基于"心肌桥-冠状动脉"模拟装置的周向应力研究

研制一种心肌桥压迫冠状动脉的模拟装置,用以研究壁冠状动脉近端与远端周向应力的动态变化,并可实现其独立调节.制作"心肌桥-冠状动脉"模拟装置,分别改变模拟冠状动脉外压和心肌桥压迫程度并记录周向应力的变化情况.结果表明,周向应力的异常主要位于壁冠状动脉近端,随着心肌桥压迫程度加剧,近端的周向应力平均值与震荡值(最大值一最小值)明显增大."心肌桥-冠状动脉"模拟装置能提供体外研究周向应力对血管影响的实验手段.     

壁冠状动脉周向应力体外加载装置的研制

目的设计并研制壁冠状动脉周向应力体外模拟装置,实现不同程度心肌桥压迫下壁冠状动脉周向应力的体外加载。方法利用心肌桥冠状动脉血液动力学体外模拟装置,实现壁冠状动脉周向应力的体外测量。依托上述实验数据,实现不同程度心肌桥压迫下壁冠状动脉周向应力的体外加载。结果通过体外测量实验发现,壁冠状动脉近心段周向应力最大值、平均值以及波动值都会随着心肌桥压迫程度的增加而显著增大。通过壁冠状动脉周向应力的体外加载实验,验证加载波形与周向应力体外测量实验波形基本吻合。结论该装置可以实现壁冠状动脉周向应力的体外加载,为探究壁冠状动脉近端血液动力学异常对动脉粥样硬化产生及斑块破裂的影响,提供一个尽量接近在体环境、多种参数可调控的体外模拟平台。     

基于“心肌桥-冠状动脉”模拟装置的切应力研究

背景:在动脉粥样硬化的研究领域,由于人体血液动力学环境的复杂性,动脉粥样硬化与血流动力学壁面切应力的相关性难以作出确切定论。目的:模拟心肌桥-冠状动脉装置,分析壁冠状动脉血液动力学参数的变化特征与动脉粥样硬化间的关系。方法:采用心肌桥-冠状动脉模拟装置进行体外模拟实验,保持系统温度、平均流量和心率等相关参数不变,调节心肌桥对壁冠状动脉的压迫程度,观察并记录壁冠状动脉近端和远端切应力平均值和震荡值的变化情况。结果与结论:0%压迫时,壁冠状动脉近端和远端的切应力平均值和震荡值差异均不显著;50%压迫时,近端切应力震荡值明显大于远端;80%压迫时,远端切应力平均值大于近端,近端切应力震荡值大于远端。随压迫程度的增加,切应力的平均值远端高于近端,而震荡值近端高于远端。提示壁冠状动脉近端切应力震荡值的升高是导致其动脉粥样硬化发生的重要因素。     

壁冠状动脉血流动力学特性的实验模拟与理论研究

目的临床研究、动物实验和模拟试验都证实心肌桥在收缩期的压迫作用,可引起壁冠状动脉管腔狭窄,从而使流量、流速及压力发生变化,导致血流动力学特性的异常现象。作者从"水击"理沦的角度探讨冠状动脉心肌桥前端的压力和流速变化这一异常现象的力学背景。方法利用心肌桥模拟装置在收缩期中和舒张期初"水击"发生前后对壁冠状动脉血流动力学进行模拟并用一维水击波理论模型进行分析、计算,与正常情况下实验数据对比分析。结果壁冠状动脉近端收缩压的升高幅度、舒张期流速的升高幅度计算值与实验值基本一致。结论证实了壁冠状动脉血流动力学特性异常现象是由扰动引起的"水击"波。     

心肌桥壁冠状动脉血液动力学数值模拟

目的数值模拟心肌桥壁冠状动脉血液动力学,探索心肌桥壁冠状动脉近心端易发生动脉粥样硬化的血液动力学机理。方法建立随心搏运动的局部狭窄直圆管模型模拟心肌桥壁冠状动脉形态学,管壁为薄壁线弹性体,血流遵循不可压缩牛顿流体的一维管流方程组,用Lax-Wendroff方法数值求解。结果心肌桥壁冠状动脉血液动力学与正常冠状动脉血液动力学相比有很大差异,血流量#壁切应力和壁切应力梯度均不同。在心肌桥壁冠状动脉中,近心端壁切应力及壁切应力梯度的变化要远大于远心端。对于有两段心肌桥的情况,它们的壁切应力和壁切应力梯度变化趋势基本一致,但距心室较远的心肌桥,其壁切应力和壁切应力梯度要大于靠近心室的那段心肌桥,且随时间的变化程度也更剧烈。结论数值模拟结果表明,心肌桥壁冠状动脉血液动力学不同于正常冠状动脉血液动力学,近心端壁切应力及壁切应力梯度的变化要远大于远心端,从而对动脉管内皮细胞产生重要影响,这可能是心肌桥壁冠状动脉近心端易发生动脉粥样硬化的血液动力学机理。     

心肌桥-壁冠状动脉血流动力学模型的设计和制作

根据流体力学原理并结合冠状动脉血流的特点,设计并研制心肌桥-壁冠状动脉血流动力学模型,使得能够在有效设定和控制各种不同参数的实验条件下,全面和系统地模拟心肌桥对壁冠状动脉血流动力学的影响,为进一步研究不同条件下心肌桥对壁冠状动脉血流的影响提供前期工作基础。     

心肌桥形态学的研究现状

心肌桥是指覆盖在冠状动脉及其主要分支上的心肌纤维,是一种较普遍的解剖现象,其肌纤维在组织学上有区别于普通心肌纤维而有类似于骨骼肌倾向结构的特点。。心肌桥的结构差异很大,部分可以压迫壁冠状动脉导致相应的血流动力学的变化,造成心肌缺血,这可能和部分心肌桥较厚和较宽,距离冠状动脉窦距离较近,和壁冠状动脉的距离不大等因素有关。尽管壁冠状动脉本身很少发生动脉粥样硬化,但其近段血管却有容易发生动脉粥样硬化的倾向,已经得到临床上越来越广泛的重胡。     

壁冠状动脉与心肌桥的应用解剖学

本文在 50例心脏上测量了心肌桥位置的长、宽、厚度 ;并在光镜下观察了壁冠状动脉的结构。发现桥前段血管内膜较桥下、后段的内膜显著增厚 (P<0 .0 1) ,讨论了它与冠状动脉粥样硬化间的关系。     

维医沙疗对股动脉分支的血流动力学影响

目的研究维医沙疗对人体股动脉分叉血管血流动力学及受力的影响,进而揭示维医沙疗对人体股动脉血栓成因的作用机制。方法在室内维医沙疗系统中对受试者进行维医沙疗,用飞利浦便携式彩色多普勒超声诊断仪分别测试受试者维医沙疗前后的股动脉血流速度峰值、内径和阻力指数(resistant index,RI),并进行统计学分析;重构股动脉分支的三维流-固耦合有限元模型,采用ANSYS workbench模拟计算维医沙疗前后流场的血流速度、压力、壁面切应力和股动脉壁的应力、应变、总位移。结果维医沙疗后股动脉血流速度峰值的平均值和内径分别增大了32.43%和2.63%,RI降低了4.88%,股动脉血流速度峰值和RI维医沙疗前后差异均具有统计学意义(P0.05),股动脉内径维医沙疗前后差异没有统计学意义(P0.05)。维医沙疗后股动脉血流速度、压力和壁面切应力最大值分别增大29.91%、68.52%和46.55%;维医沙疗后股动脉壁的总位移、应力和应变最大值分别增大65.85%、45.45%和44%。结论维医沙疗对加快血流速度、降低RI有显著影响,能增大股动脉血管内径,从而改善股动脉内血液的循环;并且维医沙疗后股动脉壁面切应力、血流速度、压力以及股动脉壁所受应力、应变和总位移有所增大,分叉处的高压力区域有所减少,维医沙疗对降低股动脉粥样硬化及血栓形成有一定的积极作用。     

缝合式和机械吻合式搭桥模型的血流动力学数值模拟

为了说明机械吻合器的引入对冠状动脉搭桥术近端吻合区血流动力学因素的影响,运用Solidworks软件构造了缝合式和机械吻合式两种搭桥模型。运用有限单元数值模拟的方法和Fluent6.3软件,对两种模型移植血管中脉动流进行数值化模拟和可视化分析。获得了吻合区在一个心动周期内不同时刻的速度场、二次流、压力及壁面切应力的分布情况。结果表明,机械吻合器的引入在增大移植血管中血流速度（大于缝合模型约0.2 m/s）的同时使得低速区范围增大,吻合区壁面切应力变化范围为0～50 Pa,应力集中现象明显,壁面切应力变化剧烈,易引起血小板活化和内膜增生。为了提高冠状动脉搭桥术的通畅率,对机械吻合器进行优化设计很有必要。     

犬左冠状动脉前室间支心肌桥的形态学特征

目的探讨犬壁冠状动脉和心肌桥的形态学特点,为比较解剖学提供资料。方法取犬心41例,10%甲醛溶液固定,解剖显示冠状动脉及其分支,观测心肌桥及壁冠状动脉的出现率。结果犬冠状动脉心肌桥多出现于前室间支、后室间支和左室前支。心肌桥出现率70.7%,前室间支79.3%,心肌桥厚度为0.56±0.61 mm。前室间支前段内径1.64±0.46 mm,厚度0.18±0.06 mm;壁冠状动脉内径1.35±0.46 mm,厚度0.13±0.04 mm。心肌桥近段距第一对角支距离为19.78±8.20 mm,距前室间支起始部距离为24.49±12.37mm,距右冠起始部距离为24.21±5.80 mm。心肌桥纤维走向与壁冠状动脉夹角为68.94±14.38。结论犬冠状动脉心肌桥出现率及位置与人相似,可作为科研动物模型。     

心肌桥的观测及其解剖生理学意义分析

目的：探讨心肌桥的存在及其存在的解剖生理学意义。方法：不同年龄段的尸体心脏128例，作年龄、性别记录，比较观察心肌桥的出现率、出现位置、壁冠状动脉所在动脉的形态特点及其与年龄、性别间的关系。结果：心肌桥的解剖检出率随年龄和性别呈阶梯样增加，心肌桥出现的区域位置相对稳定集中，心肌桥所在的冠状动脉在形态匕存在显差异，并随年龄而增强。结论：心肌桥为一良性解剖结构，可能具有支持、固定冠状动脉，局部增大冠状动脉血压，提高心肌血供的“心肌瓣膜”作用。     

Collagen alteration in vascular remodeling by hemodynamic factors

The collagen alterations in the vascular wall remodeled by hemodynamic change were investigated by electron microscopy and immunohistochemistry. The left anterior descending coronary artery (LAD) without a myocardial bridge (MB) showed both lower matrix metalloproteinase-1 (MMP-1) expression and a smaller extent of spiraled collagen (SC) distribution than the LAD wall with MB, in which the intima was influenced by high shear stress. In the wall of the varicose great saphenous vein (GSV) the expression of MMP-1 was lower, while the expression of prolyl 4-hydroxylase was higher, than in the normal GSV. The extent of SC distribution in the intima and media of the varicose GSV was smaller than that in the normal GSV. An analogous difference in results was demonstrated between the portal vein (PV) of patients with liver cirrhosis and normal PV. However, the levels of expression of MMP-2, MMP-9 and tissue inhibitors of MMP (TIMPs) in these pathologic vessels were not different from those in the corresponding normal vessels. The results indicate that hemodynamic forces such as shear stress and increased intravascular blood pressure contribute to the collagen alterations in the vascular wall, which may lead to vascular wall remodeling. Received: 22 October 1999 / Accepted: 20 January 2000     

Atherosclerosis suppression in the left anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study

Ultrastructural changes of the left anterior descending coronary artery (LAD) by the presence of myocardial bridge (MB) were studied. In contrast with various atherosclerotic lesions in the intima both proximal to MB and in the whole length of the LAD having no MB, intimal thickness beneath MB was remarkably thin. Neither lipid deposition nor foam cells were present there even in the aged. The intima beneath MB consisted of only normal smooth muscle cells (SMCs) in some layers. Collagen fibrils loosely stuffed among SMCs showed a spiraled appearance. The intima distal to MB was thicker than that beneath MB. Modified SMCs were present along with normal SMCs, and foam cells were intermingled with them. By scanning electron microscopy, endothelial cells proximal to MB were arranged in a pavement-like appearance, and they were polygonal and flat. Endothelial cells beneath MB became spindle-shaped and regularly engorged along the direction of blood flow. Such regularity was lost in endothelial cells distal to MB. These endothelial changes indicate that the intima beneath MB is stressed by high shear and that intima proximal or distal to MB is stressed by low shear. It is, thus, suggested that alteration of hemodynamic factors that arise from contraction of MB greatly affects the evolution of atherosclerosis through the regulation of intimal lipid infiltration within the LAD.     

3D flow study in a mildly stenotic coronary artery phantom using a whole volume PIV method

Blood flow dynamics has an important role in atherosclerosis initiation, progression, plaque rupture and thrombosis eventually causing myocardial infarction. In particular, shear stress is involved in platelet activation, endothelium function and secondary flows have been proposed as possible variables in plaque erosion. In order to investigate these three-dimensional flow characteristics in the context of a mild stenotic coronary artery, a whole volume PIV method has been developed and applied to a scaled-up transparent phantom. Experimental three-dimensional velocity data was processed to estimate the 3D shear stress distributions and secondary flows within the flow volume. The results show that shear stress reaches values out of the normal and atheroprotective range at an early stage of the obstructive pathology and that important secondary flows are also initiated at an early stage of the disease. The results also support the concept of a vena contracta associated with the jet in the context of a coronary artery stenosis with the consequence of higher shear stresses in the post-stenotic region in the blood domain than at the vascular wall.     

Three-Dimensional Computational Fluid Dynamics Modeling of Alterations in Coronary Wall Shear Stress Produced by Stent Implantation

Rates of coronary restenosis after stent implantation vary with stent design. Recent evidence suggests that alterations in wall shear stress associated with different stent types and changes in local vessel geometry after implantation may account for this disparity. We tested the hypothesis that wall shear stress is altered in a three-dimensional computational fluid dynamics (CFD) model after coronary implantation of a 16 mm slotted-tube stent during simulations of resting blood flow and maximal vasodilation. Canine left anterior descending coronary artery blood flow velocity and interior diameter were used to construct CFD models and evaluate wall shear stress proximal and distal to and within the stented region. Channeling of adjacent blood layers due to stent geometry had a profound affect on wall shear stress. Stagnation zones were localized around stent struts. Minimum wall shear stress decreased by 77% in stented compared to unstented vessels. Regions of low wall shear stress were extended at the stent outlet and localized to regions where adjacent axial strut spacing was minimized and the circumferential distance between struts was greatest within the stent. The present results depict alterations in wall shear stress caused by a slotted-tube stent and support the hypothesis that stent geometry may be a risk factor for restenosis by affecting local wall shear stress distributions. © 2003 Biomedical Engineering Society. PAC2003: 8719Rr, 8710+e, 8780Rb, 8719Uv