Declining Incidence of Postoperative Neonatal Brain Injury in Congenital Heart Disease.

BACKGROUND

Brain injury is common in neonates with complex neonatal congenital heart disease (CHD) and affects neurodevelopmental outcomes.

OBJECTIVES

Given advancements in perioperative care, we sought to determine if the rate of preoperative and postoperative brain injury detected by using brain magnetic resonance imaging (MRI) and associated clinical risk factors have changed over time in complex CHD.

METHODS

A total of 270 term newborns with complex CHD were prospectively enrolled for preoperative and postoperative brain MRIs between 2001 and 2021 with a total of 466 MRI scans. Brain injuries in the form of white matter injury (WMI) or focal stroke and clinical factors were compared across 4 epochs of 5-year intervals with logistic regression.

RESULTS

Rates of preoperative WMI and stroke did not change over time. After adjusting for timing of the postoperative MRI, site, and cardiac group, the odds of newly acquired postoperative WMI were significantly lower in Epoch 4 compared with Epoch 1 (OR: 0.29; 95% CI: 0.09-1.00; P = 0.05). The adjusted probability of postoperative WMI declined significantly by 18.7% from Epoch 1 (24%) to Epoch 4 (6%). Among clinical risk factors, lowest systolic, mean, and diastolic blood pressures in the first 24 hours after surgery were significantly higher in the most recent epoch.

CONCLUSIONS

The prevalence of postoperative WMI has declined, whereas preoperative WMI rates remain constant. More robust postoperative blood pressures may explain these findings by minimizing periods of ischemia and supporting cerebral perfusion. These results suggest potential modifiable clinical targets in the postoperative time period to minimize the burden of WMI.

Informations de copyright

Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This work was supported by grants K23 NS099422, R01 NS40117, R01NS063876, R01EB009756, R01HD07274, and P01 NS082330 from the National Institutes of Health; grant MOP93780 from the Canadian Institutes of Health Research; grant 5-M01-RR-01271 from the National Center for Research Resources; grants 5-FY05-1231 and 6-FY2009-303 from the March of Dimes Foundation; and grant 0365018Y from the American Heart Association. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.