Hemodynamic Characterization of Spontaneous Isolated Superior Mesenteric Artery Dissection Revealed by Patient-Specific Computational Fluid Dynamics

Hemodynamic Characterization of Spontaneous Isolated Superior Mesenteric Artery Dissection Revealed by Patient-Specific Computational Fluid Dynamics | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Hemodynamic Characterization of Spontaneous Isolated Superior Mesenteric Artery Dissection Revealed by Patient-Specific Computational Fluid Dynamics Runze Wei, Zhaolei Chen This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6595461/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 13 You are reading this latest preprint version Abstract Background Spontaneous isolated superior mesenteric artery dissection (SISMAD) is a rare but potentially lethal vascular emergency with unclear pathogenesis. While hemodynamic forces are implicated in its development, current understanding remains limited by the lack of patient-specific data. This study aimed to characterize the detailed hemodynamic environment in SISMAD using patient-specific computational fluid dynamics modeling. Results Analysis of a three-dimensional model reconstructed from computed tomography angiography of a Yun Type I SISMAD revealed complex flow patterns with marked hemodynamic differences between the true lumen (TL) and false lumen (FL). The TL exhibited high-velocity flow concentrated near the entry tear and significantly elevated wall shear stress along the intimal flap. In contrast, the FL demonstrated markedly lower velocities, regions of flow stasis, and low wall shear stress. A substantial pressure gradient existed across the intimal flap, with higher pressure in the TL compared to the FL. These findings provide quantitative confirmation of the theorized hemodynamic forces contributing to dissection progression and potential thrombosis formation. Conclusions Patient-specific computational modeling reveals a complex and heterogeneous hemodynamic environment within the dissected superior mesenteric artery. The high-velocity flow and elevated wall shear stress in the true lumen may contribute to flap instability and inflammation, while the low-flow, stagnant conditions in the false lumen likely promote thrombogenesis. This patient-specific approach provides valuable insights into SISMAD pathophysiology and demonstrates potential for personalized ris assessment and treatment planning in this rare but serious vascular condition. Spontaneous Isolated Superior Mesenteric Artery Dissection Computational Fluid Dynamics Hemodynamics Patient-Specific Model Wall Shear Stress Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Background Spontaneous isolated superior mesenteric artery dissection (SISMAD) is an uncommon yet life-threatening vascular emergency. Characterized by an insidious onset and potential for rapid progression, SISMAD presents diagnostic challenges and can lead to severe complications, including intestinal ischemia, infarction, and hemorrhage, thereby contributing to significant morbidity and mortality. Although the precise etiology of SISMAD remains elusive, hemodynamic forces, particularly at the origin and branching points of the superior mesenteric artery (SMA), are considered major contributing factors. Specifically, the acute angulation between the SMA and the aorta (SMA-aorta angle, SMA-AA) is postulated to generate elevated hemodynamic wall shear stress, potentially precipitating intimal disruption and subsequent dissection [ 1 , 2 ]. Other potential risk factors encompass hypertension, atherosclerosis, and fibromuscular dysplasia, although robust evidence supporting these associations is limited [ 3 , 4 ]. Diagnosis is typically confirmed using computed tomography angiography (CTA), which facilitates visualization of the intimal flap, distinct true and false lumens, and assessment of potential intestinal ischemia. Current management strategies for SISMAD range from conservative medical therapy (including anticoagulation, antiplatelet agents, and blood pressure control) to endovascular stenting and open surgical repair [ 5 , 6 ]. The optimal treatment approach remains controversial, with decisions frequently individualized based on clinical presentation, dissection extent, and the presence of complications [ 7 , 8 ]. Critically, the absence of patient-specific hemodynamic data hinders precise treatment planning and the ability to predict disease progression [ 9 , 10 ]. Previous computational fluid dynamics (CFD) studies investigating SMA hemodynamics have often relied on simplified or idealized geometric models. Such models may inadequately represent the complex and variable anatomy of individual patients, consequently limiting their clinical applicability. Moreover, few studies have specifically investigated the hemodynamic characteristics within dissected SMAs using patient-specific anatomical data. Therefore, this study aimed to construct patient-specific, three-dimensional (3D) hemodynamic numerical simulation models of SISMAD derived from individual patient CT data. This methodology allows for accurate representation of the unique anatomy of the dissected SMA, including the intimal flap and the true and false lumens. Through the analysis of hemodynamic parameters within these models, we seek to enhance the understanding of SISMAD pathogenesis and contribute to the development of more personalized treatment strategies. Methods Acquisition of patient three-dimensional CT data This study enrolled patients diagnosed with SISMAD at a hospital in Jiangsu Province, China. CTA data were acquired using a Siemens SOMATOM dual-source scanner employing the following parameters: voltage, 120 kV; tube current range, 200–400 mA; slice thickness, 1 mm; and slice interval, 0.8 mm. The resultant CT images were saved in the Digital Imaging and Communications in DICOM format for subsequent processing. The study protocol was approved by the Institutional Ethics Committee of Northern Jiangsu People's Hospital Affiliated to Yangzhou University (Approval No. 2024ky144) in accordance with the Declaration of Helsinki. Written informed consent was obtained from each participant. A representative case classified as Yun Type I SISMAD was selected for computational modeling. This selection was based on the subtype's relatively high incidence and distinct anatomical feature-an entry tear without a re-entry tear-which was anticipated to provide informative hemodynamic insights upon simulation [11]. Image segmentation and geometric model generation The generation of a high-fidelity geometric model is crucial for accurate CFD simulations. The process began with image segmentation and 3D reconstruction from the DICOM-formatted CT images using Mimics software (Materialise NV, Belgium). This software facilitated the delineation of vessel boundaries for the abdominal aorta and SMA through grayscale thresholding and a region-growing algorithm, effectively isolating the vascular geometry from adjacent non-target tissues (Fig.1). The segmented 2D image stack was then converted into a 3D surface model and exported as a Standard Tessellation Language (STL) file. The resulting patient-specific model provided detailed anatomical representation suitable for CFD analysis (Fig.2). Subsequently, Geomagic Studio (3D Systems, USA) was employed to refine the initial STL file. This refinement involved removing artifacts, smoothing surfaces, and filling gaps to ensure geometric integrity and continuity. The final stage utilized SolidWorks (Dassault Systèmes, France) for further geometric corrections and finalization, producing the computational domain suitable for CFD analysis. This multi-software approach ensured the creation of a geometrically accurate and simulation-ready model derived directly from patient-specific medical imaging data. Computational methods and boundary conditions Hemodynamic simulations of the SISMAD model were conducted using ANSYS Fluent (ANSYS Inc., USA). An unstructured tetrahedral mesh was generated for the SISMAD geometry, incorporating local refinement in critical regions, such as the dissection entry tear and aorta bifurcations, to enhance computational accuracy in areas anticipated to exhibit high flow gradients (Fig.3). Grid independence studies were performed to ensure mesh convergence, resulting in an optimal mesh comprising 172,160 elements with an average quality metric of 0.8. Blood was modeled as an incompressible Newtonian fluid with a density of 1045 kg/m³ and a dynamic viscosity of 0.0035 Pa·s. The characteristic Reynolds number was approximately 1800, which is below the critical threshold for turbulence, thus justifying the use of a laminar flow model. The governing Navier-Stokes equations were solved numerically using the finite volume method, ensuring mass conservation. Gravitational forces and energy dissipation were considered negligible. Transient simulations were performed using time-dependent boundary conditions: a time-varying velocity waveform, derived either from literature or patient-specific data, was applied at the inlet (Fig.4), while a constant relative pressure of 0 mmHg was imposed at the outlet. The simulations spanned two to three cardiac cycles, with data for analysis extracted from the final cycle to ensure results represented a periodically stable state, free from initial transient effects. A convergence tolerance of 1 × 10⁻⁴ was maintained for all residuals. Subsequent post-processing using CFD-Post (ANSYS Inc., USA) enabled the generation of quantitative flow field maps and detailed topographical distributions of hemodynamic parameters, including wall shear stress (WSS) and pressure gradients. This approach facilitated a comprehensive analysis of the intricate flow dynamics inherent to SISMAD pathophysiology. Results Blood flow dynamics, including velocity distributions, pressure differentials, and WSS within the true lumen (TL) and false lumen (FL) of the SISMAD model, were analyzed. The analysis focused on five critical phases of the cardiac cycle: maximum acceleration (t = 0.10 s), peak velocity (t = 0.22 s), maximum deceleration (t = 0.25 s), minimum velocity (t = 0.38 s), and the mid-diastolic phase (t = 0.72 s). This approach allowed for the elucidation of complex flow patterns within the dissected SMA, as depicted in Fig.5. Velocity distributions Velocity streamlines revealed complex flow patterns within both the TL and FL of the dissected SMA (Fig.5, top row). Maximum velocities were observed near the entry tear region within the TL, with velocity progressively attenuating distally. The FL exhibited markedly lower flow velocities and contained regions of flow stasis, particularly prominent in its distal segment. Quantitative assessment revealed peak velocities reaching 2.673 m/s within the TL, whereas the FL exhibited substantially reduced flow, with velocity magnitudes ranging from approximately 9.202 × 10⁻² m/s to 9.471 × 10⁻² m/s. Pressure distributions Analysis of pressure distribution revealed significant pressure differentials across the dissection flap and between the TL and FL (Fig.5, middle row). Maximum relative pressure values (approximately 4.198 × 10² Pa) were observed proximally in the SMA near the aortic ostium, with pressure progressively decreasing distal to the entry tear. The FL consistently exhibited lower pressure values compared to the TL. The minimum relative pressure within the FL reached approximately -9.430 × 10² Pa. Wall shear stress distributions Topographical analysis of WSS identified regions subjected to elevated shear forces, particularly near the entry tear and along the intimal flap within the TL (Fig.5, bottom row). The maximum WSS magnitude observed in these high-stress regions reached 7.264 × 10¹ Pa. Conversely, the FL generally exhibited zones of significantly lower WSS, potentially fostering conditions conducive to thrombogenesis. This spatial heterogeneity in WSS distribution likely contributes to differential endothelial responses and subsequent pathophysiological remodeling processes within the dissected vessel. Discussion Hemodynamic insights from a patient-specific SISMAD model Our CFD analysis revealed significant spatial heterogeneity in WSS distribution within the dissected SMA, corroborating and extending previous findings on the role of hemodynamics in SISMAD pathophysiology [1, 2, 12]. Specifically, markedly elevated WSS, peaking at 72.64 Pa, was concentrated near the primary entry tear and along the TL aspect of the intimal flap, consistent with hypotheses linking high shear forces to endothelial injury and potential tear propagation [2, 4]. Such elevated mechanical stimuli are known potent activators of endothelial mechanotransduction pathways, including NF-κB and MAPK signaling, which upregulate adhesion molecules like VCAM-1 and ICAM-1 [13-16]. While often studied in atherogenesis, these mechanisms suggest the high WSS environment near the flap could foster a pro-inflammatory state contributing to maladaptive remodeling or flap instability in SISMAD. Conversely, the FL predominantly exhibited regions of substantially lower WSS, a finding consistent with hemodynamic principles associating low shear with blood stasis and a pro-thrombotic milieu conducive to platelet aggregation and fibrin deposition [17, 18]. This observed low WSS environment within the FL likely underlies the common clinical finding of FL thrombosis and significantly influences disease progression [19, 20]. Therefore, the pronounced WSS dichotomy between the high-stress environment potentially driving inflammation and remodeling near the flap in the TL, and the low-stress, pro-thrombotic conditions within the FL, highlights the complex interplay of biomechanical forces in dictating the divergent pathophysiological remodeling pathways and clinical evolution characteristic of SISMAD. The velocity and pressure distributions derived from our CFD analysis further illuminate the complex hemodynamic environment characteristic of SISMAD. The observed velocity patterns, featuring high-velocity flow (peak 2.673 m/s) concentrated near the entry tear within the TL juxtaposed with markedly reduced velocities (approx. 0.09 m/s) and flow stasis within the FL, align with previous computational and clinical observations [2]. The elevated velocities in the TL, particularly near the tear, likely contribute significantly to the high wall shear stress discussed previously and may represent a key hemodynamic factor influencing tear propagation and flap dynamics. Conversely, the profoundly diminished flow and stasis within the FL directly support the propensity for thrombogenesis frequently observed in this compartment [19, 21]. Complementing these velocity findings, the significant pressure differential observed, with the TL maintaining substantially higher pressure than the FL (minimum relative pressure -943 Pa), provides the driving force influencing intimal flap behavior and FL perfusion dynamics [2, 21]. Taken together, these results depict a hemodynamically challenging environment where high-velocity, higher-pressure flow in the TL interacts with the dissection flap, while the low-velocity, lower-pressure, stagnant environment in the FL promotes thrombosis—collectively dictating the complex pathophysiology and evolution of SISMAD. Patient-specific CFD approach compared to previous studies This investigation employed a patient-specific CFD methodology, constructing the model directly from the clinical imaging data of the SISMAD patient. This approach represents a significant advancement over studies relying on idealized or generic arterial geometries, which, while useful for elucidating fundamental hemodynamic principles, inherently lack the anatomical specificity crucial for understanding individual patient pathophysiology [2, 17, 21]. The primary strength of our patient-specific approach lies in its ability to incorporate the unique anatomical intricacies of the individual’s SMA, including its specific curvature, branching pattern, the precise location and morphology of the entry tear, and the complex, often tortuous configuration of the dissection flap. Previous research has indeed utilized CFD to explore SISMAD hemodynamics, often identifying key factors like WSS, pressure gradients, and flow patterns [2, 4, 21]. However, simulations based on simplified geometries may fail to capture the localized hemodynamic extremes driven by patient-specific anatomical features. For instance, the precise angle of SMA origin, subtle variations in lumen diameter, or the specific shape and extent of the intimal flap can substantially alter local velocity jets, recirculation zones, and WSS distributions [4]. Our detailed, patient-specific model allowed for the direct observation and quantification of these phenomena, such as the focal peak WSS (72.64 Pa) near the primary entry tear and the distinct regions of flow stasis within the FL. While earlier patient-specific SISMAD studies have provided invaluable insights [2, 21], our work contributes by applying this methodology to capture the detailed interplay of velocity, pressure, and WSS within this particular complex dissection morphology. This high-fidelity simulation reinforces the concept that hemodynamic forces are highly sensitive to individual vascular geometry. Therefore, the use of patient-specific CFD is not merely an incremental refinement but a critical step towards understanding the variability in SISMAD presentation and progression, potentially paving the way for more personalized risk stratification and treatment planning in the future. Limitations of the study This study is subject to several limitations inherent to its design and methodology. Primarily, the findings are derived from a single patient case, which limits the generalizability of the specific hemodynamic results. Validation necessitates investigation across larger, multi-center cohorts encompassing diverse SISMAD morphologies and clinical presentations. Furthermore, the CFD model incorporated simplifications necessary for computational feasibility: blood was modeled as a Newtonian fluid, which may not fully capture non-Newtonian effects in low-flow regions such as the false lumen, and vessel walls were assumed rigid, thus excluding fluid-structure interaction (FSI). While common in CFD analyses, these assumptions affect the accuracy of the predicted hemodynamic parameters. Finally, direct in vivo validation of the simulated flow fields and WSS values is currently infeasible, highlighting the importance of model fidelity and the accuracy of the applied boundary conditions. Conclusion Despite these limitations, this investigation demonstrates the feasibility and potential utility of patient-specific CFD for analyzing SISMAD. By elucidating significant hemodynamic differences between the true and false lumens and identifying regions of elevated WSS, our findings reinforce the critical role of local hemodynamics in SISMAD pathophysiology and progression. This approach provides a valuable foundation for future, larger-scale studies aimed at refining personalized risk assessment and therapeutic strategies for SISMAD management. Declarations Ethics approval and consent to participate The study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Ethics Committee of Northern Jiangsu People's Hospital Affiliated to Yangzhou University (Approval No. 2024ky144). Written informed consent was obtained from each participants. Consent for publication Not applicable. Availability of data and materials The DICOM datasets used in this study are not publicly available due to patient privacy regulations but can be obtained from the corresponding author upon reasonable request with appropriate ethics committee approval. Competing interests The authors declare no competing interests. Funding The authors acknowledge funding support from the Jiangsu Province Subei People's Hospital Support Special Project (SBQN23012). Author contributions R-W. conceptualized the study and prepared the original draft while Z.C. contributed to conceptualization, review and editing, and project administration. Acknowledgements Thanks to all the authors who participated in the design and literature analysis of this paper. References Mei J, Ding W, Yu H, Zhao X, Xu H, Wang K, et al. Different hemodynamic factors cause the occurrence of superior mesenteric atherosclerotic stenosis and superior mesenteric artery dissection. Front Cardiovasc Med 2023;10:1121224. Park YJ, Park CW, Park KB, Roh YN, Kim DI, Kim YW. Inference from clinical and fluid dynamic studies about underlying cause of spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2011;53:80-6. Hau SF, Chan YC, Cheung GC, Cheng SW. Risk factor analysis and treatment outcome of patients with spontaneous isolated celiac axis or superior mesenteric artery dissection. J Vasc Surg 2023;77:150-7. Wu Z, Yi J, Xu H, Guo W, Wang L, Chen D, et al. The Significance of the Angle between Superior Mesenteric Artery and Aorta in Spontaneous Isolated Superior Mesenteric Artery Dissection. Ann Vasc Surg 2017;45:117-26. Park YJ, Park KB, Kim DI, Do YS, Kim DK, Kim YW. Natural history of spontaneous isolated superior mesenteric artery dissection derived from follow-up after conservative treatment. J Vasc Surg 2011;54:1727-33. Hou L, Wang T, Wang J, Yuan D. Isolated superior mesenteric artery dissection in China: A systematic review and meta-analysis. Asian J Surg 2022;45:1070-4. Heo SH, Kim YW, Woo SY, Park YJ, Park KB, Kim DK. Treatment strategy based on the natural course for patients with spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2017;65:1142-51. Björck M, Koelemay M, Acosta S, Bastos Goncalves F, Kölbel T, Kolkman JJ, et al. Editor's Choice - Management of the Diseases of Mesenteric Arteries and Veins: Clinical Practice Guidelines of the European Society of Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2017;53:460-510. Ye M, Zhou Q, Wu J, Zhang Z, Li B, Zheng T, et al. Conservative Versus Endovascular Treatment for Spontaneous Isolated Superior Mesenteric Artery Dissection: A Clinical and Imaging Follow-up Study. J Endovasc Ther 2024;31:840-52. Morgan CE, Mansukhani NA, Eskandari MK, Rodriguez HE. Ten-year review of isolated spontaneous mesenteric arterial dissections. J Vasc Surg 2018;67:1134-42. Yun WS, Kim YW, Park KB, Cho SK, Do YS, Lee KB, et al. Clinical and angiographic follow-up of spontaneous isolated superior mesenteric artery dissection. Eur J Vasc Endovasc Surg 2009;37:572-7. Xiaoq Z, Hao M, Lin L, Jiao Y, Zou J, Zhang X, et al. Clinical and CT Angiographic Follow-Up Outcome of Spontaneous Isolated Intramural Hematoma of the Superior Mesenteric Artery. Cardiovasc Intervent Radiol 2019;42:1088-94. Fan J, Liu D, He C, Li X, He F. Inhibiting adhesion events by Panax notoginseng saponins and Ginsenoside Rb1 protecting arteries via activation of Nrf2 and suppression of p38 - VCAM-1 signal pathway. J Ethnopharmacol 2016;192:423-30. Bryan MT, Duckles H, Feng S, Hsiao ST, Kim HR, Serbanovic-Canic J, et al. Mechanoresponsive networks controlling vascular inflammation. Arterioscler Thromb Vasc Biol 2014;34:2199-205. Zhou M, Yu Y, Chen R, Liu X, Hu Y, Ma Z, et al. Wall shear stress and its role in atherosclerosis. Front Cardiovasc Med 2023;10:1083547. Yan B, Yu X, Cai X, Huang X, Xie B, Lian D, et al. A Review: The Significance of Toll-Like Receptors 2 and 4, and NF-κB Signaling in Endothelial Cells during Atherosclerosis. Front Biosci (Landmark Ed) 2024;29:161. Jeays AD, Lawford PV, Gillott R, Spencer P, Barber DC, Bardhan KD, et al. Characterisation of the haemodynamics of the superior mesenteric artery. J Biomech 2007;40:1916-26. Mei J, Yuan Y, Yan H, Zhao X, Xue T, Su H, et al. Factors associated with false lumen changes in patients with superior mesenteric artery dissection. Vasc Med 2024;29:274-85. Kim YW. Current Understandings of Spontaneous Isolated Superior Mesenteric Artery Dissection. Vasc Specialist Int 2016;32:37-43. Mei J, Yan H, Zhao X, Yuan Y, Su H, Xue T, et al. In-stent Restenosis After Stenting for Superior Mesenteric Artery Dissection Is Associated With Stent Landing Zone: From Clinical Prediction to Hemodynamic Mechanisms. J Endovasc Ther 2024:15266028241241494. Jia Z, Mei J, Ding W, Zhao X, Gong W, Yu H, et al. The pathogenesis of superior mesenteric artery dissection: An in-depth study based on fluid-structure interaction and histology analysis. Comput Methods Programs Biomed 2022;226:107187. Additional Declarations No competing interests reported. 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10:51:35","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":116811,"visible":true,"origin":"","legend":"\u003cp\u003eVelocity inlet boundary condition with a time-dependent blood flow profile.\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-6595461/v1/2003f0293b68ef30a644d49f.png"},{"id":83605934,"identity":"c8c04d90-4a3e-489f-909b-a64b89bcc929","added_by":"auto","created_at":"2025-05-29 10:43:35","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":569829,"visible":true,"origin":"","legend":"\u003cp\u003eTemporal evolution of flow fields, wall shear stress , and pressure distributions in the true and false lumens of the SISMAD’s model.\u003c/p\u003e","description":"","filename":"5.png","url":"https://assets-eu.researchsquare.com/files/rs-6595461/v1/5fecbfa9ea585b37eb1909ac.png"},{"id":83606184,"identity":"d3358c35-7ef0-4c1e-af96-de178626151a","added_by":"auto","created_at":"2025-05-29 10:51:40","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2082391,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6595461/v1/9f3737ff-604e-4c04-803c-83e6320dec11.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Hemodynamic Characterization of Spontaneous Isolated Superior Mesenteric Artery Dissection Revealed by Patient-Specific Computational Fluid Dynamics","fulltext":[{"header":"Background","content":"\u003cp\u003eSpontaneous isolated superior mesenteric artery dissection (SISMAD) is an uncommon yet life-threatening vascular emergency. Characterized by an insidious onset and potential for rapid progression, SISMAD presents diagnostic challenges and can lead to severe complications, including intestinal ischemia, infarction, and hemorrhage, thereby contributing to significant morbidity and mortality. Although the precise etiology of SISMAD remains elusive, hemodynamic forces, particularly at the origin and branching points of the superior mesenteric artery (SMA), are considered major contributing factors. Specifically, the acute angulation between the SMA and the aorta (SMA-aorta angle, SMA-AA) is postulated to generate elevated hemodynamic wall shear stress, potentially precipitating intimal disruption and subsequent dissection [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Other potential risk factors encompass hypertension, atherosclerosis, and fibromuscular dysplasia, although robust evidence supporting these associations is limited [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Diagnosis is typically confirmed using computed tomography angiography (CTA), which facilitates visualization of the intimal flap, distinct true and false lumens, and assessment of potential intestinal ischemia.\u003c/p\u003e \u003cp\u003eCurrent management strategies for SISMAD range from conservative medical therapy (including anticoagulation, antiplatelet agents, and blood pressure control) to endovascular stenting and open surgical repair [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. The optimal treatment approach remains controversial, with decisions frequently individualized based on clinical presentation, dissection extent, and the presence of complications [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Critically, the absence of patient-specific hemodynamic data hinders precise treatment planning and the ability to predict disease progression [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Previous computational fluid dynamics (CFD) studies investigating SMA hemodynamics have often relied on simplified or idealized geometric models. Such models may inadequately represent the complex and variable anatomy of individual patients, consequently limiting their clinical applicability. Moreover, few studies have specifically investigated the hemodynamic characteristics within dissected SMAs using patient-specific anatomical data.\u003c/p\u003e \u003cp\u003eTherefore, this study aimed to construct patient-specific, three-dimensional (3D) hemodynamic numerical simulation models of SISMAD derived from individual patient CT data. This methodology allows for accurate representation of the unique anatomy of the dissected SMA, including the intimal flap and the true and false lumens. Through the analysis of hemodynamic parameters within these models, we seek to enhance the understanding of SISMAD pathogenesis and contribute to the development of more personalized treatment strategies.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003e\u003cstrong\u003eAcquisition of patient three-dimensional CT data\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study enrolled patients diagnosed with SISMAD at a hospital in Jiangsu Province, China. CTA data were acquired using a Siemens SOMATOM dual-source scanner employing the following parameters: voltage, 120 kV; tube current range, 200\u0026ndash;400 mA; slice thickness, 1 mm; and slice interval, 0.8 mm. The resultant CT images were saved in the Digital Imaging and Communications in DICOM format for subsequent processing. The study protocol was approved by the Institutional Ethics Committee of Northern Jiangsu People\u0026apos;s Hospital Affiliated to Yangzhou University (Approval No. 2024ky144) in accordance with the Declaration of Helsinki. Written informed consent was obtained from each participant. A representative case classified as Yun Type I SISMAD was selected for computational modeling. This selection was based on the subtype\u0026apos;s relatively high incidence and distinct anatomical feature-an entry tear without a re-entry tear-which was anticipated to provide informative hemodynamic insights upon simulation [11].\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eImage segmentation and geometric model generation\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe generation of a high-fidelity geometric model is crucial for accurate CFD simulations. The process began with image segmentation and 3D reconstruction from the DICOM-formatted CT images using Mimics software (Materialise NV, Belgium). This software facilitated the delineation of vessel boundaries for the abdominal aorta and SMA through grayscale thresholding and a region-growing algorithm, effectively isolating the vascular geometry from adjacent non-target tissues (Fig.1). The segmented 2D image stack was then converted into a 3D surface model and exported as a Standard Tessellation Language (STL) file. The resulting patient-specific model provided detailed anatomical representation suitable for CFD analysis (Fig.2). Subsequently, Geomagic Studio (3D Systems, USA) was employed to refine the initial STL file. This refinement involved removing artifacts, smoothing surfaces, and filling gaps to ensure geometric integrity and continuity. The final stage utilized SolidWorks (Dassault Syst\u0026egrave;mes, France) for further geometric corrections and finalization, producing the computational domain suitable for CFD analysis. This multi-software approach ensured the creation of a geometrically accurate and simulation-ready model derived directly from patient-specific medical imaging data.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eComputational methods and boundary conditions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHemodynamic simulations of the SISMAD model were conducted using ANSYS Fluent (ANSYS Inc., USA). An unstructured tetrahedral mesh was generated for the SISMAD geometry, incorporating local refinement in critical regions, such as the dissection entry tear and aorta bifurcations, to enhance computational accuracy in areas anticipated to exhibit high flow gradients (Fig.3). Grid independence studies were performed to ensure mesh convergence, resulting in an optimal mesh comprising 172,160 elements with an average quality metric of 0.8. Blood was modeled as an incompressible Newtonian fluid with a density of 1045 kg/m\u0026sup3; and a dynamic viscosity of 0.0035 Pa\u0026middot;s. The characteristic Reynolds number was approximately 1800, which is below the critical threshold for turbulence, thus justifying the use of a laminar flow model. The governing Navier-Stokes equations were solved numerically using the finite volume method, ensuring mass conservation. Gravitational forces and energy dissipation were considered negligible. Transient simulations were performed using time-dependent boundary conditions: a time-varying velocity waveform, derived either from literature or patient-specific data, was applied at the inlet (Fig.4), while a constant relative pressure of 0 mmHg was imposed at the outlet. The simulations spanned two to three cardiac cycles, with data for analysis extracted from the final cycle to ensure results represented a periodically stable state, free from initial transient effects. A convergence tolerance of 1 \u0026times; 10⁻⁴ was maintained for all residuals. Subsequent post-processing using CFD-Post (ANSYS Inc., USA) enabled the generation of quantitative flow field maps and detailed topographical distributions of hemodynamic parameters, including wall shear stress (WSS) and pressure gradients. This approach facilitated a comprehensive analysis of the intricate flow dynamics inherent to SISMAD pathophysiology.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eBlood flow dynamics, including velocity distributions, pressure differentials, and WSS within the true lumen (TL) and false lumen (FL) of the SISMAD model, were analyzed. The analysis focused on five critical phases of the cardiac cycle: maximum acceleration (t = 0.10 s), peak velocity (t = 0.22 s), maximum deceleration (t = 0.25 s), minimum velocity (t = 0.38 s), and the mid-diastolic phase (t = 0.72 s). This approach allowed for the elucidation of complex flow patterns within the dissected SMA, as depicted in Fig.5.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eVelocity distributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eVelocity streamlines revealed complex flow patterns within both the TL and FL of the dissected SMA (Fig.5, top row). Maximum velocities were observed near the entry tear region within the TL, with velocity progressively attenuating distally. The FL exhibited markedly lower flow velocities and contained regions of flow stasis, particularly prominent in its distal segment. Quantitative assessment revealed peak velocities reaching 2.673 m/s within the TL, whereas the FL exhibited substantially reduced flow, with velocity magnitudes ranging from approximately 9.202 \u0026times; 10⁻\u0026sup2; m/s to 9.471 \u0026times; 10⁻\u0026sup2; m/s.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePressure distributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAnalysis of pressure distribution revealed significant pressure differentials across the dissection flap and between the TL and FL (Fig.5, middle row). Maximum relative pressure values (approximately 4.198 \u0026times; 10\u0026sup2; Pa) were observed proximally in the SMA near the aortic ostium, with pressure progressively decreasing distal to the entry tear. The FL consistently exhibited lower pressure values compared to the TL. The minimum relative pressure within the FL reached approximately -9.430 \u0026times; 10\u0026sup2; Pa.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eWall shear stress distributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eTopographical analysis of WSS identified regions subjected to elevated shear forces, particularly near the entry tear and along the intimal flap within the TL (Fig.5, bottom row). The maximum WSS magnitude observed in these high-stress regions reached 7.264 \u0026times; 10\u0026sup1; Pa. Conversely, the FL generally exhibited zones of significantly lower WSS, potentially fostering conditions conducive to thrombogenesis. This spatial heterogeneity in WSS distribution likely contributes to differential endothelial responses and subsequent pathophysiological remodeling processes within the dissected vessel.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003e\u003cstrong\u003eHemodynamic insights from a patient-specific SISMAD model\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur CFD analysis revealed significant spatial heterogeneity in WSS distribution within the dissected SMA, corroborating and extending previous findings on the role of hemodynamics in SISMAD pathophysiology [1, 2, 12]. Specifically, markedly elevated WSS, peaking at 72.64 Pa, was concentrated near the primary entry tear and along the TL aspect of the intimal flap, consistent with hypotheses linking high shear forces to endothelial injury and potential tear propagation [2, 4]. Such elevated mechanical stimuli are known potent activators of endothelial mechanotransduction pathways, including NF-\u0026kappa;B and MAPK signaling, which upregulate adhesion molecules like VCAM-1 and ICAM-1 [13-16]. While often studied in atherogenesis, these mechanisms suggest the high WSS environment near the flap could foster a pro-inflammatory state contributing to maladaptive remodeling or flap instability in SISMAD. Conversely, the FL predominantly exhibited regions of substantially lower WSS, a finding consistent with hemodynamic principles associating low shear with blood stasis and a pro-thrombotic milieu conducive to platelet aggregation and fibrin deposition [17, 18]. This observed low WSS environment within the FL likely underlies the common clinical finding of FL thrombosis and significantly influences disease progression [19, 20]. Therefore, the pronounced WSS dichotomy between the high-stress environment potentially driving inflammation and remodeling near the flap in the TL, and the low-stress, pro-thrombotic conditions within the FL, highlights the complex interplay of biomechanical forces in dictating the divergent pathophysiological remodeling pathways and clinical evolution characteristic of SISMAD.\u003c/p\u003e\n\u003cp\u003eThe velocity and pressure distributions derived from our CFD analysis further illuminate the complex hemodynamic environment characteristic of SISMAD. The observed velocity patterns, featuring high-velocity flow (peak 2.673 m/s) concentrated near the entry tear within the TL juxtaposed with markedly reduced velocities (approx. 0.09 m/s) and flow stasis within the FL, align with previous computational and clinical observations [2]. The elevated velocities in the TL, particularly near the tear, likely contribute significantly to the high wall shear stress discussed previously and may represent a key hemodynamic factor influencing tear propagation and flap dynamics. Conversely, the profoundly diminished flow and stasis within the FL directly support the propensity for thrombogenesis frequently observed in this compartment [19, 21]. Complementing these velocity findings, the significant pressure differential observed, with the TL maintaining substantially higher pressure than the FL (minimum relative pressure -943 Pa), provides the driving force influencing intimal flap behavior and FL perfusion dynamics [2, 21]. Taken together, these results depict a hemodynamically challenging environment where high-velocity, higher-pressure flow in the TL interacts with the dissection flap, while the low-velocity, lower-pressure, stagnant environment in the FL promotes thrombosis\u0026mdash;collectively dictating the complex pathophysiology and evolution of SISMAD.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePatient-specific CFD approach compared to previous studies\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis investigation employed a patient-specific CFD methodology, constructing the model directly from the clinical imaging data of the SISMAD patient. This approach represents a significant advancement over studies relying on idealized or generic arterial geometries, which, while useful for elucidating fundamental hemodynamic principles, inherently lack the anatomical specificity crucial for understanding individual patient pathophysiology [2, 17, 21]. The primary strength of our patient-specific approach lies in its ability to incorporate the unique anatomical intricacies of the individual\u0026rsquo;s SMA, including its specific curvature, branching pattern, the precise location and morphology of the entry tear, and the complex, often tortuous configuration of the dissection flap. Previous research has indeed utilized CFD to explore SISMAD hemodynamics, often identifying key factors like WSS, pressure gradients, and flow patterns [2, 4, 21]. However, simulations based on simplified geometries may fail to capture the localized hemodynamic extremes driven by patient-specific anatomical features. For instance, the precise angle of SMA origin, subtle variations in lumen diameter, or the specific shape and extent of the intimal flap can substantially alter local velocity jets, recirculation zones, and WSS distributions [4]. Our detailed, patient-specific model allowed for the direct observation and quantification of these phenomena, such as the focal peak WSS (72.64 Pa) near the primary entry tear and the distinct regions of flow stasis within the FL. While earlier patient-specific SISMAD studies have provided invaluable insights [2, 21], our work contributes by applying this methodology to capture the detailed interplay of velocity, pressure, and WSS within this particular complex dissection morphology. This high-fidelity simulation reinforces the concept that hemodynamic forces are highly sensitive to individual vascular geometry. Therefore, the use of patient-specific CFD is not merely an incremental refinement but a critical step towards understanding the variability in SISMAD presentation and progression, potentially paving the way for more personalized risk stratification and treatment planning in the future.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLimitations of the study\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study is subject to several limitations inherent to its design and methodology. Primarily, the findings are derived from a single patient case, which limits the generalizability of the specific hemodynamic results. Validation necessitates investigation across larger, multi-center cohorts encompassing diverse SISMAD morphologies and clinical presentations. Furthermore, the CFD model incorporated simplifications necessary for computational feasibility: blood was modeled as a Newtonian fluid, which may not fully capture non-Newtonian effects in low-flow regions such as the false lumen, and vessel walls were assumed rigid, thus excluding fluid-structure interaction (FSI). While common in CFD analyses, these assumptions affect the accuracy of the predicted hemodynamic parameters. Finally, direct \u003cem\u003ein vivo\u003c/em\u003e validation of the simulated flow fields and WSS values is currently infeasible, highlighting the importance of model fidelity and the accuracy of the applied boundary conditions.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eDespite these limitations, this investigation demonstrates the feasibility and potential utility of patient-specific CFD for analyzing SISMAD. By elucidating significant hemodynamic differences between the true and false lumens and identifying regions of elevated WSS, our findings reinforce the critical role of local hemodynamics in SISMAD pathophysiology and progression. This approach provides a valuable foundation for future, larger-scale studies aimed at refining personalized risk assessment and therapeutic strategies for SISMAD management.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Ethics Committee of Northern Jiangsu People\u0026apos;s Hospital Affiliated to Yangzhou University (Approval No. 2024ky144). Written informed consent was obtained from each participants.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe DICOM datasets used in this study are not publicly available due to patient privacy regulations but can be obtained from the corresponding author upon reasonable request with appropriate ethics committee approval.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors acknowledge funding support from the Jiangsu Province Subei People\u0026apos;s Hospital Support Special Project (SBQN23012).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eR-W. conceptualized the study and prepared the original draft while Z.C. contributed to conceptualization, review and editing, and project administration.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThanks to all the authors who participated in the design and literature analysis of this paper.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eMei J, Ding W, Yu H, Zhao X, Xu H, Wang K, et al. Different hemodynamic factors cause the occurrence of superior mesenteric atherosclerotic stenosis and superior mesenteric artery dissection. Front Cardiovasc Med 2023;10:1121224.\u003c/li\u003e\n\u003cli\u003ePark YJ, Park CW, Park KB, Roh YN, Kim DI, Kim YW. Inference from clinical and fluid dynamic studies about underlying cause of spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2011;53:80-6.\u003c/li\u003e\n\u003cli\u003eHau SF, Chan YC, Cheung GC, Cheng SW. Risk factor analysis and treatment outcome of patients with spontaneous isolated celiac axis or superior mesenteric artery dissection. J Vasc Surg 2023;77:150-7.\u003c/li\u003e\n\u003cli\u003eWu Z, Yi J, Xu H, Guo W, Wang L, Chen D, et al. The Significance of the Angle between Superior Mesenteric Artery and Aorta in Spontaneous Isolated Superior Mesenteric Artery Dissection. Ann Vasc Surg 2017;45:117-26.\u003c/li\u003e\n\u003cli\u003ePark YJ, Park KB, Kim DI, Do YS, Kim DK, Kim YW. Natural history of spontaneous isolated superior mesenteric artery dissection derived from follow-up after conservative treatment. J Vasc Surg 2011;54:1727-33.\u003c/li\u003e\n\u003cli\u003eHou L, Wang T, Wang J, Yuan D. Isolated superior mesenteric artery dissection in China: A systematic review and meta-analysis. Asian J Surg 2022;45:1070-4.\u003c/li\u003e\n\u003cli\u003eHeo SH, Kim YW, Woo SY, Park YJ, Park KB, Kim DK. Treatment strategy based on the natural course for patients with spontaneous isolated superior mesenteric artery dissection. J Vasc Surg 2017;65:1142-51.\u003c/li\u003e\n\u003cli\u003eBj\u0026ouml;rck M, Koelemay M, Acosta S, Bastos Goncalves F, K\u0026ouml;lbel T, Kolkman JJ, et al. Editor\u0026apos;s Choice - Management of the Diseases of Mesenteric Arteries and Veins: Clinical Practice Guidelines of the European Society of Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2017;53:460-510.\u003c/li\u003e\n\u003cli\u003eYe M, Zhou Q, Wu J, Zhang Z, Li B, Zheng T, et al. Conservative Versus Endovascular Treatment for Spontaneous Isolated Superior Mesenteric Artery Dissection: A Clinical and Imaging Follow-up Study. J Endovasc Ther 2024;31:840-52.\u003c/li\u003e\n\u003cli\u003eMorgan CE, Mansukhani NA, Eskandari MK, Rodriguez HE. Ten-year review of isolated spontaneous mesenteric arterial dissections. J Vasc Surg 2018;67:1134-42.\u003c/li\u003e\n\u003cli\u003eYun WS, Kim YW, Park KB, Cho SK, Do YS, Lee KB, et al. Clinical and angiographic follow-up of spontaneous isolated superior mesenteric artery dissection. Eur J Vasc Endovasc Surg 2009;37:572-7.\u003c/li\u003e\n\u003cli\u003eXiaoq Z, Hao M, Lin L, Jiao Y, Zou J, Zhang X, et al. Clinical and CT Angiographic Follow-Up Outcome of Spontaneous Isolated Intramural Hematoma of the Superior Mesenteric Artery. Cardiovasc Intervent Radiol 2019;42:1088-94.\u003c/li\u003e\n\u003cli\u003eFan J, Liu D, He C, Li X, He F. Inhibiting adhesion events by Panax notoginseng saponins and Ginsenoside Rb1 protecting arteries via activation of Nrf2 and suppression of p38 - VCAM-1 signal pathway. J Ethnopharmacol 2016;192:423-30.\u003c/li\u003e\n\u003cli\u003eBryan MT, Duckles H, Feng S, Hsiao ST, Kim HR, Serbanovic-Canic J, et al. Mechanoresponsive networks controlling vascular inflammation. Arterioscler Thromb Vasc Biol 2014;34:2199-205.\u003c/li\u003e\n\u003cli\u003eZhou M, Yu Y, Chen R, Liu X, Hu Y, Ma Z, et al. Wall shear stress and its role in atherosclerosis. Front Cardiovasc Med 2023;10:1083547.\u003c/li\u003e\n\u003cli\u003eYan B, Yu X, Cai X, Huang X, Xie B, Lian D, et al. A Review: The Significance of Toll-Like Receptors 2 and 4, and NF-\u0026kappa;B Signaling in Endothelial Cells during Atherosclerosis. Front Biosci (Landmark Ed) 2024;29:161.\u003c/li\u003e\n\u003cli\u003eJeays AD, Lawford PV, Gillott R, Spencer P, Barber DC, Bardhan KD, et al. Characterisation of the haemodynamics of the superior mesenteric artery. J Biomech 2007;40:1916-26.\u003c/li\u003e\n\u003cli\u003eMei J, Yuan Y, Yan H, Zhao X, Xue T, Su H, et al. Factors associated with false lumen changes in patients with superior mesenteric artery dissection. Vasc Med 2024;29:274-85.\u003c/li\u003e\n\u003cli\u003eKim YW. Current Understandings of Spontaneous Isolated Superior Mesenteric Artery Dissection. Vasc Specialist Int 2016;32:37-43.\u003c/li\u003e\n\u003cli\u003eMei J, Yan H, Zhao X, Yuan Y, Su H, Xue T, et al. In-stent Restenosis After Stenting for Superior Mesenteric Artery Dissection Is Associated With Stent Landing Zone: From Clinical Prediction to Hemodynamic Mechanisms. J Endovasc Ther 2024:15266028241241494.\u003c/li\u003e\n\u003cli\u003eJia Z, Mei J, Ding W, Zhao X, Gong W, Yu H, et al. The pathogenesis of superior mesenteric artery dissection: An in-depth study based on fluid-structure interaction and histology analysis. Comput Methods Programs Biomed 2022;226:107187.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"biomedical-engineering-online","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmeo","sideBox":"Learn more about [BioMedical Engineering OnLine](http://biomedical-engineering-online.biomedcentral.com/)","snPcode":"12938","submissionUrl":"https://submission.nature.com/new-submission/12938/3","title":"BioMedical Engineering OnLine","twitterHandle":"@BioMedCentral","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Spontaneous Isolated Superior Mesenteric Artery Dissection, Computational Fluid Dynamics, Hemodynamics, Patient-Specific Model, Wall Shear Stress","lastPublishedDoi":"10.21203/rs.3.rs-6595461/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6595461/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eSpontaneous isolated superior mesenteric artery dissection (SISMAD) is a rare but potentially lethal vascular emergency with unclear pathogenesis. While hemodynamic forces are implicated in its development, current understanding remains limited by the lack of patient-specific data. This study aimed to characterize the detailed hemodynamic environment in SISMAD using patient-specific computational fluid dynamics modeling.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eAnalysis of a three-dimensional model reconstructed from computed tomography angiography of a Yun Type I SISMAD revealed complex flow patterns with marked hemodynamic differences between the true lumen (TL) and false lumen (FL). The TL exhibited high-velocity flow concentrated near the entry tear and significantly elevated wall shear stress along the intimal flap. In contrast, the FL demonstrated markedly lower velocities, regions of flow stasis, and low wall shear stress. A substantial pressure gradient existed across the intimal flap, with higher pressure in the TL compared to the FL. These findings provide quantitative confirmation of the theorized hemodynamic forces contributing to dissection progression and potential thrombosis formation.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003ePatient-specific computational modeling reveals a complex and heterogeneous hemodynamic environment within the dissected superior mesenteric artery. The high-velocity flow and elevated wall shear stress in the true lumen may contribute to flap instability and inflammation, while the low-flow, stagnant conditions in the false lumen likely promote thrombogenesis. This patient-specific approach provides valuable insights into SISMAD pathophysiology and demonstrates potential for personalized ris assessment and treatment planning in this rare but serious vascular condition.\u003c/p\u003e","manuscriptTitle":"Hemodynamic Characterization of Spontaneous Isolated Superior Mesenteric Artery Dissection Revealed by Patient-Specific Computational Fluid Dynamics","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-29 10:43:30","doi":"10.21203/rs.3.rs-6595461/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-06-25T11:58:42+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-06-08T09:43:03+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"200775869992809975483748966037916946781","date":"2025-06-03T14:36:23+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-05-29T13:34:50+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"323965731847342209218569836710284855691","date":"2025-05-29T12:44:18+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"284558199977779361043472122504779979029","date":"2025-05-29T10:32:05+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-05-29T06:31:50+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"85288133315946159942463532208008118319","date":"2025-05-29T03:21:56+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"174537260567701982726383660557000279008","date":"2025-05-27T14:01:18+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-05-27T09:40:08+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-05-15T16:19:42+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-05-13T22:18:47+00:00","index":"","fulltext":""},{"type":"submitted","content":"BioMedical Engineering OnLine","date":"2025-05-05T14:40:24+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"biomedical-engineering-online","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmeo","sideBox":"Learn more about [BioMedical Engineering OnLine](http://biomedical-engineering-online.biomedcentral.com/)","snPcode":"12938","submissionUrl":"https://submission.nature.com/new-submission/12938/3","title":"BioMedical Engineering OnLine","twitterHandle":"@BioMedCentral","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"16583b25-7c37-442c-9488-dc22c9a46fac","owner":[],"postedDate":"May 29th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2025-08-05T14:08:57+00:00","versionOfRecord":[],"versionCreatedAt":"2025-05-29 10:43:30","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6595461","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6595461","identity":"rs-6595461","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}