基于影像的全心脏血流模拟,可精准还原健康与先天性心脏病患者的血流动态。
Image-Based Whole-Heart Cardiac Flow Simulations in Health and Congenital Heart Disease

- 用机器学习重建动态心脏结构,结合阻力浸入表面模拟瓣膜开闭
- 模拟结果与导管测量和4D-MRI一致,揭示先天性心脏病患者血流异常
- 兼顾生理真实性和计算效率,适合临床研究与治疗评估
心腔内血流模式由心腔与心脏瓣膜的耦合运动塑造,为心脏功能提供重要信息。然而临床血流成像受限于检查时间、噪声、分辨率及三维流场不完整等问题。计算流体动力学(CFD)有望实现高精度血流量化与治疗预判,但临床转化需兼顾患者特异性、生理真实性、计算成本与建模复杂度。本文提出一种基于影像的、患者特异性的全心脏血流仿真框架,在保证生理保真度的同时提升计算效率。该框架首先利用基于机器学习的分割与网格传播技术,从时相图像中重建动态心脏解剖结构;随后在变形域上进行CFD仿真,并采用阻力浸入表面(RIS)模型模拟四个瓣膜的生理开闭行为。该方法应用于一名健康成人和一名患有复杂先天性心脏病(CHD)的儿童患者。在健康案例中,模拟重现了生理压力-容积关系、瓣膜开启时机及心室涡旋形成;在CHD案例中,模拟的腔室与血管压力与心导管测量值吻合良好。模拟流场与4D-Flow MRI定性一致,且揭示了因成像伪影遮蔽而模糊的精细流结构。健康与CHD病例对比显示,后者舒张期流场组织紊乱,黏性耗散率显著升高。
原文摘要 · Abstract (English)
Intracardiac flow patterns are shaped by the coupled motion of the cardiac chambers and heart valves and provide important information about cardiac function. However, clinical flow imaging remains limited by exam times, noise, resolution, and incomplete details of the three-dimensional flow. Computational fluid dynamics (CFD) can potentially provide detailed flow quantification and predictive insight into treatment outcomes, but clinical translation requires frameworks that reproduce patient-specific measurements while balancing physiological realism, computational cost, and modeling effort. Herein, we present an image-based, patient-specific computational framework for simulating whole-heart intracardiac hemodynamics that balances physiological fidelity with computational efficiency. The framework first employs machine learning-based segmentation and mesh propagation to reconstruct moving cardiac anatomies from time-resolved images. CFD simulations are then performed to resolve blood flow in deforming domains, while resistive immersed surfaces (RIS) are used to model all four cardiac valves with physiologically realistic opening and closing dynamics. The framework was applied to model hemodynamics in a healthy adult and a pediatric patient with complex congenital heart disease (CHD). In the healthy case, the simulations reproduced physiologic pressure-volume behavior, valve timing, and ventricular vortex formation. In the CHD case, simulated chamber and vessel pressures showed agreement with cardiac catheterization measurements. Simulated flow fields were qualitatively consistent with 4D-Flow MRI, while providing higher-resolution visualization of flow structures that were partially obscured by imaging artifacts. Comparison between the healthy and CHD cases further revealed altered diastolic flow organization and elevated normalized viscous dissipation in the CHD heart.
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