Glial fibrillary acidic protein in children with congenital heart disease undergoing cardiopulmonary bypass

Abstract

There are significant increases in glial fibrillary acidic protein levels in children undergoing cardiopulmonary bypass for repair of congenital heart disease. The highest values were seen during the re-warming phase. Elevations are significantly associated with younger age, bypass and cross-clamp times, and temperature nadir. Owing to the fact that glial fibrillary acidic protein is the most brain-specific biomarker identified to date, it may act as a rapid diagnostic marker of brain injury during cardiac surgery.

Association of intraoperative circulating-brain injury biomarker and neurodevelopmental outcomes at 1 year among neonates who have undergone cardiac surgery

“…8 Elevations in levels of GFAP are detectable within 30 minutes of CPB and are not affected by ultrafiltration. 19 GFAP levels have been associated with neurological disability in adults with traumatic brain injury and those surviving cardiac arrest. [9][10][11] In the pediatric population, circulating GFAP has been shown to be a significant predictor of neurologic injury and hospital survival in children receiving extracorporeal membrane oxygenation, of abnormal magnetic resonance imaging and functional outcomes at discharge in neonates with birth-related hypoxic ischemic encephalopathy, and of periventricular white matter injury on 6-week head ultrasound imaging in premature infants.…”

Rewarming Rate During Cardiopulmonary Bypass Is Associated With Release of Glial Fibrillary Acidic Protein

“…(20, 34) In a prior study in pediatric patients undergoing congenital heart surgery (median age, 0.67 years; range, 0.005-17.2 years), our group has reported that plasma GFAP levels were elevated during and after CPB in 70% of cases, peaking during the rewarming phase (p=0.0001). (35) Elevation of plasma GFAP levels are associated with the extent of brain injury in adults with acute stroke and pediatric patients with hypoxic ischemic injury. (22, 27) Detection of plasma GFAP, thus may allow for the early identificatoin of brain injury in a variety of settings.…”

Glial fibrillary acidic protein as a biomarker for brain injury in neonatal CHD

“…[3][4][5][6][7][8] It is released from glial cells within the central nervous system as a result of cell necrosis. 9 According to Brunetti et al, 10 an ideal biomarker for brain injury is specific to brain tissue and is released into the bloodstream immediately after neurological injury and accurately reflects the location and degree of injury. As the glial fibrillary acidic protein is released into the blood after astrocyte death, it is a suitable biomarker to predict neonatal brain injury.…”

“…As the glial fibrillary acidic protein is released into the blood after astrocyte death, it is a suitable biomarker to predict neonatal brain injury. 9 Glial fibrillary acidic protein has been previously utilised as a diagnostic and prognostic tool in both children and adults; it has been shown to correspond with abnormal brain imaging in neonates, 10 and to predict neurodevelopmental outcomes in neonates with hypoxic ischaemic encephalopathy, prematurity-related intracranial haemorrhage, extracorporeal membrane oxygenation, and cardiopulmonary bypass during repair of neonatal CHD. 8,10 The aim of this study was to determine whether there is a difference in serum glial fibrillary acidic protein levels at birth and the immediate postnatal period between neonates with major CHD and two groups of controls: neonates with hypoxic ischaemic encephalopathy serving as positive controls, and neonates without brain injury serving as negative controls.…”

“…9 Glial fibrillary acidic protein has been previously utilised as a diagnostic and prognostic tool in both children and adults; it has been shown to correspond with abnormal brain imaging in neonates, 10 and to predict neurodevelopmental outcomes in neonates with hypoxic ischaemic encephalopathy, prematurity-related intracranial haemorrhage, extracorporeal membrane oxygenation, and cardiopulmonary bypass during repair of neonatal CHD. 8,10 The aim of this study was to determine whether there is a difference in serum glial fibrillary acidic protein levels at birth and the immediate postnatal period between neonates with major CHD and two groups of controls: neonates with hypoxic ischaemic encephalopathy serving as positive controls, and neonates without brain injury serving as negative controls. The secondary objectives of this study were to determine whether glial fibrillary acidic protein levels can elucidate the timing of brain injury in neonates with CHD, and to evaluate the association between glial fibrillary acidic protein levels, abnormal head size, and brain structural abnormalities by head ultrasounds in the major CHD group.…”