protein (CRP). Propensity-weighted models analyzed the association between beta-blocker exposure and biomarker levels.Results
Among 450 patients, 31 (7%) received beta-blockers (BB+). The mean (SD) age of BB+ patients was 51.4 (16.2) years, compared to 39.5 (17.0) years for unexposed patients (BB-). BB+ group was associated with a decreased NSE level on day 3 (ratio = 0.71, 95% CI 0.52-0.96, p = 0.026), although this was not significant after adjusting for multiple comparisons (p = 0.13). For secondary outcomes, UCH-L1 levels increased on day 5 in the BB+ group (ratio = 1.62, 95% CI 1.12- 2.36, p = 0.011), but this was not significant after adjustment (p = 0.55). The NSE level on day 14 decreased in the BB+ group (ratio 0.45, 95% CI 0.30-0.66, p < 0.001) and remained significant after adjustment (p = 0.005).Conclusions
There was no association between early beta-blocker exposure and the primary outcome which was blood-based brain injury biomarker levels on day 3. In exploratory analysis, we found that early beta-blocker may associated with decreased NSE level on day 14. Due to the retrospective nature of the study and the use of propensity-weighted analysis to identify associations, direct clinical practice changes cannot be recommended. However, the significant association with NSE level warrants further investigation through prospective studies or randomized controlled trials to confirm the potential neuroprotective effect of early beta-blocker exposure on neuronal cellular injury.Type
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Wongsripuemtet, Pattrapun, Tetsu Ohnuma, Nancy Temkin, Jason Barber, Jordan Komisarow, Geoffrey T Manley, Jordan Hatfield, Miriam Treggiari, et al. (2025). Early beta-blocker exposure and association with brain injury biomarkers following moderate to severe traumatic brain injury: A TRACK-TBI study. Journal of the Intensive Care Society. p. 17511437251349680. 10.1177/17511437251349680 Retrieved from https://hdl.handle.net/10161/33516.
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Scholars@Duke
Tetsu Ohnuma
Jordan Komisarow
Miriam Treggiari
Cina Sasannejad
Daniel Todd Laskowitz
Our laboratory uses molecular biology, cell culture, and animal modeling techniques to examine the CNS response to acute injury. In particular, our laboratory examines the role of microglial activation and the endogenous CNS inflammatory response in exacerbating secondary injury following acute brain insult. Much of the in vitro work in this laboratory is dedicated to elucidating cellular responses to injury with the ultimate goal of exploring new therapeutic interventions in the clinical setting of stroke, intracranial hemorrhage, and closed head injury.
In conjunction with the Multidisciplinary Neuroprotection Laboratories, we also focus on clinically relevant small animal models of acute CNS injury. For example, we have recently characterized murine models of closed head injury, subarachnoid hemorrhage, intracranial hemorrhage and perinatal hypoxia-ischemia, in addition to the standard rodent models of focal stroke and transient forebrain ischemia. Recently we have adapted several of these models from the rat to the mouse to take advantage of murine transgenic technology. The objective of these studies are two-fold: to gain better insight into the cellular responses and pathophysiology of acute brain injury, and to test novel therapeutic strategies for clinical translation. In both cell culture systems and animal models, our primary focus is on examining the role of oxidative stress and inflammatory mechanism in mediating brain injury following acute brain insult, and examining the neuroprotective effects of endogenous apolipoprotein E in the injured mammalian central nervous system.
Our laboratory is committed to translational research, and has several active clinical research protocols, which are designed to bring the research performed in the Multidisciplinary Research Laboratories to the clinical arena. These protocols are centered around patients following stroke and acute brain injury, and are primarily based out of the Emergency Room and Neurocritical Care Unit. For example, we are currently examining the role of inflammatory mediators for use as a point-of-care diagnostic marker following stroke, intracranial hemorrhage, and closed head injury. We have recently translated a novel apoE mimetic from the preclinical setting to a multi center Phase 2 trial evaluating efficacy in intracranial hemorrhage. We are also examining the functional role of different polymorphisms of of inflammatory cytokines in the setting of acute brain injury and neurological dysfunction following cardiopulmonary bypass.
Joseph P. Mathew
Current research interests include:
1. The relationship between white matter patency, functional connectivity (fMRI) and neurocognitive function following cardiac surgery.
2. The relationship between global and regional cortical beta-amyloid deposition and postoperative cognitive decline.
3. The effect of lidocaine infusion upon neurocognitive function following cardiac surgery.
4. The association between genotype and outcome after cardiac surgery.
5. Atrial fibrillation following cardiopulmonary bypass.
Michael Lucas James
With a clinical background in neuroanesthesia and neurointensive care, I have a special interest in translational research in intracerebral hemorrhage and traumatic brain injury. I am fortunate to be part of a unique team of highly motivated and productive individuals who allow me to propel ideas from bench to bedside and the ability to reverse translate ideas from the bedside back to the bench.
Karthik Raghunathan
Dr. Karthik Raghunathan is an Associate Professor with Tenure in the Department of Anesthesiology, with a secondary appointment in the Department of Population Health Sciences, at the Duke University School of Medicine. He is also a Staff Physician at the Durham Veterans Affairs Healthcare System. He is co-director of the Critical care And Perioperative population hEalth Research (CAPER) Program at Duke Anesthesiology.
In addition to clinical practice as an anesthesiologist and intensive care physician, Dr. Raghunathan is an epidemiologist and health services researcher with over $2 Million in funding from Federal, Industry, and Non-Profit entities since 2015. His research is focused on intravenous fluid resuscitation, acute postoperative pain management, the implementation and effectiveness of nonpharmacologic treatments, sources of bias in anesthesia care, and perioperative medicine. He collaborates with investigators at Duke, and at VA Healthcare Systems nationwide. He also works with colleagues outside the US. He can be reached at kr118@duke.edu.
Benjamin Alan Goldstein
I study the meaningful use of Electronic Health Records data. My research interests sit at the intersection of biostatistics, biomedical informatics, machine learning and epidemiology. I collaborate with researchers both locally at Duke as well as nationally. I am interested in speaking with any students, methodologists or collaborators interested in EHR data.
Please find more information at: https://biostat.duke.edu/goldstein-lab
Vijay Krishnamoorthy
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