Toward Patient-Specific Hemodynamic Decision-Making in Cerebral Aneurysms: The Maturation of Computational Fluid Dynamics and Fluid-Structure Interaction

Article information

Neurointervention. 2026;21(2):63-66
Publication date (electronic) : 2026 June 9
doi : https://doi.org/10.5469/neuroint.2026.00549
Department of Neurosurgery, Yongin Severance Hospital, Yonsei University College of Medicine, Yongin, Korea
Correspondence to: Kwang-Chun Cho, MD, PhD Department of Neurosurgery, Yongin Severance Hospital, Yonsei University College of Medicine, 363 Dongbaekjukjeon-daero, Giheung-gu, Yongin 16995, Korea E-mail: ulyanminz@gmail.com
Received 2026 May 26; Revised 2026 June 1; Accepted 2026 June 2.

INTRODUCTION

Cerebral aneurysms present a persistent clinical paradox: although detected in roughly 3% of adults and only a minority rupture, aneurysmal subarachnoid hemorrhage still carries case-fatality rates approaching 30–35% and substantial longterm disability among survivors [1,2]. For decades, clinicians have determined whether to treat an aneurysm based mainly on its size, location, and shape. However, these factors alone remain insufficiently reliable. Some small aneurysms rupture unexpectedly, while many large aneurysms treated prophylactically may never have ruptured if left untreated [3]. Computational hemodynamics has long promised to narrow this gap, and advances over the past several years have brought the field substantially closer to clinically meaningful application.

FROM CLASSICAL COMPUTATIONAL FLUID DYNAMICS TO PATIENT-SPECIFIC HEMODYNAMIC MODELING

Computational fluid dynamics (CFD) has matured from idealized, rigid-wall, steady-flow simulations into patient-specific pulsatile models reconstructed from rotational angiography or magnetic resonance angiography [4]. Wall shear stress (WSS), oscillatory shear index, and WSS gradient have become the dominant hemodynamic descriptors linked to aneurysm pathology [4,5]. Although debate persists regarding whether high or low WSS is more closely associated with rupture, a more nuanced consensus has emerged: both extremes appear capable of driving endothelial dysfunction through distinct mechanobiological pathways, and the local distribution of these stresses may be more important than their global average. To improve the limited specificity of single-parameter analyses, several groups have proposed composite indices integrating WSS with oscillatory shear and normalized hemodynamic metrics. These approaches have shown promising correlation with thin-walled aneurysm regions identified intraoperatively [6]. Collectively, these developments suggest that aneurysm rupture may ultimately depend less on flow alone than on the interaction between hemodynamic stress and intrinsic wall vulnerability.

THE EMERGENCE OF FLUID-STRUCTURE INTERACTION

The most consequential shift, however, is the move from CFD toward fluid-structure interaction (FSI). Rigid-wall CFD inherently neglects the compliant, often pathologically thinned aneurysm wall, where rupture ultimately occurs. Patient-specific FSI studies have shown that wall-strain based metrics can discriminate ruptured from unruptured aneurysms more reliably than WSS alone, while elevated strain appears to correlate more closely with aneurysm formation in certain anatomical locations [7,8]. Recent FSI analyses of middle cerebral artery aneurysms extended these findings: descriptors such as High Equivalent Stress Area and Gaussian curvature independently predicted rupture in cohorts of more than 100 patients, outperforming traditional morphological scores [9]. High-fidelity FSI has additionally begun to characterize aneurysm wall vibrations and flow-induced sound, opening a mechanobiological window into wall remodeling that rigid-wall models cannot access [10]. However, important limitations remain. Most contemporary FSI studies still rely on assumed wall thickness and constitutive material properties rather than true patient-specific measurements, limiting physiologic fidelity and cross-study reproducibility. In addition, the computational expense and technical expertise required for high-fidelity simulations continue to limit widespread clinical implementation.

COMPUTATIONAL HEMODYNAMICS IN TREATMENT PLANNING

Computational modeling is also beginning to reshape endo-vascular treatment planning. Virtual deployment of flow diverters and braided stents, coupled with CFD or FSI post-processing, permits estimation of intra-aneurysmal flow reduc tion, residual WSS, and the hemodynamic consequences of incomplete stent expansion before treatment [11]. Such simulations offer the possibility of individualized procedural optimization rather than empiric device selection alone.

For computational hemodynamics to meaningfully influence treatment selection, however, simulations must become sufficiently automated, rapid, and interpretable for integration into routine neurovascular workflows. Current methodologies remain highly dependent on operator expertise, segmentation technique, and solver configuration.

MACHINE LEARNING AS AN ACCELERATOR

Machine learning is another great accelerator. In a 504-patient multicenter study, classifiers trained on computed tomography angiography-derived hemodynamic and morphological features achieved areas under the curve of 0.88–0.91 for rupture status of small aneurysms, with hemodynamic descriptors emerging as the most informative predictors [12]. Convolutional neural networks now permit rupture risk prediction directly from aneurysm geometry [13], and physics-constrained graph neural networks reproduce full-field aneurysmal hemodynamics in minutes rather than hours [14].

Importantly, however, many current machine-learning studies classify rupture status retrospectively rather than prospectively predicting future rupture risk. This distinction remains clinically critical. Negative findings in some cohorts further highlight the limited external validity of existing models and their tendency to generalize poorly outside the populations and imaging protocols on which they were trained [15]. External validation across institutions, imaging platforms, and patient populations therefore remains an essen tial unmet need

THE NEED FOR STANDARDIZATION AND VALIDATION

Three priorities should now guide the field. First, standardization remains urgently needed. Segmentation, meshing, solver settings, and source-imaging modality remain heterogeneous across centers, undermining cross-study com parability [4,5]. Second, validation must become more rigorous and systematic. Four-dimensional flow magnetic resonance imaging and patient-specific experimental phantoms should increasingly serve as benchmark references for computational studies. Without standardized in vivo validation, discrepancies between simulated and physiologic flow fields remain difficult to quantify. Third, integration into clinical decision-making must remain the ultimate objective. CFD and FSI outputs are clinically meaningful only when embedded within interpretable, prospectively validated tools that align with contemporary aneurysm management guidelines [2] and can guide bedside decision-making.

CONCLUSION

CFD told us where the blood goes; FSI is beginning to tell us when the wall will give way. Coupled with machine learning and rigorous validation, patient-specific computational hemodynamics is evolving from an experimental methodology into a potentially actionable instrument of personalized cere brovascular care. The challenge now is not whether these technologies can model aneurysm behavior, but whether they can do so robustly enough to meaningfully change clinical decisions. In addition, the future of aneurysm modeling may not lie in hemodynamics alone, but in coupling hemodynamic forces with biological markers of wall vulnerability, including inflammation, matrix degradation, and vessel wall imaging.

Notes

Fund

This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) (No. RS-2025-00559038).

Ethics Statement

This was not a human population study; therefore, neither approval from the Institutional Review Board nor the obtainment of informed consent was required.

Conflicts of Interest

KCC has been an assistant editor of the Neurointervention since 2022. No potential conflict of interest relevant to this article was reported.

Author Contributions

Concept and design: KCC. Analysis and interpretation: KCC. Data collection: none. Writing the article: KCC. Critical revision of the article: KCC. Final approval of the article: KCC. Statistical analysis: none. Obtained funding: KCC. Overall responsibility: KCC.

References

1. Etminan N, Chang HS, Hackenberg K, de Rooij NK, Vergouwen MDI, Rinkel GJE, et al. Worldwide incidence of aneurysmal subarachnoid hemorrhage according to region, time period, blood pressure, and smoking prevalence in the population: a systematic review and meta-analysis. JAMA Neurol 2019;76:588–597.
2. Hoh BL, Ko NU, Amin-Hanjani S, Chou SH-Y, Cruz-Flores S, Dan-gayach NS, et al. 2023 Guideline for the management of patients with aneurysmal subarachnoid hemorrhage: a guideline from the American Heart Association/American Stroke Association. Stroke 2023;54:e314–e370.
3. Etminan N, Ruigrok YM, Hackenberg KAM, Vergouwen MDI, Krings T, Rinkel GJE. Epidemiology, pathogenesis, and emerging concepts in unruptured intracranial aneurysms. Lancet Neurol 2025;24:945–957.
4. Cho KC. The current limitations and advanced analysis of hemodynamic study of cerebral aneurysms. Neurointervention 2023;18:107–113.
5. Meng H, Tutino VM, Xiang J, Siddiqui A. High WSS or low WSS? Complex interactions of hemodynamics with intracranial aneurysm initiation, growth, and rupture: toward a unifying hypothesis. AJNR Am J Neuroradiol 2014;35:1254–1262.
6. Cho KC, Choi JH, Oh JH, Kim YB. Prediction of thin-walled areas of unruptured cerebral aneurysms through comparison of normalized hemodynamic parameters and intraoperative images. Biomed Res Int 2018;2018:3047181.
7. Cho KC, Yang H, Kim JJ, Oh JH, Kim YB. Prediction of rupture risk in cerebral aneurysms by comparing clinical cases with fluid-structure interaction analyses. Sci Rep 2020;10:18237.
8. Kim JJ, Yang H, Kim YB, Oh JH, Cho KC. The quantitative comparison between high wall shear stress and high strain in the formation of paraclinoid aneurysms. Sci Rep 2021;11:7947.
9. Nagy J, Fenz W, Thumfart S, Maier J, Major Z, Stefanits H, et al. Fluid structure Interaction analysis for rupture risk assessment in patients with middle cerebral artery aneurysms. Sci Rep 2025;15:1965.
10. Bruneau DA, Steinman DA, Valen-Sendstad K. Understanding intracranial aneurysm sounds via high-fidelity fluid-structure-interaction modelling. Commun Med (Lond) 2023;3:163.
11. Fujimura S, Yuzawa K, Otani K, Karagiozov K, Takao H, Ishibashi T, et al. Hemodynamics in cerebral aneurysms and parent arteries with incompletely expanded flow diverter stents. Int J Numer Method Biomed Eng 2025;41e70033.
12. Shi Z, Chen GZ, Mao L, Li XL, Zhou CS, Xia S, et al. Machine learning-based prediction of small intracranial aneurysm rupture status using CTA-derived hemodynamics: a multicenter study. AJNR Am J Neuroradiol 2021;42:648–654.
13. Yang H, Cho KC, Kim JJ, Kim JH, Kim YB, Oh JH. Rupture risk prediction of cerebral aneurysms using a novel convolutional neural network-based deep learning model. J Neurointerv Surg 2023;15:200–204.
14. Suk J, Alblas D, Hutten BA, Wiegman A, Brune C, van Ooij P, et al. Physics-informed graph neural networks for flow field estimation in carotid arteries. Med Image Anal 2026;110:103974.
15. Swiatek VM, Voss S, Sprenger F, Fischer I, Kader H, Stein KP, et al. Predictive modeling and machine learning show poor performance of clinical, morphological, and hemodynamic parameters for small intracranial aneurysm rupture. Sci Rep 2025;15:24051.

Article information Continued