ABSTRACT
Mechanical circulatory support (MCS) devices can bridge the gap to transplant whilst awaiting a viable donor heart. The Realheart Total Artificial Heart is a novel positive-displacement MCS that generates pulsatile flow via bileaflet mechanical valves. This study developed a combined computational fluid dynamics and fluid-structure interaction (FSI) methodology for simulating positive displacement bileaflet valves. Overset meshing discretised the fluid domain, and a blended weak-strong coupling FSI algorithm was combined with variable time-stepping. Four operating conditions of relevant stroke lengths and rates were assessed. The results demonstrated this modelling strategy is stable and efficient for modelling positive-displacement artificial hearts.
Subject(s)
Heart Transplantation , Heart Valve Prosthesis , Humans , Models, Cardiovascular , Tissue Donors , Pulsatile Flow , Prosthesis DesignABSTRACT
To identify predictors of left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used along with serial cardiac magnetic resonance imaging (CMRI) up to 5-6 weeks post-MI. Changes in myocardial strain and strain rates were derived from CMRI data. Tissue proteomics was compared between infarcted and non-infarcted territories. Peak values of left ventricular (LV) apical circumferential strain (ACS) changed over time together with peak global circumferential strain (GCS) while peak GLS epicardial strains or strain rates did not change over time. Early LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories, 21 of which correlated with LV equatorial circumferential strain rate. The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2, and secreted frizzled-related protein 1 (sFRP1). This study shows that early changes in regional peak ACS persist at 5-6 weeks post-MI, when early LVR is observed along with increased tissue levels of D-3PGDH and sFRP1. More studies are needed to ascertain if the observed increase in tissue levels of D-3PGDH and sFRP1 might be casually involved in the pathogenesis of adverse LV remodelling.
Subject(s)
Myocardial Infarction/pathology , Myocardial Infarction/physiopathology , Myocardium/pathology , Ventricular Remodeling , Animals , Biomarkers , Computational Biology/methods , Data Analysis , Data Interpretation, Statistical , Disease Models, Animal , Disease Susceptibility , Female , Image Processing, Computer-Assisted , Magnetic Resonance Imaging/methods , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/metabolism , Myocardium/metabolism , Proteome , Proteomics/methods , Reproducibility of Results , Swine , Translational Research, Biomedical , Ventricular Function, LeftABSTRACT
Abdominal aortic aneurysm disease progression is probably influenced by tissue stresses and blood flow conditions and so accurate estimation of these will increase understanding of the disease and may lead to improved clinical practice. In this work the blood flow and tissue stresses in axially symmetric aneurysms are calculated using a complete fluid-structure interaction as a benchmark for calculating the error introduced by simpler calculations: rigid walled for the blood flow, homogeneous pressure for the tissue stress, as well as one-way-coupled interactions. The error in the peak von Mises stress in a homogeneous pressure calculation compared with a fluid-structure interaction calculation was less than 3.5 per cent for aneurysm diameters up to 7 cm. The error in the mean wall shear stress, in a rigid-walled calculation compared with a fluid-structure interaction calculation, varied from 30 per cent to 60 per cent with increasing aneurysm diameter. These results suggest that incorporation of the fluid-structure interaction is unnecessary for purely mechanical modelling, with the aim of evaluating the current rupture probability. However, for more complex biological modelling, perhaps with the aim of predicting the progress of the disease, where accurate estimation of the wall shear stress is essential, some form of fluid-structure interaction is necessary.