血管壁弹性模量对颈动脉狭窄血流储备分数的影响

目的探索将血流储备分数(fractional flow reserve,FFR)引入颈动脉狭窄评估的可行性,并且分析血管壁弹性模量对颈动脉狭窄中血液动力学参数和FFR计算结果的影响。方法利用计算机辅助设计软件建立颈动脉分叉标准模型并获得不同狭窄率的模型。假设血管壁为线弹性材料,血液为不可压缩牛顿流体,在脉动流条件下,利用有限元分析软件进行颈动脉狭窄模型中血液流动的流固耦数值模拟,获得各种血液动力学参数,并计算相应的FFR值。结果当弹性模量固定时,随着狭窄率增加,模型中狭窄部位的FFR逐渐减小,且此时其弹性壁与刚性壁的FFR相对差异随着狭窄率的增加而增加;当狭窄率固定为70%时,随着弹性模量增加,FFR会逐渐减小。结论采用FFR对颈动脉狭窄程度进行功能性评估需要考虑血管壁弹性的影响;狭窄率越大,血管壁弹性模量对FFR的影响越大。     

锥度角对非定常的动脉血流的压力分布的影响

应用Navier-Stokes方程和质量连续原理对具有锥度角的动脉血管中非定常状态下的血液发展流动建立了一组数学模型，采用贝塞尔函数方法进行了解析求解，获得了非定常状态下的动脉血液发展流动的速度分布和压力分布公式。并与定常状态下动脉血管中的血液发展流动做了比较。结果表明，非定常状态下动脉血液发展流动的压力分布和定常状态下的动脉血管中的血液发展流动的压力分布差别很大。     

分叉和狭窄对颅内动脉血液流体动力学的影响

目的 基于颅内动脉数量众多且影响因素较多,本文重点研究了分叉角度、对称分支动脉狭窄度、不对称分支动脉狭窄度和斑块尺寸对颅内动脉粥样硬化形成和生长的影响作用,以期利用血流动力学参数的评估为动脉粥样硬化的预警、诊断及选择合适的血管内治疗等提供一定的指导作用.方法 基于计算流体动力学方法,构建主支动脉连接分支动脉的几何模型和有限元模型的边界条件,设计45°～135°区间共7种分叉角度,依托狭窄度λ来表征血管的狭窄程度,通过血液压力、流速和剪切力等血液流体力学参数对比分析各因素对颅内动脉粥样硬化的产生及发展过程的机制.结果 分叉角度对速度比最大值和剪切力最大值基本没有影响,对压力最小值影响也较小,最大振幅不超过5％.随着狭窄度的增加,最小压力下降而速度比最大值增加,当λ从0增加到0.5、0.67和0.75时,最小压力分别下降了1.6 Pa、1.8 Pa和3.6 Pa,速度比最大值分别上升了48％、1.2倍和1.9倍;狭窄度对最大剪切力的影响很小,直到当狭窄度增大到0.75时,最大剪切力提升了5％.非对称两个支路狭窄度的比值φ增加时,3个参数均逐渐增加且增加的幅度随φ的增加而增大.随着斑块长度的增加,压力最小值呈线性增加,速度比最大值则逐渐增加,剪切力最大值则是逐渐下降,最后趋势趋于平缓.结论 分叉角度对血液流体力学参数的影响较小;对称分支动脉狭窄度越大,或者不对称分支动脉的狭窄度比值越大,或者斑块长度越短,均引起血管壁剪切力越大,越容易造成血管内壁损伤,加速动脉粥样硬化.本研究为颅内动脉粥样硬化的形成机制、影响因素以及预测转归等方面提供有用信息.     

锥度角对弯曲动脉血管的血流动力学影响

运用血流动力学的基本原理和计算流体力学方法,对具有锥度角的弯曲血管内的血液二维定常流动流场进行数值模拟和分析.计算出具有锥度角的弯曲动脉内血液流动的压力和速度的分布情况.计算结果表明由于弯曲血管的曲率和沿血管渐缩的锥度角使得血管截面血流速度分布尤其是径向速度分布发生较大畸变;锥度角对弯曲动脉血管的血流动力学影响主要体现在对血流径向速度分布的影响.     

椎动脉狭窄临床病例介入治疗前后椎基底动脉血流状况分析

目的:基于血液和弹性血管壁相互作用的流固耦合方法,探究1例椎动脉颅内段狭窄的临床病例支架植入前后椎基底动脉的血流动力学特性。方法:应用医学建模软件对二维CT数据进行三维重建,得到支架植入前后的椎基底动脉血管模型,采用流固耦合方法对支架植入前后的椎基底动脉血流特性进行数值模拟,分析椎基底动脉的血流动力学特性。结果:支架植入前后椎基底动脉的血液流场、血液压力、血管壁面切应力以及管壁形变量有显著的变化。在支架植入后,基底动脉中间部位两侧受力变得均匀,椎基底动脉内血流速度明显增大,支架植入处压力增大,支架上游压力和支架处切应力减小。结论:在介入治疗后,椎基底动脉内的血流环境及受力情况得到明显改善,当椎动脉发生狭窄后应及时干预治疗,避免累及基底动脉和后循环系统。     

狭窄动脉中的非线性脉动流的数值研究

本文应用ANSYS有限元分析软件对颈动脉狭窄中的非线性的血液流进行数值模拟研究。在该研究中假定颈动脉是刚性轴对称的狭窄管,血液是粘性不可压缩的牛顿流体。该研究对稳态和非稳态两种情况进行了计算。探讨在稳忘情况下,本文对雷诺数、狭窄长度、狭窄程度、狭窄上、下游的3渤称性等几何参数和生理参数对血流流动的影响进行了计算模拟。而在Iffe态情况下,除以上这些因素外,而且还考虑了WOMERSLEY数的作用。通过采用数值方法对Nayier－Stokes方程的求解,得到流经狭窄动脉的流场及压力和剪应力的分布。计算结果表明,狭窄输入端的…     

中央分流术中血管弹性壁和刚性壁对血管中血流动力学的影响

目的 通过数值模拟仿真研究中央分流手术（central shunt, CS）的血流动力学环境,并分别研究弹性与刚性血管壁条件对其血管内血流动力学参数分布的影响。方法 建立两个理想化的CS搭桥模型,其中一个假设为刚性血管壁,另一个为弹性血管壁。利用有限元方法进行数值计算,其中弹性血管壁模型采用流固耦合方法。结果 两个模型中的流速和压力分布总体大致相同。刚性血管壁模型中大约有68.9%血液从主动脉分流进入肺动脉中,弹性血管壁模型中该值增加到了70%。弹性模型和刚性模型中搭桥血管两端的压降分别为7.668 8 kPa和7.222 3 kPa。弹性模型中搭桥管各处的横截面积有一定变化,最大变化率约为2.2%,出现在近心端吻合口处。提取两个模型中的5个关键区域进行壁面切应力比较,其数值差别最多约为16.1%。结论 总体来说两个模型的血液流动形态没有大的改变;血管的弹性因素轻微影响了流量的分布和搭桥管两端的压降;搭桥管上血管的弹性对近心段吻合口处的影响高于对远心端吻合口处的影响。在CS术治疗法洛四联症的数值模拟仿真中血管壁为刚性这一假设是可以接受的,而流固耦合的数值模拟将得到更为可信的仿真结果。     

血流动力学的医学应用与发展

血流动力学是指血液在血管系统中流动的力学,主要研究血流量、血流阻力、血压、切应力、扰动流等,以及它们之间的相互关系,对人类生命健康具有重要的影响。血流动力学在血管的弯曲、狭窄、堵塞、分叉以及肿瘤的治疗等方面具有重要的临床研究意义。目前,血流动力学在动脉血管搭桥、冠状动脉狭窄、腹主动脉瘤、动脉粥样硬化、脑动脉肿瘤以及旋动流等方面引起广泛研究。伴随着血流动力学的深入研究,心脑血管的手术规划、介入治疗等得到快速发展,基于血流动力学的临床检测和治疗仪器也越来越多。血流动力学因素,如血管压力、血管阻力、血流量、壁面切应力、血液黏度、流动分离、湍流、涡流等对常见血管疾病以及术后并发症的影响机理正在逐步深入探索之中,并已经取得了一定成果。     

动脉锥度角对非定常血流速度分布的影响

从动脉血管具有1°左右的锥度角的实际情况出发,应用Navier-Stokes方程和质量连续原理对非定常状态下动脉中血液流动的锥度角效应问题建立了一组数学模型,继而采用贝塞尔函数方法进行了解析求解,获得了非定常状态下的动脉血液发展流动的速度分布公式.和无锥度角的动脉血管中的血液发展流动做了比较.得出了一些颇为新颖而重要的结论.     

基于流固耦合计算机流体力学模拟分析人体主动脉弓内血液流动

目的比较分析应用弹性血管壁的流固耦合计算流体力学（CFD）方法和刚性血管壁的CFD方法模拟获得的正常主动脉弓内血流动力学参数,同时比较两种方法的优劣,为深入研究血液流动状态与动脉疾病的关系提供帮助。方法取46岁男性,胸主动脉正常CT图像,格式为Dicom,层间距为0.5mm,每片图像的平面分辨率为512×512,像素大小为0.5mm。应用医学图像后处理软件,对通过临床获得正常人体主动脉CT二维医学图像数据进行重构,得到主动脉血流及血管壁的三维立体模型并应用于模拟计算。结果在设定边界条件和初始条件的基础上,经多次迭代耦合计算,获得血管壁形变、等效应力、血流速度、壁面振荡切应力等相关血流动力学参数。结论在心动周期内弹性血管壁的主动脉内血流情况较刚性血管壁主动脉内血流情况更为复杂,管壁等效压力变化较大,血管壁的振荡切应力更高,表明弹性血管壁的流固耦合的CFD模拟更能体现真实主动脉内复杂血流情况,为深入研究血流动力学与心脑血管疾病的关系提供了一定的技术支持。     

Coupled fluid-wall modelling of steady flow in stenotic carotid arteries

Arterial stenoses may cause critical blood flow and wall conditions leading to clinical complications. In this paper computational models of stenotic carotid arteries are proposed and the vessel wall collapse phenomenon is studied. The models are based on fluid-structure interactions (FSI) between blood and the arterial walls. Coupled finite element and computational fluid dynamics methods are used to simultaneously solve for stress and displacement in the solid, and for pressure, velocity and shear stress in the fluid domain. Results show high wall shear stress at the stenosis throat and low (negative) values accompanied by disturbed flow patterns downstream of the stenosis. The wall circumferential stress varies abruptly from tensile to compressive along the stenosis with high stress concentration on the plaque shoulders showing regions of possible plaque rupture. Wall compression and collapse are observed for severe cases. Post-stenotic collapse of the arterial wall occurs for stenotic severity as low as 50%, with the assumption that a given amount of blood flow needs to pass the stenotic artery; whereas if constant pressure drop should be maintained across a constriction, then collapse happens at severity of 75% and above. The former assumption is based on the requirement of adequate blood supply to the downstream organs/tissue, while the latter stems from the fact that the pumping mechanism of the body has a limited capacity in regulating blood pressure, in case a stenosis appears in the vasculature.     

Platelet deposition in rabbit common carotid arteries promoted by arterial stenosis and spasm

Coronary arteriograhy in patients with ischemic heart disease often shows spasm of the coronary arteries. The question is whether spasm is a triggering factor for thrombosis in a stenotic artery. If so, what are the mechanisms for this? A stenosing teflon ring was applied to the right common carotid artery of anesthetized rabbits and l‐nor‐epinephrine was dripped over the outer surface of both carotid arteries, causing spasm. In control animals an indifferent solution did not cause spasm. Nineteen rabbits were killed 30 min or 24 h after treatment. Microscopically, arteries with stenosis and spasm contained thrombi nearby the stenosis significantly more often than arteries in control animals. In another 14 rabbits, killed at 30 min, the number of platelets on the intimal surface away from the stenosis was quantified. In arteries with both stenosis and spasm the counts were significantly greater than in arteries with no treatment. The intimal surface in stenotic and spastic arteries showed assumed imprints of eddying flow and endothelial injury downstream and upstream of the stenosis. Spastic arteries showed increased folding of the internal elastic membrane, altered endothelial cells, and adhering platelets. Spasm in a rabbit artery with a preformed stenosis facilitates thrombosis probably by creating increased flow disturbances. Spasm may induce endothelial injury, causing adherence of platelets.     

Dilatation in the femoral vascular bed does not cause retrograde relaxation of the iliac artery in the anaesthetized pig

Aim: We tested the hypothesis that dilatation of a feeding artery may be elicited by transmission of a signal through the tissue of the arterial wall from a vasodilated peripheral vascular bed. Methods: In eight pentobarbital anaesthetized pigs, acetylcholine (ACh, an endothelium‐dependent vasodilator) was injected intra‐arterially above (upstream) and below (downstream) a test segment of the left iliac artery, the diameter of which was measured continuously by sonomicrometry. Results: Under control conditions, ACh injections upstream and downstream of the test segment caused dilatation. Downstream injection dilated the peripheral arterioles, resulting in increased blood flow and proximal dilatation. This is a shear stress, nitric oxide (NO)‐dependent response. The experiment was then repeated after applying a stenosis to prevent the increased flow caused by downstream injection of ACh; the stenosis was placed either above the site of diameter measurement to allow retrograde conduction, or below that site to prevent distally injected ACh reaching the measurement site. Under these conditions, downstream injection of ACh had a minimal effect on the shear stress of the test segment with no increase in test segment diameter. This was not due to endothelial damage or dysfunction as injection of ACh upstream still caused a large increase in test segment diameter. Conclusions: Our results indicate that dilatation of the feeding artery of a vasodilated bed is caused by increased shear stress within the feeding artery and not via a signal transmitted through the arterial wall from below.     

The influences of stenosis on the downstream flow pattern in curved arteries

The influence of stenosis on the pulsatile blood flow pattern in curved arteries with stenosis at inner wall was investigated by computer simulations. Numerical calculations were performed with various values of physiological parameters to examine the effect of a stenosis on the hemodynamic characteristics such as secondary flow, flow separation, wall shear stress (WSS) and pressure drop. The results demonstrated that when the severity of a stenosis at the inner wall of a curved artery reaches a certain level, the flow pattern in the downstream of the artery shows a dramatic change compared to that of a curved artery with no stenosis. According to previous studies, a flow separation occurs at the inner wall of the bend in a curved artery. The present work reports an analysis of such a flow separation area at the inner wall of the post stenosis region in curved arteries with a stenosis. In addition, another area of flow separation with low and oscillating WSS and blood pressure at the outer wall in a downstream tube was also found and investigated. The observed characteristic change of the flow downstream may suggest a formation of a new plaque at the outer wall downstream.     

Numerical simulations of unsteady flows in a stenosed coronary bypass graft

Using the finite element method, physiological blood flows through a three-dimensional model of a coronary graft are numerically analysed. The model includes a stenosis shape in the host artery upstream from the anastomosis. Recirculating areas, secondary flows, wall shear stress (WSS) and spatial wall shear stress gradients (WSSGs) are studied for different flow repartitions and at different times in the cycle. The temporal and spatial evolutions of the recirculating areas downstream from the stenosis, their interactions with the flow issued from the graft and their associated WSSs highlight that the presence of the stenosis in the recipient artery is essential for prediction of the evolution of a grafting at the beginning of its implantation. The areas downstream from the stenosis expansion, non-existent for a host artery without stenosis, are submitted to low and oscillating WSS between −0.5 and 0 Nm⁻². The stagnation point on the recipient artery floor is subjected to high positive and negative WSSG_nd values, and its location is dependent on the residual flow through the stenosis.     

Increase in the calculated resistance of anatomically fixed stenosis in vitro in association with decrease in distal resistance

The effects of changes in distal resistance on stenotic resistance were studied in vitro. Physiological saline was passed through the left carotid artery obtained from the dog, flexible rubber tubing, or through solid polyethylene tubing with a constant perfusion pressure or with a constant flow rate. Various stenotic resistances were established using a screw type constrictor and the distal resistance was varied by allowing physiological saline to pass through either a 23 gauge hypodermic needle (high peripheral resistance) or 23 and 20 gauge needles (low peripheral resistance ). For arteries with anatomically fixed stenosis, the calculated resistance was increased in association with reduction of the distal resistance. The stenotic resistance in the flexible rubber tubing changed in the same manner as that of the carotid artery, while the solid polyethylene tubing showed no significant stenotic resistance changes due to altering the distal resistance. These findings suggest that the stenotic resistance change of the artery correlates with the elasticity of the vessel wall and also indicate that resistance values were of little usefulness for evaluating the effects of vasodilating stimuli on the vessel segment with a significant stenosis.     

Computational modelling of blood flow through curved stenosed arteries

A computational model of three-dimensional blood flow in curved arteries with elliptic stenosis was developed. Two groups of models, (a) different angles of curvature and (b) degrees of stenosis, have been studied under typical conditions for stenosed coronary artery. Useful information on the haemodynamics has been obtained. Results of pressure drop show that the presence of the curvature augments the increased flow resistance due to stenotic lesions. The study also demonstrates the significant presence of secondary flow in a curved artery. In addition, the results have shown that the secondary flow in a curved artery brings about elevated shear stress on the vessel wall. These results indicated that both curvature and stenosis should be considered together by cardiologists to assess or quantify the severity of the stenosis. This study employed a powerful computer-aided design (CAD) package to construct the model and a commercial computational fluid dynamics (CFD) code for the analysis of blood flow in stenosed arteries. The long-term application of this form of research promises to be an effective tool for gaining insights into the pathology of arterial diseases.     

Computational modelling of blood flow through curved stenosed arteries

A computational model of three-dimensional blood flow in curved arteries with elliptic stenosis was developed. Two groups of models, (a) different angles of curvature and (b) degrees of stenosis, have been studied under typical conditions for stenosed coronary artery. Useful information on the haemodynamics has been obtained. Results of pressure drop show that the presence of the curvature augments the increased flow resistance due to stenotic lesions. The study also demonstrates the significant presence of secondary flow in a curved artery. In addition, the results have shown that the secondary flow in a curved artery brings about elevated shear stress on the vessel wall. These results indicated that both curvature and stenosis should be considered together by cardiologists to assess or quantify the severity of the stenosis. This study employed a powerful computer-aided design (CAD) package to construct the model and a commercial computational fluid dynamics (CFD) code for the analysis of blood flow in stenosed arteries. The long-term application of this form of research promises to be an effective tool for gaining insights into the pathology of arterial diseases.     

Evaluation of renal artery stenosis by echocardiography

Renovascular hypertension and renal hypertension are two major secondary forms of hypertension due to renal disease. Diagnosis of renovascular hypertension is important because revascularization therapy is an effective treatment for patients with renal artery stenosis. Doppler echocardiogaphy is a useful noninvasive test to detect renal artery stenosis. There are two Doppler echocardiographic methods to detect renal artery stenosis. The first is to measure flow velocity at the stenotic area. Pulse-Doppler and/or continuous Doppler methods are used to measure flow velocity. Significant stenosis is diagnosed by maximum flow velocity (Vmax) at the stenotic area: > 1.5m/sec or > 1.8-2.0m/sec. Flow waves of segmental and interlober arteries are assessed by the pulse-Doppler method. Decreased Vmax, early systolic acceleration, resistive index and pulsatility index indicate decreased renal artery blood flow and hence, renal artery stenosis.