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      The effect of Dean, Reynolds and Womersley numbers on the flow in a spherical cavity on a curved round pipe. Part 2. The haemodynamics of intracranial aneurysms treated with flow-diverting stents

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          Abstract

          The flow in a spherical cavity on a curved round pipe is a canonical flow that describes well the flow inside a sidewall aneurysm on an intracranial artery. Intracranial aneurysms are often treated with a flow-diverting stent (FDS), a low-porosity metal mesh that covers the entrance to the cavity, to reduce blood flow into the aneurysm sac and exclude it from mechanical stresses imposed by the blood flow. Successful treatment is highly dependent on the degree of reduction of flow inside the cavity, and the resulting altered fluid mechanics inside the aneurysm following treatment. Using stereoscopic particle image velocimetry, we characterize the fluid mechanics in a canonical configuration representative of an intracranial aneurysm treated with a FDS: a spherical cavity on the side of a curved round pipe covered with a metal mesh formed by an actual medical FDS. This porous mesh coverage is the focus of Part 2 of the paper, characterizing the effects of parent vessel $Re\(, \)De\( and pulsatility, \)Wo\(, on the fluid dynamics, compared with the canonical configuration with no impediments to flow into the cavity that is described in Part 1 (Chassagne et al., J. Fluid Mech., vol. 915, 2021, A123). Coverage with a FDS markedly reduces the flow \)Re\( in the aneurysmal cavity, creating a viscous-dominated flow environment despite the parent vessel \)Re>100\(. Under steady flow conditions, the topology that forms inside the cavity is shown to be a function of the parent vessel \)De\(. At low values of \)De\(, flow enters the cavity at the leading edge and remains attached to the wall before exiting at the trailing edge, a novel behaviour that was not found under any conditions of the high- \)Re\(, unimpeded cavity flow described in Part 1. Under these conditions, flow in the cavity co-rotates with the direction of the free-stream flow, similar to Stokes flow in a cavity. As \)De\( increases, the flow along the leading edge begins to separate, and the recirculation zone grows with increasing \)De\(, until, above \)De \approx 180\(, the flow inside the cavity is fully recirculating, counter-rotating with respect to the free-stream flow. Under pulsatile flow conditions, the vortex inside the cavity progresses through the same cycle – switching from attached and co-rotating with the free-stream flow at the beginning of the cycle (low velocity and positive acceleration) to separated and counter-rotating as \)De\( reaches a critical value. The location of separation within the harmonic cycle is shown to be a function of both \)De\( and \)Wo\(. The values of aneurysmal cavity \)Re\( based on both the average velocity and the circulation inside the cavity are shown to increase with increasing values of \)De\(, while \)Wo\( is shown to have little influence on the time-averaged metrics. As \)De\( increases, the strength of the secondary flow in the parent vessel grows, due to the inertial instability in the curved pipe, and the flow rate entering the cavity increases. Thus, the effectiveness of FDS treatment to exclude the aneurysmal cavity from the haemodynamic stresses is compromised for aneurysms located on high-curvature arteries, i.e. vessels with high \)De$ , and this can be a fluid mechanics criterion to guide treatment selection.

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          High WSS or low WSS? Complex interactions of hemodynamics with intracranial aneurysm initiation, growth, and rupture: toward a unifying hypothesis.

          Increasing detection of unruptured intracranial aneurysms, catastrophic outcomes from subarachnoid hemorrhage, and risks and cost of treatment necessitate defining objective predictive parameters of aneurysm rupture risk. Image-based computational fluid dynamics models have suggested associations between hemodynamics and intracranial aneurysm rupture, albeit with conflicting findings regarding wall shear stress. We propose that the "high-versus-low wall shear stress" controversy is a manifestation of the complexity of aneurysm pathophysiology, and both high and low wall shear stress can drive intracranial aneurysm growth and rupture. Low wall shear stress and high oscillatory shear index trigger an inflammatory-cell-mediated pathway, which could be associated with the growth and rupture of large, atherosclerotic aneurysm phenotypes, while high wall shear stress combined with a positive wall shear stress gradient trigger a mural-cell-mediated pathway, which could be associated with the growth and rupture of small or secondary bleb aneurysm phenotypes. This hypothesis correlates disparate intracranial aneurysm pathophysiology with the results of computational fluid dynamics in search of more reliable risk predictors.
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            The burden, trends, and demographics of mortality from subarachnoid hemorrhage.

            The objective of this study was to describe the recent epidemiology of mortality from subarachnoid hemorrhage in the United States. Subarachnoid hemorrhage is distinct from other forms of stroke in its risk factors, demographics, and treatment. However, it is often clustered with other stroke subtypes, obscuring its unique epidemiology. We analyzed subarachnoid hemorrhage mortality data from the National Center for Health Statistics of the United States for the years 1979 to 1994 and compared it with other stroke subtypes. Age-adjusted mortality rates of subarachnoid hemorrhage were 62% greater in females than in males and 57% greater in blacks than in whites. The median age of death from subarachnoid hemorrhage was 59 years compared with 73 years for intracerebral hemorrhage and 81 years for ischemic stroke. Mortality rates of subarachnoid hemorrhage have decreased by approximately 1% per year since 1979, and the mean age of death has steadily increased from 57 years in 1979 to 60 years in 1994. Subarachnoid hemorrhage accounted for 4.4% of stroke mortality but 27.3% of all stroke-related years of potential life lost before age 65, a measure of premature mortality. The proportion of years of potential life lost due to subarachnoid hemorrhage was comparable with ischemic stroke (38.5%) and intracranial hemorrhage (34.2%). Subarachnoid hemorrhage is an uncommon cause of stroke mortality but occurs at a young age, producing a relatively large burden of premature mortality, comparable with ischemic stroke.
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              Flow effects on coagulation and thrombosis.

              Thrombosis occurs in a dynamic rheological field that constantly changes as the thrombus grows to occlusive dimensions. In the initiation of thrombosis, flow conditions near the vessel wall regulate how quickly reactive components are delivered to the injured site and how rapidly the reaction products are disseminated. Whereas the delivery and removal of soluble coagulation factors to the vessel is thought to occur via classic convection-diffusion phenomena, the movement of cells and platelets to the injured wall is strongly augmented by flow-dependent cell-cell collisions that enhance their ability to interact with the wall. In addition, increased shear conditions have been shown to activate platelets, alter the cellular localization of proteins such as tissue factor (TF) and TF pathway inhibitor, and regulate gene production. In the absence of high shearing forces, red cells, leukocytes, and platelets can form stable aggregates with each other or cells lining the vessel wall, which, in addition to altering the biochemical makeup of the aggregate or vessel wall, effectively increases the local blood viscosity. Thus, hemodynamic forces not only regulate the predilection of specific anatomic sites to thrombosis, but they strongly influence the biochemical makeup of thrombi and the reaction pathways involved in thrombus formation.
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                Journal
                Journal of Fluid Mechanics
                J. Fluid Mech.
                Cambridge University Press (CUP)
                0022-1120
                1469-7645
                May 25 2021
                March 31 2021
                May 25 2021
                : 915
                Article
                10.1017/jfm.2020.1115
                aa6d6647-cf81-492d-b853-10fea0b4f8ae
                © 2021

                https://www.cambridge.org/core/terms

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