Surface Crack Monitoring by Rayleigh Waves with a Piezoelectric-Polymer-Film Ultrasonic Transducer Array.

This paper presents a method for measuring surface cracks based on the analysis of Rayleigh waves in the frequency domain. The Rayleigh waves were detected by a Rayleigh wave receiver array made of a piezoelectric polyvinylidene fluoride (PVDF) film and enhanced by a delay-and-sum algorithm. This method employs the determined reflection factors of Rayleigh waves scattered at a surface fatigue crack to calculate the crack depth. In the frequency domain, the inverse scattering problem is solved by comparing the reflection factor of the Rayleigh waves between the measured and the theoretical curves. The experimental measurement results quantitatively matched the simulated surface crack depths. The advantages of using the low-profile Rayleigh wave receiver array made of a PVDF film for detecting the incident and reflected Rayleigh waves were analyzed in contrast with those of a Rayleigh wave receiver using a laser vibrometer and a conventional lead zirconate titanate (PZT) array. It was found that the Rayleigh waves propagating across the Rayleigh wave receiver array made of the PVDF film had a lower attenuation rate of 0.15 dB/mm compared to that of 0.30 dB/mm of the PZT array. Multiple Rayleigh wave receiver arrays made of the PVDF film were applied for monitoring surface fatigue crack initiation and propagation at welded joints under cyclic mechanical loading. Cracks with a depth range of 0.36-0.94 mm were successfully monitored.

Fluid-structure interaction in a fully coupled three-dimensional mitral-atrium-pulmonary model.

This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid-structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

Analysis of a coupled fluid-structure interaction model of the left atrium and mitral valve.

We present a coupled left atrium-mitral valve model based on computed tomography scans with fibre-reinforced hyperelastic materials. Fluid-structure interaction is realised by using an immersed boundary-finite element framework. Effects of pathological conditions, eg, mitral valve regurgitation and atrial fibrillation, and geometric and structural variations, namely, uniform vs non-uniform atrial wall thickness and rule-based vs atlas-based fibre architectures, on the system are investigated. We show that in the case of atrial fibrillation, pulmonary venous flow reversal at late diastole disappears, and the filling waves at the left atrial appendage orifice during systole have reduced magnitude. In the case of mitral regurgitation, a higher atrial pressure and disturbed flows are seen, especially during systole, when a large regurgitant jet can be found with the suppressed pulmonary venous flow. We also show that both the rule-based and atlas-based fibre defining methods lead to similar flow fields and atrial wall deformations. However, the changes in wall thickness from non-uniform to uniform tend to underestimate the atrial deformation. Using a uniform but thickened wall also lowers the overall strain level. The flow velocity within the left atrial appendage, which is important in terms of appendage thrombosis, increases with the thickness of the left atrial wall. Energy analysis shows that the kinetic and dissipation energies of the flow within the left atrium are altered differently by atrial fibrillation and mitral valve regurgitation, providing a useful indication of the atrial performance in pathological situations.

On the chordae structure and dynamic behaviour of the mitral valve.

We develop a fluid-structure interaction (FSI) model of the mitral valve (MV) that uses an anatomically and physiologically realistic description of the MV leaflets and chordae tendineae. Three different chordae models-complex, 'pseudo-fibre' and simplified chordae-are compared to determine how different chordae representations affect the dynamics of the MV. The leaflets and chordae are modelled as fibre-reinforced hyperelastic materials, and FSI is modelled using an immersed boundary-finite element method. The MV model is first verified under static boundary conditions against the commercial finite element software ABAQUS and then used to simulate MV dynamics under physiological pressure conditions. Interesting flow patterns and vortex formulation are observed in all three cases. To quantify the highly complex system behaviour resulting from FSI, an energy budget analysis of the coupled MV FSI model is performed. Results show that the complex and pseudo-fibre chordae models yield good valve closure during systole but that the simplified chordae model leads to poorer leaflet coaptation and an unrealistic bulge in the anterior leaflet belly. An energy budget analysis shows that the MV models with complex and pseudo-fibre chordae have similar energy distribution patterns but the MV model with the simplified chordae consumes more energy, especially during valve closing and opening. We find that the complex chordae and pseudo-fibre chordae have similar impact on the overall MV function but that the simplified chordae representation is less accurate. Because a pseudo-fibre chordal structure is easier to construct and less computationally intensive, it may be a good candidate for modelling MV dynamics or interaction between the MV and heart in patient-specific applications.

A coupled mitral valve-left ventricle model with fluid-structure interaction.

Understanding the interaction between the valves and walls of the heart is important in assessing and subsequently treating heart dysfunction. This study presents an integrated model of the mitral valve (MV) coupled to the left ventricle (LV), with the geometry derived from in vivo clinical magnetic resonance images. Numerical simulations using this coupled MV-LV model are developed using an immersed boundary/finite element method. The model incorporates detailed valvular features, left ventricular contraction, nonlinear soft tissue mechanics, and fluid-mediated interactions between the MV and LV wall. We use the model to simulate cardiac function from diastole to systole. Numerically predicted LV pump function agrees well with in vivo data of the imaged healthy volunteer, including the peak aortic flow rate, the systolic ejection duration, and the LV ejection fraction. In vivo MV dynamics are qualitatively captured. We further demonstrate that the diastolic filling pressure increases significantly with impaired myocardial active relaxation to maintain a normal cardiac output. This is consistent with clinical observations. The coupled model has the potential to advance our fundamental knowledge of mechanisms underlying MV-LV interaction, and help in risk stratification and optimisation of therapies for heart diseases.

Modelling mitral valvular dynamics-current trend and future directions.

Dysfunction of mitral valve causes morbidity and premature mortality and remains a leading medical problem worldwide. Computational modelling aims to understand the biomechanics of human mitral valve and could lead to the development of new treatment, prevention and diagnosis of mitral valve diseases. Compared with the aortic valve, the mitral valve has been much less studied owing to its highly complex structure and strong interaction with the blood flow and the ventricles. However, the interest in mitral valve modelling is growing, and the sophistication level is increasing with the advanced development of computational technology and imaging tools. This review summarises the state-of-the-art modelling of the mitral valve, including static and dynamics models, models with fluid-structure interaction, and models with the left ventricle interaction. Challenges and future directions are also discussed.