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Title: Numerical simulation of mitral valve function
Author: Lau, K. D.
ISNI:       0000 0004 2728 9529
Awarding Body: University College London (University of London)
Current Institution: University College London (University of London)
Date of Award: 2012
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In the mammalian heart there are four heart valves (HV), of which the largest is the mitral valve (MV). Key components in the circulatory system, correct HV function is vital to cardiovascular health. A tethered and asymmetric structure, the MV regulates unidirectional flow between the left atrium and left ventricle. MVfunction is divided between systole/closure, where theMVis required to sustain a pressure load ~120 mmHg whilst minimising flow reversal, and diastole/opening in which the MV is required to rapidly transition from closed to open in order to maximise the transport of blood. Directly affecting the heart, dysfunction of the MV can affect either opening or closing through stenoses or prolapse/regurgitation respectively. Complementing experimental techniques, numerical simulation of theMVoffers additional insights into MV function as unmeasurable variables such as the stresses can be approximated. Due to the immersed nature of the HVs, numerical simulation of the MV requires an approach that is able to model both the large deformation of the MV and non–uniform haemodynamics pressure load resulting from the blood/HV contact. In this work the finite element solver LS–DYNA has been used as it addresses both issues. Using this framework, anatomically sized MV models have been used to characterise the current methodology of reported HV simulations, showing that the fluid–structure interaction (FSI) modelling of the blood/HV contact is essential in the simulation of MV dynamics. Application of this FSI method has been applied to surgical repair technique of the MV known as the edge–to–edge repair, showing that more invasive procedures result in greater stress concentrations but impaired the flow rates. Further advances in this model have been used to examine growth and remodelling effect of the MV tissue in both normal and dysfunctional states.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available