Cerebral oxygen saturation and cerebrovascular instability in newborn infants with congenital heart disease compared to healthy controls.

Nhu N Tran,Paula M Murray,Matthew Borzage,Choo Phei Wee,Bradley S Peterson,Lisa Paquette,S Ram Kumar,Mary-Lynn Brecht,Ashok Panigrahy,Jodie K Votava-Smith,John C Wood,Kenneth M Brady,Kazumichi Fujioka

doi:10.1371/journal.pone.0251255

Abstract

ObjectiveInfants with Congenital Heart Disease (CHD) are at risk for developmental delays, though the mechanisms of brain injury that impair development are unknown. Potential causes could include cerebral hypoxia and cerebrovascular instability. We hypothesized that we would detect significantly reduced cerebral oxygen saturation and greater cerebrovascular instability in CHD infants compared to the healthy controls.MethodsWe performed a secondary analysis on a sample of 43 term infants (28 CHD, 15 healthy controls) that assessed prospectively in temporal cross-section before or at 12 days of age. CHD infants were assessed prior to open-heart surgery. Cerebral oxygen saturation levels were estimated using Near-Infrared Spectroscopy, and cerebrovascular stability was assessed with the response of cerebral oxygen saturation after a postural change (supine to sitting).ResultsCerebral oxygen saturation was 9 points lower in CHD than control infants in both postures (β = -9.3; 95%CI = -17.68, -1.00; p = 0.028), even after controlling for differences in peripheral oxygen saturation. Cerebrovascular stability was significantly impaired in CHD compared to healthy infants (β = -2.4; 95%CI = -4.12, -.61; p = 0.008), and in CHD infants with single ventricle compared with biventricular defects (β = -1.5; 95%CI = -2.95, -0.05; p = 0.04).ConclusionCHD infants had cerebral hypoxia and decreased cerebral oxygen saturation values following a postural change, suggesting cerebrovascular instability. Future longitudinal studies should assess the associations of cerebral hypoxia and cerebrovascular instability with long-term neurodevelopmental outcomes in CHD infants.

Highlights

Infants with Congenital Heart Disease (CHD) are at high risk for developmental delays [1,2,3], with up to 75% experiencing delays in cognitive or motor development in pre-school to school-age years [4, 5], and 65% requiring remedial academic or behavioral services [6]
Cerebrovascular stability was significantly impaired in CHD compared to healthy infants (β = -2.4; 95%CI = -4.12, -.61; p = 0.008), and in CHD infants with single ventricle compared with biventricular defects (β = -1.5; 95%CI = -2.95, -0.05; p = 0.04)
Our data show that cerebral oxygenation declines with a postural change in CHD infants, thereby providing evidence for the presence of cerebrovascular instability

Summary

Introduction

Infants with Congenital Heart Disease (CHD) are at high risk for developmental delays [1,2,3], with up to 75% experiencing delays in cognitive or motor development in pre-school to school-age years [4, 5], and 65% requiring remedial academic or behavioral services [6]. Two potential causes of delayed development that have not been examined extensively include cerebral hypoxia [8] and cerebrovascular instability [9, 10]—i.e., dysfunction of the brain’s homeostatic response that maintains stable cerebral blood flow during a change in posture. Cerebral hypoxia and impaired perfusion from cerebrovascular instability are plausible consequences of the profoundly altered blood flow and systemic hypoxemia associated with CHD. We assessed these characteristics in CHD and healthy control infants, hypothesizing the detection of significantly reduced cerebral oxygen saturation and greater cerebrovascular instability in CHD compared to healthy control infants

Methods

Discussion

Conclusion