Numerical Study on Diastolic Left Ventricular Hemodynamics Using Motion Models of Mitral Valve With/Without Edge-to-Edge Repair

2010 ◽  
Author(s):  
Yingying Hu ◽  
Liang Shi ◽  
Siva Parameswaran ◽  
Sergey A. Smirnov ◽  
Zhaoming He
Keyword(s):  
Shear Stress ◽  
Mitral Valve ◽  
Left Ventricle ◽  
Platelet Activation ◽  
Numerical Study ◽  
Left Ventricular ◽  
High Shear ◽  
High Shear Stress ◽  
Orifice Area ◽  
Motion Models

Edge-to-edge repair (ETER) is a newly developed technique to correct such mitral valve (MV) malfunctions as regurgitation [1,2]. This technique changes MV geometric configuration by suturing the anterior and posterior leaflets at central or commissural edges, and consequently alters MV and left ventricle (LV) dynamics. For instance, stress in the MV elevated due to ETER may cause leaflets tearing near suture. Little has been known about shear stress on the MV and LV walls under MV ETER conditions, where high shear stress might cause platelet activation or hemolysis [3]. When ETER is done at the central leaflet edges, it generates two MV orifices, leads to two deflected jets, and completely changes vortices in the LV. ETER also reduces the orifice area, and increases jet velocity and transmitral pressure [1,2,4]. Flow patterns in the LV and ETER effects on the LV and MV functions have not been understood well.

Novel Platelet Antagonists

2006 ◽  
Author(s):  
Richard C. Becker ◽  
Frederick A. Spencer
Keyword(s):  
Shear Stress ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Adenosine Monophosphate ◽  
Stress Conditions ◽  
Platelet Glycoprotein ◽  
High Shear ◽  
High Shear Stress ◽  
Surface Receptor ◽  
Pharmacologic Agents

The development of pharmacologic agents that inhibit platelet performance could not have proceeded without a fundamental knowledge of normal biology and a clear understanding of the laws that govern cellular events in the circulatory system. The adhesion of platelets to a site of vessel wall injury is mediated by von Willebrand factor (vWF), which binds to the platelet glycoprotein (GP) Ib/IX-V complex receptor (and the GPIIb/IIIa receptor under high shear stress conditions). Monoclonal antibodies to vWF have been developed and tested in animal models, as has aurintricarboxylic acid (Strony et al., 1990), a triphenylmethyl compound that inhibits vWF binding. To date, investigation in humans has not taken place, perhaps because of concerns regarding the potential risk for hemorrhagic complications. Nevertheless, the scientific community remains interested in vWF and its platelet surface receptor as potential pharmacology-directed targets. Although the GPIIb/IIIa receptor antagonists are best known for their ability to inhibit platelet aggregation, under high shear stress conditions vWF can also bind the GPIIb/IIIa receptor, facilitating adhesion. As a result, GPIIb/IIIa antagonists may have an impact on both platelet adhesion and aggregation. As previously discussed, platelet activation is followed by a series of intracellular events that culminate in the release of calcium and substances that augment platelet aggregation and support coagulation protease binding. Thus, pharmacologic agents that inhibit initial surface receptor–mediated activation may also impair platelet aggregation. Several natural prostanoids (prostaglandin [PG] E1 and PGI2) can inhibit platelet activation and aggregation by elevating cyclic adenosine monophosphate (cAMP) levels. Although the mechanism is complex, the primary mode of inhibition is through the activation of adenylate cyclase (with a subsequent rise in cAMP concentrations), which in turn prevents calcium mobilization. The clinical application of PGE1 and PGI2 has been limited by their effect on vascular tone, producing substantial systemic hypotension (Emmons et al., 1967; Terres et al., 1989), and by extensive first-pass metabolism in the lungs (70% of the active compound is rapidly cleared) (Kleiman et al., 1994).

A Computational Study of a Thin-Walled Three-Dimensional Left Ventricle During Early Systole

1994 ◽  
Vol 116 (3) ◽  
pp. 307-314 ◽  
Author(s):  
Ajit P. Yoganathan ◽  
Jack D. Lemmon ◽  
Young H. Kim ◽  
Peter G. Walker ◽  
Robert A. Levine ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Ventricle ◽  
Numerical Study ◽  
Three Dimensional ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Model Parameters ◽  
Septal Wall ◽  
Early Systole ◽  
Thin Walled

A numerical study was conducted to solve the three-dimensional Navier-Stokes equations for time-dependent flow in a compliant thin-walled, anatomically correct left ventricle during early systole. Model parameters were selected so that the simulation results could be compared to clinical data. The results produced endocardial wall motion which was consistent with human heart data, and velocity fields consistent with those occurring in a normally-contracting left ventricle. During isovolumetric contraction the posterior wall moved basally and posteriorly, while the septal wall moved apically and anteriorly. During ejection, the short axis of the left ventricle decreased 1.1 mm and the long axis increased 4.2 mm. At the end of the isovolumetric contraction, most of the flow field was moving form the apex toward the base with recirculation regions at the small pocket formed by the concave anterior leaflet, adjacent to the septal wall and near the left ventricular posterior wall. Fluid velocities in the outflow tract matched NMR data to within 10 percent. The results were also consistent with clinical measurements of mitral valve-papillary muscle apparatus displacement, and changes in the mitral valve annular area. The results of the present study show that the thin-walled, three-dimensional left ventricular model simulates observed normal heart phenomena. Validation of this model permits further studies to be performed which involve altered ventricular function due to a variety of cardiac diseases.

Effects of Mitral Valve Suture Position on Left Ventricular Vortex and Energy Under Edge-to-Edge Repair

2012 ◽  
Author(s):  
Song Jiang ◽  
Ze Wang ◽  
Yingying Hu ◽  
Zhaoming He
Keyword(s):  
Mitral Valve ◽  
Left Ventricle ◽  
Energy Loss ◽  
Fluid Mechanics ◽  
Position Effect ◽  
Left Ventricular ◽  
Orifice Area ◽  
Pumping Efficiency ◽  
Early Closure ◽  
Repair Techniques

Mitral valve (MV) asymmetry in the left ventricle causes a large anterior vortex during left ventricle (LV) filling which is considered to store kinematic energy. This vortex persists in the end of diastole and may facilitate early closure of the mitral valve and transfer kinetic energy in the anterior vortex to help blood ejection through the aortic valve. Washout effect from the anterior vortex may prevent thrombosis in the left ventricle. Recently one of the repair techniques, the mitral valve edge-to-edge repair (ETER) procedure, has been used for the correction of mitral regurgitation. According to this procedure, MV’s competence is restored by suturing the edges of the leaflets, at the central, lateral or commissural position, depending on the mechanism of the regurgitation and the site of valvular lesions. Changes in the mitral valve geometry, due to ETER, alter LV fluid mechanics. Our group has investigated suture length effect on LV fluid mechanics. MV ETER increased energy loss and lowered LV filling efficiency. The larger orifice area after ETER might prevent significant energy loss and transmitral pressure drop during diastole. However, suture position effect is unknown. In this study, we aim to investigate the effect of different MV suture position on LV fluid mechanics, especially the vortex, LV pumping efficiency.

Platelet Aggregation and Activation under Complex Patterns of Shear Stress

2002 ◽  
Vol 88 (11) ◽  
pp. 817-821 ◽  
Author(s):  
Jian-ning Zhang ◽  
Angela Bergeron ◽  
Qinghua Yu ◽  
Carol Sun ◽  
Larry McIntire ◽  
...  
Keyword(s):  
Shear Stress ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Low Flow ◽  
High Shear ◽  
High Shear Stress ◽  
Fast Flow ◽  
Low Shear

SummaryArterial stenosis results in a complex pattern of blood flow containing an extremely fast flow in the throat of stenosis and a post-stenosis low flow. The fast flow generates high shear stress that has been demonstrated in vitro to activate and aggregate platelets. One potential problem of these in vitro studies is that platelets are invariably exposed to a high shear stress for a period that is significantly longer than they would have experienced in vivo. More importantly, the role of the poststenosis low flow in platelet activation and aggregation has not been determined. By exposing platelets to a shear profile that contains both high and low shear segments, we found that platelets aggregate when they are exposed to a high shear stress of 100 dyn/cm2 for as short as 2.5 s, a period that is significantly shorter than those previously reported (30–120 s). Platelet aggregation under this condition requires a low shear exposure immediately after a high shear pulse, suggesting that post-stenosis low flow enhances platelet aggregation. Furthermore, platelet aggregation under this condition is not activation-dependent because the CD62P expression of sheared platelets is significantly less than that of platelets treated with ADP. Based on these findings, we propose that shear-induced platelet aggregation may be a process of mechanical crosslinking of platelets, requiring minimal platelet activation. This process may function as a protective mechanism to prevent in vivo irreversible platelet activation and aggregation under temporary high shear.

scholarly journals 5065Platelet desialylation induced by high shear-stress mechanical circulatory support

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
H Spillemaeker ◽  
A Dupont ◽  
A Kauskot ◽  
A Rauch ◽  
F Vincent ◽  
...  
Keyword(s):  
Shear Stress ◽  
Mechanical Circulatory Support ◽  
Circulatory Support ◽  
High Shear ◽  
High Shear Stress
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