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Effects of hemodynamic alterations and oxygen saturation on cerebral perfusion in congenital heart disease
Alexandra De Silvestro1,2,3,4, Giancarlo Natalucci4,5,6, Maria Feldmann3,7
1Pediatric Cardiology, Pediatric Heart Center, Department of Surgery, University Children's Hospital Zurich, Zurich, Switzerland.
Insights
Severe congenital heart disease (CHD) alters brain blood flow. A systemic-to-pulmonary shunt affects cortical gray matter perfusion, but overall cerebral perfusion is increased in infants with CHD.
Area of Science:
- Neuroscience
- Cardiology
- Medical Imaging
Background:
- Severe congenital heart disease (CHD) poses a risk for neurodevelopmental impairment.
- Altered cerebral blood supply in CHD can hinder optimal brain development.
- Understanding cerebral perfusion in infants with CHD is crucial for neuroprotection.
Purpose of the Study:
- To evaluate the impact of systemic-to-pulmonary shunts, aortic arch obstruction, and arterial oxygen saturation on cerebral perfusion in severe CHD.
- To compare cerebral perfusion in infants with severe CHD to healthy controls.
Main Methods:
- Utilized pseudocontinuous arterial spin labeling MRI to assess cerebral perfusion.
- Included patients with severe CHD requiring early cardiac surgery and healthy controls.
- Analyzed perfusion in deep and cortical gray matter.
Main Results:
- Systemic-to-pulmonary shunts correlated with reduced cortical gray matter perfusion (p=0.003) but not deep gray matter (p=0.031).
- Aortic arch obstruction and arterial oxygen saturation did not significantly affect cerebral perfusion.
- Adjusted analysis revealed increased deep (p=0.018) and cortical (p=0.012) gray matter perfusion in CHD patients compared to controls.
Conclusions:
- Patients with severe CHD exhibit altered postnatal brain hemodynamics.
- Regional differences in compensating for the cerebral steal effect were observed.
- Increased cerebral perfusion in CHD patients, after adjustment, highlights complex hemodynamic adaptations.
Background:
Patients with severe congenital heart disease (CHD) are at risk for neurodevelopmental impairment. An abnormal cerebral blood supply caused by the altered cardiac physiology may limit optimal brain development. The aim of this study was to evaluate the effect of a systemic-to-pulmonary shunt, aortic arch obstruction and arterial oxygen saturation on cerebral perfusion in patients with severe CHD.
Methods:
Patients with severe CHD requiring cardiac surgery within the first six weeks of life, who underwent pre- and/or postoperative brain magnetic resonance imaging (MRI), and healthy controls with one postnatal scan were included. Cerebral perfusion in deep and cortical gray matter was assessed by pseudocontinuous arterial spin labeling MRI.
Results:
We included 59 CHD and 23 healthy control scans. The presence of a systemic-to-pulmonary shunt was associated with decreased perfusion in cortical (p = 0.003), but not in deep gray matter (p = 0.031). No evidence for an effect of aortic arch obstruction and arterial oxygen saturation on cerebral perfusion was found. After adjusting for hemodynamic and oxygen saturation parameters, deep (p = 0.018) and cortical (p = 0.012) gray matter perfusion was increased in patients with CHD compared to controls.
Conclusion:
We detected regional differences in compensation to the cerebral steal effect in patients with severe CHD.
Impact:
Patients with severe congenital heart disease (CHD) have altered postnatal brain hemodynamics. A systemic-to-pulmonary shunt was associated with decreased perfusion in cortical gray matter but preserved perfusion in deep gray matter, pointing towards regional differences in compensation to the cerebral steal effect. No effects of aortic arch obstruction and arterial oxygenation on cerebral perfusion were seen. Cerebral perfusion was increased in patients with CHD compared to healthy controls after adjusting for hemodynamic alterations and oxygen saturation. To improve neuroprotection and neurodevelopmental outcomes, it is important to increase our understanding of the factors influencing cerebral perfusion in neonates with severe CHD.
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