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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]

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]

Coronary artery disease, caused by the buildup of atherosclerotic plaques in the coronary vessel wall, is one of the leading causes of death in the world. For high-risk patients, coronary artery bypass graft is the preferred treatment. Despite overall excellent patency rates, bypasses may fail due to restenosis. In this context, the purpose of this work was to perform a parametric computational study of the fluid dynamics in patient-specific geometries with the aim of investigating a possible relationship between coronary stenosis degree and risk of graft failure. Firstly, we propose a strategy to prescribe realistic boundary conditions in the absence of measured data, based on an extension of Murray's law to provide the flow division at bifurcations in case of stenotic vessels and non-Newtonian blood rheology. Then, we carry out numerical simulations in three patients affected by severe coronary stenosis and treated with a graft, in which the stenosis degree is virtually varied in order to compare the resulting fluid dynamics in terms of hemodynamic indices potentially involved in restenosis development. Our findings suggest that low degrees of coronary stenosis produce a more disturbed fluid dynamics in the graft, resulting in hemodynamic conditions that may promote a higher risk of graft failure. [ABSTRACT FROM AUTHOR]