Background and objective

Coronary artery diseases and aortic valve stenosis are two of the main causes of mortality and morbidity worldwide. Stenosis of the aortic valve develops due to calcium deposition on the aortic valve leaflets during the cardiac cycle. Clinical investigations have demonstrated that aortic valve stenosis not only affects hemodynamic parameters inside the aortic root but also has a significant influence on the coronary artery hemodynamics and leads to the initiation of coronary artery disease. The aim of this study is to investigate the effect of calcification of the aortic valve on the variation of hemodynamic parameters in the aortic root and coronary arteries in order to find potential locations for initiation of the coronary stenoses.

Methods

Fluid structure interaction modelling methodology was used to simulate aortic valve hemodynamics in the presence of coronary artery flow. A 2-D model of the aortic valve leaflets was developed in ANSYS Fluent based on the available echocardiography images in literature. The k-ω SST turbulence model was utilised to model the turbulent flow downstream of the leaflets.

Results

The effects of calcification of the aortic valve on aortic root hemodynamics including transvalvular pressure gradient, valve orifice dimeter, vorticity magnitude in the sinuses and wall shear stress on the ventricularis and fibrosa layers of the leaflets were studied. Results revealed that the transvalvular pressure gradient increases from 792 Pa (∼ 6 mmHg) for a healthy aortic valve to 2885 Pa (∼ 22 mmHg) for a severely calcified one. Furthermore, the influence of the calcification of the aortic valve leaflets on the velocity profile and the wall shear stress in the coronary arteries was investigated and used for identification of potential locations of initiation of the coronary stenoses. Obtained results show that the maximum velocity inside the coronary arteries at early diastole decreases from 1 m/s for the healthy valve to 0.45 m/s for the severely calcified case.

Conclusions

Calcification significantly decreases the wall shear stress of the coronary arteries. This reduction in the wall shear stress can be a main reason for initiation of the coronary atherosclerosis process and eventually results in coronary stenoses.

中文翻译：

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主动脉瓣狭窄的流体结构相互作用模型：瓣膜钙化对冠状动脉血流和主动脉根部血流动力学的影响。

背景和目标

冠状动脉疾病和主动脉瓣狭窄是世界范围内死亡率和发病率的两个主要原因。由于在心动周期期间钙沉积在主动脉瓣小叶上而导致主动脉瓣狭窄。临床研究表明，主动脉瓣狭窄不仅影响主动脉根内的血流动力学参数，而且对冠状动脉血流动力学有重大影响，并导致冠状动脉疾病的发作。这项研究的目的是调查主动脉瓣钙化对主动脉根和冠状动脉血流动力学参数变化的影响，以便找到引发冠状动脉狭窄的潜在位置。

方法

在冠状动脉血流存在的情况下，使用流体结构相互作用建模方法来模拟主动脉瓣血流动力学。基于文献中可获得的超声心动图图像，在ANSYS Fluent中开发了主动脉瓣小叶的二维模型。利用k - ωSST湍流模型来模拟小叶下游的湍流。

结果

研究了主动脉瓣钙化对主动脉根部血流动力学的影响，包括跨瓣压力梯度，瓣膜口径直径，鼻窦的涡度大小以及小叶的心室和纤维层的壁切应力。结果表明，跨瓣压力梯度从健康主动脉瓣的792 Pa（〜6 mmHg）增加到严重钙化的2885 Pa（〜22 mmHg）。此外，研究了主动脉瓣小叶钙化对冠状动脉速度分布和壁切应力的影响，并将其用于识别冠状动脉狭窄的潜在起始位置。获得的结果表明，舒张早期早期冠状动脉内部的最大速度从健康瓣膜的1 m / s降低到0。

结论

钙化显着降低了冠状动脉的壁切应力。壁切应力的降低可能是引发冠状动脉粥样硬化过程的主要原因，并最终导致冠状动脉狭窄。