Angulation of the inflow cannula >7° from the apical axis (axis connecting mitral valve and ventricular apex) leads to markedly unfavorable hemodynamics as determined by computational fluid dynamics. Computational hemodynamic simulations incorporating Lagrangian and Eulerian metrics are a powerful tool for studying optimization of LVAD implantation strategies, with the long-term potential of improving outcomes.
This study quantifies thrombogenic potential of a wide range of LVAD outflow graft anastomosis angles through. This study aims at clarifying the influence of a single parameter (outflow graft angle) on the thrombogenesis associated with flow patterns in the aortic root after LVAD implantation. This is an important and poorly-understood aspect of LVAD therapy, because several studies have shown strong inter-and intra-patient thrombogenic variability and current LVAD implantation strategies do not incorporate outflow graft angle optimization. Accurate platelet-level investigation, enabled by statistical treatment of outliers in Lagrangian particle tracking, demonstrate a strong influence of outflow graft anastomoses angle on thrombogenicity (platelet residence times and activation state characterized by shear stress accumulation) with significantly reduced thrombogenic potential for acutely-angled anastomosed outflow grafts. The methodology presented in this study provides a device-neutral platform for conducting comprehensive thrombogenicity evaluation of LVAD surgical configurations, empowering optimal patient-focused surgical strategies for long-term treatment and care for advanced heart failure patients.
Blood flow is inherently linked to embryonic cardiac development, as haemodynamic forces exerted by flow stimulate mechanotransduction mechanisms that modulate cardiac growth and remodelling. This study evaluated blood flow in the embryonic heart outflow tract (OFT) during normal development at each stage between HH13 and HH18 in chicken embryos, in order to characterize changes in haemodynamic conditions during critical cardiac looping transformations. Two-dimensional optical coherence tomography was used to simultaneously acquire both structural and Doppler flow images, in order to extract blood flow velocity and structural information and estimate haemodynamic measures. From HH13 to HH18, peak blood flow rate increased by 2.4-fold and stroke volume increased by 2.1-fold. Wall shear rate (WSR) and lumen diameter data suggest that changes in blood flow during HH13-HH18 may induce a shear-mediated vasodilation response in the OFT. Embryo-specific four-dimensional computational fluid dynamics modelling at HH13 and HH18 complemented experimental observations and indicated heterogeneous WSR distributions over the OFT. Characterizing changes in haemodynamics during cardiac looping will help us better understand the way normal blood flow impacts proper cardiac development.
The prevalence of ventricular assist device (VAD) therapy has continued to increase due to a stagnant donor supply and growing advanced heart failure (HF) population. We hypothesize that left ventricular (LV) size strongly influences biocompatibility and risk of thrombosis. Unsteady computational fluid dynamics (CFD) was used in conjunction with patient-derived computational modeling and virtual surgery with a standard, apically implanted inflow cannula. A dual-focus approach of evaluating thrombogenicity was employed: platelet-based metrics to characterize the platelet environment and flow-based metrics to investigate hemodynamics. Left ventricular end-diastolic dimensions (LVEDds) ranging from 4.5 to 6.5 cm were studied and ranked according to relative thrombogenic potential. Over 150,000 platelets were individually tracked in each LV model over 15 cardiac cycles. As LV size decreased, platelets experienced markedly increased shear stress histories (SHs), whereas platelet residence time (RT) in the LV increased with size. The complex interplay between increased SH and longer RT has profound implications on thrombogenicity, with a significantly higher proportion of platelets in small LVs having long RT times and being subjected to high SH, contributing to thrombus formation. Our data suggest that small LV size, rather than decreased VAD speed, is the primary pathologic mechanism responsible for the increased incidence of thrombosis observed in VAD patients with small LVs.
Over 90% of cancer deaths result not from primary tumor development, but from metastatic tumors that arise after cancer cells circulate to distal sites via the circulatory system. While it is known that metastasis is an inefficient process, the effect of hemodynamic parameters such as fluid shear stress (FSS) on the viability and efficacy of metastasis is not well understood. Recent work has shown that select cancer cells may be able to survive and possibly even adapt to FSS in vitro. The current research seeks to characterize the effect of FSS on the mechanical properties of suspended cancer cells in vitro. Nontransformed prostate epithelial cells (PrEC LH) and transformed prostate cancer cells (PC-3) were used in this study. The Young’s modulus was determined using micropipette aspiration. We examined cells in suspension but not exposed to FSS (unsheared) and immediately after exposure to high (6,400 dyn/cm2) and low (510 dyn/cm2) FSS. The PrEC LH cells were ~140% stiffer than the PC-3 cells not exposed to FSS. Post-FSS exposure, there was an increase of ~77% in Young’s modulus after exposure to high FSS and a ~47% increase in Young’s modulus after exposure to low FSS for the PC-3 cells. There was no significant change in the Young’s modulus of PrEC LH cells post-FSS exposure. Our findings indicate that cancer cells adapt to FSS, with an increased Young’s modulus being one of the adaptive responses, and that this adaptation is specific only to PC-3 cells and is not seen in PrEC LH cells. Moreover, this adaptation appears to be graded in response to the magnitude of FSS experienced by the cancer cells. This is the first study investigating the effect of FSS on the mechanical properties of cancer cells in suspension, and may provide significant insights into the mechanism by which some select cancer cells may survive in the circulation, ultimately leading to metastasis at distal sites. Our findings suggest that biomechanical analysis of cancer cells could aid in identifying and diagnosing cancer in the future.
Blood flow plays a critical role in regulating embryonic cardiac growth and development, with altered flow leading to congenital heart disease. Progress in the field, however, is hindered by a lack of quantification of hemodynamic conditions in the developing heart. In this study, we present a methodology to quantify blood flow dynamics in the embryonic heart using subject-specific computational fluid dynamics (CFD) models. While the methodology is general, we focused on a model of the chick embryonic heart outflow tract (OFT), which distally connects the heart to the arterial system, and is the region of origin of many congenital cardiac defects. Using structural and Doppler velocity data collected from optical coherence tomography (OCT), we generated 4D (3D + time) embryo-specific CFD models of the heart OFT. To replicate the blood flow dynamics over time during the cardiac cycle, we developed an iterative inverse-method optimization algorithm, which determines the CFD model boundary conditions such that differences between computed velocities and measured velocities at one point within the OFT lumen are minimized. Results from our developed CFD model agree with previously measured hemodynamics in the OFT. Further, computed velocities and measured velocities differ by less than 15% at locations that were not used in the optimization, validating the model. The presented methodology can be used in quantifications of embryonic cardiac hemodynamics under normal and altered blood flow conditions, enabling an in depth quantitative study of how blood flow influences cardiac development.
Background Computational modeling of intracranial aneurysms provides insights into the influence of hemodynamics on aneurysm growth, rupture, and treatment outcome. Standard modeling of coiled aneurysms simplifies the complex geometry of the coil mass into a homogeneous porous medium that fills the aneurysmal sac. We compare hemodynamics of coiled aneurysms modeled from high-resolution imaging with those from the same aneurysms modeled following the standard technique, in an effort to characterize sources of error from the simplified model. Materials Physical models of two unruptured aneurysms were created using three-dimensional printing. The models were treated with coil embolization using the same coils as those used in actual patient treatment and then scanned by synchrotron X-ray microtomography to obtain high-resolution imaging of the coil mass. Computational modeling of each aneurysm was performed using patient-specific boundary conditions. The coils were modeled using the simplified porous medium or by incorporating the X-ray imaged coil surface, and the differences in hemodynamic variables were assessed. Results X-ray microtomographic imaging of coils and incorporation into computational models were successful for both aneurysms. Porous medium calculations of coiled aneurysm hemodynamics overestimated intraaneurysmal flow, underestimated oscillatory shear index and viscous dissipation, and over- or underpredicted wall shear stress (WSS) and WSS gradient compared with X-ray- based coiled computational fluid dynamics models. Conclusions Computational modeling of coiled intracranial aneurysms using the porous medium approach may inaccurately estimate key hemodynamic variables compared with models incorporating high-resolution synchrotron X-ray microtomographic imaging of complex aneurysm coil geometry.
This study evaluates quantitatively the impact that intermittent Aortic Valve opening has on the thrombogenicity in the aortic arch region for patients under Left Ventricular Assist Device therapy. The influence of flow through the Aortic Valve, opening once every five cardiac cycles, on the flow patterns in the ascending aortic is measured in a patient-derived CT-image-based model, after LVAD implantation. The mechanical environment of flowing platelets is investigated, by statistical treatment of outliers in Lagrangian particle tracking, and thrombogenesis metrics (platelet residence times and activation state characterized by shear stress accumulation) are compared for the cases of no Aortic Valve opening and intermittent Aortic Valve opening. All hemodynamics metrics are improved by Aortic Valve opening, even at a reduced frequency and flow rate. Residence times of platelets or microthrombi are reduced significantly by transvalvular flow, as are the shear stress history experienced and the shear stress magnitude and gradients on the aortic root endothelium. The findings of this device-neutral study support the multiple advantages of management that enables Aortic Valve opening, providing a rationale for establishing this as a standard in long-term treatment and care for advanced heart failure patients.
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