Effects of congenital heart disease on brain development

McQuillen, Patrick S.; Goff, Donna A.; Licht, Daniel J.

doi:10.1016/j.ppedcard.2010.06.011

Cited by 120 publications

(99 citation statements)

References 61 publications

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“…The altered circulation in congenital cardiovascular malformations possibly affects cerebral development by decreasing oxygen saturation of cerebral arterial blood (hypoxemia) (4,6); decreasing cerebral energy substrate (glucose) supply; or decreasing cerebral blood flow with reduced oxygen and substrate supply (9,10).…”

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Impaired cerebral development in fetuses with congenital cardiovascular malformations: Is it the result of inadequate glucose supply?

Rudolph

2016

Pediatr Res

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Cerebral development may be impaired in fetuses with congenital cardiovascular malformations, particularly hypoplastic left heart syndrome (HLHS) and aortopulmonary transposition (APT). The decreased cerebral arterial pusatility index observed in some of these fetuses led to the belief that cerebral vascular resistance was reduced as a result of arterial hypoxemia and cerebral hypoxia is thought to be responsible for impaired cerebral growth. However, other hemodynamic factors could affect pulsatility index. I propose that cerebral blood flow is reduced in fetuses with HLHS and that reduced glucose, rather than oxygen, delivery interferes with cerebral development. This is based on the fact that most of these fetuses do not have lactate accumulation in the brain. In fetuses with APT, umbilical venous blood, containing oxygen and glucose derived across the placenta, is distributed to the lungs and lower body; venous blood, with low oxygen and glucose content, is delivered to the ascending aorta and brain. Oxygen and glucose delivery may further be reduced by decreased cerebral blood flow resulting from run-off of aortic blood through the ductus arteriosus to the pulmonary circulation during diastole. In APT fetuses, lack of lactate in the brain also supports my proposal that glucose deficiency interferes with cerebral development. Increased frequency of neurodevelopmental disabilities has been noted in children born with congenital cardiovascular malformations. It had been attributed to cerebral damage resulting from cardiac failure or hypoxemia during the neonatal period, or following complicated surgical procedures (1-3). Recently, it has been recognized that abnormalities in cerebral development may occur before birth in association with congenital cardiovascular malformations.Unfortunately, most studies have grouped a variety of malformations and compared the observations with those in normal fetuses (4-6). However, it did appear that the most significant abnormalities were noted in fetuses with aortopulmonary transposition (APT) and hypoplastic left heart syndrome (HLHS). Head size at birth was noted to be reduced in infants with APT and particularly in those with HLHS (7).Hinton et al. (8) noted a significant reduction of head growth in fetuses with HLHS during the latter half of gestation; also, in 11 fetuses aborted electively, histopathology revealed diffuse cerebral white matter injury. Quantitative magnetic resonance imaging at 25-37 wk gestation showed a decrease in brain volume in fetuses with various congenital cardiovascular malformations compared with normal fetuses. These differences were most prominent in those with HLHS (5) This evidence of prenatal disturbance in cerebral development has raised questions regarding possible mechanisms. Genetic disturbances with which the cardiovascular malformations are associated could be responsible; this requires further study. Recently, there has been considerable interest in the possibility that altered circulatory dynamics could result in cerebral injury....

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Impaired cerebral development in fetuses with congenital cardiovascular malformations: Is it the result of inadequate glucose supply?

Rudolph

2016

Pediatr Res

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“…An explanation for the interchangeable cerebral rSO 2 and FTOE values in infants with antegrade and infants with retrograde blood flow in the ascending aorta might be the persistence of antenatal circulatory alterations in favor of brain perfusion after birth. Fetuses with CHD often show signs of brain sparing [6,7,8], with fetuses with LSOL with retrograde blood flow being more affected than fetuses with LSOL with antegrade blood flow in the ascending aorta [9]. Furthermore, fetuses with CHD and a cerebroplacental ratio <1.0 (brain sparing) had higher cerebral blood flow after birth compared with fetuses with CHD and cerebroplacental ratio >1.0 [21].…”

Section: Discussionmentioning

confidence: 99%

“…Prolonged and repeated episodes of hypoxia and/or ischemia might be a major risk factor for developing brain injury [2,3]. Recent evidence suggests that such episodes occur already during early postnatal life or even before birth [4,5,6]. …”

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Cerebral and Renal Oxygen Saturation Are Not Compromised in the Presence of Retrograde Blood Flow in either the Ascending or Descending Aorta in Term or Near-Term Infants with Left-Sided Obstructive Lesions

Laan

Mebius²,

Roofthooft³

et al. 2017

Neonatology

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Background: In infants with left-sided obstructive lesions (LSOL), the presence of retrograde blood flow in either the ascending or descending aorta may lead to diminished cerebral and renal blood flow, respectively. Objectives: Our aim was to compare cerebral and renal tissue oxygen saturation (rSO₂) between infants with LSOL with antegrade and retrograde blood flow in the ascending aorta and with and without diastolic backflow in the descending aorta. Methods: Based on 2 echocardiograms, the study group was categorized according to the direction of blood flow in the ascending and descending aorta. We measured cerebral and renal rSO₂ using near-infrared spectroscopy and calculated fractional tissue oxygen extraction (FTOE). Results: Nineteen infants with LSOL, admitted to the NICU between 0 and 28 days after birth, were included. Infants with antegrade blood flow (n = 12) and infants with retrograde blood flow in the ascending aorta (n = 7) had similar cerebral rSO₂ and FTOE during both echocardiograms. Only during the first echocardiogram, infants with retrograde blood flow in the ascending aorta had lower renal FTOE (0.14 vs. 0.32, p = 0.04) and tended to have higher renal rSO₂ (80 vs. 65%, p = 0.09). The presence of diastolic backflow in the descending aorta was not associated with cerebral or renal rSO₂ and FTOE during the first (n = 8) as well as the second echocardiogram (n = 10). Conclusions: Retrograde blood flow in the ascending aorta was not associated with cerebral oxygenation, while diastolic backflow in the descending aorta was not associated with renal oxygenation in infants with LSOL.

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“…7 Even before surgery, infants born with HPLHS have brains that are smaller and structurally less mature than expected. 11 Brain development in these neonates even at term appears to be delayed by B1 month. Although the causes of these conditions are almost certainly multifactorial, Licht notes it is likely that altered fetal blood flow patterns and diminished oxygen delivery in utero has a role in the developmental delays.…”

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confidence: 93%

Physician counseling, informed consent and parental decision making for infants with hypoplastic left-heart syndrome

Schreiber

2012

J Perinatol

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Effects of congenital heart disease on brain development

Cited by 120 publications

References 61 publications

Impaired cerebral development in fetuses with congenital cardiovascular malformations: Is it the result of inadequate glucose supply?

Impaired cerebral development in fetuses with congenital cardiovascular malformations: Is it the result of inadequate glucose supply?

Cerebral and Renal Oxygen Saturation Are Not Compromised in the Presence of Retrograde Blood Flow in either the Ascending or Descending Aorta in Term or Near-Term Infants with Left-Sided Obstructive Lesions

Physician counseling, informed consent and parental decision making for infants with hypoplastic left-heart syndrome

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