11,140 research outputs found
Computational modeling of acute myocardial infarction
This is an Accepted Manuscript of an article published by Taylor & Francis Group in Computer Methods in Biomechanics and Biomedical Engineering on October, 2016, available online at: http://www.tandfonline.com/10.1080/10255842.2015.1105965Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.Peer ReviewedPostprint (author's final draft
Computational modeling of hypertensive growth in the human carotid artery
The final publication is available at Springer via http://dx.doi.org/10.1007/s00466-013-0959-zArterial hypertension is a chronic medical condition associated with an elevated blood pressure. Chronic arterial hypertension initiates a series of events, which are known to collectively initiate arterial wall thickening. However, the correlation between macrostructural mechanical loading, microstructural cellular changes, and macrostructural adaptation remains unclear. Here, we present a microstructurally motivated computational model for chronic arterial hypertension through smooth muscle cell growth. To model growth, we adopt a classical concept based on the multiplicative decomposition of the deformation gradient into an elastic part and a growth part. Motivated by clinical observations, we assume that the driving force for growth is the stretch sensed by the smooth muscle cells. We embed our model into a finite element framework, where growth is stored locally as an internal variable. First, to demonstrate the features of our model, we investigate the effects of hypertensive growth in a real human carotid artery. Our results agree nicely with experimental data reported in the literature both qualitatively and quantitatively.Peer ReviewedPostprint (author's final draft
A modeling framework for contact, adhesion and mechano-transduction between excitable deformable cells
Cardiac myocytes are the fundamental cells composing the heart muscle. The
propagation of electric signals and chemical quantities through them is
responsible for their nonlinear contraction and dilatation. In this study, a
theoretical model and a finite element formulation are proposed for the
simulation of adhesive contact interactions between myocytes across the
so-called gap junctions. A multi-field interface constitutive law is proposed
for their description, integrating the adhesive and contact mechanical response
with their electrophysiological behavior. From the computational point of view,
the initial and boundary value problem is formulated as a structure-structure
interaction problem, which leads to a straightforward implementation amenable
for parallel computations. Numerical tests are conducted on different couples
of myocytes, characterized by different shapes related to their stages of
growth, capturing the experimental response. The proposed framework is expected
to have impact on the understanding how imperfect mechano-transduction could
lead to emergent pathological responses.Comment: 31 pages, 17 figure
Modelling mitral valvular dynamics–current trend and future directions
Dysfunction of mitral valve causes morbidity and premature mortality and remains a leading medical problem worldwide. Computational modelling aims to understand the biomechanics of human mitral valve and could lead to the development of new treatment, prevention and diagnosis of mitral valve diseases. Compared with the aortic valve, the mitral valve has been much less studied owing to its highly complex structure and strong interaction with the blood flow and the ventricles. However, the interest in mitral valve modelling is growing, and the sophistication level is increasing with the advanced development of computational technology and imaging tools. This review summarises the state-of-the-art modelling of the mitral valve, including static and dynamics models, models with fluid-structure interaction, and models with the left ventricle interaction. Challenges and future directions are also discussed
Non-linear modeling of active biohybrid materials
Recent advances in engineered muscle tissue attached to a synthetic substrate motivates the development of appropriate constitutive and numerical models. Applications of active materials can be expanded by using robust, non-mammalian muscle cells, such as those of Manduca sexta. In this study, we propose a model to assist in the analysis of biohybrid constructs by generalizing a recently proposed constitutive law for Manduca muscle tissue. The continuum model accounts (i) for the stimulation of muscle fibers by introducing multiple stress-free reference configurations for the active and passive states and (ii) for the hysteretic response by specifying a pseudo-elastic energy function. A simple example representing uniaxial loading-unloading is used to validate and verify the characteristics of the model. Then, based on experimental data of muscular thin films, a more complex case shows the qualitative potential of Manduca muscle tissue in active biohybrid constructs
Modelling the evolution of cerebral aneurysms: biomechanics, mechanobiology and multiscale modelling
Intracranial aneurysms (IAs) are abnormal dilatations of the cerebral vasculature. Computational modelling may shed light on the aetiology of the disease and lead to improved criteria to assist diagnostic decisions. We briefly review models of aneurysm evolution to date and present a novel fluid-solid-growth (FSG) framework for patient-specific modelling of IA evolution. We illustrate its application to 4 clinical cases depicting an IA. The section of arterial geometry containing the IA is removed and replaced with a cylindrical section: this represents an idealised section of healthy artery upon which IA evolution is simulated. The utilisation of patient-specific geometries enables G&R to be explicitly linked to physiologically realistic spatial distributions and magnitudes of haemodynamic stimuli. In this study, we investigate the hypothesis that elastin degradation is driven by locally low wall shear stress (WSS). In 3 out of 4 cases, the evolved model IA geometry is qualitatively similar to the corresponding in vivo IA geometry. This suggests some tentative support for the hypothesis that low WSS plays a role in the mechanobiology of IA evolution
Continuum Modeling and Simulation in Bone Tissue Engineering
Bone tissue engineering is currently a mature methodology from a research perspective.
Moreover, modeling and simulation of involved processes and phenomena in BTE have been proved
in a number of papers to be an excellent assessment tool in the stages of design and proof of concept
through in-vivo or in-vitro experimentation. In this paper, a review of the most relevant contributions
in modeling and simulation, in silico, in BTE applications is conducted. The most popular in silico
simulations in BTE are classified into: (i) Mechanics modeling and sca old design, (ii) transport and
flow modeling, and (iii) modeling of physical phenomena. The paper is restricted to the review of the
numerical implementation and simulation of continuum theories applied to di erent processes in
BTE, such that molecular dynamics or discrete approaches are out of the scope of the paper. Two main
conclusions are drawn at the end of the paper: First, the great potential and advantages that in silico
simulation o ers in BTE, and second, the need for interdisciplinary collaboration to further validate
numerical models developed in BTE.Ministerio de Economía y Competitividad del Gobierno España DPI2017-82501-
Competing mechanisms of stress-assisted diffusivity and stretch-activated currents in cardiac electromechanics
We numerically investigate the role of mechanical stress in modifying the
conductivity properties of the cardiac tissue and its impact in computational
models for cardiac electromechanics. We follow a theoretical framework recently
proposed in [Cherubini, Filippi, Gizzi, Ruiz-Baier, JTB 2017], in the context
of general reaction-diffusion-mechanics systems using multiphysics continuum
mechanics and finite elasticity. In the present study, the adapted models are
compared against preliminary experimental data of pig right ventricle
fluorescence optical mapping. These data contribute to the characterization of
the observed inhomogeneity and anisotropy properties that result from
mechanical deformation. Our novel approach simultaneously incorporates two
mechanisms for mechano-electric feedback (MEF): stretch-activated currents
(SAC) and stress-assisted diffusion (SAD); and we also identify their influence
into the nonlinear spatiotemporal dynamics. It is found that i) only specific
combinations of the two MEF effects allow proper conduction velocity
measurement; ii) expected heterogeneities and anisotropies are obtained via the
novel stress-assisted diffusion mechanisms; iii) spiral wave meandering and
drifting is highly mediated by the applied mechanical loading. We provide an
analysis of the intrinsic structure of the nonlinear coupling using
computational tests, conducted using a finite element method. In particular, we
compare static and dynamic deformation regimes in the onset of cardiac
arrhythmias and address other potential biomedical applications
The role of topology and mechanics in uniaxially growing cell networks
In biological systems, the growth of cells, tissues, and organs is influenced
by mechanical cues. Locally, cell growth leads to a mechanically heterogeneous
environment as cells pull and push their neighbors in a cell network. Despite
this local heterogeneity, at the tissue level, the cell network is remarkably
robust, as it is not easily perturbed by changes in the mechanical environment
or the network connectivity. Through a network model, we relate global tissue
structure (i.e. the cell network topology) and local growth mechanisms (growth
laws) to the overall tissue response. Within this framework, we investigate the
two main mechanical growth laws that have been proposed: stress-driven or
strain-driven growth. We show that in order to create a robust and stable
tissue environment, networks with predominantly series connections are
naturally driven by stress-driven growth, whereas networks with predominantly
parallel connections are associated with strain-driven growth
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