Cardiology journal · 2016
Estimation of shear stress by using a myocardial bridge-mural coronary artery simulating device.
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Ding Hao, Yang Qian, Shang Kun, Lan Hailian, Lv Jie, Liu Zhilin, Liu Yang, Sheng Lixing, Zeng Yanjun
Аннотация
BACKGROUND: This study was aimed at developing a myocardial bridge-mural coronary artery simulative device and analyzing the relationship between shear stress on the mural coronary artery and atherosclerosis.
METHODS: A myocardial bridge-mural coronary artery simulative device was used to simulate experiments in vitro. In the condition of maintaining any related parameters such as system temperature, average flow rate, and heart rate, we calculated and observed changes in proximal and distal mean values, and oscillatory value of shear stress on the mural coronary artery by regulating the compression level of the myocardial bridge to the mural coronary artery.
RESULTS: Under 0% compression, no significant differences were observed in distal and proximal mean values and oscillatory value of the shear stress on the mural coronary artery. With the increase in the degree of compression, the mean shear stress at the distal end was greater than that at the proximal end, but the oscillatory value of the shear stress at the proximal end was greater than that at the distal end.
CONCLUSIONS: The experimental results of this study indicate that myocardial bridge compression leads to abnormal hemodynamics at the proximal end of the mural coronary artery. This abnormal phenomenon is of great significance in the study of atherosclerosis hemodynamic pathogenesis, which has potential clinical value for pathological effects and treatments of myocardial bridge.
METHODS: A myocardial bridge-mural coronary artery simulative device was used to simulate experiments in vitro. In the condition of maintaining any related parameters such as system temperature, average flow rate, and heart rate, we calculated and observed changes in proximal and distal mean values, and oscillatory value of shear stress on the mural coronary artery by regulating the compression level of the myocardial bridge to the mural coronary artery.
RESULTS: Under 0% compression, no significant differences were observed in distal and proximal mean values and oscillatory value of the shear stress on the mural coronary artery. With the increase in the degree of compression, the mean shear stress at the distal end was greater than that at the proximal end, but the oscillatory value of the shear stress at the proximal end was greater than that at the distal end.
CONCLUSIONS: The experimental results of this study indicate that myocardial bridge compression leads to abnormal hemodynamics at the proximal end of the mural coronary artery. This abnormal phenomenon is of great significance in the study of atherosclerosis hemodynamic pathogenesis, which has potential clinical value for pathological effects and treatments of myocardial bridge.