Publications by authors named "Chi-Pei Li"

The closing velocity of the leaflets of mechanical heart valves is excessively rapid and can cause the cavitation phenomenon. Cavitation bubbles collapse and produce high pressure which then damages red blood cells and platelets. The closure mechanism of the trileaflet valve uses the vortices in the aortic sinus to help close the leaflets, which differs from that of the monoleaflet or bileaflet mechanical heart valves which mainly depends on the reverse flow.

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Bubble cavitation occurs in the flow field when local pressure drops below vapor pressure. One hypothesis states that low-pressure regions in vortices created by instantaneous valve closure and occluder rebound promote bubble formation. To quantitatively analyze the role of vortices in cavitation, we applied particle image velocimetry (PIV) to reduce the instantaneous fields into plane flow that contains information about vortex core radius, maximum tangential velocity, circulation strength, and pressure drop.

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Design limitations of current mechanical heart valves cause blood flow to separate at the leaflet edges and annular valve base, forming downstream vortex mixing and high turbulent shear stresses. The closing behavior of a bileaflet valve is associated with reverse flow and may lead to cavitation phenomenon. The new trileaflet (TRI) design opens similar to a physiologic valve with central flow and closes primarily due to the vortices in the aortic sinus.

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When studying mechanical heart valve cavitation, a physical model allows direct flow field and pressure measurements that are difficult to perform with actual valves, as well as separate testing of water hammer and squeeze flow effects. Movable rods of 5 and 10 mm diameter impinged same-sized stationary rods to simulate squeeze flow. A 24 mm piston within a tube simulated water hammer.

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Among the clinical complications of mechanical heart valves (MHVs), hemolysis was previously thought to result from Reynolds stresses in turbulent flows. A more recent hypothesis suggests viscous dissipative stresses at spatial scales similar in size to red blood cells may be related to hemolysis in MHVs, but the resolution of current instrumentation is insufficient to measure the smallest eddy sizes. We studied the St.

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Background And Aim Of The Study: Cavitation occurs during mechanical heart valve closure when the local pressure drops below vapor pressure. The formation of stable gas bubbles may result in gaseous emboli, and secondarily cause transient ischemic attacks or strokes. It is noted that instantaneous valve closure, occluder rebound and high-speed leakage flow generate vortices that promote low-pressure regions in favor of stable bubble formation; however, to date no studies have been conducted for the quantitative measurement and analysis of these vortices.

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Accelerated testing provides a substantial amount of data on mechanical heart valve durability in a short period of time, but such conditions may not accurately reflect in vivo performance. Cavitation, which occurs during mechanical heart valve closure when local flow field pressure decreases below vapor pressure, is thought to play a role in valve damage under accelerated conditions. The underlying flow dynamics and mechanisms behind cavitation bubble formation are poorly understood.

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High-speed squeeze flow during mechanical valve closure is often thought to cause cavitation, either between the leaflet tip and flat contact area in the valve housing, seating lip, or strut flat seat stop, depending on design. These sites have been difficult to measure within the housing, limiting earlier research to study of squeeze flow outside the housing or with computational fluid dynamics. We directly measured squeeze flow velocity with laser Doppler velocimetry at its site of occurrence within the St.

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