von Willebrand Factor and Management of Heart Valve Disease

Belle, Éric Van; Vincent, Flavien; Casari, Caterina; Jeanpierre, Emmanuelle; Loobuyck, Valentin; Rosa, Mickaël; Delhaye, Cédric; Spillemaeker, Hughes; Paris, Camille; Debry, Nicolas; Verdier, Basile; Vincentelli, André; Dupont, Annabelle; Lenting, Peter J.; Susen, Sophie

doi:10.1016/j.jacc.2018.12.045

Cited by 38 publications

(42 citation statements)

References 44 publications

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“…At near valve closure, flow dynamics can be considered analogous to transient valve stenosis, whereby regurgitation is increasingly constrained until complete, motionless, closed-valve conditions occur. During brief crucial moments preceding valve closure, localized prothrombotic microenvironments may be relevant to generation of high velocity leakage jets, flow unsteadiness, valve flutter, cyclic variability of PDVA, turbulence, and excessive shear forces that may induce blood element damage [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31]. These influences may impact multiple valve types for:…”

Section: Resultsmentioning

confidence: 99%

Violin plot data: A concerto of crucial information on valve thrombogenicity categorized in vitro by valve motion and inferred flow velocity

Scotten

Blundon

Deutsch

et al. 2019

Preprint

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Objectives: We hypothesize that prosthetic valve thrombogenic potential may be inferred by valve regional flow velocity. This metric was used to compare two clinical valves and two experimental prototypes. Methods: Four our clinical and experimental prototype valve models were tested in aortic and mitral sites under pulsatile circulation in a pulse duplicator. An optical approach measuring projected dynamic valve area to gauge valve motion was implemented. Pulsatile pressures and flow rates were measured by conventional techniques and a quasi-steady flow tester was used to measure valve leakage. Regurgitant flow velocity was derived using time-dependent volumetric flow rate / projected dynamic valve area. Since flow velocity and fluid shear force are related through flow velocity gradient, thrombogenic potential for valves that achieve near closure during the forward flow deceleration phase were determined as regurgitant flow velocities relative to the control mechanical valve regurgitant flow velocity of -126 m/s. Analysis of the flow velocity data made use of Vioplot R* and VISIO software packages to provide split violin plots that represent probability of recurrence of data. Results: Thrombogenic potential was made dimensionless and ranged between -0.45 and +1.0. Negative thrombogenic potentials arise when transient rebound of valve occluder is accompanied by water-hammer phenomena. Positive thrombogenic potentials occur during decelerating forward flow. Bioprostheses had lowest thrombogenic potential transient of 0.15. A mock-transcatheter aortic valve replacement incorporating by design a trivial paravalvular leak (~1.35 ml/s) demonstrated a high transient thrombogenic potential of 0.95. Conclusions: Our data reveals distinct thrombogenic potential profile differences between valve models. If our study methods are verifiable, the design of future valves may utilize currently available experimental tools to produce advanced devices with significantly reduced thrombogenic potential.

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Section: Resultsmentioning

confidence: 99%

Violin plot data: A concerto of crucial information on valve thrombogenicity categorized in vitro by valve motion and inferred flow velocity

Scotten

Blundon

Deutsch

et al. 2019

Preprint

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“…Altogether, this predisposes to the propagation of the inflammatory process. vWF is considered a risk factor of arterial thrombosis and might contribute to the development of adverse events in atherosclerosis and other cardiovascular diseases [ 5 , 6 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Shear Stress-Induced Activation of von Willebrand Factor and Cardiovascular Pathology

Okhota

Melnikov

Avtaeva

et al. 2020

IJMS

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The von Willebrand factor (vWF) is a plasma protein that mediates platelet adhesion and leukocyte recruitment to vascular injury sites and carries coagulation factor VIII, a building block of the intrinsic pathway of coagulation. The presence of ultra-large multimers of vWF in the bloodstream is associated with spontaneous thrombosis, whereas its deficiency leads to bleeding. In cardiovascular pathology, the progression of the heart valve disease results in vWF deficiency and cryptogenic gastrointestinal bleeding. The association between higher plasma levels of vWF and thrombotic complications of coronary artery disease was described. Of note, it is not the plasma levels that are crucial for vWF hemostatic activity, but vWF activation, triggered by a rise in shear rates. vWF becomes highly reactive with platelets upon unfolding into a stretched conformation, at shear rates above the critical value (more than 5000 s−1), which might occur at sites of arterial stenosis and injury. The activation of vWF and its counterbalance by ADAMTS-13, the vWF-cleaving protease, might contribute to complications of cardiovascular diseases. In this review, we discuss vWF involvement in complications of cardiovascular diseases and possible diagnostic and treatment approaches.

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“…This proangiogenic mechanism of vWF degradation fragments may be the factor linking shear stress, lack of pulsatility, angiodysplasias, and gastrointestinal bleeding. [6][7][8] Acquired vWF deficiency and gastrointestinal bleeding are not unique to patients receiving continuous-flow LVAD support. These conditions have also been described in patients with valvular heart disease (aortic and mitral stenosis, regurgitant valve lesions, and structural and nonstructural valve deterioration), congenital heart disease, and pulmonary hypertension.…”

mentioning

confidence: 99%

“…These conditions have also been described in patients with valvular heart disease (aortic and mitral stenosis, regurgitant valve lesions, and structural and nonstructural valve deterioration), congenital heart disease, and pulmonary hypertension. [7][8][9] The severity of acquired vWF deficiency increases as these lesions progress and usually reverses after treatment either by surgery or by transcatheter procedures. [7][8][9] Similar to the conditions in valvular heart disease, preventing the development of acquired vWF deficiency by restoring pulse pressure and decreasing shear stress may lead to lower rates of gastrointestinal bleeding.…”

mentioning

confidence: 99%

“…[7][8][9] The severity of acquired vWF deficiency increases as these lesions progress and usually reverses after treatment either by surgery or by transcatheter procedures. [7][8][9] Similar to the conditions in valvular heart disease, preventing the development of acquired vWF deficiency by restoring pulse pressure and decreasing shear stress may lead to lower rates of gastrointestinal bleeding. 5 Furthermore, advances in hemocompatibility, pump design and management may similarly achieve this goal.…”

mentioning

confidence: 99%

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