182 research outputs found
Effects of forcing in three dimensional turbulent flows
We present the results of a numerical investigation of three-dimensional
homogeneous and isotropic turbulence, stirred by a random forcing with a power
law spectrum, . Numerical simulations are performed at
different resolutions up to . We show that at varying the spectrum slope
, small-scale turbulent fluctuations change from a {\it forcing independent}
to a {\it forcing dominated} statistics. We argue that the critical value
separating the two behaviours, in three dimensions, is . When the
statistics is forcing dominated, for , we find dimensional scaling, i.e.
intermittency is vanishingly small. On the other hand, for , we find the
same anomalous scaling measured in flows forced only at large scales. We
connect these results with the issue of {\it universality} in turbulent flows.Comment: 4 pages, 4 figure
A Practical Approach for Wall Shear Stress Topological Skeleton Analysis Applied to Intracranial Aneurysm Hemodynamics
The physiopathological role of Wall Shear Stress (WSS) in intracranial aneurysm development/rupture and the action of contraction/expansion played by shear forces on vessel wall make topological skeleton analysis of the WSS vector field of great interest. Here we present a practical way to analyze WSS topological skeleton through the identification and classification of WSS fixed points and manifolds. The method is based on the calculation of the WSS vector field divergence and Poincarè index, and it is here successfully applied to a dataset computational hemodynamic models of intracranial aneurysms
A Eulerian method to analyze wall shear stress fixed points and manifolds in cardiovascular flows
Based upon dynamical systems theory, a fixed point of a vector field such as the wall shear stress (WSS) at the luminal surface of a vessel is a point where the vector field vanishes. Unstable/stable manifolds identify contraction/expansion regions linking fixed points. The significance of such WSS topological features lies in their strong link with “disturbed” flow features like flow stagnation, separation and reversal, deemed responsible for vascular dysfunction initiation and progression. Here, we present a Eulerian method to analyze WSS topological skeleton through the identification and classification of WSS fixed points and manifolds in complex vascular geometries. The method rests on the volume contraction theory and analyzes the WSS topological skeleton through the WSS vector field divergence and Poincare´ index. The method is here applied to computational hemodynamics models of carotid bifurcation and intracranial aneurysm. An in-depth analysis of the time dependence of the WSS topological skeleton along the cardiac cycle is provided, enriching the information obtained from cycle-average WSS. Among the main findings, it emerges that on the carotid bifurcation, instantaneous WSS fixed points co-localize with cycle-average WSS fixed points for a fraction of the cardiac cycle ranging from 0 to 14.5 % ; a persistent instantaneous WSS fixed point confined on the aneurysm dome does not co-localize with the cycle-average low-WSS region. In conclusion, the here presented approach shows the potential to speed up studies on the physiological significance of WSS topological skeleton in cardiovascular flows, ultimately increasing the chance of finding mechanistic explanations to clinical observations
Deciphering ascending thoracic aortic aneurysm hemodynamics in relation to biomechanical properties
The degeneration of the arterial wall at the basis of the ascending thoracic aortic aneurysm (ATAA) is a complex multifactorial process, which may lead to clinical complications and, ultimately, death. Individual genetic, biological or hemodynamic factors are inadequate to explain the heterogeneity of ATAA development/progression mechanisms, thus stimulating the analysis of their complex interplay. Here the disruption of the hemodynamic environment in the ATAA is investigated integrating patient-specific computational hemodynamics, CT-based in vivo estimation of local aortic stiffness and advanced fluid mechanics methods of analysis. The final aims are (1) deciphering the ATAA spatiotemporal hemodynamic complexity and its link to near-wall topological features, and (2) identifying the existing links between arterial wall degeneration and hemodynamic insult. Technically, two methodologies are applied to computational hemodynamics data, the wall shear stress (WSS) topological skeleton analysis, and the Complex Networks theory. The same analysis was extended to the healthy aorta. As main findings of the study, we report that: (1) different spatiotemporal heterogeneity characterizes the ATAA and healthy hemodynamics, that markedly reflect on their WSS topological skeleton features; (2) a link (stronger than canonical WSS-based descriptors) emerges between the variation of contraction/expansion action exerted by WSS on the endothelium along the cardiac cycle, and ATAA wall stiffness. The findings of the study suggest the use of advanced methods for a deeper understanding of the hemodynamics disruption in ATAA, and candidate WSS topological skeleton features as promising indicators of local wall degeneration
Exploring novel arterio-venous graft designs to reduce vascular access failure risk
Although arterio-venous grafts (AVGs) are the second best option as permanent vascular access for hemodialysis, this solution is still affected by a relevant failure rate associated with neointimal hyperplasia (IH), mainly located at the venous anastomosis, where abnormal hemodynamics occurs. In this study we use computational fluid dynamics (CFD) to investigate the impact of six innovative AVG designs on reducing the IH risk at the distal anastomosis in AVGs. Findings from simulations clearly show that using a helical shaped flow divider located in the venous side of the graft could assure a reduced hemodynamic risk of failure at the distal anastomosis, with a clinically irrelevant increase in pressure drop over the graft
Coronary Artery Stenting Affects Wall Shear Stress Topological Skeleton
Despite the important advancements in the stent technology for the treatment of diseased coronary arteries, major complications still affect the postoperative long-term outcome. The stent-induced flow disturbances, and especially the altered wall shear stress (WSS) profile at the strut level, play an important role in the pathophysiological mechanisms leading to stent thrombosis (ST) and in-stent restenosis (ISR). In this context, the analysis of the WSS topological skeleton is gaining more and more interest by extending the current understanding of the association between local hemodynamics and vascular diseases. This study aims to analyze the impact that a deployed coronary stent has on the WSS topological skeleton. Computational fluid dynamics (CFD) simulations were performed in three stented human coronary artery geometries reconstructed from clinical images. The selected cases presented stents with different designs (i.e., two contemporary drug-eluting stents and one bioresorbable scaffold) and included regions with stent malapposition or overlapping. A recently proposed Eulerian-based approach was applied to analyze the WSS topological skeleton features. The results highlighted that the presence of single or multiple stents within a coronary artery markedly impacts the WSS topological skeleton. In particular, repetitive patterns of WSS divergence were observed at the luminal surface, highlighting a WSS contraction action exerted proximal to the stent struts and a WSS expansion action distal to the stent struts. This WSS action pattern was independent from the stent design. In conclusion, these findings could contribute to a deeper understanding of the hemodynamics-driven processes underlying ST and ISR
Blood Flow Energy Identifies Coronary Lesions Culprit of Future Myocardial Infarction.
The present study establishes a link between blood flow energy transformations in coronary atherosclerotic lesions and clinical outcomes. The predictive capacity for future myocardial infarction (MI) was compared with that of established quantitative coronary angiography (QCA)-derived predictors. Angiography-based computational fluid dynamics (CFD) simulations were performed on 80 human coronary lesions culprit of MI within 5 years and 108 non-culprit lesions for future MI. Blood flow energy transformations were assessed in the converging flow segment of the lesion as ratios of kinetic and rotational energy values (KER and RER, respectively) at the QCA-identified minimum lumen area and proximal lesion sections. The anatomical and functional lesion severity were evaluated with QCA to derive percentage area stenosis (%AS), vessel fractional flow reserve (vFFR), and translesional vFFR (ΔvFFR). Wall shear stress profiles were investigated in terms of topological shear variation index (TSVI). KER and RER predicted MI at 5 years (AUC = 0.73, 95% CI 0.65-0.80, and AUC = 0.76, 95% CI 0.70-0.83, respectively; p < 0.0001 for both). The predictive capacity for future MI of KER and RER was significantly stronger than vFFR (p = 0.0391 and p = 0.0045, respectively). RER predictive capacity was significantly stronger than %AS and ΔvFFR (p = 0.0041 and p = 0.0059, respectively). The predictive capacity for future MI of KER and RER did not differ significantly from TSVI. Blood flow kinetic and rotational energy transformations were significant predictors for MI at 5 years (p < 0.0001). The findings of this study support the hypothesis of a biomechanical contribution to the process of plaque destabilization/rupture leading to MI
Aggressive thyroid cancer: targeted therapy with sorafenib
Sorafenib (Nexavar), is a multikinase inhibitor, which has demonstrated both anti proliferative and anti-angiogenic properties in vitro and in vivo, inhibiting the activity of targets present in the tumoral cells [c-RAF (proto-oncogene serine/threonine-protein kinase), BRAF, (V600E)BRAF, c-KIT, and FMS-like tyrosine kinase 3] and in tumor vessels [c-RAF, vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, and platelet-derived growth factor receptor β]. Sorafenib was initially approved for the treatment of hepatocellular carcinoma and advanced renal cell carcinoma. Experimental studies have demonstrated that sorafenib has both anti-proliferative and anti-angiogenic properties in vitro and in vivo, against thyroid cancer cells. Furthermore, several completed (or ongoing) studies have evaluated the long-term efficacy and tolerability of sorafenib in patients with papillary, follicular and medullary aggressive thyroid cancer. The results of the different studies showed good clinical responses and stabilization of the disease and suggested that sorafenib is a promising therapeutic option in patients with advanced thyroid cancer that is not responsive to traditional therapeutic strategies (such as radioiodine). Currently, USA Food and Drug Administration has approved the use of sorafenib for metastatic differentiated thyroid cancer
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