Mortality is Reduced for Heart Rate 80 to 89 After Traumatic Brain Injury

Ley, Eric J.; Berry, Cherisse; Mirocha, James; Salim, Ali

doi:10.1016/j.jss.2010.04.046

Cited by 20 publications

(17 citation statements)

References 25 publications

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“…We excluded 32 of those citations. Ten studies were excluded as the key exposure or outcome was not reported (16–25). Three were excluded due to the study population (26–28).…”

Section: Resultsmentioning

confidence: 99%

“…The increased CMR in the injured brain, with defective autoregulation, can exacerbate the pre-existing ischemia and metabolic crisis following TBI (2). This hyperadrenergic state may contribute to increased mortality after TBI (3) and, conversely, patients with low levels of adrenergic stress as evidenced by a normal heart rate may have reduced mortality after TBI (4). …”

Section: Introductionmentioning

confidence: 99%

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Beta-blockers and Traumatic Brain Injury

et al. 2017

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OBJECTIVE To determine if beta-(β)-blockers improve outcomes after acute traumatic brain injury (TBI). BACKGROUND There have been no new inpatient pharmacologic therapies to improve TBI outcomes in a half-century. Treatment of TBI patients with β-blockers offers a potentially beneficial approach. METHODS Using MEDLINE, EMBASE, and CENTRAL databases, eligible articles for our systematic review and meta-analysis (PROSPERO CRD42016048547) included adult (age≥16 years) blunt trauma patients admitted with TBI. The exposure of interest was β-blocker administration initiated during the hospitalization. Outcomes were mortality, functional measures, quality of life, cardiopulmonary morbidity (e.g. hypotension, bradycardia, bronchospasm, and/or congestive heart failure). Data were analyzed using a random-effects model, and represented by pooled odds ratio (OR) with 95% confidence intervals (CI) and statistical heterogeneity (I2). RESULTS Data were extracted from 9 included studies encompassing 2005 unique TBI patients with β-blocker treatment and 6240 unique controls. Exposure to β-blockers after TBI was associated with a reduction of in-hospital mortality (pooled OR 0.39, 95%CI: 0.27–0.56; I2=65%, p<0.00001). None of the included studies examined functional outcome or quality of life measures, and cardiopulmonary adverse events were rarely reported. No clear evidence of reporting bias was identified. CONCLUSIONS In adults with acute TBI, observational studies reveal a significant mortality advantage with β-blockers; however, quality of evidence is very low. We conditionally recommend the use of in-hospital β-blockers. However, we recommend further high-quality trials to answer questions about the mechanisms of action, effectiveness on subgroups, dose-response, length of therapy, functional outcome, and quality of life after β-blocker use for TBI.

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“…We excluded 32 of those citations. Ten studies were excluded as the key exposure or outcome was not reported (16–25). Three were excluded due to the study population (26–28).…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Beta-blockers and Traumatic Brain Injury

et al. 2017

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“…HR variability was not examined for this study. The optimal HR after trauma or TBI is unknown although adjusted mortality was lowest with an HR between 70 and 110 bpm and a range between 80 and 89 bpm may be ideal [33,34].…”

Section: Discussionmentioning

confidence: 99%

Prospective evaluation of early propranolol after traumatic brain injury

Murry

Hoang

Barmparas

et al. 2016

Journal of Surgical Research

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“…3–5 The hyperadrenergic state observed in moderate to severe TBI patients contributes to increased mortality and may guide surgical therapy 22 .…”

Section: Discussionmentioning

confidence: 99%

Cardiac Reactive Oxygen Species After Traumatic Brain Injury

Larson

Stockwell

Boas

et al. 2012

Journal of Surgical Research

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Background Cardiovascular complications after traumatic brain injury (TBI) contribute to morbidity and mortality and may provide a target for therapy. We examined blood pressure and left ventricle contractility after TBI, and tested the hypothesis that beta-adrenergic blockade would decrease oxidative stress after TBI. Material and Methods Rodents received fluid-percussion injury or sham surgery, confirmed with magnetic resonance imaging (MRI) and histopathology. We followed recovery with sensorimotor coordination testing and blood pressure measurements. We assessed left ventricular ejection fraction using ECG-gated cardiac MRI and measured myocardial reactive oxygen species (ROS) with dihydroethidium. We randomized additional TBI and sham animals to post-operative treatment with propranolol or control, for measurement of ROS. Results Blood pressure and cardiac contractility were elevated 48 hours after TBI. Myocardial tissue sections showed increased ROS. Treatment with propranolol diminished ROS levels following TBI. Conclusions TBI is associated with increased cardiac contractility and myocardial ROS; decreased myocardial ROS after beta-blockade suggests that sympathetic stimulation is a mechanism of oxidative stress.

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Mortality is Reduced for Heart Rate 80 to 89 After Traumatic Brain Injury

Cited by 20 publications

References 25 publications

Beta-blockers and Traumatic Brain Injury

Beta-blockers and Traumatic Brain Injury

Prospective evaluation of early propranolol after traumatic brain injury

Cardiac Reactive Oxygen Species After Traumatic Brain Injury

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