Two-Dimensional Simulation of Platelet Activation in the Hinge Region of a Mechanical Heart Valve

2007 ◽  
Author(s):  
V. Govindarajan ◽  
H. S. Udaykumar ◽  
K. B. Chandran
Keyword(s):  
Platelet Activation ◽  
Complex Geometry ◽  
Thrombus Formation ◽  
Mechanical Heart Valve ◽  
Mechanical Valve ◽  
Hinge Region ◽  
Valve Closure ◽  
Flow Through ◽  
Valve Housing ◽  
Squeezed Flow

The proper functioning of the leaflets of a bi-leaflet mechanical valve requires the use of the hinge mechanism which lets the leaflets pivot to the valve housing and lets it rotate at a specified angle. It has been pointed that the hinge design directly affects the durability of the valve [1]. In Bi-leaflet valves the thrombus formation is mostly observed in the hinge region and also on the valve housing [2]. This may be due to the complex geometry presented by the hinge region, which makes the flow complex making the hinge region a potential site for thrombus formation and accumulation which could pose a threat to the efficient functioning of the valve itself. It was hypothesized that the flow fields with in the hinge region played a major role in thrombus accumulation in the Medtronic parallel valve [3]. Studies have demonstrated that fluid dynamics in the vicinity of valve leaflet and housing at the instant of valve closure may lead to large negative pressure transients across the leaflets [4]. These large pressure gradients present for a small duration of time induces very high velocity squeezed flow through the clearance region between the valve housing and the leaflet tip and through the gaps in the hinge region which has been provided for rotation of the leaflet and washout. The wall shear stress in these regions can be relatively high during the closure phase resulting in platelet activation. This study will focus on the flow through the hinge region and its effect on the platelet activation during the valve closure under Mitral conditions which is the harshest environment for a valve.

scholarly journals Two-Dimensional FSI Simulation of Closing Dynamics of a Tilting Disk Mechanical Heart Valve

2010 ◽  
Vol 4 (1) ◽  
Author(s):  
V. Govindarajan ◽  
H. S. Udaykumar ◽  
L. H. Herbertson ◽  
S. Deutsch ◽  
K. B. Manning ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Interaction Analysis ◽  
Mechanical Heart Valve ◽  
Shear Stresses ◽  
Particle Dynamic ◽  
Valve Closure ◽  
Two Dimensional ◽  
Disk Valve ◽  
Bileaflet Mechanical Valve ◽  
Valve Housing

The fluid dynamics during valve closure resulting in high shear flows and large residence times of particles has been implicated in platelet activation and thrombus formation in mechanical heart valves. Our previous studies with bileaflet valves have shown that large shear stresses induced in the gap between the leaflet edge and valve housing results in relatively high platelet activation levels, whereas flow between the leaflets results in shed vortices not conducive to platelet damage. In this study we compare the result of closing dynamics of a tilting disk valve with that of a bileaflet valve. The two-dimensional fluid-structure interaction analysis of a tilting disk valve closure mechanics is performed with a fixed grid Cartesian mesh flow solver with local mesh refinement, and a Lagrangian particle dynamic analysis for computation of potential for platelet activation. Throughout the simulation the flow remains in the laminar regime, and the flow through the gap width is marked by the development of a shear layer, which separates from the leaflet downstream of the valve. Zones of recirculation are observed in the gap between the leaflet edge and valve housing on the major orifice region of the tilting disk valve and are seen to be migrating toward the minor orifice region. Jet flow is observed at the minor orifice region and a vortex is formed, which sheds in the direction of fluid motion, as observed in experiments using PIV measurements. The activation parameter computed for the tilting disk valve at the time of closure was found to be 2.7 times greater than that of the bileaflet mechanical valve and was found to be in the vicinity of the minor orifice region, mainly due to the migration of vortical structures from the major to the minor orifice region during the leaflet rebound of the closing phase.

scholarly journals Two-Dimensional Simulation of Flow and Platelet Dynamics in the Hinge Region of a Mechanical Heart Valve

2008 ◽  
Vol 131 (3) ◽  
Author(s):  
V. Govindarajan ◽  
H. S. Udaykumar ◽  
K. B. Chandran
Keyword(s):  
Complex Geometry ◽  
Interaction Analysis ◽  
Thrombus Formation ◽  
Fluid Dynamic ◽  
Mechanical Heart Valve ◽  
Hinge Region ◽  
Shear Stresses ◽  
Two Dimensional ◽  
Bileaflet Mechanical Valve ◽  
Bileaflet Valve

The hinge region of a mechanical bileaflet valve is implicated in blood damage and initiation of thrombus formation. Detailed fluid dynamic analysis in the complex geometry of the hinge region during the closing phase of the bileaflet valve is the focus of this study to understand the effect of fluid-induced stresses on the activation of platelets. A fixed-grid Cartesian mesh flow solver is used to simulate the blood flow through a two-dimensional geometry of the hinge region of a bileaflet mechanical valve. Use of local mesh refinement algorithm provides mesh adaptation based on the gradients of flow in the constricted geometry of the hinge. Leaflet motion is specified from the fluid-structure interaction analysis of the leaflet dynamics during the closing phase from a previous study, which focused on the fluid mechanics at the gap between the leaflet edges and the valve housing. A Lagrangian particle tracking method is used to model and track the platelets and to compute the magnitude of the shear stress on the platelets as they pass through the hinge region. Results show that there is a boundary layer separation in the gaps between the leaflet ear and the constricted hinge geometry. Separated shear layers roll up into vortical structures that lead to high residence times combined with exposure to high-shear stresses for particles in the hinge region. Particles are preferentially entrained into this recirculation zone, presenting the possibility of platelet activation, aggregation, and initiation of thrombi.

scholarly journals A numerical study of hemodynamic effects on the bileaflet mechanical heart valve

2019 ◽  
Vol 213 ◽  
pp. 02103
Author(s):  
Jan Zbavitel ◽  
Simona Fialová
Keyword(s):  
Numerical Simulation ◽  
Heart Valve ◽  
Transient Flow ◽  
Numerical Study ◽  
Thrombus Formation ◽  
Fluid Model ◽  
Mechanical Heart Valve ◽  
Mechanical Valve ◽  
Physiological Data ◽  
Dimensional Solution

The work is focused on calculating hemodynamically negative effects of a flow through bileaflet mechanical heart valves (BMHV). Open-source FOAM-extend and cfMesh libraries were used for numerical simulation, the leaflet movement was solved as a fluid-structure interaction. A real model of the Sorin Bicarbon heart valve was employed as the default geometry for the following shape improvement. The unsteady boundary conditions correspond to physiological data of a cardiac cycle. It is shown how the modification of the shape of the original valve geometry positively affected the size of backflow areas. Based on numerical results, a significant reduction of shear stress magnitude is shown. The outcome of a direct numerical simulation (DNS) of transient flow was compared with results of low-Reynolds URANS model k-ω SST. Despite the limits of the two-dimensional solution and Newtonian fluid model, the suitability of models frequently used in literature was reviewed. Use of URANS models can suppress the formation of some relevant vortex structures which may affect the BMHV’s dynamics. The results of this analysis can find use in optimizing the design of the mechanical valve that would cause less damage to the blood cells and lower risk of thrombus formation.

Flow and Thrombosis at Orifices Simulating Mechanical Heart Valve Leakage Regions

2005 ◽  
Vol 128 (1) ◽  
pp. 30-39 ◽  
Author(s):  
Anna M. Fallon ◽  
Nisha Shah ◽  
Ulla M. Marzec ◽  
James N. Warnock ◽  
Ajit P. Yoganathan ◽  
...  
Keyword(s):  
Present Method ◽  
Heart Valves ◽  
Antithrombin Iii ◽  
Thrombus Formation ◽  
Mechanical Heart Valve ◽  
Critical Threshold ◽  
Valve Leakage ◽  
Study Interval ◽  
Flow Through ◽  
Blood Elements

Background: While it is established that mechanical heart valves (MHVs) damage blood elements during leakage and forward flow, the role in thrombus formation of platelet activation by high shear flow geometries remains unclear. In this study, continuously recalcified blood was used to measure the effects of blood flow through orifices, which model MHVs, on the generation of procoagulant thrombin and the resulting formation of thrombus. The contribution of platelets to this process was also assessed. Method of Approach: 200, 400, 800, and 1200μm orifices simulated the hinge region of bileaflet MHVs, and 200, 400, and 800μm wide slits modeled the centerline where the two leaflets meet when the MHV is closed. To assess activation of coagulation during blood recirculation, samples were withdrawn over 0-47min and the plasmas assayed for thrombin-antithrombin-III (TAT) levels. Model geometries were also inspected visually. Results: The 200 and 400μm round orifices induced significant TAT generation and thrombosis over the study interval. In contrast, thrombin generation by the slit orifices, and by the 800 and 1200μm round orifices, was negligible. In additional experiments with nonrecalcified or platelet-depleted blood, TAT levels were markedly reduced versus the studies with fully anticoagulated whole blood (p<0.05). Conclusions: Using the present method, a significant increase in TAT concentration was found for 200 and 400μm orifices, but not 800 and 1200μm orifices, indicating that these flow geometries exhibit a critical threshold for activation of coagulation and resulting formation of thrombus. Markedly lower TAT levels were produced in studies with platelet-depleted blood, documenting a key role for platelets in the thrombotic process.

Computational hemodynamic investigation of a new bileaflet mechanical heart valve

SIMULATION ◽  
2019 ◽  
Vol 96 (5) ◽  
pp. 459-469
Author(s):  
Belkhiri Khellaf ◽  
Boumeddane Boussad
Keyword(s):  
Heart Valve ◽  
Heart Valves ◽  
Stokes Equations ◽  
Thrombus Formation ◽  
Mechanical Heart Valve ◽  
Navier Stokes ◽  
Two Dimensional ◽  
Navier Stokes Equations ◽  
Blood Damage ◽  
Flow Through

In this paper, we perform a numerical analysis for simulating steady, two-dimensional, laminar blood flow through our proposed design, known as the Butterfly mechanical heart valve, where the leaflets are fully opened. Blood has been assumed to be Newtonian and non-Newtonian fluid using the Casson model for shear-thinning behavior. A non-uniform Cartesian grid generation technique is presented to generate a two-dimensional grid for the irregular geometry of the Butterfly valve. The governing Navier–Stokes equations of flow, written in a stream function–vorticity formulation, are solved by the finite difference method with hybrid differencing of the convective terms. The computed results show that the blood’s non-Newtonian nature significantly affects the flow field with the existence of recirculation and consequently stagnation causing thrombus formation, as well as an increase of the shear stress along the wall, which contributes to hemolytic blood damage. The results demonstrate that the model is capable of predicting the hemodynamic features most interesting to physiologists. It can be used to assess thromboembolic problems occurring with heart valves and in the design of cardiac prostheses.

Two-Dimensional Dynamic Simulation of Platelet Activation During Mechanical Heart Valve Closure

2006 ◽  
Vol 34 (10) ◽  
pp. 1519-1534 ◽  
Author(s):  
S. Krishnan ◽  
H. S. Udaykumar ◽  
J. S. Marshall ◽  
K. B. Chandran
Keyword(s):  
Dynamic Simulation ◽  
Heart Valve ◽  
Platelet Activation ◽  
Mechanical Heart Valve ◽  
Valve Closure ◽  
Two Dimensional

scholarly journals Entecavir as a P2X7R antagonist ameliorates platelet activation and thrombus formation

2020 ◽  
Vol 144 (1) ◽  
pp. 43-51
Author(s):  
Yue Ming ◽  
Guang Xin ◽  
Beihong Ji ◽  
Chengji Ji ◽  
Zeliang Wei ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Thrombus Formation

scholarly journals Dietary α-Linolenic Acid Inhibits Arterial Thrombus Formation, Tissue Factor Expression, and Platelet Activation

2011 ◽  
Vol 31 (8) ◽  
pp. 1772-1780 ◽  
Author(s):  
Erik W. Holy ◽  
Marc Forestier ◽  
Eva K. Richter ◽  
Alexander Akhmedov ◽  
Florian Leiber ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Linolenic Acid ◽  
Platelet Activation ◽  
Thrombus Formation ◽  
Tissue Factor Expression ◽  
Arterial Thrombus ◽  
Factor Expression

GPIb-dependent platelet activation is dependent on Src kinases but not MAP kinase or cGMP-dependent kinase

Blood ◽  
2004 ◽  
Vol 103 (7) ◽  
pp. 2601-2609 ◽  
Author(s):  
Stuart J. Marshall ◽  
Yotis A. Senis ◽  
Jocelyn M. Auger ◽  
Robert Feil ◽  
Franz Hofmann ◽  
...  
Keyword(s):  
Map Kinase ◽  
Platelet Activation ◽  
Map Kinases ◽  
Thrombus Formation ◽  
Critical Role ◽  
Rabbit Model ◽  
Guanosine Monophosphate ◽  
Src Kinases ◽  
Aggregate Formation ◽  
No Donor

Abstract Glycoprotein Ib-IX-V (GPIb-IX-V) mediates platelet tethering to von Willebrand factor (VWF), recruiting platelets into the thrombus, and activates integrin αIIbβ3 through a pathway that is dependent on Src kinases. In addition, recent reports indicate that activation of αIIbβ3 by VWF is dependent on protein kinase G (PKG) and mitogen-activated protein (MAP) kinases. The present study compares the importance of these signaling pathways in the activation of αIIbβ3 by GPIb-IX-V. In contrast to a recent report, VWF did not promote an increase in cyclic guanosine monophosphate (cGMP), while agents that elevate cGMP, such as the nitrous oxide (NO) donor glyco–SNAP-1 (N-(β-D-glucopyranosyl)-N2-acetyl-S-nitroso-D,L-penicillaminamide) or the type 5 phosphosdiesterase inhibitor, sildenafil, inhibited rather than promoted activation of αIIbβ3 by GPIb-IX-V and blocked aggregate formation on collagen at an intermediate rate of shear (800 s-1). Additionally, sildenafil increased blood flow in a rabbit model of thrombus formation in vivo. A novel inhibitor of the MAP kinase pathway, which is active in plasma, PD184161, had no effect on aggregate formation on collagen under flow conditions, whereas a novel inhibitor of Src kinases, which is also active in plasma, PD173952, blocked this response. These results demonstrate a critical role for Src kinases but not MAP kinases in VWF-dependent platelet activation and demonstrate an inhibitory role for cGMP-elevating agents in regulating this process.

Abstract 803: Diesel Exhaust Inhalation Enhances Thrombus Formation In Man

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew J Lucking ◽  
Magnus Lundback ◽  
Nicholas L Mills ◽  
Dana Faratian ◽  
Fleming Cassee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Air Pollution ◽  
Platelet Activation ◽  
Diesel Exhaust ◽  
Intermittent Exercise ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Ex Vivo Model ◽  
Double Blind

Background: Transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction although the mechanism is unclear. The aim of this study was to investigate the effect of diesel exhaust inhalation on thrombus formation in man using an ex vivo model of thrombosis. Methods and Results: In a double-blind randomized cross-over study, 20 healthy volunteers were exposed to diluted diesel exhaust (300 μg/m3) or filtered air during intermittent exercise for 1 or 2 hours. Thrombus formation, coagulation, platelet activation and inflammatory markers were measured at 2 and 6 hours after exposure. Thrombus formation was measured using the Badimon ex vivo perfusion chamber at low (212 /s) and high (1,690 /s) shear rates with porcine aortic tunica media as the thrombogenic substrate. Specimens were fixed, stained and thrombus area measured using computerized planimetry. Compared to filtered air, diesel exhaust increased thrombus formation in the low and high shear chambers by 24.2% (p<0.001) and 19.1% (p<0.001) respectively. This increased thrombogenicity was seen at two and six hours, and using two different types of diesel exposure. Although there were no effects on coagulation variables, diesel exhaust inhalation increased platelet-neutrophil (6.5% to 9.2%; P<0.05) and platelet-monocyte (21.0% to 25.0%; P<0.05) aggregates 2 hours following exposure. Conclusions: Inhalation of diesel exhaust increases ex vivo thrombus formation and causes platelet activation in man. These findings provide a potential mechanism that links exposure to traffic-derived air pollution with acute atherothrombotic events including acute myocardial infarction.

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