ArticleBiomedical engineering and computational biology2026
Fluid-Structure Interaction Analysis of Hyoid Bone-Induced Compression on Carotid Artery Hemodynamics.
Article in Biomedical engineering and computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The carotid bifurcation plays a crucial role in cerebral perfusion, and its hemodynamic behavior is influenced by external factors, including interactions with surrounding anatomical structures. This study investigates the impact of hyoid bone-induced compression on carotid artery hemodynamics using computational fluid dynamics (CFD) and fluid-structure interaction (FSI) modeling. The results reveal significant alterations in time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), velocity distribution, and Von-Mises stress, highlighting the biomechanical effects of external compression at various arterial locations. Compression of the common carotid artery results in a marked reduction in downstream TAWSS, dropping from 3.68 Pa to 1.70 Pa, and a substantial increase in OSI, reaching up to 0.46, suggesting disturbed flow patterns that may contribute to pathological vessel remodeling. In contrast, compression at the internal carotid artery leads to localized elevations in TAWSS, reaching approximately 6.90 Pa at the contact site and 7.80 Pa at the bifurcation, while OSI remains relatively low (around 0.22). Similarly, high oscillatory low magnitude shear index (HOLMES) levels decrease significantly after compression of the common carotid artery, from 1.23 Pa to 0.41 Pa, but increase when the internal carotid artery is compressed, peaking at 3.30 Pa at the contact site and 2.60 Pa downstream within the external carotid artery. Velocity streamline analysis demonstrates prominent vortex formation at the bifurcation, particularly in cases where direct compression occurs at this site, indicating disrupted and recirculating flow. Von-Mises stress analysis shows the highest stress concentration at the contact region across all cases. The lowest stress is observed with common carotid compression (approximately 0.6 MPa), while higher stresses occur in the bifurcation and internal carotid cases (around 1.5 MPa). The greatest mechanical stress, reaching approximately 1.9 MPa, is seen when the external carotid artery is compressed, indicating a higher risk of structural damage in this region. These results improve understanding of the effects of external anatomical interactions on carotid artery hemodynamics and motivate further investigation of their clinical significance. Future investigations should prioritize patient-specific modeling and in vivo validation to better assess the long-term vascular health impacts of hyoid bone-induced compression.
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