Numerical comparison of the closing dynamics of a new trileaflet and a bileaflet mechanical aortic heart valve

[[abstract]]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. We used the commercial software program Fluent to run numerical simulations of the St. Jude Medical bileaflet valve and a new trileaflet mechanical heart valve. The results of these numerical simulations were validated with flow field experiments. The closing velocity of the trileaflet valve was clearly slower than that of the St. Jude Medical bileaflet valve, which would effectively reduce the occurrence of cavitation. The findings of this study are expected to advance the development of the trileaflet valve.[[incitationindex]]SCI[[booktype]]電子版[[booktype]]紙

Cardiac valves

[[abstract]]The article covers some historical investigation of mammalian heart. The basic anatomy and natural function of heart valves, heart valve disease, and its treatment with replacement prostheses are described. The FDA regulatory requirements of mechanical heart valves, biological prosthetic heart valves, and tissue engineered replacements are discussed

On accelerated fatigue testing of prosthetic heart valves

[[abstract]]Accelerated testing (AT) of prosthetic heart valves allows simulation of wear and fatigue sustained by the replacement heart valves, and to estimate the valves’ life expectancy in human body. At accelerated test rates, sufficient amounts of data can be collected within a reasonably short time period, after repeated opening and closing cycles, to predict the valve durability. The U.S. Food and Drug Administration (FDA) Replacement Heart Valve Guidance (Version 4.1, 1994) requires that mechanical heart valves (MHV) must be tested at least 600 million cycles (equivalent to 15 years in vivo), while biological heart valve prostheses (BHV) must be tested at least 200 million cycles (equivalent to 5 years in vivo) in pulsatile flow simulators. The cyclic test must meet two basic FDA requirements: 1) the test valve open and close fully each cycle; and 2) the average transvalvular pressure is kept at least 100 mmHg at closure. At accelerated test rates, the valves were subjected to non-physiologic dynamic force loads and often damaged under excessive conditions, such as cavitation. AT may pinpoint early flaws in the design and in the manufacturing processes, and deflects regions of materials weakness. Hence the design of AT must follow the principles of engineering testing such as the law of dynamic similarities. One must first identify dimensionless parameters that are physiologically meaningful and those much be specific to heart valve testing. The main goal of this paper is to present an AT system and an experimental protocol so that in vitro accelerated testing may be carried out without creating these excess forces on the test valves and to predict the durability of prosthetic heart valves with physiological considerations.[[booktype]]紙

Role of vortices in cavitation formation in the flow at the closure of a bileaflet mitral mechanical heart valve

[[abstract]]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. Assuming symmetrical flow along the center of the St. Jude Medical 25-mm valve, flow fields downstream of the closing valve were measured using PIV in the mitral position of a circulatory mock loop. Flow measurements were made during successive time phases immediately following the impact of the occluder with the housing (O/H impact) at valve closing. The velocity profile near the vortex core clearly shows a typical Rankine vortex. The vortex strength reaches maximum immediately after closure and rapidly decreases at about 10 ms, indicating viscous dissipation; vortex strength also intensifies with rising pulse rate. The maximum pressure drop at the vortex center is approximately 20 mmHg, an insignificant drop relative to atmospheric vapor pressures, which implies vortices play a minor role in cavitation formation.[[incitationindex]]SCI[[booktype]]紙本[[booktype]]電子

Cavitation Phenomena in Mechanical Heart Valves: Studied by Using a Physical Impinging Rod System

[[abstract]]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. Adding a 5 mm stationary rod within the tube generated both effects simultaneously. Charged-coupled device (CCD) laser displacement sensors, strobe lighting technique, laser Doppler velocimetry (LDV), particle image velocimetry (PIV) and high fidelity piezoelectric pressure transducers measured impact velocities, cavitation images, squeeze flow velocities, vortices, and pressure changes at impact, respectively. The movable rods created cavitation at critical impact velocities of 1.6 and 1.2 m/s; squeeze flow velocities were 2.8 and 4.64 m/s. The isolated water hammer created cavitation at 1.3 m/s piston speed. The combined piston and stationary rod created cavitation at an impact speed of 0.9 m/s and squeeze flow of 3.2 m/s. These results show squeeze flow alone caused cavitation, notably at lower impact velocity as contact area increased. Water hammer alone also caused cavitation with faster displacement. Both effects together were additive. The pressure change at the vortex center was only 150 mmHg, which cannot generate the magnitude of pressure drop required for cavitation bubble formation. Cavitation occurred at 3–5 m/s squeeze flow, significantly different from the 14 m/s derived by Bernoulli’s equation; the temporal acceleration of unsteady flow requires further study.[[incitationindex]]SCI[[booktype]]紙