Design and Validation of a Novel Bioreactor to Expose Aortic Valve Leaflets to Side-Specific Shear Stress

2011 ◽  
Author(s):  
Ling Sun ◽  
Nalini M. Rajamannan ◽  
Philippe Sucosky
Keyword(s):  
Shear Stress ◽  
Aortic Valve ◽  
Fluid Shear Stress ◽  
Left Ventricular ◽  
Calcific Aortic Valve Disease ◽  
Aortic Valve Leaflets ◽  
Left Ventricular Outflow ◽  
Pulsatile Shear Stress ◽  
Plate Geometry

Calcific aortic valve disease (CAVD), the most common aortic valve disorder, is characterized by an accumulation of calcium on the valve leaflets that contributes to the obstruction of the left ventricular outflow and progressive heart failure. CAVD follows an active process presumably triggered by atherogenic risk factors and hemodynamic cues1,2. Resulting from the relative motion between the deforming leaflets and the surrounding blood flow, fluid shear stress is an important component of the valve hemodynamic environment. The ventricular surface of the leaflets is exposed to a unidirectional pulsatile shear stress, while the aortic surface experiences a bidirectional oscillatory shear stress3. The characterization of the effects of shear stress on valvular pathogenesis, which requires the replication of the native valvular shear stress in the laboratory setting, has been hampered by this hemodynamic complexity. In an effort to address this challenge, the goal of this study was to design and validate a novel apparatus capable of exposing simultaneously but independently both surfaces of aortic valve leaflets to native side-specific shear stress. The device based on a cone-and-plate geometry was validated with respect to its ability to expose each surface of aortic valve leaflets to its native, time-varying shear stress waveform, while maintaining the tissue under sterile conditions for 96 hours.

Contribution of Hemodynamic Shear Stress Magnitude and Frequency Abnormalities to Calcific Aortic Valve Disease Pathogenesis

2013 ◽  
Author(s):  
Ling Sun ◽  
Philippe Sucosky
Keyword(s):  
Shear Stress ◽  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Fluid Shear Stress ◽  
Ex Vivo ◽  
Valve Disease ◽  
Molecular Signaling ◽  
Fluid Shear ◽  
Calcific Aortic Valve Disease ◽  
Hemodynamic Shear Stress

Calcific aortic valve disease (CAVD) is an active process presumably triggered by interplays between atherogenic risk factors, molecular signaling networks and hemodynamic cues. While our earlier work demonstrated that progressive alterations in fluid shear stress (FSS) on the fibrosa could trigger valvular inflammation [1], the mechanisms of CAVD pathogenesis secondary to side-specific FSS abnormalities are poorly understood. Supported by our previous studies, we hypothesize that valve leaflets are sensitive to both WSS magnitude and pulsatility and that abnormalities in either promote CAVD development. This study aims at elucidating ex vivo the contribution of isolated and combined alterations in FSS magnitude and pulsatility to valvular calcification.

Structural Deformation of Native Aortic Valve Leaflet Under Hypertension: An In Vitro Study

2009 ◽  
Author(s):  
C. H. Yap ◽  
H. S. Kim ◽  
L. P. Dasi ◽  
M. J. Weiler ◽  
K. Balachandran ◽  
...  
Keyword(s):  
Shear Stress ◽  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Fluid Shear Stress ◽  
Complex Structure ◽  
Valve Disease ◽  
Structural Deformation ◽  
Fluid Shear ◽  
Calcific Aortic Valve Disease ◽  
Increased Risk

The aortic valve (AV) is a complex structure that functions in a complex dynamic environment. During systole, the valve leaflets bend at the base to open and experience fluid shear stress on both ventricular and aortic sides of the leaflet. During diastole, adverse pressure gradient closes the valve causing it to structurally support the systemic afterload pressure. Ex vivo experiments has shown that isolated mechanical forces such as pressure, membrane tension, and fluid shear stress affects the remodeling activities of the valve leaflets and also elicit pathological responses [1], potentially leading to calcific aortic valve disease in the long term. Clinically, patients with hypertension have increased risk of developing calcific aortic valve disease [2], which could be a result of the increased pressure or the increased stretch on the valve leaflets.

Low and Unsteady Shear Stresses Upregulate Calcification Response of the Aortic Valve Leaflets

2011 ◽  
Author(s):  
Swetha Rathan ◽  
Choon Hwai Yap ◽  
Elizabeth Morris ◽  
Sivakkumar Arjunon ◽  
Hanjoong Jo ◽  
...  
Keyword(s):  
Shear Stress ◽  
Aortic Valve ◽  
Mechanical Loading ◽  
Causes Of Death ◽  
Fluid Shear Stress ◽  
Degenerative Disease ◽  
Shear Stresses ◽  
Fluid Shear ◽  
Cellular Processes ◽  
Aortic Valve Leaflets

Aortic Valve (AV) calcification is a degenerative disease that results in AV sclerosis and is one of the major causes of death. AV is subjected to mechanical conditions such as fluid shear stress, transvalvular pressure and membrane tension1. Normal hemodynamic conditions constantly renew and remodel the valve, whereas altered mechanical loading has been implicated to be the cause of AV disease2. Studies have shown that adverse hemodynamics such as hypertension and altered shear stress can cause tissue inflammation that leads to calcification and stenosis3, 4, and ultimately result in valve failure. However, the molecular and cellular processes that lead to calcification are not very well understood.

Echocardiographic assessment of the aortic valve and left ventricular outflow tract

2005 ◽  
Vol 15 (S1) ◽  
pp. 27-36 ◽  
Author(s):  
Alfred Asante-Korang ◽  
Robert H. Anderson
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Left Heart ◽  
Transesophageal Echocardiogram ◽  
Left Ventricular Outflow ◽  
Echocardiographic Assessment

The previous reviews in this section of our Supplement1,2 have summarized the anatomic components of the ventriculo-arterial junctions, and then assessed the echocardiographic approach to the ventriculo-arterial junction or junctions as seen in the morphologically right ventricle. In this complementary review, we discuss the echocardiographic assessment of the comparable components found in the morphologically left ventricle, specifically the outflow tract and the arterial root. We will address the echocardiographic anatomy of the aortic valvar complex, and we will review the causes of congenital arterial valvar stenosis, using the aortic valve as our example. We will also review the various lesions that, in the outflow of the morphologically left ventricle, can produce subvalvar and supravalvar stenosis. We will then consider the salient features of the left ventricular outflow tract in patients with discordant ventriculo-arterial connections, and double outlet ventricles. To conclude the review, we will briefly address some rarer anomalies that involve the left ventricular outflow tract, showing how the transesophageal echocardiogram is used to assist the surgeon preparing for repair. The essence of the approach will be to consider the malformations as seen at valvar, subvalvar, or supravalvar levels,1 but we should not lose sight of the fact that aortic coarctation or interruption, hypoplasia of the left heart, and malformations of the mitral valve are all part of the spectrum of lesions associated with obstruction to the left ventricular outflow tract. These additional malformations, however, are beyond the scope of this review.

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