Choice of a hemodynamic model for occlusive thrombosis in arteries

Intravascular thrombosis can lead to heart attacks and strokes that together are the leading causes of death in the US (Kochanek, K.D., Murphy, S.L., Xu, J.Q., 2014). The ability to identify the offending biofluid mechanical conditions and predict the timescale of thrombotic occlusion in vessels and devices may improve patient outcomes. A computational model was developed to describe the growth of thrombus based on the local hemodynamic shear rate. The model predicts thrombus deposition based on initial geometric and fluid mechanical conditions, which are updated throughout the simulation to reflect the changing lumen dimensions. Thrombus growth and occlusion from whole blood was measured in in vitro experiments using stenotic glass capillary tubes, a PDMS microfluidic channel, and a PTFE stenotic aorto-iliac graft. Comparison of the predicted occlusion times to experimental results shows excellent agreement. The results indicate that local shear rate plays a critical role in acute thrombosis, and that hemodynamic characterization may have clinical utility.     

Inertial particle dynamics in large artery flows – Implications for modeling arterial embolisms

The complexity of inertial particle dynamics through swirling chaotic flow structures characteristic of pulsatile large-artery hemodynamics renders significant challenges in predictive understanding of transport of such particles. This is specifically crucial for arterial embolisms, where knowledge of embolus transport to major vascular beds helps in disease diagnosis and surgical planning. Using a computational framework built upon image-based CFD and discrete particle dynamics modeling, a multi-parameter sampling-based study was conducted on embolic particle dynamics and transport. The results highlighted the strong influence of material properties, embolus size, release instance, and embolus source on embolus distribution to the cerebral, renal and mesenteric, and ilio-femoral vasculature beds. The study also isolated the importance of shear-gradient lift, and elastohydrodynamic contact, in affecting embolic particle transport. Near-wall particle re-suspension due to lift alters aortogenic embolic particle dynamics significantly as compared to cardiogenic. The observations collectively indicated the complex interplay of particle inertia, fluid–particle density ratio, and wall collisions, with chaotic flow structures, which render the overall motion of the particles to be non-trivially dispersive in nature.     

Brain protective effect and hemodynamics of dexmedetomidine hydrochloride in patients with intracranial aneurysm

ObjectiveThe purpose of the study was to investigate the effect of dexmedetomidine hydrochloride (Dex) on the recovery of cognitive function, hemodynamics, and postoperative analgesia in patients undergoing intracranial aneurysm craniotomy. Methods: general anesthesia was performed on patients undergoing intracranial aneurysm craniotomy in neurosurgery. Patients were randomly divided into three groups: Dex 1 group (Dex dose: 1 μg/kg), Dex 2 group (Dex dose: 0.5 μg/kg), and blank control group (normal saline). The changes of heart rate, arterial pressure, intraoperative brain function index, and postoperative pain score were recorded and compared. Results: in Dex 1 group and Dex 2 group, the heart rate of T1 and T2 phase was significantly lower than that of T3-T7 phases (P < 0.05); compared with the control group, the heart rate of Dex 1 group and Dex 2 group was significantly lower (P < 0.05). The average arterial pressure of the control group and Dex groups was significantly different (P < 0.05). Compared with the control group, there were significant differences between Dex 1 group and Dex 2 group: S100 β protein in T7-T10, NSE (neuron specific enolase) in T9 and T10, pain score in T8, T9 and T10 after operation. Conclusion: the application of Dex in the resection of intracranial aneurysms can protect the brain of patients, minimize the influence of operation on hemodynamics, and relieve postoperative pain, which is worthy of clinical application.     

Hemodynamics of patient-specific aorta-pulmonary shunt configurations

Optimal hemodynamics in aorta-pulmonary shunt reconstruction is essential for improved post-operative recovery of the newborn congenital heart disease patient. However, prior to in vivo execution, the prediction of post-operative hemodynamics is extremely challenging due to the interplay of multiple confounding physiological factors. It is hypothesized that the post-operative performance of the surgical shunt can be predicted through computational blood flow simulations that consider patient size, shunt configuration, cardiac output and the complex three-dimensional disease anatomy. Utilizing only the routine patient-specific pre-surgery clinical data sets, we demonstrated an intelligent decision-making process for a real patient having pulmonary artery atresia and ventricular septal defect. For this patient, a total of 12 customized candidate shunt configurations are contemplated and reconstructed virtually using a sketch-based computer-aided anatomical editing tool. Candidate shunt configurations are evaluated based on the parameters that are computed from the flow simulations, which include 3D flow complexity, outlet flow splits, shunt patency, coronary perfusion and energy loss. Our results showed that the modified Blalock-Taussig (mBT) shunt has 12% higher right pulmonary artery (RPA) and 40% lower left pulmonary artery (LPA) flow compared to the central shunt configuration. Also, the RPA flow regime is distinct from the LPA, creating an uneven flow split at the pulmonary arteries. For all three shunt sizes, right mBT innominate and central configurations cause higher pulmonary artery (PA) flow and lower coronary artery pressure than right and left mBT subclavian configurations. While there is a trade-off between energy loss, flow split and coronary artery pressure, overall, the mBT shunts provide sufficient PA perfusion with higher coronary artery pressures and could be preferred for similar patients having PA overflow risk. Central shunts would be preferred otherwise particularly for cases with very low PA overflow risk.     

A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique

A rat model of electrically-induced ventricular fibrillation followed by cardiac resuscitation using a closed chest technique that incorporates the basic components of cardiopulmonary resuscitation in humans is herein described. The model was developed in 1988 and has been used in approximately 70 peer-reviewed publications examining a myriad of resuscitation aspects including its physiology and pathophysiology, determinants of resuscitability, pharmacologic interventions, and even the effects of cell therapies. The model featured in this presentation includes: (1) vascular catheterization to measure aortic and right atrial pressures, to measure cardiac output by thermodilution, and to electrically induce ventricular fibrillation; and (2) tracheal intubation for positive pressure ventilation with oxygen enriched gas and assessment of the end-tidal CO₂. A typical sequence of intervention entails: (1) electrical induction of ventricular fibrillation, (2) chest compression using a mechanical piston device concomitantly with positive pressure ventilation delivering oxygen-enriched gas, (3) electrical shocks to terminate ventricular fibrillation and reestablish cardiac activity, (4) assessment of post-resuscitation hemodynamic and metabolic function, and (5) assessment of survival and recovery of organ function. A robust inventory of measurements is available that includes – but is not limited to – hemodynamic, metabolic, and tissue measurements. The model has been highly effective in developing new resuscitation concepts and examining novel therapeutic interventions before their testing in larger and translationally more relevant animal models of cardiac arrest and resuscitation.     

A One-dimensional Finite Element Method for Simulation-based Medical Planning for Cardiovascular Disease

We have previously described a new approach to planning treatments for cardiovascular disease, Simulation-Based Medical Planning, whereby a physician utilizes computational tools to construct and evaluate a combined anatomic/physiologic model to predict the outcome of alternative treatment plans for an individual patient. Current systems for Simulation-Based Medical Planning utilize finite element methods to solve the time-dependent, three-dimensional equations governing blood flow and provide detailed data on blood flow distribution, pressure gradients and locations of flow recirculation, low wall shear stress and high particle residence. However, these methods are computationally expensive and often require hours of time on parallel computers. This level of computation is necessary for obtaining detailed information about blood flow, but likely is unnecessary for obtaining information about mean flow rates and pressure losses. We describe, herein, a space-time finite element method for solving the one-dimensional equations of blood flow. This method is applied to compute flow rate and pressure in a single segment model, a bifurcation, an idealized model of the abdominal aorta, in three alternate treatment plans for a case of aorto-iliac occlusive disease and in a vascular bypass graft. All of these solutions were obtained in less than 5 min of computation time on a personal computer.     

构建基于患者个体化的Stanford B型主动脉夹层计算流体力学数值模拟分析模型

目的:探索简便、高效、精确的构建基于真实人体解剖形态结构的Stanford B型主动脉夹层计算流体力学数值模拟分析模型的方法.方法:利用Siemens Sensation Cardiac 64层螺旋CT薄层扫描技术,基于1mm层厚获取6例Stanford B型主动脉夹层连续断层DICOM格式图像,导入Materialise MIMICS v12.11软件,界定目标区域后生成三维动脉模型,经网格优化处理去除低质量及相交面网格,保存结果输出,导入TGrid 5.0软件,对主动脉面网格模型进行几何修复,使面网格扭曲率<0.75,采用自由分网方式生成Stanford B型主动脉夹层计算流体力学分析体网格模型,并对所构建模型进行血流属性、流场边界等界定,初步验证模型的有效性.结果:通过初步计算求解,确定所构建的6例Stanford B型主动脉夹层计算流体力学分析模型分别包含1857030,1820501,1844181,1849651,1858246及1814914个四面体单元.结论:利用64层螺旋CT薄层扫描技术获取DICOM格式连续断层CT图像可快速、准确地构建Stanford B型主动脉夹层计算流体力学数值模拟分析模型,为进一步的计算流体力学分析奠定了良好的基础.     

Mathematical model for the estimation of hemodynamic and oxygenation variables by tissue spectroscopy

This article presents a quasistatic, compartmental model of tissue-level hemodynamics and oxygenation that leads to a set of formulas, which is suitable to calculate important physiological variables from the mean tissue concentration and saturation of hemoglobin, measured by tissue spectroscopy. Dimensioned quantities are represented relative to their baseline value in the equations (relative value = perturbed/baseline). All model parameters are non-dimensional. The model is based and extends on a number of previous works: previous models of similar aim and scope are consolidated, and every critical assumptions and approximations are treated explicitly; extensions include for example the incorporation of the Fahraeus-effect and the separate estimation of the volume changes of the arterial and the venous compartments. The information content of spectroscopic data alone is shown to be valuable, but limited: the relative venous volume, the oxygen extraction fraction and the relative cellulovascular coupling (defined as the ratio of blood flow and oxygen consumption) can be calculated from these data, if the alterations in arterial blood volume are negligible. The number of variables estimated by the derived formulas can be increased if local blood flow is measured simultaneously: in this case, the relative arterial and venous volume and resistance, the oxygen extraction fraction, and the relative oxygen consumption can be determined. Given that this model considers arterial blood pressure, saturation and hematocrit as its inputs, when measured, the model becomes applicable in such conditions as hyper- or hypotension, hypoxic hypoxia, hemodilution and hemorrhage, where these variables do change. The estimation of the changes in arterial resistance can be applied to estimate the extent of an autoregulatory response.     

Cardioprotective and Antioxidant Effects of Apomorphine

Apomorphine is a potent antioxidant that infiltrates through biological membranes. We studied the effect of apomorphine (2?μM) on myocardial ischemic-reperfusion injury in the isolated rat heart. Since iron and copper ions (mediators in formation of oxygen-derived free radicals) are released during myocardial reperfusion, apomorphine interaction with iron and copper and its ability to prevent copper-induced ascorbate oxidation were studied. Apomorphine perfused before ischemia or at the commencement of reperfusion demonstrated enhanced restoration of hemodynamic function (i.e. recovery of the work index (LVDP?×?HR) was 69.2±4.0% with apomorphine pre-ischemic regimen vs. 43.4±9.01% in control hearts, p<0.01, and 76.3±8.0% with apomorphine reperfusion regimen vs. 30.4±11.1% in controls, p<0.001). This was accompanied by decreased release of proteins in the effluent and improved coronary flow recovery in hearts treated with apomorphine after the ischemia. Apomorphine forms stable complexes with copper and with iron, and inhibits the copper-induced ascorbate oxidation. It is suggested that these iron and copper chelating properties and the redox-inactive chelates formed by transition metals and apomorphine play an essential role in post-ischemic cardioprotection.