Turbulent Stresses in the Region of Aortic and Pulmonary Valves

Stein, Paul D.; Walburn, F. J.; Sabbah, Hani N.

doi:10.1115/1.3138355

Cited by 37 publications

(13 citation statements)

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“…The stress accumulation calculation was then performed by a summation of the instantaneous product of this scalar value of the total stress and the exposure time between successive nodal points along the platelet trajectory: σ × ∑ Δt (6) where Dt is the time step.…”

Section: Y Alemu and D Bluestein 680mentioning

confidence: 99%

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Flow‐induced Platelet Activation and Damage Accumulation in a Mechanical Heart Valve: Numerical Studies

2007

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A model for platelet activation based on the theory of damage, incorporating cumulative effects of stress history and past damage (senescence) was applied to a three-dimensional (3-D) model of blood flow through a St. Jude Medical (SJM) bileaflet mechanical heart valve (MHV), simulating flow conditions after implantation. The calculations used unsteady Reynolds-averaged Navier-Stokes formulation with non-Newtonian blood properties. The results were used to predict platelet damage from total stress (shear, turbulent, deformation), and incorporate the contribution of repeated passages of the platelets along pertinent trajectories. Trajectories that exposed the platelets to elevated levels of stress around the MHV leaflets and led them to entrapment within the complex 3-D vortical structures in the wake of the valve significantly enhanced platelet activation. This damage accumulation model can be used to quantify the thrombogenic potential of implantable cardiovascular devices, and indicate the problem areas of the device for improving their designs.

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Section: Y Alemu and D Bluestein 680mentioning

confidence: 99%

“…Patients with MHV may develop thromboembolic complications (2). Nonphysiologic flow patterns are characterized by elevated shear stresses, with portions of the flow cycle becoming turbulent (3)(4)(5)(6). MHVs may induce jet flow, elevated shear stresses, areas of flow separation and recirculation, shed vortices, and turbulence (7).…”

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confidence: 99%

Flow‐induced Platelet Activation and Damage Accumulation in a Mechanical Heart Valve: Numerical Studies

2007

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“…Hydraulic models, simulating the aortic valve, have demonstrated flow recirculation and eddy currents that swirl behind the flexible cusps during rapid flow through the valve orifice. 24 In the aortic outlet, ␤-gal activity was restricted to the valves and was undetectable in the vessel wall downstream ( Figure 3A). Sectioning through the outflow tract has shown that tie1 promoter is exclusively expressed in endothelial cells lining the inner aspect of the cup-shaped cusps but not in endothelial cells at the outer aspect of the same leaflet ( Figures 3B and 3C).…”

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confidence: 98%

Specific Induction of tie1 Promoter by Disturbed Flow in Atherosclerosis-Prone Vascular Niches and Flow-Obstructing Pathologies

Porat

Grunewald

Globerman

et al. 2004

Circulation Research

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Abstract-Nonlaminar flow is a major predisposing factor to atherosclerosis. Yet little is known regarding hemodynamic gene regulation in disease-prone areas of the vascular tree in vivo. We have determined spatial patterns of expression of endothelial cell receptors in the arterial tree and of reporter gene constructs in transgenic animals. In this study we show that the endothelial cell-specific receptor Tie1 is induced by disturbed flow in atherogenic vascular niches. Specifically, tie1 expression in the adult is upregulated in vascular bifurcations and branching points along the arterial tree. It is often confined to a single ring of endothelial cells functioning as sphincters and hence experiencing the steepest gradient in shear stress. In aortic valves, tie1 is asymmetrically induced only in endothelial cells encountering changes in flow direction. Disturbance of laminar flow by a surgical interposition of a vein into an artery led to induction of tie1, specifically in the region where the differently sized vessels adjoin. In pathological settings, tie1 expression is specifically induced in areas of disturbed flow because of the emergence of aneurysms and, importantly, in endothelial cells precisely overlying atherosclerotic plaques. Hemodynamic features of atherosclerotic lesion-prone regions, recreated in vitro with the aid of a flow chamber with a built-in step, corroborated an upregulated tie1 promoter activity only in cells residing where flow separation and recirculation take place. These defined promoter elements might be harnessed for targeting gene expression to atherosclerotic lesions. Key Words: angiogenesis Ⅲ atherosclerosis Ⅲ basic research Ⅲ blood flow Ⅲ blood vessels T he luminal surface of blood vessels is constantly exposed to hemodynamic forces, primarily to shear stress that is the tangential force engendered on endothelial cell surfaces by the blood flow. Hemodynamic forces play a fundamental remodeling role in the vascular network during its formative stage as well as in adapting the adult vasculature to pathophysiological changes in shear stress (eg, the process of arteriogenesis 1 ). Hemodynamic forces are also a considerable factor in the development of vascular pathologies such as atherosclerosis, aneurysms, poststenotic dilatations, and arteriovenous malformations. Notably, these diseases have the propensity to develop in vascular regions distinguished by disturbed flow that occurs naturally in certain vascular niches. Atherosclerosis, although clearly associated with some systemic risk factors, is a geometrically focal disease that preferentially develops at the outer edges of blood vessel bifurcations and at points of blood flow recirculation and stasis (eg, in aortic valves). In these predisposed locations, fluid shear stress on the vessel wall is significantly lower in magnitude and exhibits directional changes and flow separation, features absent from regions of the vascular tree generally spared from atherosclerosis. 2 The detrimental effects of disturbed flow have inspired e...

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“…In some cases, they overstimulate platelet thrombosis which then accelerate atherosclerosis as reported in Stein et al . [3]. On the other hand, the intimal thickening that causes the remodelling of the vessel wall relates to the presence of the low shear stresses at the throat of the stenosis, Ku et al .…”

Section: Introductionmentioning

confidence: 99%