Li Cai , Tong Zhao , Yongheng Wang , Xiaoyu Luo , Hao Gao
{"title":"Fluid–structure interaction simulation of pathological mitral valve dynamics in a coupled mitral valve-left ventricle model","authors":"Li Cai , Tong Zhao , Yongheng Wang , Xiaoyu Luo , Hao Gao","doi":"10.1016/j.imed.2022.06.005","DOIUrl":null,"url":null,"abstract":"<div><p><strong>Background</strong> Understanding the interaction between the mitral valve (MV) and the left ventricle (LV) is very important in assessing cardiac pump function, especially when the MV is dysfunctional. Such dysfunction is a major medical problem owing to the essential role of the MV in cardiac pump function. Computational modelling can provide new approaches to gain insight into the functions of the MV and LV.</p><p><strong>Methods</strong> In this study, a previously developed LV–MV model was used to study cardiac dynamics of MV leaflets under normal and pathological conditions, including hypertrophic cardiomyopathy (HOCM) and calcification of the valve. The coupled LV–MV model was implemented using a hybrid immersed boundary/finite element method to enable assessment of MV haemodynamic performance. Constitutive parameters of the HOCM and calcified valves were inversely determined from published experimental data. The LV compensation mechanism was further studied in the case of the calcified MV.</p><p><strong>Results</strong> Our results showed that MV dynamics and LV pump function could be greatly affected by MV pathology. For example, the HOCM case showed bulged MV leaflets at the systole owing to low stiffness, and the calcified MV was associated with impaired diastolic filling and much-reduced stroke volume. We further demonstrated that either increasing the LV filling pressure or increasing myocardial contractility could enable a calcified valve to achieve near-normal pump function.</p><p><strong>Conclusion</strong> The modelling approach developed in this study may deepen our understanding of the interactions between the MV and the LV and help in risk stratification of heart valve disease and <em>in silico</em> treatment planning by exploring intrinsic compensation mechanisms.</p></div>","PeriodicalId":73400,"journal":{"name":"Intelligent medicine","volume":"3 2","pages":"Pages 104-114"},"PeriodicalIF":4.4000,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Intelligent medicine","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667102622000523","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"COMPUTER SCIENCE, INTERDISCIPLINARY APPLICATIONS","Score":null,"Total":0}
引用次数: 0
Abstract
Background Understanding the interaction between the mitral valve (MV) and the left ventricle (LV) is very important in assessing cardiac pump function, especially when the MV is dysfunctional. Such dysfunction is a major medical problem owing to the essential role of the MV in cardiac pump function. Computational modelling can provide new approaches to gain insight into the functions of the MV and LV.
Methods In this study, a previously developed LV–MV model was used to study cardiac dynamics of MV leaflets under normal and pathological conditions, including hypertrophic cardiomyopathy (HOCM) and calcification of the valve. The coupled LV–MV model was implemented using a hybrid immersed boundary/finite element method to enable assessment of MV haemodynamic performance. Constitutive parameters of the HOCM and calcified valves were inversely determined from published experimental data. The LV compensation mechanism was further studied in the case of the calcified MV.
Results Our results showed that MV dynamics and LV pump function could be greatly affected by MV pathology. For example, the HOCM case showed bulged MV leaflets at the systole owing to low stiffness, and the calcified MV was associated with impaired diastolic filling and much-reduced stroke volume. We further demonstrated that either increasing the LV filling pressure or increasing myocardial contractility could enable a calcified valve to achieve near-normal pump function.
Conclusion The modelling approach developed in this study may deepen our understanding of the interactions between the MV and the LV and help in risk stratification of heart valve disease and in silico treatment planning by exploring intrinsic compensation mechanisms.