ArticleFrontiers in neurology2024
Investigating the pathophysiology and evolution of internal carotid dissection: a fluid-structure interaction simulation study.
Article in Frontiers in neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The perfect storm: autoinflammation, metabolic stress, and thrombolysis in bilateral carotid dissection-a case report.Journal of neurology · 2026Article
- A predictive surrogate model of blood haemodynamics for patient-specific carotid artery stenosis.Journal of the Royal Society, Interface · 2025Article
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Authors and funding
8 authors.
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Abstract
Background: Arterial dissection, a condition marked by the tearing of the carotid artery's inner layers, can result in varied clinical outcomes, including progression, stability, or spontaneous regression. Understanding these outcomes' underlying mechanisms is crucial for enhancing patient care, particularly with the increasing use of computer simulations in medical diagnostics and treatment planning. The aim of this study is to utilize computational analysis of blood flow and vascular wall to: (1) understand the pathophysiology of stroke-like episodes in patients with carotid artery dissection; and (2) assess the effectiveness of this method in predicting the evolution of carotid dissection. Methods: Utilizing contrast-enhanced magnetic resonance angiography (MRA), we segmented images of the patient's right internal carotid artery. These images were transformed into 3D solids for simulation in Ansys multifisic software, employing a two-way fluid structure interaction (FSI) analysis. Simulations were conducted across two wall conditions (atherosclerotic and normal) and three pressure states (hypotension, normotension, hypertension). Results: The simulations indicated a significant pressure discrepancy between the true and false lumens of the artery. This suggests that flap motion and functional occlusion under hypertensive conditions could be the cause of the clinical episodes. Thrombotic risk and potential for dissection extension were not found to be critical concerns. However, a non-negligible risk of vessel dilation was assessed, aligning with the patient's clinical follow-up data. Conclusion: This study highlights specific hemodynamic parameters that could elucidate carotid artery dissection's mechanisms, offering a potential predictive tool for assessing dissection progression and informing personalized patient care strategies.
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