A comprehensive mathematical model for cardiac perfusion

Zingaro, Alberto; Vergara, Christian; Dede’, Luca; Regazzoni, Francesco; Quarteroni, Alfio

doi:10.1038/s41598-023-41312-0

Cited by 11 publications

(5 citation statements)

References 94 publications

(131 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this regard, the recent work by Sharifi et al [ 225 ] is notable, where the authors were able to mimic important features of the physiological baroreflex, one of the body’s homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels. Regarding perfusion, the process linking the circulatory system with the myocardium, Zingaro et al [ 226 ] recently presented a mechanics model linking cardiac mechanics with perfusion. However, this is just the first step to achieve clinical translation of this type of cardiac model.…”

Section: Discussionmentioning

confidence: 99%

Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways

Rodero,

Baptiste,

Barrows

et al. 2023

Front. Phys.

View full text Add to dashboard Cite

Cardiac mechanics models are developed to represent a high level of detail, including refined anatomies, accurate cell mechanics models, and platforms to link microscale physiology to whole-organ function. However, cardiac biomechanics models still have limited clinical translation. In this review, we provide a picture of cardiac mechanics models, focusing on their clinical translation. We review the main experimental and clinical data used in cardiac models, as well as the steps followed in the literature to generate anatomical meshes ready for simulations. We describe the main models in active and passive mechanics and the different lumped parameter models to represent the circulatory system. Lastly, we provide a summary of the state-of-the-art in terms of ventricular, atrial, and four-chamber cardiac biomechanics models. We discuss the steps that may facilitate clinical translation of the biomechanics models we describe. A well-established software to simulate cardiac biomechanics is lacking, with all available platforms involving different levels of documentation, learning curves, accessibility, and cost. Furthermore, there is no regulatory framework that clearly outlines the verification and validation requirements a model has to satisfy in order to be reliably used in applications. Finally, better integration with increasingly rich clinical and/or experimental datasets as well as machine learning techniques to reduce computational costs might increase model reliability at feasible resources. Cardiac biomechanics models provide excellent opportunities to be integrated into clinical workflows, but more refinement and careful validation against clinical data are needed to improve their credibility. In addition, in each context of use, model complexity must be balanced with the associated high computational cost of running these models.

show abstract

Section: Discussionmentioning

confidence: 99%

Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways

Rodero,

Baptiste,

Barrows

et al. 2023

Front. Phys.

View full text Add to dashboard Cite

show abstract

“…Still, an accurate mathematical description of coronary hemodynamics remains a challenge because of two main reasons: firstly, the coronary circulation spans over a broad range of length scales (from few millimeters to few microns of vessel diameter), making it impossible to run even 1D fluid-dynamics simulations in the fully resolved tree; secondly, cardiac contraction deeply affects coronary flow, mainly through the well known systolic impediment effect [4], which is challenging to model in an effective way. To address the first issue, previous works have proposed either a focus on large coronaries with outflow conditions, surrogating microvasculature, based on lumped parameter models [5,6] or on extendend Murray's law [7]; or multiscale models, often treating blood dynamics in the microcirculation through Modeling cardiac microcirculation for the simulation of coronary flow and 3D myocard a homogenized porous medium approach (Darcy equations, [8]), coupled with a 1D [9] or 3D [10] description of fluid-dynamics in the large coronaries. This has been further extended with the proposal of multicompartment Darcy formulations to account for the different length scales in the microcirculation [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Modeling cardiac microcirculation for the simulation of coronary flow and 3D myocardial perfusion

Pelagi,

Regazzoni,

Huyghe

et al. 2024

Preprint

Self Cite

View full text Add to dashboard Cite

Purpose: accurate modeling of blood dynamics in the coronary microcirculation is a crucial step towards the clinical application of in silico methods for the diagnosis of coronary artery disease (CAD). In this work, we present a new mathematical model of microcirculatory hemodynamics accounting for microvasculature compliance and cardiac contraction; we also present its application to a full simulation of hyperemic coronary blood flow and 3D myocardial perfusion in real clinical cases. Methods: microvasculature hemodynamics is modeled with a compliant multi-compartment Darcy formulation, with the new compli- ance terms depending on the local intramyocardial pressure generated by cardiac contraction. Nonlinear analytical relationships for vessels distensibility are included based on experimental data, and all the parameters of the model are reformulated based on histo-logically relevant quantities, allowing a deeper model personalization. Results: Phasic flow patterns of high arterial inflow in diastole and venous outflow in systole are obtained, with flow waveforms morphology and pressure distribution along the microcirculation reproduced in accordance with experimental and in vivo measures. Phasic diameter change for arterioles and capillaries is also obtained with relevant differences depending on the depth location. Coronary blood dynamics exhibits a disturbed flow at the systolic onset, while the obtained 3D perfusion maps reproduce the systolic impediment effect and show relevant regional and transmural heterogeneities in myocardial blood flow (MBF). Conclusion: the proposed model successfully reproduces microvasculature hemodynamics over the whole heartbeat and along the entire intramural vessels. Quantification of phasic flow patterns, diameter changes, regional and transmural heterogeneities in MBF represent key steps ahead in the direction of the predictive simulation of cardiac perfusion.

show abstract

“…Vigmond et al (23) performed the first whole heart simulations in an idealized geometry to investigate the impact of bundle branch block on transvalvular flow, septal movement, and stretch-induced effects for myocytes in the left and right ventricular walls. Quarteroni et al (24) introduced multi-physics computational models of idealized LVs, which were subsequently improved to consider realistic left heart (25) and whole-heart anatomies (26). Feng et al (27) analyzed the effects of mitral valve regurgitation and AFib on LA and LAA flow in an LA-mitral valve system using their coupled fluid interaction model.…”

Section: Introductionmentioning

confidence: 99%

Patient-specific multi-physics simulations of fibrotic changes in left atrial tissue mechanics impact on hemodynamics

Gonzalo,

Augustin,

Bifulco

et al. 2024

Preprint

View full text Add to dashboard Cite

Stroke is a leading cause of death and disability worldwide. Atrial myopathy, including fibrosis, is associated with an increased risk of ischemic stroke, but the mechanisms underlying this association are poorly understood. Fibrosis modifies myocardial structure, impairing electrical propagation and tissue biomechanics, and creating stagnant flow regions where clots could form. Fibrosis can be mapped non-invasively using late gadolinium enhancement magnetic resonance imaging (LGE-MRI). However, fibrosis maps are not currently incorporated into stroke risk calculations or computational electro-mechano-fluidic models. We present multi-physics simulations of left atrial (LA) myocardial motion and hemodynamics using patient-specific anatomies and fibrotic maps from LGE-MRI. We modify tissue stiffness and active tension generation in fibrotic regions and investigate how these changes affect LA flow for different fibrotic burdens. We find that fibrotic regions and, to a lesser extent, non-fibrotic regions experience reduced myocardial strain, resulting in decreased LA emptying fraction consistent with clinical observations. Both fibrotic tissue stiffening and hypocontractility independently reduce LA function, but together, these two alterations cause more pronounced effects than either one alone. Fibrosis significantly alters flow patterns throughout the atrial chamber, and particularly, the filling and emptying jets of the left atrial appendage (LAA). The effects of fibrosis in LA flow are largely captured by the concomitant changes in LA emptying fraction except inside the LAA, where a multi-factorial behavior is observed. This work illustrates how high-fidelity, multi-physics models can be used to study thrombogenesis mechanisms in a patient-specific manner, shedding light onto the link between atrial fibrosis and ischemic stroke.Key pointsLeft atrial (LA) fibrosis is associated with arrhythmogenesis and increased risk of ischemic stroke; its extent and pattern can be quantified on a patient-specific basis using late gadolinium enhancement magnetic resonance imaging.Current stroke risk prediction tools have limited personalization, and their accuracy could be improvedfib by incorporating patient-specific information like fibrotic maps and hemodynamic patterns.We present the first electro-mechano-fluidic multi-physics computational simulations of LA flow, including fibrosis and anatomies from medical imaging.Mechanical changes in fibrotic tissue impair global LA motion, decreasing LA and left atrial appendage (LAA) emptying fractions, especially in subjects with higher fibrosis burdens.Fibrotic-mediated LA motion impairment alters LA and LAA flow near the endocardium and the whole cavity, ultimately leading to more stagnant blood regions in the LAA.

show abstract

A comprehensive mathematical model for cardiac perfusion

Cited by 11 publications

References 94 publications

Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways

Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways

Modeling cardiac microcirculation for the simulation of coronary flow and 3D myocardial perfusion

Patient-specific multi-physics simulations of fibrotic changes in left atrial tissue mechanics impact on hemodynamics

Contact Info

Product

Resources

About