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Impaired cardiac function has been described as a frequent complication of COVID-19-related pneumonia. To investigate possible underlying mechanisms, we represented the cardiovascular system by means of a lumped-parameter 0D mathematical model. The model was calibrated using clinical data, recorded in 58 patients hospitalized for COVID-19-related pneumonia, to make it patient-specific and to compute model outputs of clinical interest related to the cardiocirculatory system. We assessed, for each patient with a successful calibration, the statistical reliability of model outputs estimating the uncertainty intervals. Then, we performed a statistical analysis to compare healthy ranges and mean values (over patients) of reliable model outputs to determine which were significantly altered in COVID-19-related pneumonia. Our results showed significant increases in right ventricular systolic pressure, diastolic and mean pulmonary arterial pressure, and capillary wedge pressure. Instead, physical quantities related to the systemic circulation were not significantly altered. Remarkably, statistical analyses made on raw clinical data, without the support of a mathematical model, were unable to detect the effects of COVID-19-related pneumonia in pulmonary circulation, thus suggesting that the use of a calibrated 0D mathematical model to describe the cardiocirculatory system is an effective tool to investigate the impairments of the cardiocirculatory system associated with COVID-19. [ABSTRACT FROM AUTHOR]

The aim of this paper is to introduce a new mathematical model that simulates myocardial blood perfusion that accounts for multiscale and multiphysics features. Our model incorporates cardiac electrophysiology, active and passive mechanics, hemodynamics, valve modeling, and a multicompartment Darcy model of perfusion. We consider a fully coupled electromechanical model of the left heart that provides input for a fully coupled Navier–Stokes–Darcy model for myocardial perfusion. The fluid dynamics problem is modeled in a left heart geometry that includes large epicardial coronaries, while the multicompartment Darcy model is set in a biventricular myocardium. Using a realistic and detailed cardiac geometry, our simulations demonstrate the biophysical fidelity of our model in describing cardiac perfusion. Specifically, we successfully validate the model reliability by comparing in-silico coronary flow rates and average myocardial blood flow with clinically established values ranges reported in relevant literature. Additionally, we investigate the impact of a regurgitant aortic valve on myocardial perfusion, and our results indicate a reduction in myocardial perfusion due to blood flow taken away by the left ventricle during diastole. To the best of our knowledge, our work represents the first instance where electromechanics, hemodynamics, and perfusion are integrated into a single computational framework. [ABSTRACT FROM AUTHOR]

The aim of this paper is to introduce a new mathematical model that simulates myocardial blood perfusion that accounts for multiscale and multiphysics features. Our model incorporates cardiac electrophysiology, active and passive mechanics, hemodynamics, valve modeling, and a multicompartment Darcy model of perfusion. We consider a fully coupled electromechanical model of the left heart that provides input for a fully coupled Navier–Stokes–Darcy Model for myocardial perfusion. The fluid dynamics problem is modeled in a left heart geometry that includes large epicardial coronaries, while the multicompartment Darcy model is set in a biventricular myocardium. Using a realistic and detailed cardiac geometry, our simulations demonstrate the biophysical fidelity of our model in describing cardiac perfusion. Specifically, we successfully validate the model reliability by comparing in-silico coronary flow rates and average myocardial blood flow with clinically established values ranges reported in relevant literature. Additionally, we investigate the impact of a regurgitant aortic valve on myocardial perfusion, and our results indicate a reduction in myocardial perfusion due to blood flow taken away by the left ventricle during diastole. To the best of our knowledge, our work represents the first instance where electromechanics, hemodynamics, and perfusion are integrated into a single computational framework. [ABSTRACT FROM AUTHOR]

This work dealt with the assessment of a computational tool to estimate the electrical activation in the left ventricle focusing on the latest electrically activated segment (LEAS) in patients with left bundle branch block and possible myocardial fibrosis. We considered the Eikonal-diffusion equation and to recover the electrical activation maps in the myocardium. The model was calibrated by using activation times acquired in the coronary sinus (CS) branches or in the CS solely with an electroanatomic mapping system (EAMS) during cardiac resynchronization therapy (CRT). We applied our computational tool to ten patients founding an excellent accordance with EAMS measures; in particular, the error for LEAS location was less than 4 mm. We also calibrated our model using only information in the CS, still obtaining an excellent agreement with the measured LEAS. The proposed tool was able to accurately reproduce the electrical activation maps and in particular LEAS location in the CS branches, with an almost real-time computational effort, regardless of the presence of myocardial fibrosis, even when information only at CS was used to calibrate the model. This could be useful in the clinical practice since LEAS is often used as a target site for the left lead placement during CRT. Overall picture of the computational pipeline for the estimation of LEAS. [ABSTRACT FROM AUTHOR]

In the current work, we present a descriptive fluid-structure interaction computational study of the end-to-side radio-cephalic arteriovenous fistula. This allows us to account for the different thicknesses and elastic properties of the radial artery and cephalic vein. The core of the work consists in simulating different arteriovenous fistula configurations obtained by virtually varying the anastomosis angle, i.e. the angle between the end of the cephalic vein and the side of the radial artery. Since the aim of the work is to understand the blood dynamics in the very first days after the surgical intervention, the radial artery is considered stiffer and thicker than the cephalic vein. Our results demonstrate that both the diameter of the cephalic vein and the anastomosis angle play a crucial role to obtain a blood dynamics without re-circulation regions that could prevent fistula failure. When an anastomosis angle close to the perpendicular direction with respect to the radial artery is combined with a large diameter of the cephalic vein, the recirculation regions and the low Wall Shear Stress (WSS) zones are reduced. Conversely, from a structural point of view, a low anastomosis angle with a large diameter of the cephalic vein reduces the mechanical stress acting on the vessel walls. • Fluid-structure interaction analysis for different configurations of the arteriovenous fistula. • Mismatch of the arterial and venous Young's moduli and different vessel thicknesses. • Real reconstruction of the shape of the anastomosis region. • The diameter of the cephalic vein drastically influences the hemodynamics. [ABSTRACT FROM AUTHOR]

Purpose: Quantification of myocardial blood flow (MBF) and functional assessment of coronary artery disease (CAD) can be achieved through stress myocardial computed tomography perfusion (stress-CTP). This requires an additional scan after the resting coronary computed tomography angiography (cCTA) and administration of an intravenous stressor. This complex protocol has limited reproducibility and non-negligible side effects for the patient. We aim to mitigate these drawbacks by proposing a computational model able to reproduce MBF maps. Methods: A computational perfusion model was used to reproduce MBF maps. The model parameters were estimated by using information from cCTA and MBF measured from stress-CTP (MBFCTP) maps. The relative error between the computational MBF under stress conditions (MBFCOMP) and MBFCTP was evaluated to assess the accuracy of the proposed computational model. Results: Applying our method to 9 patients (4 control subjects without ischemia vs 5 patients with myocardial ischemia), we found an excellent agreement between the values of MBFCOMP and MBFCTP. In all patients, the relative error was below 8% over all the myocardium, with an average-in-space value below 4%. Conclusion: The results of this pilot work demonstrate the accuracy and reliability of the proposed computational model in reproducing MBF under stress conditions. This consistency test is a preliminary step in the framework of a more ambitious project which is currently under investigation, i.e., the construction of a computational tool able to predict MBF avoiding the stress protocol and potential side effects while reducing radiation exposure. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a systemic disease that leads to accumulation of deposits, known as atherosclerotic plaques, within the walls of the carotids. In particular, three types of plaque can be distinguished: soft, fibrous, and calcific. Most of the computational studies who investigated the interplay between the plaque and the blood flow on patient-specific geometries used nonstandard medical images to directly delineate and segment the plaque and its components. However, these techniques are not so widely available in the clinical practice. In this context, the aim of our work was twofold: (i) to propose a new geometric tool that allowed to reconstruct a plausible plaque in the carotids from standard images and (ii) to perform three-dimensional (3D) fluid-structure interaction (FSI) simulations where we compared some fluid-dynamic and structural quantities among 15 patients characterized by different typologies of plaque. Our results highlighted that both the morphology and the mechanical properties of different plaque components play a crucial role in determining the vulnerability of the plaque. [ABSTRACT FROM AUTHOR]

We consider a loosely-coupled algorithm for fluid-structure interaction based on a Robin interface condition for the fluid problem (explicit Robin-Neumann scheme). We study the dependence of the stability of this method on the interface parameter in the Robin condition. In particular, for a model problem we find sufficient conditions for instability and stability of the method. In the latter case, we find a stability condition relating the time discretization parameter, the interface parameter, and the fluid and structure densities. Numerical experiments confirm the theoretical findings and highlight optimal choices of the interface parameter that guarantee accurate solutions. [ABSTRACT FROM AUTHOR]

We present a new model of human cardiac electromechanics for the left ventricle where electrophysiology is described by a Reaction–Eikonal model and which enables an off-line resolution of the reaction model, thus entailing a big saving of computational time. Subcellular dynamics is coupled with a model of tissue mechanics, which is in turn coupled with a Windkessel model for blood circulation. Our numerical results show that the proposed model is able to provide a physiological response to changes in certain variables (end-diastolic volume, total peripheral resistance, contractility). We also show that our model is able to reproduce with high accuracy and with a considerably lower computational time the results that we would obtain if the monodomain model should be used in place of the Eikonal model. [ABSTRACT FROM AUTHOR]

In this work, we performed a computational image-based study of blood dynamics in the whole left heart, both in a healthy subject and in a patient with mitral valve regurgitation. We elaborated multi-series cine-MRI with the aim of reconstructing the geometry and the corresponding motion of left ventricle, left atrium, mitral and aortic valves, and aortic root of the subjects. This allowed us to prescribe such motion to computational blood dynamics simulations where, for the first time, the whole left heart motion of the subject is considered, allowing us to obtain reliable subject-specific information. The final aim is to investigate and compare between the subjects the occurrence of turbulence and the risk of hemolysis and of thrombi formation. In particular, we modeled blood with the Navier–Stokes equations in the arbitrary Lagrangian–Eulerian framework, with a large eddy simulation model to describe the transition to turbulence and a resistive method to manage the valve dynamics, and we used a finite element discretization implemented in an in-house code for the numerical solution. [ABSTRACT FROM AUTHOR]

Transcatheter aortic valve implantation (TAVI) is a minimally invasive intervention for the treatment of severe aortic valve stenosis. The main cause of failure is the structural deterioration of the implanted prosthetic leaflets, possibly inducing a valvular re‐stenosis 5–10 years after the implantation. Based solely on pre‐implantation data, the aim of this work is to identify fluid‐dynamics and structural indices that may predict the possible valvular deterioration, in order to assist the clinicians in the decision‐making phase and in the intervention design. Patient‐specific, pre‐implantation geometries of the aortic root, the ascending aorta, and the native valvular calcifications were reconstructed from computed tomography images. The stent of the prosthesis was modeled as a hollow cylinder and virtually implanted in the reconstructed domain. The fluid‐structure interaction between the blood flow, the stent, and the residual native tissue surrounding the prosthesis was simulated by a computational solver with suitable boundary conditions. Hemodynamical and structural indicators were analyzed for five different patients that underwent TAVI – three with prosthetic valve degeneration and two without degeneration – and the comparison of the results showed a correlation between the leaflets' structural degeneration and the wall shear stress distribution on the proximal aortic wall. This investigation represents a first step towards computational predictive analysis of TAVI degeneration, based on pre‐implantation data and without requiring additional peri‐operative or follow‐up information. Indeed, being able to identify patients more likely to experience degeneration after TAVI may help to schedule a patient‐specific timing of follow‐up. [ABSTRACT FROM AUTHOR]

The importance of myocardial perfusion at the outset of cardiac disease remains largely understudied. To address this topic we present a mathematical model that considers the systemic circulation, the coronary vessels, the myocardium, and the interactions among these components. The core of the whole model is the description of the myocardium as a multicompartment poromechanics system. A novel decomposition of the poroelastic Helmholtz potential involved in the poromechanics model allows for a quasi-incompressible model that adequately describes the physical interaction among all components in the porous medium. We further provide a rigorous mathematical analysis that gives guidelines for the choice of the Helmholtz potential. To reduce the computational cost of our integrated model we propose decoupling the deformation of the tissue and systemic circulation from the porous flow in the myocardium and coronary vessels, which allows us to apply the model also in combination with precomputed cardiac displacements, obtained form other models or medical imaging data. We test the methodology through the simulation of a heartbeat in healthy conditions that replicates the systolic impediment phenomenon, which is particularly challenging to capture as it arises from the interaction of several parts of the model. [ABSTRACT FROM AUTHOR]

Background: We designed a retrospective computational study to evaluate the effects of hemodynamics on portal confluence remodeling in real models of patients with malignancies of the pancreatic head. Methods: Patient-specific models were created according to computed tomography data. Fluid dynamics was simulated by using finite-element methods. Computational results were compared to morphological findings. Results: Five patients underwent total pancreatectomy, one had duodenopancreatectomy. Vein resection was performed en-bloc with the specimen. Histopathological findings showed that in patients without a vein stenosis and a normal hemodynamics, the three-layered wall of the vein was preserved. In patients with a stenosis > 70% of vein diameter and modified hemodynamics, the three-layered structure of the resected vein was replaced by a dense inflammatory infiltrate in absence of tumor infiltration. Conclusions: The portal confluence involved by malignancies of the pancreatic head undergoes a remodeling that is not mainly due to a wall infiltration by the tumor but instead to a persistent pathological hemodynamics that disrupts the balance between eutrophic remodeling and degradative process of the vein wall that can lead to the complete upheaval of the three-layered vein wall. This finding can have useful surgical application in planning resection of the vein involved by tumor growth. [ABSTRACT FROM AUTHOR]

Numerical simulations of cardiac blood pump systems are integral to the optimization of device design, hydraulic performance and hemocompatibility. In wave membrane blood pumps, blood propulsion arises from the wave propagation along an oscillating immersed membrane, which generates small pockets of fluid that are pushed towards the outlet against an adverse pressure gradient. We studied the Fluid–Structure Interaction between the oscillating membrane and the blood flow via three‐dimensional simulations using the Extended Finite Element Method (XFEM), an unfitted numerical technique that avoids remeshing by using a fluid fixed mesh. Our three‐dimensional numerical simulations in a realistic pump geometry highlighted, for the first time in this field of application, that XFEM is a reliable strategy to handle complex industrial problems. Moreover, they showed the role of the membrane deformation in promoting a blood flow towards the outlet despite an adverse pressure gradient. We also simulated the pump system at different pressure conditions and we validated the numerical results against in‐vitro experimental data. [ABSTRACT FROM AUTHOR]

We present a loosely coupled scheme for the numerical simulation of the cardiac electro-fluid-structure interaction problem, whose solution is typically computationally intensive due to the need to suitably treat the coupling of the different submodels. Our scheme relies on a segregated treatment of the subproblems, in particular on an explicit Robin-Neumann algorithm for the fluid-structure interaction, aiming at reducing the computational burden of numerical simulations. The results, both in an ideal and a realistic cardiac setting, show that the proposed scheme is stable at the regimes typical of cardiac simulations. From a comparison with a scheme with implicit fluid-structure interaction, it emerges that, while conservation properties are not fully preserved, computational times significantly benefit from the explicit scheme. Overall, the explicit discretization represents a good trade-off between accuracy and cost, and is a valuable alternative to implicit schemes for fast large-scale simulations. • We present an explicit scheme for the simulation of cardiac electro-fluid-structure interaction. • The scheme uses Robin-Neumann fluid-structure interface conditions. • We analyze the stability, accuracy and efficiency of the explicit scheme. • The explicit scheme provides a compromise between accuracy and computational cost. [ABSTRACT FROM AUTHOR]

In this special issue, we collect some recent works in this field. In the recent years, there have been remarkable developments in the field of numerical simulations of the cardiovascular system. In particular, the works presented here cover both methodological and applicative issues in two fields of great interest, such as cardiac electrophysiology and hemodynamics. [Extracted from the article]

Two crucial factors for accurate numerical simulations of cardiac electromechanics, which are also essential to reproduce the synchronous activity of the heart, are: (i) accounting for the interaction between the heart and the circulatory system that determines pressures and volumes loads in the heart chambers; (ii) reconstructing the muscular fiber architecture that drives the electrophysiology signal and the myocardium contraction. In this work, we present a 3D biventricular electromechanical model coupled with a 0D closed-loop model of the whole cardiovascular system that addresses the two former crucial factors. With this aim, we introduce a boundary condition for the mechanical problem that accounts for the neglected part of the domain located on top of the biventricular basal plane and that is consistent with the principles of momentum and energy conservation. We also discuss in detail the coupling conditions behind the 3D and the 0D models. We perform electromechanical simulations in physiological conditions using the 3D–0D model and we show that our results match the experimental data of relevant mechanical biomarkers available in the literature. Furthermore, we investigate different arrangements in cross-fibers active contraction. We prove that an active tension along the sheet direction counteracts the myofiber contraction, while the one along the sheet-normal direction enhances the cardiac work. Finally, several myofiber architectures are analyzed. We show that a different fiber field in the septal area and in the transmural wall affects the pumping functionality of the left ventricle. • 3D electromechanical biventricular model coupled with a 0D hemodynamic closed-loop model. • A novel effective mechanical boundary condition for the biventricular basal plane. • Numerical results on a realistic biventricular model matching the experimental data. • Study of different configurations in cross-fibers active contraction. • Evaluation of the impact of different myofibers architectures on biventricular electromechanics. [ABSTRACT FROM AUTHOR]