Predicting the Outcome of TEVAR for Aortic Dissection

主动脉夹层是一种潜在的危及生命的疾病，它始于主动脉壁最内层--内膜的最初撕裂。当血液穿过这个撕裂口时，主动脉壁的各层分开，形成一个不需要的次要血液通道，称为假腔。继发性和/或折返性撕裂可形成在胸主动脉远端、腹主动脉或分叉下的髂动脉。夹层发生的原因尚不完全清楚，但最常见的危险因素是无法控制的高血压和动脉粥样硬化。易患因素也可导致解剖(Salameh和Ratchford，2016)。由于主动脉是向身体供应含氧血液的主要血管，系统的故障可能会导致一系列并发症，包括缺血(最终导致主要器官衰竭)、主动脉瘤和破裂。主动脉夹层的严重程度和由此产生的并发症导致了很高的死亡率。斯坦福A型夹层的死亡率为每小时1%，到第3天的死亡率为50%，而斯坦福B型夹层的30天死亡率较低，为10%(对于最高风险组，死亡率高达70%)(Frank J.Criado，2011)。通常，A型夹层需要立即手术治疗，而B型夹层通常使用血管内治疗或药物治疗，具体取决于患者可能表现出的其他并发症(Salameh和Ratchford，2016)。鉴于血栓形成对患者预后的重要性，在进行治疗时能够预测血栓形成过程是非常必要的。一个基于热力学的数学模型(Menichini and Xu，2016)是在理想化模型中发展起来的，用于预测B型夹层的血栓形成过程。自那以后，它已被应用于患者特定的几何形状，以研究模型的准确性(Menichini等人，2016)，并产生了令人振奋的结果，模型输出与从患者收集的体内数据相当。展望当前博士学位的第二年及以后，目标之一将是对这一模式进行批判性分析。这将包括对所做的假设进行深入的敏感性分析，这可能会导致模型的扩展-例如，需要研究并可能包括的一个理想因素是流体-结构相互作用，以模拟主动脉的非刚性壁。也产生了许多基于动力学的模型，纳入了血栓形成所涉及的复杂生物和化学机制(Anand等人，2006年；Biasetti等人，2012年；Tolenaar等人，2014年；Filipovic等人，2008年；Leiderman和Fogelson，2011年)。将对这些模型进行深入回顾，并与前面讨论的血流动力学模型进行比较，以确定所有模型产生的结果的关键差异。

Aortic dissection is a potentially life threatening disease that begins with an initial tear in the inner most layer of the aortic wall, the intima. When blood passes through this tear the layers of the aortic wall separate creating a secondary, unwanted, channel of blood, known as the false lumen. Secondary and/or reentry tears can form in the distal thoracic aorta, abdominal aorta or the iliac arteries below the bifurcation. The reasoning for why a dissection occurs is not completely understood, however the most common risk factors are uncontrolled hypertension and atherosclerosis. Dissection can also occur due to predisposing factors (Salameh and Ratchford, 2016). As the aorta is the primary vessel for supplying oxygenated blood to the body a fault in the system can lead to a range of complications, including ischemia (and ultimately major organ failure), aortic aneurysm and rupture. The severity of aortic dissection and the resulting complications leads to a high mortality rate. Stanford Type A dissection has a mortality rate of 1% per hour from onset with a rate of 50% by day 3, while Stanford Type B has a lower, but still significant, 30-day rate of 10% (and up to 70% for the highest-risk groups) (Frank J. Criado, 2011). Typically, a Type A dissection requires immediate surgical treatment, while Type B dissections are normally treated using either endovascular or medical therapies, with the decision for which dependent on other complications the patient may be exhibiting (Salameh and Ratchford, 2016).Given the importance of thrombosis to patient prognosis, it is highly desirable to be able to predict the thrombosis process when treatment is administered. A mathematical thermodynamics-based model (Menichini and Xu, 2016) was developed in idealized models to predict the thrombosis process in Type B dissections. It has since been applied to patient specific geometries to investigate the accuracy of the model (Menichini et al., 2016), and produced promising results with model outputs being comparable to in vivo data collected from the patients. Looking at the second year and onwards of the current PhD, one of the objectives will be to critically analyse this model. This will include carrying out an in-depth sensitivity analysis of the assumptions made, which may lead to the expansion of the model - for example, one desirable factor to investigate and potentially include is fluid-structure interactions to simulate the non-rigid wall of the aorta. There have also been numerous kinetic-based models produced, incorporating the complex biological and chemical mechanisms involved in thrombosis formation (Anand et al., 2006; Biasetti et al., 2012; ?; Tolenaar et al., 2014; Filipovic et al., 2008; Leiderman and Fogelson, 2011). An in-depth review of these models and comparison to the previously discussed hemodynamic model will be conducted to determine key differences in results produced by all models.