Aortic dissection is where the medial layer of the arterial wall is separated by a tear leading to intramural bleeding. The blood forms an alternate channel of flow known as the false lumen. Thrombosis of the false lumen (FL) is common in cases of dissection as flow conditions are typically more stagnant than in the true lumen (TL). Central to the process of thrombosis is the activation and aggregation of platelets in the blood. Therefore, the aim of this work is to simulate the transport of platelets in a case of Type-B aortic dissection in a clinically-relevant timeframe.
We investigated a 38-year-old female with Type-B aortic dissection. After reconstructing the contrast-enhanced computed tomography (CT) scans into three dimensions, we created a computational mesh of polyhedral and prism elements. We used realistic boundary conditions at the inlet and at the outlets via 3-element Windkessel models. A one-way Lagrangian method was used to model the trajectories of platelets and particles were injected for 11 s over 16 cardiac cycles. The total number of injected particles was 1.5M. We ran our simulations on 512 cores of the MAGNUS supercomputer at the Pawsey Supercomputing Centre.
We observed elevated residence times of these particles in regions of both stagnant (low TAWSS) and recirculating flow (high OSI), emphasising the need to consider both TAWSS and OSI in thrombus susceptibility predictions for dissection. Tear geometry was seen to have a dominating effect on TL haemodynamics, with platelets colliding and adhering to the wall primarily around the proximal entry tears and supra-aortic branching vessels.
The complex flow patterns support the need for computational modelling to reveal flow conditions and prognosis for Type-B aortic dissection patients. Furthermore, high-performance computing enables computationally expensive patient-specific simulations to be carried out within a clinical timescale.
Computational fluid dynamics Particle residence time Wall shear stress
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We would like to acknowledge funding from the National Health and Medical Research Council (grants APP106986 and APP1083572) and the William and Marlene Schrader Trust. This work was supported by resources provided by the Pawsey Supercomputing Centre with funding from the Australian Government and the Government of Western Australia. The patient was imaged for the Liège Study on Dissected Aorta (LIDIA) partially funded by ‘Fonds pour la chirurgie cardiaque, Belgium’ and unrestricted research grant from Medtronic.
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