Fluid-structure interaction modelling in type B aortic dissection: Effect of intimal flap and aortic wall motion on hemodynamics / Chong Mei Yan

Chong , Mei Yan (2022) Fluid-structure interaction modelling in type B aortic dissection: Effect of intimal flap and aortic wall motion on hemodynamics / Chong Mei Yan. PhD thesis, Universiti Malaya.

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Abstract

Aortic dissection is a life-threatening vascular disease that is initiated by the development of a tear in the intima aortic wall layer, allowing high pressure blood to enter the aortic wall and separate the wall layers, forming a true lumen (TL) and a false lumen (FL), which are separated by the intimal flap. During the acute phase of type B aortic dissection (TBAD), the first two weeks since symptom onset, uncomplicated patient is preferentially treated medically, and thus naturally transitions into the chronic state. However, patient follow-ups continue to show a high number of late complications mainly caused by incomplete FL thrombosis, despite best medical treatments. While computational fluid dynamics (CFD) is a promising modelling technique to assist the clinical management of TBAD by providing insight into the complex hemodynamics of TBAD, most CFD studies reported so far are based on rigid wall simulations, assuming wall motion has a minor effect on the hemodynamics. Hence, this thesis aims to develop and validate a monolithic, fully coupled fluid-structure interaction (FSI) computational framework to account for realistic flap motion in TBAD. To achieve this aim, an idealised phantom geometry, relevant to anatomical measurements of acute dissected human aorta was constructed. Large flap motion of up to 4.6 mm is examined, and the influence of flap motion on flow has been quantitatively analysed in terms of TL and FL flow splits, disturbed flow in the FL, luminal pressure difference, wave propagation and time-averaged WSS indices. Next, the developed FSI model was combined with a shear-driven thrombosis model described by a series of convection-diffusion reaction equations. The integrated FSI-thrombosis model aimed to investigate the interaction between vessel wall motion and growing thrombus, which has not been reported elsewhere in TBAD. Further extension of the FSI approach was performed on patient-specific cases to validate computational results with 4D flow MRI and Doppler-wire pressure measurements. In comparison with CFD model, the substantial movement of flap mostly increases the flow resistance in the TL and causes more disturbed flow in the FL. The flap-induced luminal pressure is dampened, thereby affecting pressure measures. Regarding FL thrombosis, the wall compliance and flap motion sped up the progression of thrombus growth and formation. The continuous development of vortices caused by drastic flap motion, induced high shear stress and shear rates around tears. This helped to transport activated platelets further to the neighbouring region, thus accelerating thrombus formation in the FSI models. In the end, the FSI results have been validated and good agreement between FSI models and in-vivo data was observed. The high jet velocity entering the primary entry tear was captured accurately by the FSI models, while the average pressures predicted by the FSI models matched closely with the Doppler-wire readings. The incorporation of drastic aortic wall motion as reported in the TBAD patients can be reproduced in the patient-specific FSI models. The movement of the aortic wall and flap influenced the TL/FL flow splits, pulse pressure and pressure difference between the TL and the FL.

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