主动脉瓣狭窄对左心室血流特性的影响

基于CT断层扫描数据,对心脏左心室进行三维重构和模型优化。结合心肌壁面的运动特性,建立左心室几何模型过流边界运动的数学模型。通过水力半径表征主动脉瓣的狭窄程度,采用动网格技术研究主动脉瓣狭窄对左心室血液流动的影响。研究发现不同程度主动脉瓣狭窄时,水力半径与主动脉瓣狭窄程度负相关,出口面积减小,收缩期出口处速度与压力升高,剪切应力增加。舒张期,速度与压力出现先增大后减小的规律。当水力半径较小时,左心室瓣膜处剪切应力较大,收缩初期剪切应力最大为0.81 Pa。通过动态模拟对心脏的仿真研究,为后续心脏的研究提供重要的参考价值。     

人体左心室三维有限元模型构建及流-固耦合动力学分析

有限元分析是研究心血管动力学问题的重要手段。本文基于中国数字人体心脏断层解剖图像,采用Visu-al C++可视化工具包对心脏外形及内腔结构进行三维重建,进一步基于结构模型构建了左心室、血液耦合有限元模型。在通用有限元分析软件ANSYS环境下使用双向流-固耦合方法对心脏灌注期心室壁受力与血液流动过程进行了动力学仿真。仿真结果成功实现了对心脏灌注期心室两阶段充盈过程中室壁应力与血液流体动态特性的定量分析。本研究提供了一种基于二维医学图像信息构建心室有限元模型,并进行心室血液流体力学模拟的新方法,为心脏生理及病理过程的定量有限元分析提供了一套可行的技术方案。     

左心室射血动力学的一个理论和计算研究

本文提出了一个新的理论模型来研究和分析心脏左心室的射血动力学。在该模型中，假设血液是不可压缩粘性牛顿流体，而左心室是一个有缺口的椭球体，且在射血过程当中，左心室始终按照椭球形状变形和运动。在这些假设下，作者根据生物流体力学的基本原理，推导了一个采用椭球坐标表达的左心室射血动力学的基本方程组。该方程组由不可压流体的涡量方程、流函数方程、速度与流函数关系方程以及友。动室内壁收缩运动方程等组成。为了描述左心室内壁的运动，作者用多普勒彩色超声心动仪对人体心脏在不同时刻的图像进行了测量，并将所获得的数据进…     

心力衰竭犬跨室壁心肌复极时间和不应期离散度的致心律失常机制研究

目的：从复极和不应期两个角度,观察不同部位起搏对心力衰竭犬三层心肌跨室壁复极和不应期离散度的影响及其可能的致心律失常机制。方法：正常犬8只和心力衰竭模型犬5只,模拟临床上充血性心力衰竭患者接受心脏再同步治疗的情况,分别从右心室心内膜、左心室心外膜和双心室发放刺激,在体记录和比较犬三层心肌的单相动作电位时程、不应期及其跨室壁离散度。在心力衰竭犬组,给予维拉帕米进行干预并重复上述实验。结果：心力衰竭犬三层心肌的动作电位时程与不应期均有延长,中层心肌动作电位时程延长最明显 [(279.30±54.81) ms vs (270.03±57.58) ms,P<0.01],跨室壁复极离散显著增大 [(29.80±25.67) ms vs (20.60±12.65) ms,P<0.01],不应期离散有所减小 [(29.21±15.83) ms vs (31.25±20.83) ms,P>0.05];左心室心外膜和双心室刺激增加跨室壁复极离散度,但对跨室壁不应期离散度无明显影响;维拉帕米能在一定程度上延长中层和心外膜下心肌的动作电位时程与不应期,减小跨室壁复极和不应期离散 [心力衰竭犬给予维拉帕米后 (24.50±15.18) ms vs 正常犬 (31.25±20.83) ms,P<0.05]。结论：心力衰竭犬跨室壁复极离散增大、不应期离散减小;维拉帕米减小心力衰竭犬跨室壁复极与不应期离散;左心室心外膜参与的起搏方式对心肌不应期无明显影响,但增大跨室壁复极离散,且这一效应不能被维拉帕米矫正。     

应用MRI对心脏进行平面有限元应变解析

近年来随着医疗检测影像技术的发展,MRI技术不断改进,特别是SPAMM磁化空间调制法的出现,在收缩末期对心脏壁进行格子状的磁标记,使得磁标记格子点在整个心动周期随心脏壁同步运动,以显示心肌内部成分和收缩期室壁运动情况,从而对标记的物质粒子的移动进行追踪,使得心脏壁的变形、应变的计测、解析成为可能,为定量。客观地评价心功能提供了必要的手段。本研究应用上述的磁标记法,对志愿者的心脏左心室短轴断面像进行多时相连续摄像,在心脏壁画像上密集地取一些要素节点,对它们进行平面应变解析。为了对心脏左心是在体内的约束…     

013 用于评价心脏功能的计算生物力学

[日]/Sawaki K…∥BME.－2000，14(10).－28～30 心脏是维持血液在体内循环的重要器官之一，从力学的角度来，其泵血功能对定量或客观提供各种心疾患的诊断信息是极为重要的。在这种背景下，为了对各种心疾患提供定量且客观的诊断信息，开发了采用三维有限元法评价心脏左心室力学功能的数字模拟系统及其图像显示系统。为了能分析三维电刺激传导系统的影响、三维复杂分布的心肌纤维的构造及由此而产生的三维应力及变形分布等，系统引入了三维有限元法。研究所采用的数字模拟器由左心室有限元模型及与此相关的循环系统模型构成。在左心室三维有限元模型中引入了心肌的力学特性模型、电刺激传导路径及心肌纤维的分布模型。在进行模拟时，首先要确定循环系统的参数及心肌的杨氏模量和泊松比等材料特性，并将这些值参照以往研究中所使用的参数调整到正常心脏的心内压-容积关系。为了能得到更接近实际心脏的变形情况，应在健康志愿者心脏的短轴断面MRI图像的基础上加以重叠，作成左心室实际形状数据。此外，由于在分析中是以舒张末期为计算的始点，因此，在制作左心室实际形状数据时，应使用舒张末期的MRI图像。应用这一系统可替代部分基础医学中的动物实验等多种实验，且可预测假设疾患心尤其是心肌肥大(HCM)的人类心脏左心室壁内应力及变形分布，并通过与MR tagging法获得的室壁变形信息进行比较，定量评价疾患心的心肌纤维收缩功能。 (刘士新摘)     

血管脉动对骨单元内液体流动行为的影响

骨组织内部存在两大类液体,一类是血液,一类是间隙流。骨细胞新陈代谢主要依赖于间隙流微环境。在骨组织的微观结构下,骨单元壁中液体的渗流行为是研究的热点。本文的主要目的是考察中央哈弗管的血管脉动对骨单元壁中的间隙流流动行为的影响。本文利用COMSOL Multiphysics软件分别建立了中空的和考虑哈弗管中血管脉动的骨单元多孔弹性力学有限元模型,并对比了轴向载荷下两种模型中骨单元壁中的液体渗流行为。结果表明:当考虑哈弗管中的血管脉动时,骨单元壁中液体的压力会明显增大,而流速几乎没有影响。具体地,骨单元孔隙组织液的压力幅值随着血压脉动幅值的增大而增大,受脉动频率的变化影响不大,而血压脉动幅值及频率对骨单元孔隙组织液的流速基本没有影响。该有限元模型可用来进一步研究非轴对称载荷及微裂缝等复杂应力状态下骨单元的多孔弹性力学行为,并为研究骨的力传导及力-电传导机制提供新方法。     

血流图——一种新的诊断技术

心脏不断跳动,促使血液循环以维持机体生存。当心室收缩时,左心室的血液射入主动脉,流到颈动脉,股动脉和肝、肾等动脉。右心室的血液射入肺动脉;与此同时,血管内的压力增加,血管扩张。心室舒张时、动脉瓣关闭,血管回缩。各动脉的这种扩张和收缩变化是有节奏和有规律的,而当脏器有病,使外周阻力增大,血管顺应性变差     

基于左心辅助的血液循环系统的控制研究

本文提出一种基于左心辅助的血液循环系统控制模型,该模型由左心血液循环系统和旋转式心脏泵模型耦合而成。考虑心脏泵的水力特性,根据泵相似性原理提出了新型旋转式心脏泵的数学模型。泵模型耦合心血管系统后采用七阶集总参数非线性空间状态方程表示,控制变量为电机转速。本文采用泵心脏舒张期最小流量变化斜率作为反馈机制,确保最大灌注量的同时避免抽吸。通过Matlab对模型进行仿真,结果显示在开环控制下,心衰患者的血液循环系统各项血液动力特性均有改善。当转速为9 000r/min时,经左心辅助的患者每搏心输出量由最初34mL/s提高至正常水平82mL/s,左心室压力-容积环向左偏移并且面积减小,说明辅助装置能够明显改善泵血不足并帮助心室卸载。若持续提高泵转速,当转速达到12 800r/min时,会发生抽吸异常状况,这是因为转速过高导致静脉回流量不足而形成的。经采用反馈控制后,系统可有效避免抽吸现象。本文研究结果表明,基于左心辅助的血液循环系统的控制模型能在确保足量灌注量的同时避免抽吸异常状态。该模型反映了左心辅助装置与心血管系统的交互作用,为左心辅助心衰治疗和生理控制策略设计提供理论依据。     

基于CT影像的人体心脏三维重构

三维重构是研究心脏血流机理及特性等问题的有效手段,本文基于CT断层扫描数据,利用Mimics处理工具对心脏进行三维重构,并对左心室优化模型进行偏差分析,优化改变了重构模型的粗糙度,对左心室结构的影响较小为后续探究心脏内部血流模式及特性、血液生理学参数异变和组织结构病变提供了基础研究。     

Realistic three-dimensional left ventricular ejection determined from computational fluid dynamics

A realistic model of the left ventricle of the human heart was constructed using a cast from a dog heart which was in diastole. A coordinate measuring machine was used to measure and digitize the coordinates of the left ventricle. From the complex measured left ventricle shape values, a three-dimensional finite volume representation was constructed using a simulation package. The left ventricular walls moved towards the centre of the aortic outlet in order to study the effects of time-varying left ventricular ejection. The left ventricular wall motion was assumed to follow the blood flow and the wall grid was reformed 25 times during the calculation. The 25.8 cm³ ventricular volume was reduced by 75% in 0.25 s. Centreline and cross-sectional velocity vectors greatly increased in magnitude at the aortic outlet, and most of the pressure occurred in the top 15% of the heart. The computational method should make it possible to compare simulation results with important measurement techniques such as ultrasound and magnetic resonance imaging, and this should allow a finer detail of flow understanding than is presently available using either a modelling or imaging method alone.     

Analysis of the isovolumic pressure in the canine left ventricle

Summary Some of the factors which influence the shape of left ventricular isometric pressure are discussed. Complete isometric recordings were obtained in dogs by raising the afterload (aortic pressure) with a special blood pump of own design. The effects of ventricular geometry, myocardial wall thickness and finite velocity of the depolarization wave are discussed. The relation between active state of muscle fibers and isometrically developed pressure in the left ventricle is derived analytically. The commonly used velocity of the contractile element was computed in a new way by differentiation of logarithmically transformed pressure data. This derived function is compared with the simple derivative (dp/dt) with regard to their potential value as indices of myocardial contractility. Contractile element velocity as based on a 3-component model was not found sensitive to so-called contractility changes in the intact heart.     

A two phase harmonic model for left ventricular function

A minimal model for mechanical motion of the left ventricle is proposed. The model assumes the left ventricle to be a harmonic oscillator with two distinct phases, simulating the systolic and diastolic phases, at which both the amplitude and the elastic constant of the oscillator are different. Taking into account the pressure within the left ventricle, the model shows qualitative agreement with functional parameters of the left ventricle. The model allows for a natural explanation of heart failure with preserved systolic left ventricular function, also termed diastolic heart failure. Specifically, the rise in left ventricular filling pressures following increased left-ventricular wall stiffness is attributed to a mechanism aimed at preserving heart rate and cardiac output.     

An Integrative Model of the Cardiovascular System Coupling Heart Cellular Mechanics with Arterial Network Hemodynamics

The current study proposes a model of the cardiovascular system that couples heart cell mechanics with arterial hemodynamics to examine the physiological role of arterial blood pressure (BP) in left ventricular hypertrophy (LVH). We developed a comprehensive multiphysics and multiscale cardiovascular model of the cardiovascular system that simulates physiological events, from membrane excitation and the contraction of a cardiac cell to heart mechanics and arterial blood hemodynamics. Using this model, we delineated the relationship between arterial BP or pulse wave velocity and LVH. Computed results were compared with existing clinical and experimental observations. To investigate the relationship between arterial hemodynamics and LVH, we performed a parametric study based on arterial wall stiffness, which was obtained in the model. Peak cellular stress of the left ventricle and systolic blood pressure (SBP) in the brachial and central arteries also increased; however, further increases were limited for higher arterial stiffness values. Interestingly, when we doubled the value of arterial stiffness from the baseline value, the percentage increase of SBP in the central artery was about 6.7% whereas that of the brachial artery was about 3.4%. It is suggested that SBP in the central artery is more critical for predicting LVH as compared with other blood pressure measurements.     

人工心脏泵辅助对左心室血流动力学影响的数值研究

目的采用数值模拟方法研究人工心脏辅助装置植入对左心室内血流动力学的影响。方法首先利用心血管集中参数模型获取了健康状态、心衰状态以及人工心脏泵辅助状态下收缩末期左心室三维几何模型,其中选取超弹性材料Ogden为心肌材料,以左心房压力,主动脉压力以及通过左心室容积计算获取的左心室壁面位移作为边界条件,利用CFD方法对上述三种情况进行左心室的数值模拟。同时对比了健康时的模拟结果和生理状态下的左心室压力,以及心衰和人工心脏泵辅助两种状态下的血流动力学指标的差别。通过左心室压力和流速等评价灌注和负荷的情况,通过壁面切应力和涡流,评价人工心脏泵辅助后的左心室血流动力学变化规律。结果健康状态下模拟的左心室压力与生理指标相符合。在心衰和人工心脏泵辅助状态下,收缩期内左心室压力与健康状态比分别降低了1718 Pa和8455 Pa,辅助后左心室最大压力下降速度高于心衰时。人工心脏泵辅助后,舒张期壁面切应力峰值由4.3 Pa降低至3.8 Pa,收缩期壁面切应力峰值由4.1 Pa降低至1.3 Pa,射血速度峰值由1.61 m/s降低至0.68 m/s,主动脉瓣开放时间由0.25 s增加至0.65 s,左室射血分数由43.6%增加至52.7%,心室底端漩涡持续时间由0.35 s增加至0.51 s,顶端漩涡出现血流分离。结论左心室压力对比表明本研究方法可以用来模拟左心室的行为。人工心脏泵辅助能够快速降低心室内压力和心室负荷,增加灌注时间,提高器官灌注,降低左心室壁面切应力以及提高左心室内血液流场的涡流强度,延长涡流持续时间。     

Regional three-dimensional geometry of the normal human left ventricle using cine computed tomography

The aim of this study is to provide accurate three-dimensional measurements of left ventricular geometrical indices in relation to regional myocardial function. The analysis of the three-dimensional regional geometry and function of left ventricles of ten normal human volunteers is based on three-dimensional reconstructions of the left ventricle from cine computed tomography images, at end diastole and end systole, demonstrating normal left ventricular spatial, geometrical, and functional variability. Regional wall thickness, curvature and surface normals, as well as wall thickening and endocardial wall motion, are calculated and mapped for the entire left ventricle. The circumferential asymmetry of the left ventricle is reflected by the smaller circumferential and meridional curvatures at the septum. Thickening is highest at the anterior and lateral walls. Longitudinally, circumferential curvature increases toward the apex, whereas both wall thickness and wall thickening at end systole are largest at the midventricular level, decreasing toward the apex and base. This study describes the circumferential and apex-to-base variations in regional left ventricular geometric parameters of the normal human left ventricle, using three-dimensional imaging and analysis. Dr. Marcus is deceased. He was at the University of Iowa, Iowa City, IA     

The influence of coronary pressure and coronary flow on intracoronary blood volume and geometry of the left ventricle

Summary Intracoronary blood volume in relation to coronary perfusion pressure was estimated in dog hearts in situ with cannulated left coronary arteries. Electromagnetically measured inflow into coronary arteries times mean transit time, obtained by a dye dilution technique determined the intracoronary blood volume. Within the range from 70 and 170 mm Hg coronary perfusion pressure the mean value of intracoronary blood volume increases from 11.0 to 17.8 ml per 100 g wet weight; an increase of about 62%. The mycocardial wall at 70 mm Hg consists of 10.4% intracoronary blood and at 170 mm Hg of 15.1%. A significant increase in intracoronary blood volume is seen with increasing coronary perfusion pressure at constant coronary flow.With increasing coronary perfusion pressure the outer volume of the heart and the volume of the myocardial wall increases while the inner volume of the left ventricle decreases in blood perfused dog hearts in situ and in isolated cat hearts. The mean radius of the left ventricle is not changed by the coronary perfusion pressure. This change in the geometry of the left ventricle influences the pressurevolume relation of the heart and can explain the effect of coronary perfusion pressure on the performance of the heart.     

Hyperfunction with normal inotropic state of the hypertrophied left ventricle.

Conscious dogs were instrumented with an inflatable cuff around the ascending aorta, a high-fidelity micromanometer in the left ventricle (LV), and pairs of ultrasonic crystals for measurements of LV wall thickness and internal LV diameter. Wall stress (WSt) and mean velocity of wall shortening (VCF) were calculated. Mean force-velocity relations and WSt-diameter loops in single contractions were then analyzed over a range of matched systolic pressures during acute aortic constrictions both before and after induction of chronic hypertrophy by sustained aortic constriction. At normal LV systolic pressures and at each matched level of systolic LV pressure, wall shortening velocity was increased in the hypertrophied ventricle. However, force-velocity relations obtained by relating mean VCF to mean WSt at various stress levels fell on the same relation as during control. The linear relation between LV diameter and pressure at the end of ventricular ejection was shifted to the left in the hypertrophied ventricle, indicating enhanced shortening. However, linear WSt-diameter relations at end-ejection were not different in control and hypertrophied hearts. These findings indicate that the ventricle hypertrophied by pressure overload exhibited hyperfunction as a pump but that its myocardium had a normal level of inotropic state.     

Analysis of cardiac ventricular wall motion based on a three-dimensional electromechanical biventricular model

This paper describes a biventricular model, which couples the electrical and mechanical properties of the heart, and computer simulations of ventricular wall motion and deformation by means of a biventricular model. In the constructed electromechanical model, the mechanical analysis was based on composite material theory and the finite-element method; the propagation of electrical excitation was simulated using an electrical heart model, and the resulting active forces were used to calculate ventricular wall motion. Regional deformation and Lagrangian strain tensors were calculated during the systole phase. Displacements, minimum principal strains and torsion angle were used to describe the motion of the two ventricles. The simulations showed that during the period of systole, (1) the right ventricular free wall moves towards the septum, and at the same time, the base and middle of the free wall move towards the apex, which reduces the volume of the right ventricle; the minimum principle strain (E3) is largest at the apex, then at the middle of the free wall and its direction is in the approximate direction of the epicardial muscle fibres; (2) the base and middle of the left ventricular free wall move towards the apex and the apex remains almost static; the torsion angle is largest at the apex; the minimum principle strain E3 is largest at the apex and its direction on the surface of the middle wall of the left ventricle is roughly in the fibre orientation. These results are in good accordance with results obtained from MR tagging images reported in the literature. This study suggests that such an electromechanical biventricular model has the potential to be used to assess the mechanical function of the two ventricles, and also could improve the accuracy of ECG simulation when it is used in heart-torso model-based body surface potential simulation studies.