模拟人体心脏的心肌流体动力学

Marshall Davey, Charles Puelz, Simone Rossi, Margaret Anne Smith, David R Wells, Gregory M Sturgeon, William Paul Segars, John P Vavalle, Charles S Peskin, Boyce E Griffith
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摘要

心脏流体动力学从根本上涉及复杂血流与肌肉心壁和薄瓣膜叶结构变形之间的相互作用。长期以来,科学界、工程界和医学界一直致力于创建心脏数学模型,以捕捉、解释和预测这些流体与结构之间的相互作用。然而,现有的考虑血液、活跃收缩的心肌和瓣膜之间相互作用的计算模型在预测瓣膜性能、捕捉细尺度流动特征或使用组织生物力学的现实描述方面能力有限。在这里,我们介绍了一个全面的人体心脏流体与结构相互作用(FSI)数学模型,并对其进行了基准测试。该模型的独特之处在于它包含了对所有主要心脏结构的生物力学详细描述,并通过人体组织标本的拉伸试验进行校准,以反映心脏的微观结构。此外,它还是首个从解剖学和生理学角度详细描述所有四个心脏瓣膜的 FSI 心脏模型。我们证明,该综合模型可生成生理动态,包括自动捕捉等容收缩和松弛的逼真压力-容积环路,而且其对负荷条件变化的反应与弗兰克-斯塔林机制一致。这些复杂的关系是在我们对心脏生理学的全面描述中通过相互作用内在产生的。这些模型可以作为预测医疗干预影响的工具。它们还能为心脏病理生理学和功能障碍(包括先天性缺陷、心肌病和心力衰竭)的机理研究提供平台,而这些研究很难或不可能在患者身上进行。
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Simulating cardiac fluid dynamics in the human heart
Cardiac fluid dynamics fundamentally involves interactions between complex blood flows and the structural deformations of the muscular heart walls and the thin valve leaflets. There has been longstanding scientific, engineering, and medical interest in creating mathematical models of the heart that capture, explain, and predict these fluid-structure interactions. However, existing computational models that account for interactions among the blood, the actively contracting myocardium, and the valves are limited in their abilities to predict valve performance, capture fine-scale flow features, or use realistic descriptions of tissue biomechanics. Here we introduce and benchmark a comprehensive mathematical model of cardiac fluid-structure interaction (FSI) in the human heart. A unique feature of our model is that it incorporates biomechanically detailed descriptions of all major cardiac structures that are calibrated using tensile tests of human tissue specimens to reflect the heart's microstructure. Further, it is the first FSI model of the heart that provides anatomically and physiologically detailed representations of all four cardiac valves. We demonstrate that this integrative model generates physiologic dynamics, including realistic pressure-volume loops that automatically capture isovolumetric contraction and relaxation, and that its responses to changes in loading conditions are consistent with the Frank-Starling mechanism. These complex relationships emerge intrinsically from interactions within our comprehensive description of cardiac physiology. Such models can serve as tools for predicting the impacts of medical interventions. They also can provide platforms for mechanistic studies of cardiac pathophysiology and dysfunction, including congenital defects, cardiomyopathies, and heart failure, that are difficult or impossible to perform in patients.
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