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. Jude Medical (SJM) 27 mm valve in the aortic position of a pulsatile circulatory mock loop under physiologic conditions with particle image velocimetry (PIV). Assuming a dynamic equilibrium assumption between the resolved and sub-grid-scale (SGS) energy flux, the SGS energy flux was calculated from the strain rate tensor computed from the resolved velocity fields and the SGS stress was determined by the Smagorinsky model, from which the turbulence dissipation rate and then the viscous dissipative stresses were estimated. Our results showed Reynolds stresses up to 80 N/m2 throughout the cardiac cycle, and viscous dissipative stresses below 12 N/m2. The viscous dissipative stresses remain far below the threshold of red blood cell hemolysis, but could potentially damage platelets, implying the need for further study in the phenomenon of MHV hemolytic complications.

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.

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.

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. In this study, we measured the St. Jude Medical 27 mm and the TRI 27 mm valves in the aortic position of a pulsatile circulatory mock loop under physiologic conditions with digital particle image velocimetry (DPIV). Our results showed the major principal Reynolds shear stresses were <100 N/m2 for both valves, and turbulent viscous shear stresses were smaller than 15 N/m2. The TRI valve closed more slowly than the St. Jude Medical valve. As the magnitudes of the shear stresses were similar, the closing velocity of the valves should be considered as an important factor and might reduce the risks of thrombosis and thromboembolism.

After a chronic ligation of the common bile duct (BDL), Long-Evans rats are hypotensive and have elevated saline intake during both sodium-depleted and nondepleted conditions. We tested whether BDL rats have exaggerated hypotension during sodium depletion or an elevated dipsogenic response to angiotensin II (ANG II) that might help to explain the saline intake. After 4 wk of BDL, rats were hypotensive at baseline and developed exaggerated hypotension during acute furosemide-induced diuresis. Without saline to drink, BDL rats increased water intake during depletion equal to sham-ligated rats. However, with saline solution available at 22 h after sodium depletion, the BDL rats drank more water and saline than did sham-ligated rats. This rapid intake temporarily increased their mean arterial pressure to equal that of sham-ligated rats. Intravenous infusion of ANG II induced equal drinking responses despite reduced pressor responses in the BDL rats relative to sham-ligated rats during both ad libitum and sodium-depleted conditions. Thus BDL rats have exaggerated hypotension during diuresis, and their hypotension is corrected by drinking an exaggerated volume of saline, but they do not have an increased drinking response to ANG II.