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JOURNAL ARTICLE

Role of vortices in cavitation formation in the flow across a mechanical heart valve

Chi-Pei Li, Po-Chien Lu, Jia-Shing Liu, Chi-Wen Lo, Ned H Hwang
Journal of Heart Valve Disease 2008, 17 (4): 435-45
18751474

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.

METHODS: A Björk-Shiley Monostrut (BSM) monoleaflet valve was placed in the mitral position of a pulsatile mock circulatory loop. Particle image velocimetry (PIV) and pico coulomb (PCB) pressure measurements were applied. Flow field measurements were carried out at t = -5, -3, -1, -0.5, 0 (valve closure), 0.3, 0.5, 0.75, 1.19, 1.44, 1.69, 1.94, 2, 2.19, 2.54, 2.79, 3.04, 3.29, 3.54, 5 and 10 ms. The vortices were quantitatively analyzed using the Rankine vortex model.

RESULTS: A single counter-clockwise vortex was The instantaneous formation of cavitation bubbles at mechanical heart valve (MHV) closure, which subsequently damage blood cells and valve integrity, is a well-known and widely studied phenomenon (1-4). Contributing factors seem to include the water-hammer, squeeze flow and Venturi effects, all of which are short-lived. Both, Dauzat et al. (5) and Sliwka et al. (6) have detected high-intensity transient signals (HITS) with transcranial Doppler ultrasound in the carotid and cerebral arteries of MHV recipients, while Deklunder (7) observed clinical occurrences of cerebral gas emboli that were not seen with bioprosthetic valves. These detected over the major orifice, while a pair of counter-rotating vortices was found over the minor orifice. Velocity profiles were consistent with Rankine vortices. The vortex strength and magnitude of the pressure drop peaked shortly after initial occluder-housing impact and rapidly decreased after 0.5 ms, indicating viscous dissipation, with a less significant contribution from the occluder rebound effect. The maximum pressure drop was on the order of magnitude of 40 mmHg.

CONCLUSION: Detailed PIV measurements and quantitative analysis of the BSM mechanical heart valve revealed large-scale vortex formation immediately after valve closure. Of note, the vortices were typical of a Rankine vortex and the maximum pressure change at the vortex center was only 40 mmHg. These data support the conclusion that vortex formation alone cannot generate the magnitude of pressure drop required for cavitation bubble formation.

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