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Updated: Mar 24, 2026
Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
Published on: June 22, 2012
Original Research: Sickle cell anemia and pediatric strokes: Computational fluid dynamics analysis in the middle
Christian P Rivera1, Alessandro Veneziani2, Russell E Ware3
1Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332, USA.
Insights
Children with sickle cell anemia (SCA) experience high stroke rates. Computational modeling revealed that uneven cerebral artery walls, not just stenosis, may increase blood flow velocity, highlighting new therapeutic targets.
Area of Science:
- Biomedical Engineering
- Pediatric Neurology
- Hematology
Background:
- Children with sickle cell anemia (SCA) face a high risk of stroke.
- Transcranial Doppler (TCD) identifies high-risk patients by measuring elevated blood flow velocities in cerebral arteries, typically above 200 cm/s, necessitating blood transfusions.
Purpose of the Study:
- To investigate the fluid dynamics and arterial wall properties that contribute to elevated blood flow velocities in children with SCA.
- To simulate scenarios that could cause significantly increased arterial blood velocities using computational fluid dynamics.
Main Methods:
- Two-dimensional and three-dimensional computational fluid dynamics (CFD) simulations were employed.
- Patient-specific three-dimensional reconstructions of the middle cerebral artery (MCA), internal carotid artery (ICA), and anterior cerebral artery (ACA) were generated from MRAs of children with SCA.
- Finite element method was used to simulate blood flow with realistic velocity waveforms.
Main Results:
- In silico stenoses (up to 75%) in 2D models did not reach the critical velocity threshold (>200 cm/s).
- 3D reconstructions from children with SCA showed uneven internal arterial walls and higher mean MCA velocities (up to 145 cm/s) compared to non-SCA models.
- SCA models exhibited increased flow recirculation and larger regions of low wall shear stress.
Conclusions:
- Uneven cerebral artery wall surfaces in SCA patients may cause local flow disturbances that collectively elevate blood velocities.
- These findings suggest that microstructural changes in cerebral arteries, potentially due to adhered blood cells or endothelial hyperplasia, are critical factors in SCA-related stroke risk.
- Patient-specific 3D vascular reconstructions are crucial for understanding the interplay between vascular geometry and altered rheological properties in SCA.
Abstract:
Children with sickle cell anemia (SCA) have a high incidence of strokes, and transcranial Doppler (TCD) identifies at-risk patients by measuring blood velocities in large intracerebral arteries; time-averaged mean velocities greater than 200 cm/s confer high stroke risk and warrant therapeutic intervention with blood transfusions. Our objective was to use computational fluid dynamics to alter fluid and artery wall properties, to simulate scenarios causative of significantly elevated arterial blood velocities. Two-dimensional simulations were created and increasing percent stenoses were created in silico, with their locations varied among middle cerebral artery (MCA), internal carotid artery (ICA), and anterior cerebral artery (ACA). Stenoses placed in the MCA, ICA, or ACA generated local increases in velocity, but not sufficient to reach magnitudes > 200 cm/s, even up to 75% stenosis. Three-dimensional reconstructions of the MCA, ICA, and ACA from children with SCA were generated from magnetic resonance angiograms. Using finite element method, blood flow was simulated with realistic velocity waveforms to the ICA inlet. Three-dimensional reconstructions revealed an uneven, internal arterial wall surface in children with SCA and higher mean velocities in the MCA up to 145 cm/s compared to non-SCA reconstructions. There were also greater areas of flow recirculation and larger regions of low wall shear stress. Taken together, these bumps on the internal wall of the cerebral arteries could create local flow disturbances that, in aggregate, could elevate blood velocities in SCA. Identifying cellular causes of these microstructures as adhered blood cells or luminal narrowing due to endothelial hyperplasia induced by disturbed flow would provide new targets to treat children with SCA. The preliminary qualitative results provided here point out the critical role of 3D reconstruction of patient-specific vascular geometries and provide qualitative insight to complex interplay between vascular geometry and rheological properties possibly altered by SCA.
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