Mahalingam Arun, Gawandalkar Udhav Ulhas, Kini Girish, Buradi Abdulrajak, Araki Tadashi, Ikeda Nobutaka, Nicolaides Andrew, Laird John R, Saba Luca, Suri Jasjit S
1 Department of Mechanical Engineering, National Institute of Technology Karnataka, Surathkal, Mangalore, India ; 2 Division of Cardiovascular Medicine, Toho University Ohashi Medical Center, Tokyo, Japan ; 3 Division of Cardiovascular Medicine, National Center for Global Health and Medicine (NCGM), Tokyo, Japan ; 4 Vascular Diagnostic Center, University of Cyprus, Nicosia, Cyprus ; 5 Division of Cardiology, University of Davis, Sacramento, California, USA ; 6 Department of Radiology, Azienda Ospedaliero Universitaria di Cagliari, Cagliari, Italy ; 7 Diagnostic and Monitoring Division, AtheroPoint, Roseville, California, USA ; 8 Department of Electrical Engineering (Affl.), Idaho State University, Pocatello, ID, USA.
Cardiovasc Diagn Ther. 2016 Jun;6(3):208-20. doi: 10.21037/cdt.2016.03.08.
Local hemodynamics plays an important role in atherogenesis and the progression of coronary atherosclerosis disease (CAD). The primary biological effect due to blood turbulence is the change in wall shear stress (WSS) on the endothelial cell membrane, while the local oscillatory nature of the blood flow affects the physiological changes in the coronary artery. In coronary arteries, the blood flow Reynolds number ranges from few tens to several hundreds and hence it is generally assumed to be laminar while calculating the WSS calculations. However, the pulsatile blood flow through coronary arteries under stenotic condition could result in transition from laminar to turbulent flow condition.
In the present work, the onset of turbulent transition during pulsatile flow through coronary arteries for varying degree of stenosis (i.e., 0%, 30%, 50% and 70%) is quantitatively analyzed by calculating the turbulent parameters distal to the stenosis. Also, the effect of turbulence transition on hemodynamic parameters such as WSS and oscillatory shear index (OSI) for varying degree of stenosis is quantified. The validated transitional shear stress transport (SST) k-ω model used in the present investigation is the best suited Reynolds averaged Navier-Stokes turbulence model to capture the turbulent transition. The arterial wall is assumed to be rigid and the dynamic curvature effect due to myocardial contraction on the blood flow has been neglected.
Our observations shows that for stenosis 50% and above, the WSSavg, WSSmax and OSI calculated using turbulence model deviates from laminar by more than 10% and the flow disturbances seems to significantly increase only after 70% stenosis. Our model shows reliability and completely validated.
Blood flow through stenosed coronary arteries seems to be turbulent in nature for area stenosis above 70% and the transition to turbulent flow begins from 50% stenosis.
局部血流动力学在动脉粥样硬化形成及冠状动脉粥样硬化疾病(CAD)进展中起重要作用。血液湍流产生的主要生物学效应是内皮细胞膜上壁面剪应力(WSS)的变化,而血流的局部振荡特性影响冠状动脉的生理变化。在冠状动脉中,血流雷诺数范围从几十到几百,因此在计算WSS时通常假定为层流。然而,狭窄条件下通过冠状动脉的脉动血流可能导致从层流到湍流状态的转变。
在本研究中,通过计算狭窄远端的湍流参数,对不同狭窄程度(即0%、30%、50%和70%)的冠状动脉脉动血流中湍流转变的起始进行了定量分析。此外,还量化了不同狭窄程度下湍流转变对诸如WSS和振荡剪切指数(OSI)等血流动力学参数的影响。本研究中使用的经过验证的过渡剪切应力输运(SST)k-ω模型是最适合捕捉湍流转变的雷诺平均纳维-斯托克斯湍流模型。假定动脉壁是刚性的,忽略了心肌收缩对血流的动态曲率效应。
我们的观察结果表明,对于50%及以上的狭窄,使用湍流模型计算的WSSavg、WSSmax和OSI与层流偏差超过10%,并且似乎仅在狭窄70%后流动干扰才显著增加。我们的模型显示出可靠性并得到了充分验证。
对于面积狭窄超过70%的情况,通过狭窄冠状动脉的血流似乎本质上是湍流,并且从50%狭窄开始向湍流的转变。