Abstract 15580: Impaired Pre-Operative Cerebral Autoregulation is Associated With Functional Brain Dysmaturation in Neonatal Congenital Heart Disease

Introduction: Altered hemodynamics may drive abnormal brain development in congenital heart disease (CHD). We aimed to correlate impaired cerebral autoregulation (CA) and neonatal brain connectivity using a data-driven quantitative analysis involving diffusion tensor imaging (DTI) to assess white matter microstructure and resting blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) to assess functional connections. Methods: Term neonates with complex CHD underwent pre and post-op 3T brain MRI with DTI in 42 directions and resting BOLD acquired for 5 minutes x2, and pre-op continuous mean arterial pressure (MAP), oxygen saturation (SaO2) & cerebral near infrared spectroscopy (CrSO2) for up to 72 hours. Significant low frequency coherence between MAP and CrSO2 defined impaired CA in 20 minute epochs. Calculations included pressure passivity index (PPI) = % epochs with abnormal CA, and cerebral fractional tissue oxygen extraction FTOE = (SaO2 - CrSO2)/ SaO2. Brain dysmaturation was defined as reduced network integration (DTI) and reduced network segregation (BOLD) as calculated with graph theory using 90 segmented brain regions. Multivariate mixed-effect modeling was used. Results: We evaluated 32 neonates with 47 MRI scans and hemodynamics (65 ± 34 epochs per subject). Mean PPI = 15 ± 13%, range 0-52% with abnormal CA in 88% of subjects. Impaired CA metrics (PPI and FTOE) correlated with altered functional brain network segregation nodal metrics, with significant associations seen in prefrontal, subcortical, and temporal areas ( Figure ). DTI network integration metrics showed fewer associations with CA including temporal regional efficiency (p=0.02). Conclusions: Impaired pre-op CA is associated with reduced functional network segregation metrics in neonates with complex CHD. These findings suggest a common vulnerability between compensatory hemodynamic mechanisms and functional brain dysmaturation in patients with complex CHD.