scholarly journals Impaired cerebral autoregulation and elevation in plasma glial fibrillary acidic protein level during cardiopulmonary bypass surgery for CHD

2017 ◽  
Vol 28 (1) ◽  
pp. 55-65 ◽  
Author(s):  
Ronald B. Easley ◽  
Bradley S. Marino ◽  
Jacky Jennings ◽  
Amy E. Cassedy ◽  
Kathleen K. Kibler ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiopulmonary Bypass ◽  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Lower Limit ◽  
Cerebrovascular Reactivity ◽  
Acidic Protein ◽  
Volume Index ◽  
Arterial Blood ◽  
The Mean

AbstractBackgroundCerebrovascular reactivity monitoring has been used to identify the lower limit of pressure autoregulation in adult patients with brain injury. We hypothesise that impaired cerebrovascular reactivity and time spent below the lower limit of autoregulation during cardiopulmonary bypass will result in hypoperfusion injuries to the brain detectable by elevation in serum glial fibrillary acidic protein level.MethodsWe designed a multicentre observational pilot study combining concurrent cerebrovascular reactivity and biomarker monitoring during cardiopulmonary bypass. All children undergoing bypass for CHD were eligible. Autoregulation was monitored with the haemoglobin volume index, a moving correlation coefficient between the mean arterial blood pressure and the near-infrared spectroscopy-based trend of cerebral blood volume. Both haemoglobin volume index and glial fibrillary acidic protein data were analysed by phases of bypass. Each patient’s autoregulation curve was analysed to identify the lower limit of autoregulation and optimal arterial blood pressure.ResultsA total of 57 children had autoregulation and biomarker data for all phases of bypass. The mean baseline haemoglobin volume index was 0.084. Haemoglobin volume index increased with lowering of pressure with 82% demonstrating a lower limit of autoregulation (41±9 mmHg), whereas 100% demonstrated optimal blood pressure (48±11 mmHg). There was a significant association between an individual’s peak autoregulation and biomarker values (p=0.01).ConclusionsIndividual, dynamic non-invasive cerebrovascular reactivity monitoring demonstrated transient periods of impairment related to possible silent brain injury. The association between an impaired autoregulation burden and elevation in the serum brain biomarker may identify brain perfusion risk that could result in injury.

scholarly journals Wavelet Autoregulation Monitoring Identifies Blood Pressures Associated With Brain Injury in Neonatal Hypoxic-Ischemic Encephalopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiuyun Liu ◽  
Aylin Tekes ◽  
Jamie Perin ◽  
May W. Chen ◽  
Bruno P. Soares ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Near Infrared ◽  
Brain Regions ◽  
Hypoxic Ischemic Encephalopathy ◽  
Volume Index ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Ischemic Encephalopathy

Dysfunctional cerebrovascular autoregulation may contribute to neurologic injury in neonatal hypoxic-ischemic encephalopathy (HIE). Identifying the optimal mean arterial blood pressure (MAPopt) that best supports autoregulation could help identify hemodynamic goals that support neurologic recovery. In neonates who received therapeutic hypothermia for HIE, we hypothesized that the wavelet hemoglobin volume index (wHVx) would identify MAPopt and that blood pressures closer to MAPopt would be associated with less brain injury on MRI. We also tested a correlation-derived hemoglobin volume index (HVx) and single- and multi-window data processing methodology. Autoregulation was monitored in consecutive 3-h periods using near infrared spectroscopy in an observational study. The neonates had a mean MAP of 54 mmHg (standard deviation: 9) during hypothermia. Greater blood pressure above the MAPopt from single-window wHVx was associated with less injury in the paracentral gyri (p = 0.044; n = 63), basal ganglia (p = 0.015), thalamus (p = 0.013), and brainstem (p = 0.041) after adjustments for sex, vasopressor use, seizures, arterial carbon dioxide level, and a perinatal insult score. Blood pressure exceeding MAPopt from the multi-window, correlation HVx was associated with less injury in the brainstem (p = 0.021) but not in other brain regions. We conclude that applying wavelet methodology to short autoregulation monitoring periods may improve the identification of MAPopt values that are associated with brain injury. Having blood pressure above MAPopt with an upper MAP of ~50–60 mmHg may reduce the risk of brain injury during therapeutic hypothermia. Though a cause-and-effect relationship cannot be inferred, the data support the need for randomized studies of autoregulation and brain injury in neonates with HIE.

Vasomotor waves of arterial blood pressure after cessation of cardiopulmonary bypass in man

Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi
Keyword(s):  
Blood Pressure ◽  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Heart Patients ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Epicardial Pacing

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.

Effect of chronic ANG I-converting enzyme inhibition on aging processes. IV. Cerebral blood flow regulation

1994 ◽  
Vol 267 (3) ◽  
pp. R687-R694 ◽  
Author(s):  
I. Lartaud ◽  
T. Makki ◽  
L. Bray-des-Boscs ◽  
N. Niederhoffer ◽  
J. Atkinson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Cerebrovascular Reactivity ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Age Related

Age-related changes in systemic arterial blood pressure, basal cerebral blood flow (CBF), and CBF regulatory capacity were investigated in awake 6-, 12-, 24-, and 30-mo-old male Wistar (WAG/Rij) rats, one-half of which received the angiotensin I-converting enzyme inhibitor (ACEI) perindopril from 6 mo onward. There was no age-dependent change in mean arterial blood pressure, basal CBF, or cerebrovascular reactivity to hypercapnia, but the lower limit of CBF autoregulation rose from 70 mmHg at 6 and 12 mo to 90 mmHg in 24- and 30-mo-old animals. ACEI lowered mean arterial blood pressure but had no effect on basal CBF or on cerebrovascular reactivity to hypercapnia. ACEI shifted the lower limit of CBF autoregulation to a 20-mmHg-lower level in 12- and 24-mo animals but not in rats treated for 2 yr, i.e., from the ages of 6 to 30 mo. In conclusion, the main age-related change in CBF regulation was an increase in the lower limit of CBF autoregulation to a higher blood pressure level. Treatment with ACEI partially restored the lower limit of CBF autoregulation.

scholarly journals Optimizing Cerebral Autoregulation May Decrease Neonatal Regional Hypoxic-Ischemic Brain Injury

2016 ◽  
Vol 39 (1-4) ◽  
pp. 248-256 ◽  
Author(s):  
Jennifer K. Lee ◽  
Andrea Poretti ◽  
Jamie Perin ◽  
Thierry A.G.M. Huisman ◽  
Charlamaine Parkinson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Injury ◽  
White Matter ◽  
Near Infrared ◽  
Birth Asphyxia ◽  
Neurologic Injury ◽  
Ischemic Brain ◽  
Arterial Blood ◽  
Blood Pressures ◽  
The Mean

Background: Therapeutic hypothermia provides incomplete neuroprotection for neonatal hypoxic-ischemic encephalopathy (HIE). We examined whether hemodynamic goals that support autoregulation are associated with decreased brain injury and whether these relationships are affected by birth asphyxia or vary by anatomic region. Methods: Neonates cooled for HIE received near-infrared spectroscopy autoregulation monitoring to identify the mean arterial blood pressure with optimized autoregulatory function (MAPOPT). Blood pressure deviation from MAPOPT was correlated with brain injury on MRI after adjusting for the effects of arterial carbon dioxide, vasopressors, seizures, and birth asphyxia severity. Results: Blood pressure deviation from MAPOPT related to neurologic injury in several regions independent of birth asphyxia severity. Greater duration and deviation of blood pressure below MAPOPT were associated with greater injury in the paracentral gyri and white matter. Blood pressure within MAPOPT related to lesser injury in the white matter, putamen and globus pallidus, and brain stem. Finally, blood pressures that exceeded MAPOPT were associated with reduced injury in the paracentral gyri. Conclusions: Blood pressure deviation from optimal autoregulatory vasoreactivity was associated with MRI markers of brain injury that, in many regions, were independent of the initial birth asphyxia. Targeting hemodynamic ranges to optimize autoregulation has potential as an adjunctive therapy to hypothermia for HIE.

Post-operative acute kidney injury is associated with a biomarker of acute brain injury after paediatric cardiac surgery

2020 ◽  
Vol 30 (4) ◽  
pp. 505-510
Author(s):  
Michael Parsons ◽  
Jason Greenberg ◽  
Chirag Parikh ◽  
Jeremiah Brown ◽  
Devin Parker ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Kidney Injury ◽  
Acidic Protein ◽  
Protein Levels ◽  
Post Operative Period ◽  
Galectin 3

AbstractIntroduction:Children with CHD who undergo cardiopulmonary bypass are at an increased risk of acute kidney injury. This study evaluated the association of end-organ specific injury plasma biomarkers for brain: glial fibrillary acidic protein and heart: Galectin 3, soluble suppression of tumorgenicity 2, and N-terminal pro b-type natriuretic peptide with acute kidney injury in children undergoing cardiopulmonary bypass.Materials and Methods:We enrolled consecutive children undergoing cardiac surgery with cardiopulmonary bypass. Blood samples were collected pre-bypass in the operating room and in the immediate post-operative period. Acute kidney injury was defined as a rise of serum creatinine ≥50% from pre-operative baseline within 7 days after surgery.Results:Overall, 162 children (mean age 4.05 years, sd 5.28 years) were enrolled. Post-operative acute kidney injury developed in 55 (34%) children. Post-operative plasma glial fibrillary acidic protein levels were significantly higher in patients with acute kidney injury (median 0.154 (inter-quartile range 0.059–0.31) ng/ml) compared to those without acute kidney injury (median 0.056 (inter-quartile range 0.001–0.125) ng/ml) (p = 0.043). After adjustment for age, weight, and The Society of Thoracic Surgeons-European Association for Cardio-Thoracic Surgery category, each natural log increase in post-operative glial fibrillary acidic protein was significantly associated with a higher risk for subsequent acute kidney injury (adjusted odds ratio glial fibrillary acidic protein 1.25; 95% confidence interval 1.01–1.59). Pre/post-operative levels of galectin 3, soluble suppression of tumorgenicity 2, and N-terminal pro b-type natriuretic peptide did not significantly differ between patients with and without acute kidney injury.Conclusions:Higher plasma glial fibrillary acidic protein levels measured in the immediate post-operative period were independently associated with subsequent acute kidney injury in children after cardiopulmonary bypass. Elevated glial fibrillary acidic protein likely reflects intraoperative brain injury which may occur in the context of acute kidney injury-associated end-organ dysfunction.

scholarly journals Development of a novel, sensitive translational immunoassay to detect plasma glial fibrillary acidic protein (GFAP) after murine traumatic brain injury

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Emily B. Button ◽  
Wai Hang Cheng ◽  
Carlos Barron ◽  
Honor Cheung ◽  
Asma Bashir ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Lower Limit ◽  
Limit Of Detection ◽  
Density Lipoprotein ◽  
Acidic Protein ◽  
Meso Scale Discovery ◽  
Limit Of Quantification ◽  
Plasma High Density

Abstract Background Glial fibrillary acidic protein (GFAP) has emerged as a promising fluid biomarker for several neurological indications including traumatic brain injury (TBI), a leading cause of death and disability worldwide. In humans, serum or plasma GFAP levels can predict brain abnormalities including hemorrhage on computed tomography (CT) scans and magnetic resonance imaging (MRI). However, assays to quantify plasma or serum GFAP in preclinical models are not yet available. Methods We developed and validated a novel sensitive GFAP immunoassay assay for mouse plasma on the Meso Scale Discovery immunoassay platform and validated assay performance for robustness, precision, limits of quantification, dilutional linearity, parallelism, recovery, stability, selectivity, and pre-analytical factors. To provide proof-of-concept data for this assay as a translational research tool for TBI and Alzheimer’s disease (AD), plasma GFAP was measured in mice exposed to TBI using the Closed Head Impact Model of Engineered Rotational Acceleration (CHIMERA) model and in APP/PS1 mice with normal or reduced levels of plasma high-density lipoprotein (HDL). Results We performed a partial validation of our novel assay and found its performance by the parameters studied was similar to assays used to quantify human GFAP in clinical neurotrauma blood specimens and to assays used to measure murine GFAP in tissues. Specifically, we demonstrated an intra-assay CV of 5.0%, an inter-assay CV of 7.2%, a lower limit of detection (LLOD) of 9.0 pg/mL, a lower limit of quantification (LLOQ) of 24.8 pg/mL, an upper limit of quantification (ULOQ) of at least 16,533.9 pg/mL, dilution linearity of calibrators from 20 to 200,000 pg/mL with 90–123% recovery, dilution linearity of plasma specimens up to 32-fold with 96–112% recovery, spike recovery of 67–100%, and excellent analyte stability in specimens exposed to up to 7 freeze-thaw cycles, 168 h at 4 °C, 24 h at room temperature (RT), or 30 days at − 20 °C. We also observed elevated plasma GFAP in mice 6 h after TBI and in aged APP/PS1 mice with plasma HDL deficiency. This assay also detects GFAP in serum. Conclusions This novel assay is a valuable translational tool that may help to provide insights into the mechanistic pathophysiology of TBI and AD.

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

2020 ◽  
Vol 132 (6) ◽  
pp. 1952-1960 ◽  
Author(s):  
Seung-Bo Lee ◽  
Hakseung Kim ◽  
Young-Tak Kim ◽  
Frederick A. Zeiler ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Status ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Clinical Parameters ◽  
Artifact Removal ◽  
Clinical Events ◽  
Arterial Blood ◽  
Before And After

OBJECTIVEMonitoring intracranial and arterial blood pressure (ICP and ABP, respectively) provides crucial information regarding the neurological status of patients with traumatic brain injury (TBI). However, these signals are often heavily affected by artifacts, which may significantly reduce the reliability of the clinical determinations derived from the signals. The goal of this work was to eliminate signal artifacts from continuous ICP and ABP monitoring via deep learning techniques and to assess the changes in the prognostic capacities of clinical parameters after artifact elimination.METHODSThe first 24 hours of monitoring ICP and ABP in a total of 309 patients with TBI was retrospectively analyzed. An artifact elimination model for ICP and ABP was constructed via a stacked convolutional autoencoder (SCAE) and convolutional neural network (CNN) with 10-fold cross-validation tests. The prevalence and prognostic capacity of ICP- and ABP-related clinical events were compared before and after artifact elimination.RESULTSThe proposed SCAE-CNN model exhibited reliable accuracy in eliminating ABP and ICP artifacts (net prediction rates of 97% and 94%, respectively). The prevalence of ICP- and ABP-related clinical events (i.e., systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and poor cerebrovascular reactivity) all decreased significantly after artifact removal.CONCLUSIONSThe SCAE-CNN model can be reliably used to eliminate artifacts, which significantly improves the reliability and efficacy of ICP- and ABP-derived clinical parameters for prognostic determinations after TBI.

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