No Arabic abstract
Endovascular sealing is a new technique for the repair of abdominal aortic aneurysms. Commercially available in Europe since~2013, it takes a revolutionary approach to aneurysm repair through minimally invasive techniques. Although aneurysm sealing may be thought as more stable than conventional endovascular stent graft repairs, post-implantation movement of the endoprosthesis has been described, potentially leading to late complications. The paper presents for the first time a model, which explains the nature of forces, in static and dynamic regimes, acting on sealed abdominal aortic aneurysms, with references to real case studies. It is shown that elastic deformation of the aorta and of the endoprosthesis induced by static forces and vibrations during daily activities can potentially promote undesired movements of the endovascular sealing structure.
Thoracic endovascular aortic repair (TEVAR) has become the standard treatment of a variety of aortic pathologies. The objective of this study is to evaluate the hemodynamic effects of stent-graft introducer sheath during TEVAR. Three idealized representative diseased aortas of aortic aneurysm, coarctation of the aorta, and aortic dissection were designed. Computational fluid dynamics studies were performed in the above idealized aortic geometries. An introducer sheath routinely used in the clinic was virtually-delivered into diseased aortas. Comparative analysis was carried out to evaluate the hemodynamic effects of the introducer sheath. Results show that the blood flow to the supra-aortic branches would increase above 9% due to the obstruction of the introducer sheath. The region exposed to high endothelial cell activation potential (ECAP) expands in the scenarios of coarctation of the aorta and aortic dissection, which indicates that the probability of thrombus formation may increase during TEVAR. The pressure magnitude in peak systole shows an obvious rise and a similar phenomenon is not observed in early diastole. The blood viscosity in the aortic arch and descending aorta is remarkably altered by the introducer sheath. The uneven viscosity distribution confirms the necessity of using non-Newtonian models and high viscosity region with high ECAP further promotes thrombosis. Our results highlight the hemodynamic effects of stent-graft introducer sheath during TEVAR, which may associate with perioperative complications.
Thoracic endovascular aortic repair (TEVAR) has developed to be the most effective treatment for aortic diseases. The objective of this study is to evaluate the biomechanical implications of the implanted endograft after TEVAR. We present a novel image-based, patient-specific, fluid-structure computational framework. The geometries of blood, endograft, and aortic wall were reconstructed based on clinical images. Patient-specific measurement data was collected to determine the parameters of the three-element Windkessel. We designed three postoperative scenarios with rigid wall assumption, blood-wall interaction, blood-endograft-wall interplay, respectively, where a two-way fluid-structure interaction (FSI) method was applied to predict the deformation of the composite stent-wall. Results show that flow energy loss (EL) during a cardiac cycle is underestimated by the rigid wall assumption. The complete storage and release process of blood flow energy, which consists of four phases is firstly captured. The implantation of the endograft would weaken the buffer function of the aorta and reduce mean EL by 19.1%. The closed curve area of wall pressure and aortic volume could indicate the EL caused by the interaction between blood flow and wall deformation. Both the FSI and endograft have a slight effect on wall shear stress-related-indices. The deformability of the composite stent-wall region is remarkably limited by the endograft. Our results highlight the importance of considering both the FSI method and the biomechanical implications of endograft to acquire physiologically-accurate hemodynamics in post-TEVAR computational studies and that neglecting the effect of the endograft would overestimate the blood flow EL and aortic deformability.
Presently 4T-1 luc cells were irradiated with proton under ultra-high dose rate FLASH or with gamma-ray with conventional dose rate, and then subcutaneous vaccination with or without Mn immuno-enhancing adjuvant into the mice for three times. One week later, we injected untreated 4T-1 luc cells on the other side of the vaccinated mice, and found that the untreated 4T-1 luc cells injected later nearly totally did not grow tumor (1/17) while controls without previous vaccination all grow tumors (18/18). The result is very interesting and the findings may help to explore in situ tumor vaccination as well as new combined radiotherapy strategies to effectively ablate primary and disseminated tumors. To our limited knowledge, this is the first paper reporting the high efficiency induction of systemic vaccination suppressing the metastasized/disseminated tumor progression.
Vehicle safety systems have substantially decreased motor vehicle crash-related injuries and fatalities, but injuries to the lumbar spine still have been reported. Experimental and computational analyses of upright and, particularly, reclined occupants in frontal crashes have shown that the lumbar spine can be subjected to axial compression followed by combined compression-flexion loading. Lumbar spine failure tolerance in combined compression-flexion has not been widely explored in the literature. Therefore, the goal of this study was to measure the failure tolerance of the lumbar spine in combined compression and flexion. Forty 3-vertebra lumbar spine segments were pre-loaded with axial compression and then subjected to dynamic flexion bending until failure. Clinically relevant middle vertebra fractures were observed in twenty-one of the specimens, including compression and burst fractures. The remaining nineteen specimens experienced failure at the potting grip interface. Since specimen characteristics and pre-test axial load varied widely within the sample, failure forces (mean 3.4 kN, range 1.6-5.1 kN) and moments (mean 73 Nm, range 0-181 Nm) also varied widely. Tobit univariate regressions were performed to determine the relationship between censored failure tolerance and specimen sex, segment type (upper/lower), age, and cross-sectional area. Age, sex, and cross-sectional area significantly affected failure force and moment individually (p<0.0024). These data can be used to develop injury prediction tools for lumbar spine fractures and further research in future safety systems.
In its permanent quest of mechanobiological homeostasis, our vascula-ture significantly adapts across multiple length and time scales in various physiological and pathological conditions. Computational modeling of vascular growth and remodeling (G&R) has significantly improved our insights of the mechanobio-logical processes of diseases such as hypertension or aneurysms. However, patient-specific computational modeling of ascending thoracic aortic aneurysm (ATAA) evolution, based on finite-element models (FEM), remains a challenging scientific problem with rare contributions, despite the major significance of this topic of research. Challenges are related to complex boundary conditions and geometries combined with layer-specific G&R responses. To address these challenges, in the current paper, we employed the constrained mixture model (CMM) to model the arterial wall as a mixture of different constituents such as elastin, collagen fiber families and smooth muscle cells (SMCs). Implemented in Abaqus as a UMAT, this first patient-specific CMM-based FEM of G&R in human ATAA was first validated for canonical problems such as single-layer thick-wall cylindrical and bi-layer thick-wall toric arterial geometries. Then it was used to predict ATAA evolution for a patient-specific aortic geometry, showing that the typical shape of an ATAA can be simply produced by elastin proteolysis localized in regions of deranged hemodymanics. The results indicate a transfer of stress to the adventitia by elastin loss and continuous adaptation of the stress distribution due to change of ATAA shape. Moreover, stress redistribution leads to collagen deposition where the maximum elastin mass is lost, which in turn leads to stiffening of the arterial wall. As future work, the predictions of this G&R framework will be validated on datasets of patient-specific ATAA geometries followed up over a significant number of years.