Computational modeling of left heart diastolic function: Examination of ventricular dysfunction
Computational modeling of left heart diastolic function: Examination of ventricular dysfunction
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DOI：
10.1115/1.1286559
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发表时间：
2000-08-01
影响因子：
1.7
通讯作者：
Yoganathan, AP
中科院分区：
文献类型：
--
作者：
Lemmon, JD;Yoganathan, AP
一个计算模型，占生理流动条件下的血液-组织相互作用的开发和应用到薄壁模型的左心脏。该模型由左心室、左心房和肺静脉血流组成。该模型的输入函数包括肺静脉驱动压力和模拟期间腔室组织特性变化的时间依赖关系。浸没边界法用于响应于流体力和组织病理生理学变化的组织和血液的相互作用，并且流体质量和动量守恒方程使用Patankar的压力链接方程的半隐式方法（SIMPLE）求解。该模型被用来检查左心室舒张异常条件下的流场延迟心室舒张，延迟心室舒张与心室刚度增加，延迟心室舒张与心房收缩增加。将从左心模型获得的结果与临床观察到的舒张期血流条件以及该模型中正常舒张功能的模拟结果进行比较[1]。涉及舒张功能受损的病例通过改变心室纤维舒张/收缩的输入函数进行建模。三例舒张期舒张功能不全的病例与临床观察到的舒张期流场变化一致。延迟舒张的作用是降低早期充盈幅度，且随心室僵硬度的增加而降低。此外，在心房收缩期增加心房收缩导致更高的晚期充盈速度和心房压力。结果表明，功能障碍可以通过改变纤维的静止长度和/或刚度的关系来建模。这为未来的疾病建模提供了信心，特别是改变腔室特性以检查局部功能障碍对全局流场的影响。【S0148-0731（00）00104-7】。
A computational model that accounts for blood-tissue interaction under physiological flow conditions was developed and applied to a thin-walled model of the left heart. This model consisted of the left ventricle, left atrium, and pulmonary vein flow. The input functions for the model included the pulmonary vein driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The Immersed Boundary Method was used for the interaction of the the tissue and blood in response to fluid forces and changes in tissue pathophysiology, and the fluid mass and momentum conservation equations were solved using Patankar's Semi-implicit Method for Pressure Linked Equations (SIMPLE). This model was used to examine the flow fields in the left heart under abnormal diastolic conditions of delayed ventricular relaxation, delayed ventricular relaxation with increased ventricular stiffness, and delayed ventricular relaxation with an increased atrial contraction. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions, and to the results from simulations of normal diastolic function in this model [1]. Cases involving impairment of diastolic function were modeled with changes to the input functions for fiber relaxation/contraction of the chambers. The three cases of diastolic diastolic dysfunction investigated agreed with the changes in diastolic flow fields seen clinically. The effect of delayed relaxation was to decrease the early filling magnitude, and this decrease was larger when the stiffness of the ventricle was increased. Also, increasing the contraction of the atrium during atrial systole resulted in a higher late filling velocity and atrial pressure. The results show that dysfunction can be modeled by changing the relationships for fiber resting-length and/or stiffness. This provides confidence in future modeling of disease, especially changes to chamber properties to examine the effect of local dysfunction on global flow fields. [S0148-0731(00)00104-7].