An integrated fluid\u2013structure interaction and thrombosis model for type B aortic dissection

Mei Yan Chong,Socrates Dokos,Zhi Chao Ong,Chlöe Harriet Armour,Einly Lim,Xiao Yun Xu,Boram Gu

doi:10.1007/s10237-021-01534-5

Abstract

False lumen thrombosis (FLT) in type B aortic dissection has been associated with the progression of dissection and treatment outcome. Existing computational models mostly assume rigid wall behavior which ignores the effect of flap motion on flow and thrombus formation within the FL. In this study, we have combined a fully coupled fluid–structure interaction (FSI) approach with a shear-driven thrombosis model described by a series of convection–diffusion reaction equations. The integrated FSI-thrombosis model has been applied to an idealized dissection geometry to investigate the interaction between vessel wall motion and growing thrombus. Our simulation results show that wall compliance and flap motion can influence the progression of FLT. The main difference between the rigid and FSI models is the continuous development of vortices near the tears caused by drastic flap motion up to 4.45 mm. Flap-induced high shear stress and shear rates around tears help to transport activated platelets further to the neighboring region, thus speeding up thrombus formation during the accelerated phase in the FSI models. Reducing flap mobility by increasing the Young’s modulus of the flap slows down the thrombus growth. Compared to the rigid model, the predicted thrombus volume is 25% larger using the FSI-thrombosis model with a relatively mobile flap. Furthermore, our FSI-thrombosis model can capture the gradual effect of thrombus growth on the flow field, leading to flow obstruction in the FL, increased blood viscosity and reduced flap motion. This model is a step closer toward simulating realistic thrombus growth in aortic dissection, by taking into account the effect of intimal flap and vessel wall motion.

Highlights

Aortic dissection is a severe injury caused by a tear in the inner layer of the aortic wall, the intima
Greater pressure in the proximal TL caused the flap to be pushed toward the false lumen (FL), while FL pressure predominantly exceeded the TL in the distal location, the flap moved toward the TL
After T4 the location of maximum flap displacement shifted from the distal tear toward the middle FL region where no thrombus was formed

Summary

Introduction

Aortic dissection is a severe injury caused by a tear in the inner layer of the aortic wall, the intima. Hemodynamics in the FL such as highly disturbed flow, long residence time and abnormally low wall shear stress (WSS) (Chen et al 2013; Tse et al 2011; Cheng et al 2010), which have all been identified as potential markers for predicting thrombus development (Rayz et al 2008, 2010). Rayz et al (2008) found for intracranial aneurysms that regions with increased flow residence time and low shear stress correlated strongly with areas of thrombus deposition observed in follow-up magnetic resonance scans. Dissection patients with fewer reentry tears, longer distances between the tears and a smaller aortic arch angle were observed to have higher chances of FL thrombosis. These CFD models are useful in predicting the regions which are likely to form thrombus for dissection patients

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