Aortic dissection is a disease caused by the occurrence of a rupture in the innermost layer of the aortic wall. Due to the pulsation of the heart, blood penetrates through the tear between the layers of the aortic wall, which causes a new, so-called false lumen (FL). The local haemodynamic conditions in the FL significantly contribute to clotting of blood, so the formation of a thrombus. The level of thrombosis in the FL affects patients' prognosis and chances of survival, in which a complete thrombosis is usually beneficial. In recent studies on platelet deposition in the FL, it is demonstrated that haemodynamic conditions influence on platelet activation and aggregation, effectively boosting in regions of recirculation. Blood coagulation has the highest chance of occurrence in these recirculation regions within the FL. Considering the dominant influence of shear rate in FL thrombosis, the non-Newtonian rheological properties and behaviour of blood play a crucial role. The most important rheological factor is the volume fraction of red blood cells in the blood, i.e., the haematocrit value (HCT), which affects the shear rate dependent viscosity and the yield stress observed in regions of low shear rate and stress, respectively, in the blood flow. In the current work, the influence of the haematocrit value on thrombosis in the FL is simulated. The simulations are done in idealized aortic dissection phantom models employing HCT-dependent non-Newtonian haemodynamics. The value for the HCT was varied within a physiological range. On the one hand, an increase in the total volume of thrombus in time was found for all HCT values. On the other hand, with increasing HCT values, less thrombus is formed in the FL. This suggests that high HCT values impede thrombus formation due to rheological effects and that patients with higher haematocrit values have less chance of benefiting from complete thrombosis in the FL.
Aortic dissection is a severe cardiovascular disease caused by the occurrence of a tear in the aortic wall. As a result, the blood penetrates the wall and makes a new blood channel called the false lumen. The haemodynamic conditions in the false lumen may contribute to the formation of thrombi, which influence the patient's diagnosis and outcomes. In this study, the focus is on a haemodynamic-based model of thrombus formation. Since the model construction entails uncertainties in the model parameters, a variance-based sensitivity analysis is performed. Thrombus formation at a backward-facing step is considered as a benchmark for the numerical simulations and sensitivity analysis. This geometry is capable of representing the main contributions of the model in thrombus formation. The study aims at improving the understanding of the model's structure and at preparing model simplifications to enable efficient patient-specific simulations in the future. A polynomial chaos expansion is employed as a surrogate model, from which the quantitative sensitivity indices are derived. In this study, nine model parameters are selected, whose proper values are not well known. The model responses taken into account are the maximum volume fraction of thrombus, its time development, and the thrombus growth rate. The results show that the model lends itself to model reduction since some of the model parameters show little to no influence on the model's outputs. A threshold value related to the concentration of bounded platelets and the bounded platelets reaction rate are identified as the key input parameters dominating the thrombus model predictions in the current geometry. Furthermore, the introduced thrombus characteristic growth time is driven by both the aforementioned variables.
Background: Type B aortic dissection (TBAD) is a dangerous pathological condition with a high mortality rate. TBAD is initiated by an intimal tear that allows blood to flow between the aortic wall layers, causing them to separate. As a result, alongside the original aorta (true lumen), a false lumen (FL) develops. TBAD compromises the whole cardiovascular system, in the worst case resulting in complete aortic rupture. Clinical studies have shown that dilation and rupture of the FL are related to the failure of the FL to thrombose. Complete FL thrombosis has been found to improve the clinical outcomes of patients with chronic TBAD and is the desired outcome of any treatment. Partial FL thrombosis has been associated with late dissection-related deaths and the requirement for re-intervention, thus the level of FL thrombosis is dominant in classifying the risk of TBAD patients. Therefore, it is important to investigate and understand under which conditions complete thrombosis of the FL occurs.Method: Local FL hemodynamics play an essential role in thrombus formation and growth. In this study, we developed a simplified phenomenological model to predict FL thrombosis in TBAD under physiological flow conditions. Based on an existing shear-driven thrombosis model, a comprehensive model reduction study was performed to improve computational efficiency. The reduced model has been implemented in Ansys CFX and applied to a TBAD case following thoracic endovascular aortic repair (TEVAR) to test the model. Predicted thrombus formation based on post-TEVAR geometry at 1-month was compared to actual thrombus formation observed on a 3-year follow-up CT scan.Results: The predicted FL status is in excellent agreement with the 3-year follow-up scan, both in terms of thrombus location and total volume, thus validating the new model. The computational cost of the new model is significantly lower than the previous thrombus model, with an approximate 65% reduction in computational time. Such improvement means the new model is a significant step towards clinical applicability.Conclusion: The thrombosis model developed in this study is accurate and efficient at predicting FL thrombosis based on patient-specific data, and may assist clinicians in choosing individualized treatments in the future.
Aortic dissection is caused by a tear on the aortic wall that allows blood to flow through the wall layers. Usually, this tear involves the intimal and partly the medial layer of the aortic wall. As a result, a new false lumen develops besides the original aorta, denoted then as the true lumen. The local hemodynamic conditions such as flow disturbances, recirculations and low wall shear stress may cause thrombus formation and growth in the false lumen. Since the false lumen status is a significant predictor for late-dissection-related deaths, it is of great importance in the medical management of patients with aortic dissection. The hemodynamic changes in the aorta also alter the electrical conductivity of blood. Since the blood is much more conductive than other tissues in the body, such changes can be identified with non-invasive methods such as impedance cardiography. Therefore, in this study, the capability of impedance cardiography in monitoring thrombosis in the false lumen is studied by multiphysics simulations to assist clinicians in the medical management of patients under treatment.To tackle this problem, a 3D computational fluid dynamics simulation has been set up to model thrombosis in the false lumen and its impact on the blood flow-induced conductivity changes. The electrical conductivity changes of blood have been assigned as material properties of the blood-filled aorta in a 3D finite element electric simulation model to investigate the impact of conductivity changes on the measured impedance from the body's surface.The results show remarkable changes in the electrical conductivity distribution in the measurement region due to thrombosis in the false lumen, which significantly impacts the morphology of the impedance cardiogram. Thus, frequent † Vahid Badeli and Alireza Jafarinia contributed equally to this work
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