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The deformability of blood vessels in one‐dimensional blood flow models is typically described through a pressure‐area relation, known as the tube law. The most used tube laws take into account the elastic and viscous components of the tension of the vessel wall. Accurately parametrizing the tube laws is vital for replicating pressure and flow wave propagation phenomena. Here, we present a novel mathematical‐property‐preserving approach for the estimation of the parameters of the elastic and viscoelastic tube laws. Our goal was to estimate the parameters by using ovine and human in vitro data, while constraining them to meet prescribed mathematical properties. Results show that both elastic and viscoelastic tube laws accurately describe experimental pressure‐area data concerning both quantitative and qualitative aspects. Additionally, the viscoelastic tube law can provide a qualitative explanation for the observed hysteresis cycles. The two models were evaluated using two approaches: (i) allowing all parameters to freely vary within their respective ranges and (ii) fixing some of the parameters. The former approach was found to be the most suitable for reproducing pressure‐area curves. [ABSTRACT FROM AUTHOR]

Arterial hypertension, defined as an increase in systemic arterial pressure, is a major risk factor for the development of diseases affecting the cardiovascular system. Every year, 9.4 million deaths worldwide are caused by complications arising from hypertension. Despite well‐established approaches to diagnosis and treatment, fewer than half of all hypertensive patients have adequately controlled blood pressure. In this scenario, computational models of hypertension can be a practical approach for better quantifying the role played by different components of the cardiovascular system in the determination of this condition. In the present work we adopt a global closed‐loop multi‐scale mathematical model for the entire human circulation to reproduce a hypertensive scenario. In particular, we modify the model to reproduce alterations in the cardiovascular system that are cause and/or consequence of the hypertensive state. The adaptation does not only affect large systemic arteries and the heart but also the microcirculation, the pulmonary circulation and the venous system. Model outputs for the hypertensive scenario are validated through assessment of computational results against current knowledge on the impact of hypertension on the cardiovascular system. [ABSTRACT FROM AUTHOR]

In recent years, several works have addressed the problem of modeling blood flow phenomena in veins, as a response to increasing interest in modeling pathological conditions occurring in the venous network and their connection with the rest of the circulatory system. In this context, one-dimensional models have proven to be extremely efficient in delivering predictions in agreement with in-vivo observations. Pursuing the increase of anatomical accuracy and its connection to physiological principles in haemodynamics simulations, the main aim of this work is to describe a novel closed-loop Anatomically-Detailed Arterial-Venous Network (ADAVN) model. An extremely refined description of the arterial network consisting of 2,185 arterial vessels is coupled to a novel venous network featuring high level of anatomical detail in cerebral and coronary vascular territories. The entire venous network comprises 189 venous vessels, 79 of which drain the brain and 14 are coronary veins. Fundamental physiological mechanisms accounting for the interaction of brain blood flow with the cerebrospinal fluid and of the coronary circulation with the cardiac mechanics are considered. Several issues related to the coupling of arterial and venous vessels at the microcirculation level are discussed in detail. Numerical simulations are compared to patient records published in the literature to show the descriptive capabilities of the model. Furthermore, a local sensitivity analysis is performed, evidencing the high impact of the venous circulation on main cardiovascular variables. [ABSTRACT FROM AUTHOR]

The one‐dimensional (1D) modeling of blood flow in complex networks of vessels and cardiovascular models can result in computationally expensive simulations. The complexity of such networks has significantly increased in the last years, in terms of both enhanced anatomical detail and modeling of physiological mechanisms and mechanical characteristics. To address such issue, the main goal of this work is to present a novel methodology to construct hybrid networks of coupled 1D and 0D vessels and to perform computationally efficient and accurate blood flow simulations in such networks. Departing from both the 1D and lumped‐parameter (0D) nonlinear models for blood flow, we propose high‐order numerical coupling strategies to solve the 1D, 0D, and hybrid coupling of vessels at junctions. To effectively construct hybrid networks, we explore different a‐priori model selection criteria focusing in obtaining the best possible trade‐off between computational cost of the simulations and accuracy of the computed solutions for the hybrid network with respect to the 1D network. The achievement of the expected order of accuracy is verified in several test cases. The novel methodology is applied to two different arterial networks, the 37‐artery network and the reduced ADAN56 model, where, in order to identify the best performing a‐priori model selection criteria, the quantitative assessment of CPU times and errors and the qualitative comparison between results are carried out and discussed. [ABSTRACT FROM AUTHOR]

Model‐based prediction of fractional flow reserve (FFR) in the context of stable coronary artery disease (CAD) diagnosis requires a number of modelling assumptions. One of these assumptions is the definition of a baseline coronary flow, ie, total coronary flow at rest prior to the administration of drugs needed to perform invasive measurements. Here we explore the impact of several methods available in the literature to estimate and distribute baseline coronary flow on FFR predictions obtained with a reduced‐order model. We consider 63 patients with suspected stable CAD, for a total of 105 invasive FFR measurements. First, we improve a reduced‐order model with respect to previous results and validate its performance versus results obtained with a 3D model. Next, we assess the impact of a wide range of methods to impose and distribute baseline coronary flow on FFR prediction, which proved to have a significant impact on diagnostic performance. However, none of the proposed methods resulted in a significant improvement of prediction error standard deviation. Finally, we show that intrinsic uncertainties related to stenosis geometry and the effect of hyperemic inducing drugs have to be addressed in order to improve FFR prediction accuracy. [ABSTRACT FROM AUTHOR]

There is growing interest in developing mathematical models and appropriate numerical methods for problems involving networks formed by, essentially, one-dimensional (1D) domains joined by junctions. Examples include hyperbolic equations in networks of gas tubes, water channels and vessel networks for blood and lymph transport in the human circulatory system. A key point in designing numerical methods for such applications is the treatment of junctions, i.e. points at which two or more 1D domains converge and where the flow exhibits multidimensional behaviour. This paper focuses on the design of methods for networks of water channels. Our methods adopt the finite volume approach to make full use of the two-dimensional shallow water equations on the true physical domain, locally at junctions, while solving the usual one-dimensional shallow water equations away from the junctions. In addition to mass conservation, our methods enforce conservation of momentum at junctions; the latter seems to be the missing element in methods currently available. Apart from simplicity and robustness, the salient feature of the proposed methods is their ability to successfully deal with transcritical and supercritical flows at junctions, a property not enjoyed by existing published methodologies. Systematic assessment of the proposed methods for a variety of flow configurations is carried out. The methods are directly applicable to other systems, provided the multidimensional versions of the 1D equations are available. [ABSTRACT FROM AUTHOR]

Computational models of many aspects of the mammalian cardiovascular circulation have been developed. Indeed, along with orthopaedics, this area of physiology is one that has attracted much interest from engineers, presumably because the equations governing blood flow in the vascular system are well understood and can be solved with well-established numerical techniques. Unfortunately, there have been only a few attempts to create a comprehensive public domain resource for cardiovascular researchers. In this paper we propose a roadmap for developing an open source cardiovascular circulation model. The model should be registered to the musculo-skeletal system. The computational infrastructure for the cardiovascular model should provide for near real-time computation of blood flow and pressure in all parts of the body. The model should deal with vascular beds in all tissues, and the computational infrastructure for the model should provide links into CellML models of cell function and tissue function. In this work we review the literature associated with 1D blood flow modelling in the cardiovascular system, discuss model encoding standards, software and a model repository. We then describe the coordinate systems used to define the vascular geometry, derive the equations and discuss the implementation of these coupled equations in the open source computational software OpenCMISS. Finally, some preliminary results are presented and plans outlined for the next steps in the development of the model, the computational software and the graphical user interface for accessing the model. [ABSTRACT FROM AUTHOR]

In recent years, the complexity of vessel networks for one-dimensional blood flow models has significantly increased, because of enhanced anatomical detail or automatic peripheral vasculature generation, for example. This fact, along with the application of these models in uncertainty quantification and parameter estimation poses the need for extremely efficient numerical solvers. The aim of this work is to present a finite volume solver for one-dimensional blood flow simulations in networks of elastic and viscoelastic vessels, featuring high-order space-time accuracy and local time stepping (LTS). The solver is built on (i) a high-order finite volume type numerical scheme, (ii) a high-order treatment of the numerical solution at internal vertexes of the network, often called junctions, and (iii) an accurate LTS strategy. The accuracy of the proposed methodology is verified by empirical convergence tests. Then, the resulting LTS scheme is applied to arterial networks of increasing complexity and spatial scale heterogeneity, with a number of one-dimensional segments ranging from a few tens up to several thousands and vessel lengths ranging from less than a millimeter up to tens of centimeters, in order to evaluate its computational cost efficiency. The proposed methodology can be extended to any other hyperbolic system for which network applications are relevant. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The article presents the discussion on cerebrotoxicity of antihypertensive therapy and risk factor cosmetics. Topics include patients with stiff arteries having a wide pulse pressure aggravated by bradycardia showing diastolic pressure being lower than the cuff pressure; and computer simulations using an anatomically detailed cerebrovascular architecture estimating the the blood pressure in the brachial artery.

Hæmodynamical simulations using one-dimensional (1D) computational models exhibit many of the features of the systemic circulation under normal and diseased conditions. Recent interest in verifying 1D numerical schemes has led to the development of alternative experimental setups and the use of three-dimensional numerical models to acquire data not easily measured in vivo. In most studies to date, only one particular 1D scheme is tested. In this paper, we present a systematic comparison of six commonly used numerical schemes for 1D blood flow modelling: discontinuous Galerkin, locally conservative Galerkin, Galerkin least-squares finite element method, finite volume method, finite difference MacCormack method and a simplified trapezium rule method. Comparisons are made in a series of six benchmark test cases with an increasing degree of complexity. The accuracy of the numerical schemes is assessed by comparison with theoretical results, three-dimensional numerical data in compatible domains with distensible walls or experimental data in a network of silicone tubes. Results show a good agreement among all numerical schemes and their ability to capture the main features of pressure, flow and area waveforms in large arteries. All the information used in this study, including the input data for all benchmark cases, experimental data where available and numerical solutions for each scheme, is made publicly available online, providing a comprehensive reference data set to support the development of 1D models and numerical schemes. Copyright © 2015 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

SUMMARY We present a global, closed-loop, multiscale mathematical model for the human circulation including the arterial system, the venous system, the heart, the pulmonary circulation and the microcirculation. A distinctive feature of our model is the detailed description of the venous system, particularly for intracranial and extracranial veins. Medium to large vessels are described by one-dimensional hyperbolic systems while the rest of the components are described by zero-dimensional models represented by differential-algebraic equations. Robust, high-order accurate numerical methodology is implemented for solving the hyperbolic equations, which are adopted from a recent reformulation that includes variable material properties. Because of the large intersubject variability of the venous system, we perform a patient-specific characterization of major veins of the head and neck using MRI data. Computational results are carefully validated using published data for the arterial system and most regions of the venous system. For head and neck veins, validation is carried out through a detailed comparison of simulation results against patient-specific phase-contrast MRI flow quantification data. A merit of our model is its global, closed-loop character; the imposition of highly artificial boundary conditions is avoided. Applications in mind include a vast range of medical conditions. Of particular interest is the study of some neurodegenerative diseases, whose venous haemodynamic connection has recently been identified by medical researchers. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

ABSTRACT We present a well-balanced, high-order non-linear numerical scheme for solving a hyperbolic system that models one-dimensional flow in blood vessels with variable mechanical and geometrical properties along their length. Using a suitable set of test problems with exact solution, we rigorously assess the performance of the scheme. In particular, we assess the well-balanced property and the effective order of accuracy through an empirical convergence rate study. Schemes of up to fifth order of accuracy in both space and time are implemented and assessed. The numerical methodology is then extended to realistic networks of elastic vessels and is validated against published state-of-the-art numerical solutions and experimental measurements. It is envisaged that the present scheme will constitute the building block for a closed, global model for the human circulation system involving arteries, veins, capillaries and cerebrospinal fluid. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In this work, we determined the total effective vascular compliance of a global closed-loop model for the cardiovascular system by performing an infusion test of 500 mL of blood in four minutes. Our mathematical model includes a network of arteries and veins where blood flow is described by means of a one-dimensional nonlinear hyperbolic PDE system and zero-dimensional models for other cardiovascular compartments. Some mathematical modifications were introduced to better capture the physiology of the infusion test: (1) a physiological distribution of vascular compliance and total blood volume was implemented, (2) a nonlinear representation of venous resistances and compliances was introduced, and (3) main regulatory mechanisms triggered by the infusion test where incorporated into the model. By means of presented in silico experiment, we show that effective total vascular compliance is the result of the interaction between the assigned constant physical vascular compliance and the capacity of the cardiovascular system to adapt to new situations via regulatory mechanisms. [ABSTRACT FROM AUTHOR]

Background: Induced hypertension has been used to promote cerebral blood flow under vasospastic conditions although there is no randomised clinical trial to support its use. We sought to mathematically model the effects of vasospasm on the cerebral blood flow and the effects of induced hypertension., Methods: The Anatomically Detailed Arterial Network (ADAN) model is employed as the anatomical substrate in which the cerebral blood flow is simulated as part of the simulation of the whole body arterial circulation. The pressure drop across the spastic vessel is modelled by inserting a specific constriction model within the corresponding vessel in the ADAN model. We altered the degree of vasospasm, the length of the vasospastic segment, the location of the vasospasm, the pressure (baseline mean arterial pressure [MAP] 90 mm Hg, hypertension MAP 120 mm Hg, hypotension), and the presence of collateral supply., Results: Larger decreases in cerebral flow were seen for diffuse spasm and more severe vasospasm. The presence of collateral supply could maintain cerebral blood flow, but only if the vasospasm did not occur distal to the collateral. Induced hypertension caused an increase in blood flow in all scenarios, but did not normalise blood flow even in the presence of moderate vasospasm (30%). Hypertension in the presence of a complete circle of Willis had a marginally greater effect on the blood flow, but did not normalise flow., Conclusion: Under vasospastic condition, cerebral blood flow varies considerably. Hypertension can raise the blood flow, but it is unable to restore cerebral blood flow to baseline., Competing Interests: P. Bhogal: proctoring and consultancy agreements with phenox. The other authors declare no conflict of interests. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors., (Copyright © 2019 by S. Karger AG, Basel.)

We propose a detailed CellML model of the human cerebral circulation that runs faster than real time on a desktop computer and is designed for use in clinical settings when the speed of response is important. A lumped parameter mathematical model, which is based on a one-dimensional formulation of the flow of an incompressible fluid in distensible vessels, is constructed using a bond graph formulation to ensure mass conservation and energy conservation. The model includes arterial vessels with geometric and anatomical data based on the ADAN circulation model. The peripheral beds are represented by lumped parameter compartments. We compare the hemodynamics predicted by the bond graph formulation of the cerebral circulation with that given by a classical one-dimensional Navier-Stokes model working on top of the whole-body ADAN model. Outputs from the bond graph model, including the pressure and flow signatures and blood volumes, are compared with physiological data.

Rationale: The role of hypertension in cerebral small vessel disease is poorly understood. At the base of the brain (the 'vascular centrencephalon'), short straight arteries transmit blood pressure directly to small resistance vessels; the cerebral convexity is supplied by long arteries with many branches, resulting in a drop in blood pressure. Hypertensive small vessel disease (lipohyalinosis) causes the classically described lacunar infarctions at the base of the brain; however, periventricular white matter intensities (WMIs) seen on MRI and WMI in subcortical areas over the convexity, which are often also called 'lacunes', probably have different aetiologies., Objectives: We studied pressure gradients from proximal to distal regions of the cerebral vasculature by mathematical modelling., Methods and Results: Blood flow/pressure equations were solved in an Anatomically Detailed Arterial Network (ADAN) model, considering a normotensive and a hypertensive case. Model parameters were suitably modified to account for structural changes in arterial vessels in the hypertensive scenario. Computations predict a marked drop in blood pressure from large and medium-sized cerebral vessels to cerebral peripheral beds. When blood pressure in the brachial artery is 192/113 mm Hg, the pressure in the small arterioles of the posterior parietal artery bed would be only 117/68 mm Hg. In the normotensive case, with blood pressure in the brachial artery of 117/75 mm Hg, the pressure in small parietal arterioles would be only 59/38 mm Hg., Conclusion: These findings have important implications for understanding small vessel disease. The marked pressure gradient across cerebral arteries should be taken into account when evaluating the pathogenesis of small WMIs on MRI. Hypertensive small vessel disease, affecting the arterioles at the base of the brain should be distinguished from small vessel disease in subcortical regions of the convexity and venous disease in the periventricular white matter., Competing Interests: Competing interests: None declared.