Computer model coupling hemodynamics and oxygen transport in the coronary capillary network: Pulsatile vs. non-pulsatile analysis.

Background And Objective: Oxygen transport in the heart is crucial, and its impairment can lead to pathological conditions such as hypoxia, ischemia, and heart failure. However, investigating oxygen transport in the heart using in vivo measurements is difficult due to the small size of the coronary capillaries and their deep embedding within the heart wall.

Methods: In this study, we developed a novel computational modeling framework that integrates a 0-D hemodynamic model with a 1-D mass transport model to simulate oxygen transport in/across the coronary capillary network.

Rapid estimation of left ventricular contractility with a physics-informed neural network inverse modeling approach.

Physics-based computer models based on numerical solutions of the governing equations generally cannot make rapid predictions, which in turn limits their applications in the clinic. To address this issue, we developed a physics-informed neural network (PINN) model that encodes the physics of a closed-loop blood circulation system embedding a left ventricle (LV). The PINN model is trained to satisfy a system of ordinary differential equations (ODEs) associated with a lumped parameter description of the circulatory system.

Multiscale fiber remodeling in the infarcted left ventricle using a stress-based reorientation law.

The organization of myofibers and extra cellular matrix within the myocardium plays a significant role in defining cardiac function. When pathological events occur, such as myocardial infarction (MI), this organization can become disrupted, leading to degraded pumping performance. The current study proposes a multiscale finite element (FE) framework to determine realistic fiber distributions in the left ventricle (LV).

Computational investigation of the role of ventricular remodelling in HFpEF: The key to phenotype dissection.

Recent clinical studies have reported that heart failure with preserved ejection fraction (HFpEF) can be divided into two phenotypes based on the range of ejection fraction (EF), namely HFpEF with higher EF and HFpEF with lower EF. These phenotypes exhibit distinct left ventricle (LV) remodelling patterns and dynamics. However, the influence of LV remodelling on various LV functional indices and the underlying mechanics for these two phenotypes are not well understood.

Multiscale Finite Element Modeling of Left Ventricular Growth in Simulations of Valve Disease.

Multiscale models of the cardiovascular system are emerging as effective tools for investigating the mechanisms that drive ventricular growth and remodeling. These models can predict how molecular-level mechanisms impact organ-level structure and function and could provide new insights that help improve patient care. MyoFE is a multiscale computer framework that bridges molecular and organ-level mechanisms in a finite element model of the left ventricle that is coupled with the systemic circulation.

A multiscale finite element model of left ventricular mechanics incorporating baroreflex regulation.

Cardiovascular function is regulated by a short-term hemodynamic baroreflex loop, which tries to maintain arterial pressure at a normal level. In this study, we present a new multiscale model of the cardiovascular system named MyoFE. This framework integrates a mechanistic model of contraction at the myosin level into a finite-element-based model of the left ventricle pumping blood through the systemic circulation.

Computational analysis of ventricular mechanics in hypertrophic cardiomyopathy patients.

Hypertrophic cardiomyopathy (HCM) is a genetic heart disease that is associated with many pathological features, such as a reduction in global longitudinal strain (GLS), myofiber disarray and hypertrophy. The effects of these features on left ventricle (LV) function are, however, not clear in two phenotypes of HCM, namely, obstructive and non-obstructive. To address this issue, we developed patient-specific computational models of the LV using clinical measurements from 2 female HCM patients and a control subject.

The dependency of fetal left ventricular biomechanics function on myocardium helix angle configuration.

The helix angle configuration of the myocardium is understood to contribute to the heart function, as finite element (FE) modeling of postnatal hearts showed that altered configurations affected cardiac function and biomechanics. However, similar investigations have not been done on the fetal heart. To address this, we performed image-based FE simulations of fetal left ventricles (LV) over a range of helix angle configurations, assuming a linear variation of helix angles from epicardium to endocardium.

Computational modelling of multi-temporal ventricular-vascular interactions during the progression of pulmonary arterial hypertension.

A computational framework is developed to consider the concurrent growth and remodelling (G&R) processes occurring in the large pulmonary artery (PA) and right ventricle (RV), as well as ventricular-vascular interactions during the progression of pulmonary arterial hypertension (PAH). This computational framework couples the RV and the proximal PA in a closed-loop circulatory system that operates in a short timescale of a cardiac cycle, and evolves over a long timescale due to G&R processes in the PA and RV. The framework predicts changes in haemodynamics (e.

Morphological, functional, and biomechanical progression of LV remodelling in a porcine model of HFpEF.

Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for about half of heart failure cases, but the progression of cardiac biomechanics during pathogenesis is not completely understood. We investigated a published porcine model of HFpEF, generated by progressive constriction of an aortic cuff causing progressive left ventricle (LV) pressure overload, and characterized by hypertrophy, diastolic dysfunction and overt HF with elevated plasma beta natriuretic peptide (BNP). We characterized morphological and functional features and performed image-based finite element modelling over multiple time points, so as to understand how biomechanics evolved with morphological and functional changes during pathogenesis, and to provide data for future growth and remodeling investigations.

Data-driven computational models of ventricular-arterial hemodynamics in pediatric pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a complex disease involving increased resistance in the pulmonary arteries and subsequent right ventricular (RV) remodeling. Ventricular-arterial interactions are fundamental to PAH pathophysiology but are rarely captured in computational models. It is important to identify metrics that capture and quantify these interactions to inform our understanding of this disease as well as potentially facilitate patient stratification.

Transmural Distribution of Coronary Perfusion and Myocardial Work Density Due to Alterations in Ventricular Loading, Geometry and Contractility.

Myocardial supply changes to accommodate the variation of myocardial demand across the heart wall to maintain normal cardiac function. A computational framework that couples the systemic circulation of a left ventricular (LV) finite element model and coronary perfusion in a closed loop is developed to investigate the transmural distribution of the myocardial demand (work density) and supply (perfusion) ratio. Calibrated and validated against measurements of LV mechanics and coronary perfusion, the model is applied to investigate changes in the transmural distribution of passive coronary perfusion, myocardial work density, and their ratio in response to changes in LV contractility, preload, afterload, wall thickness, and cavity volume.

Optimization of cardiac resynchronization therapy based on a cardiac electromechanics-perfusion computational model.

Cardiac resynchronization therapy (CRT) is an established treatment for left bundle branch block (LBBB) resulting in mechanical dyssynchrony. Approximately 1/3 of patients with CRT, however, are non-responders. To understand factors affecting CRT response, an electromechanics-perfusion computational model based on animal-specific left ventricular (LV) geometry and coronary vascular networks located in the septum and LV free wall is developed.

Multiscale simulations of left ventricular growth and remodeling.

Cardiomyocytes can adapt their size, shape, and orientation in response to altered biomechanical or biochemical stimuli. The process by which the heart undergoes structural changes-affecting both geometry and material properties-in response to altered ventricular loading, altered hormonal levels, or mutant sarcomeric proteins is broadly known as cardiac growth and remodeling (G&R). Although it is likely that cardiac G&R initially occurs as an adaptive response of the heart to the underlying stimuli, prolonged pathological changes can lead to increased risk of atrial fibrillation, heart failure, and sudden death.

Computational Modeling Studies of the Roles of Left Ventricular Geometry, Afterload, and Muscle Contractility on Myocardial Strains in Heart Failure with Preserved Ejection Fraction.

Global longitudinal strain and circumferential strain are found to be reduced in HFpEF, which some have interpreted that the global left ventricular (LV) contractility is impaired. This finding is, however, contradicted by a preserved ejection fraction (EF) and confounded by changes in LV geometry and afterload resistance that may also affect the global strains. To reconcile these issues, we used a validated computational framework consisting of a finite element LV model to isolate the effects of HFpEF features in affecting systolic function metrics.

Inverse modeling framework for characterizing patient-specific microstructural changes in the pulmonary arteries.

Microstructural changes in the pulmonary arteries associated with pulmonary arterial hypertension (PAH) is not well understood and characterized in humans. To address this issue, we developed and applied a patient-specific inverse finite element (FE) modeling framework to characterize mechanical and structural changes of the micro-constituents in the proximal pulmonary arteries using in-vivo pressure measurements and magnetic resonance images. The framework was applied using data acquired from a pediatric PAH patient and a heart transplant patient with normal pulmonary arterial pressure, which serves as control.