New power loss optimized Fontan connection evaluated by calculation of power loss using high resolution PC-MRI and CFD.

A new blood vessel configuration was invented to optimize blood flow efficiency and reduce the power loss in the Fontan connection. The current preferred Fontan configuration, the total cavopulmonary connection (TCPC), usually connects the venae cava (VC) to the pulmonary arteries (PA), bypassing the right ventricle. The new connection, called OptiFlo, has two vertical inlets, which both bifurcate then merge into one another to form two horizontal outlets. One of the preliminary configurations of the new OptiFlo model was used for a comparison experiment between computational fluid dynamics (CFD) and high resolution phase contrast magnetic resonance imaging (PC-MRI) with a voxel resolution of 0.23 mmx0.23 mmx0.25 mm. The thin slice thickness was achieved using the ACGI interpolation technique we have used in other applications before. The 2D PC-MRI velocity vectors were mapped into a CFD grid, enabling direct CFD and MRI data comparisons. The mean squared difference was found between the two dataset Using the viscous power dissipation function we calculated the power loss for both CFD and MRI data. The power losses, calculated with the viscous power dissipation function, were 0.66 mW for CFD and 0.46 mW for the PC-MRI data.

Surface strains in the anterior leaflet of the functioning mitral valve.

Abstract-The mitral valve (MV) is a complex anatomical structure whose function involves a delicate force balance and synchronized function of each of its components. Elucidation of the role of each component and their interactions is critical to improving our understanding of MV function, and to form the basis for rational surgical repair. In the present study, we present the first known detailed study of the surface strains in the anterior leaflet in the functioning MV. The three-dimensional spatial positions of markers placed in the central region of the MV anterior leaflet in a left ventricle-simulating flow loop over the cardiac cycle were determined. The resulting two-dimensional in-surface strain tensor was computed from the marker positions using a C0 Lagrangian quadratic finite element. Results demonstrated that during valve closure the anterior leaflet experienced large, anisotropic strains with peak stretch rates of 500%-1,000%/s. This rapid stretching was followed by a plateau phase characterized by relatively constant strain state. We hypothesized that the presence of this plateau phase was a result of full straightening of the leaflet collagen fibers upon valve closure. This hypothesis suggests that the MV collagen fibers are designed to allow leaflet coaptation followed by a dramatic increase in stiffness to prevent further leaflet deformation, which would lead to valvular regurgitation. These studies represent a first step in improving our understanding of normal MV function and to help establish the principles for repair and replacement.

Biosynthetic activity in heart valve leaflets in response to in vitro flow environments.

The development of bioreactors for tissue engineered heart valves would be aided by a thorough understanding of how mechanical forces impact cells within valve leaflets. The hypothesis of the present study is that flow may influence the biosynthetic activity of aortic valve leaflet cells. Porcine leaflets were exposed to one of several conditions for 48 h, including steady or pulsatile flow in a tubular flow system at 10 or 20 l/min, and steady shear stress in a parallel plate flow system at 1, 6, or 22 dyne/cm2. Protein, glycosaminoglycan, and DNA synthesis increased during static incubation but remained at basal levels after exposure to flow. The modulation of synthetic activity was attributed to the presence of a shear stress on the leaflet surface, which may be transmitted to cells within the leaflet matrix through tensile forces. The alpha-smooth muscle (alpha-SM) actin distribution observed in fresh leaflets was proportionately decreased after exposure to antibiotics and not recovered by either static incubation or exposure to flow. These results indicate that exposure to flow maintains leaflet synthetic activity near normal levels, but that the inclusion of another force, such as bending or backpressure, may be necessary to preserve alpha-SM actin immunoreactive cells.

Chordal cutting: a new therapeutic approach for ischemic mitral regurgitation.

BACKGROUND: Mitral regurgitation (MR) conveys adverse prognosis in ischemic heart disease. Because such MR is related to increased leaflet tethering by displaced attachments to the papillary muscles (PMs), it is incompletely treated by annular reduction. We therefore addressed the hypothesis that such MR can be reduced by cutting a limited number of critically positioned chordae to the leaflet base that most restrict closure but are not required to prevent prolapse. This was tested in 8 mitral valves: a porcine in vitro pilot with PM displacement and 7 sheep with acute inferobasal infarcts studied in vivo with three-dimensional (3D) echo to quantify MR in relation to 3D valve geometry. METHODS AND RESULTS: In all 8 valves, PM displacement restricted leaflet closure, with anterior leaflet angulation at the basal chord insertion, and mild-to-moderate MR. Cutting the 2 central basal chordae reversed this without prolapse. In vivo, MR increased from 0.8+/-0.2 to 7.1+/-0.5 mL/beat after infarction and then decreased to 0.9+/-0.1 mL/beat with chordal cutting (P<0.0001); this paralleled changes in the 3D leaflet area required to cover the orifice as dictated by chordal tethering (r(2)=0.76). CONCLUSIONS: Cutting a minimum number of basal chordae can improve coaptation and reduce ischemic MR. Such an approach also suggests the potential for future minimally invasive implementation.

Evaluation of the precision of magnetic resonance phase velocity mapping for blood flow measurements.

Evaluating the in vivo accuracy of magnetic resonance phase velocity mapping (PVM) is not straightforward because of the absence of a validated clinical flow quantification technique. The aim of this study was to evaluate PVM by investigating its precision, both in vitro and in vivo, in a 1.5 Tesla scanner. In the former case, steady and pulsatile flow experiments were conducted using an aortic model under a variety of flow conditions (steady: 0.1-5.5 L/min; pulsatile: 10-75 mL/cycle). In the latter case, PVM measurements were taken in the ascending aorta of ten subjects, seven of which had aortic regurgitation. Each velocity measurement was taken twice, with the slice perpendicular to the long axis of the aorta. Comparison between the measured and true flow rates and volumes confirmed the high accuracy of PVM in measuring flow in vitro (p > 0.85). The in vitro precision of PVM was found to be very high(steady: y = 1.00x + 0.02, r = 0.999; pulsatile: y = 0.98x + 0.72, r = 0.997; x: measurement #1, y: measurement #2) and this was confirmed by Bland-Altman analysis. Of great clinical significance was the high level of the in vivo precision (y = 1.01x - 0.04, r = 0.993), confirmed statistically (p = 1.00). In conclusion, PVM provides repeatable blood flow measurements. The high in vitro accuracy and precision, combined with the high in vivo precision, are key factors for the establishment of PVM as the "gold-standard" to quantify blood flow.

Noninvasive fluid dynamic power loss assessments for total cavopulmonary connections using the viscous dissipation function: a feasibility study.

The total cavopulmonary connection (TCPC) has shown great promise as an effective palliation for single-ventricle congenital heart defects. However, because the procedure results in complete bypass of the right-heart, fluid dynamic power losses may play a vital role in postoperative patient success. Past research has focused on determining power losses using control volume methods. Such methods are not directly applicable clinically without highly invasive pressure measurements. This work proposes the use of the viscous dissipation function as a tool for velocity gradient based estimation of fluid dynamic power loss. To validate this technique, numerical simulations were conducted in a model of the TCPC incorporating a 13.34 mm (one caval diameter) caval offset and a steady cardiac output of 2 L x min(-1). Inlet flow through the superior vena cava was 40 percent of the cardiac output, while outflow through the right pulmonary artery (RPA) was varied between 30 and 70 percent, simulating different blood flow distributions to the lungs. Power losses were determined using control volume and dissipation function techniques applied to the numerical data. Differences between losses computed using these techniques ranged between 3.2 and 9.9 percent over the range of RPA outflows studied. These losses were also compared with experimental measurements front a previous study. Computed power losses slightly exceeded experimental results due to different inlet flow conditions. Although additional experimental study is necessary to establish the clinical applicability of the dissipation function, it is believed that this method, in conjunction with velocity gradient information derived from imaging modalities such as magnetic resonance imaging, can provide a noninvasive means of assessing power losses within the TCPC in vivo.

Bileaflet aortic valve prosthesis pivot geometry influences platelet secretion and anionic phospholipid exposure.

The clinical histories of the Medtronic Parallel (MP) and St. Jude Medical (SJM) Standard valves suggest pivot geometry influences the thrombogenic characteristics of bileaflet prostheses. This work studied the effects of various pivot geometries on markers of platelet damage in a controlled, in vitro apparatus. The Medtronic Parallel valve, two St. Jude Medical valves, and two demonstration prostheses were used to study the effects of bileaflet pivot design, gap width, and size on platelet secretion and anionic phospholipid expression during leakage flow. A centrifugal pump was used to drive blood through a circuit containing a bileaflet prosthesis. Samples were taken at set time intervals after the start of the pump. These samples were analyzed by cell counting, flow cytometry, and enzyme-linked immunosorbant assay. No significant differences were observed in platelet secretion or anionic phospholipid expression between experiments with the SJM 27 Standard regular leaker, the SJM 20 regular leaker, and the MP 27 valves. Significant differences in platelet secretion and anionic phospholipid expression were observed between a SJM 27 Standard regular leaker and a SJM 27 high leaker valve. These studies suggest that leakage gap width within bileaflet valve pivots has a significant effect on platelet damage initiated by leakage flow.

Evaluation of cardiovascular parameters of a selenium-based antihypertensive using pulsed Doppler ultrasound.

The pharmacology of selenium is of much interest because selenium deficiency has been linked to cardiovascular diseases, cancer, and arthritis, and selenoenzymes are critical cellular antioxidants. We have previously reported that phenyl-2-aminoethylselenide (PAESe) and its derivatives represent a novel class of selenium-based antihypertensive agents that exhibit unique biochemical and pharmacologic properties. We now report on experiments designed to probe the hemodynamic mechanism of action of these compounds in spontaneously hypertensive rats (SHR). A noninvasive pulsed Doppler ultrasound probe was used to measure peak blood flow velocity in the aortic arch from the right second intercostal space. PAESe was found to increase peak aortic blood flow velocity (+44%), heart rate (+16%), and blood flow acceleration (+105%), while decreasing left ventricular ejection time (LVET) (-37%) concomitant with a decrease in mean arterial pressure (-54%). These results were compared with the known vasodilator hydralazine, which had similar effects on mean arterial pressure (MAP) and peak velocity but caused an increase in LVET (+42%) and a decrease in heart rate (-18%). Taken together, our results suggest that PAESe decreases blood pressure via a decrease in peripheral resistance, which overcomes the initial increase in heart rate and acceleration to give a net decrease in MAP.

Improved in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall: three-dimensional force vector measurement system.

Recent developments indicate that the forces acting on the papillary muscles can be a measure of the severity of mitral valve regurgitation. Pathological conditions, such as ischemic heart disease, cause changes in the geometry of the left ventricle and the mitral valve annulus, often resulting in displacement of the papillary muscles relative to the annulus. This can lead to increased tension in the chordae tendineae. This increased tension is transferred to the leaflets, and can disturb the coaptation pattern of the mitral valve. The force balance on the individual components governs the function of the mitral valve. The ability to measure changes in the force distribution from normal to pathological conditions may give insight into the mechanisms of mitral valve insufficiency. A unique in vitro model has been developed that allows quantification of the papillary muscle spatial position and quantification of the three-dimensional force vector applied to the left ventricular wall by the papillary muscles. This system allows for the quantification of the global force exerted on the posterior left ventricular wall from the papillary muscles during simulation of normal and diseased conditions.

The sensitivity of indicators of thrombosis initiation to a bileaflet prosthesis leakage stimulus.

BACKGROUND AND AIM OF THE STUDY: The recent clinical history and experimental studies of the Medtronic Parallel (MP) valve suggest that bileaflet valve leakage flow is a primary initiator of thrombosis. These studies investigated the effects of physiologic leakage flow through a MP valve on various markers of blood damage. METHODS: A centrifugal pump was used to drive whole, human blood anticoagulated with PPACK through a circuit containing a MP 27 mm valve in the closed position (experimental runs) or a MP 27 mm valve in the open position (control runs). Samples were taken at set time intervals after the start of the pump. These samples were analyzed by cell counting, flow cytometry, and ELISA. RESULTS: Cell counts remained relatively constant in both the experimental and control runs. Increases in plasma hemoglobin concentration and the percentage of glycophorin A-positive fragments in the cell population were not significant in either the experimental or the control runs. Plasma platelet factor 4 activity and the percentage of the CD41-positive population which was positive for annexin V increased significantly (p <0.05) in the experimental runs compared with the control runs. CONCLUSION: The results indicate that bileaflet valve leakage flow causes significant platelet disruption, that erythrocytes are more resistant to disruption by leakage flow than platelets and granulocytes, and that annexin V binding to platelets and plasma platelet factor 4 activity are more sensitive markers of leakage induced blood damage than plasma hemoglobin concentration.

In vivo flow dynamics of the total cavopulmonary connection from three-dimensional multislice magnetic resonance imaging.

BACKGROUND: The total cavopulmonary connection (TCPC) design continues to be refined on the basis of flow analysis at the connection site. These refinements are of importance for myocardial energy conservation in the univentricular supported circulation. In vivo magnetic resonance phase contrast imaging provides semiquantitative flow visualization information. The purpose of this study was to understand the in vivo TCPC flow characteristics obtained by magnetic resonance phase contrast imaging and compare the results with our previous in vitro TCPC flow experiments in an effort to further refine TCPC surgical design. METHODS: Twelve patients with TCPC underwent sedated three-dimensional, multislice magnetic resonance phase contrast imaging. Seven patients had intraatrial lateral tunnel TCPC and 5 had extracardiac TCPC. RESULTS: In all patients in both groups a disordered flow pattern was observed in the inferior caval portion of the TCPC. Flow at the TCPC site appeared to be determined by connection geometry, being streamlined at the superior vena cava-pulmonary junction when the superior vena cava was offset and flared toward the left pulmonary artery. Without caval offset, intense swirling and dominance of superior vena caval flow was observed. In TCPC with bilateral superior vena cavae, the flow patterns observed included secondary vortices, a central stagnation point, and influx of the superior vena cava flow into the inferior caval conduit. A comparative analysis of in vivo flow and our previous in vitro flow data from glass model prototypes of TCPC demonstrated significant similarities in flow disturbances. Three-dimensional magnetic resonance phase contrast imaging in multiple coronal planes enabled a comprehensive semiquantitative flow analysis. The data are presented in traditional instantaneous images and in animated format for interactive display of the flow dynamics. CONCLUSIONS: Flow in the inferior caval portion of the TCPC is disordered, and the TCPC geometry determines flow characteristics.

Harvested porcine mitral xenograft fixation: impact on fluid dynamic performance.

BACKGROUND AND AIM OF THE STUDY: Recent developments suggest that stentless bioprosthetic mitral valve heterografts should be considered in order to optimize valve hydrodynamics. The fixation process alters the mechanical properties of tissue. This study investigates the changes in mitral valve morphology and hemodynamic performance following fixation. METHODS: Porcine mitral valves were excised and attached to a physiological annular ring. Mitral valve function was studied in vitro with a rigid transparent left heart model, allowing transverse and sagittal views. Initial experiments were performed with fresh valves under physiological conditions. Three different papillary muscle positions were used, and each was recorded. After glutaraldehyde fixation, genipin fixation, and cryopreservation, the valves were re-studied while maintaining cardiac output. Performance characteristics before and after fixation were obtained from hydrodynamic pressure and flow data, high-speed video camera, digital video, Doppler ultrasound, and three-dimensional papillary muscle force measurements. Morphology changes were detected by detailed anatomic measurements of the valves before and after fixation. RESULTS: Valve length was reduced by 18.5% after fixation with genipin (p <0.001), but not with glutaraldehyde. Cryopreserved valves showed no statistically significant changes in morphology or hydrodynamic performance after preservation. The forward flow opening area was reduced by 12.2% (p <0.001) after glutaraldehyde fixation, and by 32.3% (p = 0.004) after genipin fixation. Thus, maximal forward flow velocity was increased by 33.3% (p = 0.008) after glutaraldehyde fixation and by 52.8% (p = 0.001) after genipin fixation. The flow acceleration was consistent with a funnel shape of the fixed valves causing important flow contraction beyond the orifice (vena contracta). The papillary muscle force increased with apically posterior papillary muscle displacement by 20.4% (p = 0.001) and 101.5% (p <0.001) after glutaraldehyde and genipin fixation, respectively, and total regurgitant volume was increased by 91.6% (p <0.001) and 117.3% (p <0.001), respectively. The work required by the heart simulator to maintain a constant cardiac output at constant vascular resistance increased by 24.2% (p = 0.003) and 34.2% (p = 0.004) after glutaraldehyde and genipin fixation, respectively. CONCLUSION: The present study shows that chemical fixation of porcine mitral valves adversely affects the hemodynamics of the valves, increasing overall workload. The effects were more severe after fixation with genipin than with glutaraldehyde. This suggests the need to explore other fixation agents to optimize valvular cardiac function. Cryopreservation had no detrimental effects on valvular hemodynamic performance.

Comparative hydrodynamic evaluation of bioprosthetic heart valves.

BACKGROUND AND AIM OF STUDY: Pressure gradients across cardiac valve prostheses have been identified as one of the most important performance measures in valve replacement surgery. Specifically in aortic valves, these gradients influence reduction of left ventricular hypertrophy and are postulated to influence long-term survival. The correct choice of replacement valve is hampered by a lack of uniform measures of valve performance. The aim of this study was to compare in-vitro hydrodynamic performance of commercially available bioprosthetic valves under identical test conditions. METHODS: In-vitro steady forward flow and pulsatile flow tests were performed on aortic and mitral bioprosthetic valves in accordance with ISO/FDA guidelines at two different institutions to obtain objective hemodynamic performance measures. Measurements were recorded at various flow rates, flow and pressure to obtain mean pressure gradients and effective orifice areas (EOAs). RESULTS: Wide variation in pressure gradients was found among tested valves of each size. For a given size, differences of 200 to 400% were observed; in general, the valve models' relative rankings in pressure drop were independent of size. CONCLUSION: The Carpentier-Edwards Perimount valve showed superior performance at all sizes tested. While the mean pressure gradients and EOAs reported by each institution differed for a given valve, the performance of valve models relative to each other was similar. The testing of valves under identical conditions is a valuable comparative indicator of valve hemodynamic performance.

Importance of accurate geometry in the study of the total cavopulmonary connection: computational simulations and in vitro experiments.

Previous in vitro studies have shown that total cavopulmonary connection (TCPC) models incorporating offset between the vena cavae are energetically more efficient than those without offsets. In this study, the impact of reducing simplifying assumptions, thereby producing more physiologic models, was investigated by computational fluid dynamics (CFD) and particle flow visualization experiments. Two models were constructed based on angiography measurements. The first model retained planar arrangement of all vessels involved in the TCPC but incorporated physiologic vessel diameters. The second model consisted of constant-diameter vessels with non-planar vascular features. CFD and in vitro experiments were used to study flow patterns and energy losses within each model. Energy losses were determined using three methods: theoretical control volume, simplified control volume, and velocity gradient based dissipation. Results were compared to a simplified model control. Energy loss in the model with physiologically more accurate vessel diameters was 150% greater than the simplified model. The model with nonplanar features produced an asymmetric flow field with energy losses approximately 10% higher than simplified model losses. With the velocity gradient based dissipation technique, the map of energy dissipation was plotted revealing that most of the energy was dissipated near the pulmonary artery walls.

Computational modeling of left heart diastolic function: examination of ventricular dysfunction.

A computational model that accounts for blood-tissue interaction under physiological flow conditions was developed and applied to a thin-walled model of the left heart. This model consisted of the left ventricle, left atrium, and pulmonary vein flow. The input functions for the model included the pulmonary vein driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The Immersed Boundary Method was used for the interaction of the tissue and blood in response to fluid forces and changes in tissue pathophysiology, and the fluid mass and momentum conservation equations were solved using Patankar's Semi-Implicit Method for Pressure Linked Equations (SIMPLE). This model was used to examine the flow fields in the left heart under abnormal diastolic conditions of delayed ventricular relaxation, delayed ventricular relaxation with increased ventricular stiffness, and delayed ventricular relaxation with an increased atrial contraction. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions, and to the results from simulations of normal diastolic function in this model [1]. Cases involving impairment of diastolic function were modeled with changes to the input functions for fiber relaxation/contraction of the chambers. The three cases of diastolic dysfunction investigated agreed with the changes in diastolic flow fields seen clinically. The effect of delayed relaxation was to decrease the early filling magnitude, and this decrease was larger when the stiffness of the ventricle was increased. Also, increasing the contraction of the atrium during atrial systole resulted in a higher late filling velocity and atrial pressure. The results show that dysfunction can be modeled by changing the relationships for fiber resting-length and/or stiffness. This provides confidence in future modeling of disease, especially changes to chamber properties to examine the effect of local dysfunction on global flow fields.

An in vitro study of the hinge and near-field forward flow dynamics of the St. Jude Medical Regent bileaflet mechanical heart valve.

The most widely implanted prosthetic valve is the mechanical bileaflet. Recent clinical experiences suggest that some designs are more prone to thromboembolic episodes than others. This study evaluated the hinge flow and near-field forward flow of the new St. Jude Medical Regent bileaflet mechanical heart valve. Laser Doppler velocimetry measurements were conducted within the hinge and near-field forward flow regions of the Regent valve. These pulsatile flow velocity measurements were animated in time to visualize the flow fields throughout the cardiac cycle. During forward flow, a recirculation region developed in the inflow pocket of the Regent hinge but was subsequently abolished by strong backflow during valve closure. Leakage velocities in the hinge region reached 0.72 m/s and Reynolds shear stresses reached 2,600 dyn/cm2. Velocities in the near-field region were highest in the lateral orifice jet, reaching 2.1 m/s. Small regions of separated flow were observed adjacent to the hinge region. Leaflet motion through the Regent hinge creates a washout pattern which restricts the persistence of stagnation zones in its hinge. Based upon the results of these studies, the hematological performance of the Regent series should be at least equivalent to the performance of the Standard series.

Geometric distribution of chordae tendineae: an important anatomic feature in mitral valve function.

BACKGROUND AND AIM OF THE STUDY: This study examined the geometric distribution of chordae tendineae and their importance in compensating for papillary muscle (PM) displacement. METHODS: Anatomic, chordal mechanics and hemodynamic measurements were performed with porcine mitral valves. For hemodynamic measurements, physiological pulsatile flow conditions were maintained, and PM positions varied. Leaflet coaptation was documented by 2-D echocardiography, and regurgitation measured directly. RESULTS: Anatomic measurements showed the sum of marginal leaflet and marginal chordal lengths to exceed basal chordal length (1.8+/-0.4 versus 2.8+/-0.7 cm for anterior leaflets; 1.6+/-0.3 versus 2.5+/-0.6 cm for posterior leaflets). Triangular structures existed between basal chordae and marginal chordae with the marginal leaflet as the third side. Basal chordae resisted apical PM displacement in static experiments, while marginal chordae governed leaflet closure in hemodynamic experiments. Under pulsatile flow conditions, apical PM displacement decreased leaflet coaptation length and increased regurgitation (9.4+/-2.1 versus 4.0+/-1.6 ml). When marginal chordae were fused to the basal chordae, eliminating the role of the marginal chordae, severe regurgitation resulted (28.5+/-5.0 ml with apical PM displacement). CONCLUSION: Based on triangular structures involving the basal and marginal chordae, a compensatory mechanism was described which explains how the severity of mitral regurgitation can vary following PM displacement. Basal chordae provide a constant connection between the annulus and papillary muscles, while marginal chordae maintain marginal leaflet flexibility, governing proper valve closure. This study relates chordal distribution to normal valve function, and provides a better understanding of breakdown in valve function under pathophysiological conditions.

Three-dimensional computational model of left heart diastolic function with fluid-structure interaction.

Aided by advancements in computer speed and modeling techniques, computational modeling of cardiac function has continued to develop over the past twenty years. The goal of the current study was to develop a computational model that provides blood-tissue interaction under physiologic flow conditions, and apply it to a thin-walled model of the left heart. To accomplish this goal, the Immersed Boundary Method was used to study the interaction of the tissue and blood in response to fluid forces and changes in tissue pathophysiology. The fluid mass and momentum conservation equations were solved using Patankar's Semi-Implicit Method for Pressure Linked Equations (SIMPLE). A left heart model was developed to examine diastolic function, and consisted of the left ventricle, left atrium, and pulmonary flow. The input functions for the model included the pulmonary driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions for validation. The inflow velocities through the mitral valve corresponded with clinical values (E-wave = 74.4 cm/s, A-wave = 43 cm/s, and E/A = 1.73). The pressure traces for the atrium and ventricle, and the appearance of the ventricular flow fields throughout filling, agreed with those observed in the heart. In addition, the atrial flow fields could be observed in this model and showed the conduit and pump functions that current theory suggests. The ability to examine atrial function in the present model is something not described previously in computational simulations of cardiac function.

Experimental investigation of the steady flow downstream of the St. Jude bileaflet heart valve: a comparison between laser Doppler velocimetry and particle image velocimetry techniques.

This study investigates turbulent flow, based on high Reynolds number, downstream of a prosthetic heart valve using both laser Doppler velocimetry (LDV) and particle image velocimetry (PIV). Until now, LDV has been the more commonly used tool in investigating the flow characteristics associated with mechanical heart valves. The LDV technique allows point by point velocity measurements and provides enough statistical information to quantify turbulent structure. The main drawback of this technique is the time consuming nature of the data acquisition process in order to assess an entire flow field area. Another technique now used in fluid dynamics studies is the PIV measurement technique. This technique allows spatial and temporal measurement of the entire flow field. Using this technique, the instantaneous and average velocity flow fields can be investigated for different positions. This paper presents a comparison of PIV two-dimensional measurements to LDV measurements, performed under steady flow conditions, for a measurement plane parallel to the leaflets of a St. Jude Medical (SJM) bileaflet valve. Comparisons of mean velocity obtained by the two techniques are in good agreement except for where there is instability in the flow. For second moment quantities the comparisons were less agreeable. This suggests that the PIV technique has sufficient temporal and spatial resolution to estimate mean velocity depending on the degree of instability in the flow and also provides sufficient images needed to duplicate mean flow but not for higher moment turbulence quantities such as maximum turbulent shear stress.

A comparison of the hinge and near-hinge flow fields of the St Jude medical hemodynamic plus and regent bileaflet mechanical heart valves.

OBJECTIVE: The most widely implanted prosthetic valves are the mechanical bileaflets, most of which have good forward flow hemodynamics. However, recent clinical experiences illustrate the importance of understanding the flow structures generated within the hinge. The purpose of this study was to evaluate the hinge-flow dynamics of two new variations of a 17-mm St Jude Medical bileaflet valve: the Hemodynamic Plus and the Regent (St Jude Medical, Inc, St Paul, Minn). METHODS: Clinical quality reproductions of the valves were manufactured with clear housings. Laser Doppler velocimetry velocity and turbulent shear stress measurements were conducted within the hinge and thumbnail regions of the valves. RESULTS: In the 17-mm Hemodynamic Plus hinge, a rotating flow structure developed in the inflow pocket during forward flow. During systole, velocities through the hinge pocket reached 0.70 m/s, and the turbulent shear stress reached 1000 dynes/cm(2). In the thumbnail, forward flow velocities ranged from 1.4 m/s to 1.7 m/s. In the 17-mm Regent hinge, a rotating flow structure partially developed in the inflow pocket during forward flow. During systole, velocities through the hinge pocket reached 0.75 m/s, and the turbulent shear stress reached 1300 dynes/cm(2). In the thumbnail, forward flow velocities ranged from 1.0 m/s to 1.3 m/s. CONCLUSIONS: The active leaflet motion through the St Jude Medical hinge creates a washout pattern that restricts the persistence of stagnation zones and thus may be a contributing factor to its successful clinical performance. The hinge and thumbnail flow dynamics of the 17-mm Regent valve are at least equivalent to, and possibly superior to, those of the 17-mm Hemodynamic Plus valve.