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Eur J Cardiothorac Surg 2006;29:1008-1013
© 2006 Elsevier Science NL

Turbulent stress measurements downstream of three bileaflet heart valve designs in pigs

Camilla Nyboe a , b , Jonas A. Funder a , b , Morten H. Smerup a , b , Hans Nygaard a , b , c , J. Michael Hasenkam a , b , *

a Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Skejby Sygehus, Brendstrupgaardsvej, 8200 Aarhus, Denmark
b Institute of Clinical Medicine, Aarhus University Hospital, Skejby Sygehus, Brendstrupgaardsvej, 8200 Aarhus, Denmark
c The Engineering College of Aarhus, Dalgas Avenue, 8000 Aarhus, Denmark

Received 7 December 2005; received in revised form 21 February 2006; accepted 3 March 2006.

* Corresponding author. Address: Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, Skejby Sygehus, Brendstrupgaardsvej, 8200 Aarhus N, Denmark. Tel.: +45 89495481; fax: +45 89496016. (Email: hasenkam{at}ki.au.dk).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Objective: Mechanical heart valves can cause thromboembolic complications, possibly due to abnormal flow patterns that produce turbulence downstream of the valve. The objective of this study was to investigate whether three different bileaflet valve designs would exhibit clinically relevant differences in downstream turbulent stresses. Methods: Three bileaflet mechanical heart valves (Medtronic Advantage®, CarboMedics© OrbisTM Universal and St. Jude Medical® Standard) were implanted into 19 female 90 kg pigs. Blood velocity was measured during open chest conditions in the cross sectional area downstream of the valves with 10 MHz ultrasonic probes connected to a modified Alfred® Pulsed Doppler equipment. As a measure of turbulence, Reynolds normal stress (RNS) was calculated at three different cardiac output ranges (3–4, 4.5–5.5, 6–7 L/min). Results: Data from 12 animals were obtained. RNS correlated with increasing cardiac outputs. The highest instantaneous RNS observed in these experiments was 47 N/m2, and the mean RNS taken spatially over the cross sectional area of the aorta during systole was between 3 N/m2 and 15 N/m2. In none of the cardiac output ranges RNS values exceeded the lower critical limit for erythrocyte or thrombocyte damage for any of the valve designs. Conclusions: Reynolds normal stress values were below 100 N/m2 for all three valve designs and the difference in design was not reflected in generation of turbulence. Hence, it is unlikely that any of the valve designs causes flow induced damage to platelets or erythrocytes.

Key Words: Animal model • Aortic valve • Hemodynamics • Ultrasound • Mechanical heart valve


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Implantation of mechanical heart valves is a routine treatment for valvular heart disease, which dramatically prolongs life expectancy of patients and increases their quality of life. Unfortunately, mechanical heart valves still have several shortcomings. Complications such as thromboembolisms, valve thrombosis, hemolysis, tissue overgrowth, calcification and thrombocytopenia remain problems to be solved. Thromboembolic complications account for 75% of the complications seen after implantation of a mechanical aortic valve, and even though treatment has improved, there is still an overall 10-year mortality of 30–55% [1,2].

Initiation of thromboembolic events is caused both by the artificial material of the valve and by the valves’ interference with normal blood flow [3]. Therefore, continuous evaluation and testing of mechanical heart valves in terms of material and design is needed to provide input to future valve designs which entail minimal biologic damage.

After implantation of a mechanical heart valve the blood flow is partially obstructed by the leaflets and the sewing ring of the new valve. This disturbs the flow and causes abnormal flow patterns such as turbulence. Several studies have associated the shear stresses produced by turbulence with pathophysiological changes such as platelet activation and damage [3–7] and hemolysis [4,8].

Whether the elements of the blood become activated and damaged by turbulent stresses depends both on the magnitude and the exposure time of the stresses. In healthy individuals with normal valves Reynolds normal stresses (RNS) have been measured to be below 4 N/m2 [9].

Studies have shown that the absolute minimal critical turbulent shear tress (TSS) level for altering platelet function is around 50 N/m2 for exposures times within normal physiological ranges [4,10]. For red blood cells (RBC) the critical level is around 600–800 N/m2 for any direct and immediate alteration [7,11,12]. However, it has been suggested that in the presence of a foreign material, RBCs and platelets can be damaged as well as activated at lower values [13].

The formation of TSS is thought to depend on cardiac output. When blood flow is increased, more blood passes through the obstructed area per time unit and therefore velocity increases and more turbulence is formed. Thus, TSS levels will be higher during exercise with high cardiac output, than during rest when cardiac output is low.

Several studies have tested different mechanical valves in order to identify optimal design and orientation to minimize interference with blood flow [9,13–16]. In order to minimize formation of TSS it is necessary to identify a valve design that interferes minimally with the blood flow. The Medtronic Advantage ® valve is a bileaflet valve that differentiates itself from formerly known bileaflet valves by having a larger central opening with a wider space between the two leaflets. The larger central opening is hypothesized to minimize obstruction of the blood flow and thus formation of TSS. In order to investigate whether this design optimization is reflected by less turbulence we aimed to compare turbulence levels with two widely used bileaflet valve prostheses in a porcine model.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 5. Conclusion
 References
 
2.1 Experimental animals
The study comprised of 19 female Danish Landrace/Yorkshire pigs all weighing approximately 90 kg. This size was chosen to mimic the aortic size of human beings and to ease the access to the aortic orifice [17]. According to our own unpublished experience and other previous studies, native annulus diameters were assumed to be approximately the same size and were therefore not measured in order to reduce preoperative stress on the animals [18]. Turbulence measurements were conducted right after weaning from the extracorporeal circulation and under open chest conditions. The animals were euthanized immediately after the measurements were performed. Experiments were conducted at the Institute of Clinical Medicine, Aarhus University Hospital and were performed according to the guidelines and with approval from the Inspectorate of Animal Experimentation under the Danish Ministry of Justice.

2.2 Study valves
All valves were factory labelled 21 mm bileaflet aortic mechanical heart valves (Medtronic Advantage ®, CarboMedics© OrbisTM Universal and St. Jude Medical® Standard). Since we have previously performed turbulence measurements on the SJM Standard and CM valves these were chosen as a reference for comparing with the MA valve. A fixed valve size was chosen because the pigs were of the same size and the results would therefore be easier to compare.

2.3 Experiments
General anesthesia was maintained by continuous infusion of ketamine/midazolam (Ketalar® 250 mg/Dormicum® 50 mg/h) and fentanyl (Haldid® 900 µg/h).

The heart was exposed through a midline sternotomy. ECC was established via cannulation of the aortic arch and the caval veins and a vent (Sarns®) was placed through an apical incision.

After cross clamping the ascending aorta one liter of a 4 °C crystalline cardioplegic solution (Kardioplex®) was given in the aortic root to induce cardiac arrest. The native aortic valve was removed and the mechanical valve was placed with one of the two large openings towards the non-coronary sinus. The placement of the valve is opposite recommendations on bileaflet valve placement and previous studies have shown a tendency towards higher turbulent shear stress values in this position [18,19]. Although the impact of valverotation is minor we chose this position as a marginal worst case scenario. During the operation cardioplegic solution (Kardioplex®) was given every 20 min directly into the coronary ostia. After aortic closure the cross clamp was removed and the heart was defibrillated and reperfused for approximately 60 min to allow stabilizing after the CPB. The aortic cannula and the two stage venous catheter were removed as was the left ventricular vent catheter. Micro-tip catheters (Millar Instruments Inc., Houston, TX) for ventricular pressure and aortic pressure measurements were put through the left ventricular apex and through the carotid artery. A 18 mm transit-time flow probe (Cardiomed, Norway) was placed around the pulmonary trunk to measure cardiac output. Turbulence measurements were performed as soon as the pigs had spontaneously stabilized hemodynamically in one of the required CO ranges. If CO was outside the selected range we interrupted the measurements and started the measurement series all over again for that CO range.

Further details in anesthesia and surgery has been described elsewhere [17].

2.4 Theoretical considerations
Turbulence is known as fluid motions that are random both in time and space. This means that to prove the existence of turbulence, simultaneous three-dimensional measurements of velocity fluctuations are theoretically needed. However, feasible methods of three-dimensional measurement of turbulence in vivo are not yet available. Thus, the existence of turbulence has to be disclosed otherwise.

Turbulent shear stress can be pictured as stresses acting tangentially on the surface of the elements of the blood. Since this cannot be measured directly the stresses acting normally on the blood Reynolds normal stress is measured instead. RNS is defined as


Formula

where Formula is the turbulent velocity component in any direction of the vessel and {rho} is the fluid density of blood (1060 kg/m3). Due to technical feasibilities, the measurements of the velocity component are done in the radial direction rather than in the axial direction. This can be done because the turbulent radial and axial velocity intensities are considered similar [20]. Thus, the radial velocity component is used to calculate RNS [13].

When RNS has been measured TSS can be estimated. Nygaard et al. [21] found in an in vitro study that the correlation factor between RNS and TSS is around 0.5. Thus TSS can be estimated as

Formula (1)

Results in this study will therefore be shown as RNS values rather than TSS values.

2.5 Data recording
The radial velocity components were measured by two 10 MHz ultrasonic probes. The probes were placed in a C-shaped PVC shell that was placed on top of the ascending aorta with the probes in –45° and +45° position (Fig. 1a).


Figure 1
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  		Fig. 1. Schematic drawing of a section of the aorta with the two positions of the C-shaped PVC shell placing the probes in the four different positions.

 
Each probe was used to record blood velocity in five fixed sample volumes through the diameter of the vessel. The size of the aorta was measured to find a compatible shell and to set the range gate delay (depths) of the pulsed ultrasound system. The correct position of the shell was ensured by marking 0° on the aorta. By rotating the shell from 0° to 45° the probes were positioned at 0° and 90° (Fig. 1b).

Seventeen different points of measurement were obtained by switching between the two probes, rotating the shell and changing the depth of the measurement (Fig. 1c).

Mean sample volumes were approximately 2 mm in diameter and 1 mm in axial length. The ultrasonic probes were connected to a modified pulsed Doppler ultrasound (PDU) velocimeter (ALFRED, Vingmed, Norway). The velocity measurements from the PDU as well as ECG, cardiac output, left ventricular pressure and aortic pressure were recorded on a datarecorder and digitized.

At least 20 heart cycles were recorded from each of the 17 measuring points to calculate turbulence components.

The animals were held hemodynamically stable and measurements were performed at three different cardiac outputs (3.5, 5 and 6.5 L/min, all ±0.5 L/min).

2.6 Data analysis
Data were analyzed by a specially developed LabView program (National Instruments, Austin, TX; Version 6.0i). The velocity signal was divided into eight time windows each lasting 50 ms. Each time window overlapped with the previous window by 25 ms. Thus measurements of the formation of RNS through 225 ms of peak systole were obtained. Acquisition of data was triggered by the rise of pressure in the left ventricle or by the ECG (Fig. 2 ).


Figure 2
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  		Fig. 2. The basic principles for calculating the development of turbulent stresses (RNS) are schematically shown in this figure. (A) The electrocardiogram was used as a time reference for signal analysis. (B) The velocity component from each of the 17 points recorded was computed in eight time windows (C). This was used to calculate RNS values in each of the eight time windows (D), so that RNS levels for the 17 points throughout the systole are obtained. A: anterior; P: posterior; L: left; R: right; t: time; u'(t): turbulent velocity component; w(t): time window.

 
2.7 Statistical analysis
Groups were compared by Bonferrani correlated t-test after ANOVA analysis at more than two groups.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 5. Conclusion
 References
 
Of the 19 animals in the study, the first two failed due to technical flaws in our measurement equipment. No subsequent technical difficulties were seen. Animal number three died from metabolic acidosis and four animals died from trying to obtain a high cardiac output under extreme hemodynamic conditions (experiments number 6, 7, 9 and 15). The pigs died from ventricular fibrillation or from bleeding. None of these conditions were related to the implanted valve which was normally functioning in all cases (verified by post-mortem examination). In total data from 12 animals were obtained, distributed evenly between the three valve types. Mean cross clamp time was 68.5 min (57–91) and reperfusion time was 61 min (37–150).

Measurements at each cardiac output level were performed within approximately 15 min.

The highest instantaneous RNS value observed in these experiments was 47 N/m2, which was observed at high cardiac output (Table 1 ). Mean spatial RNS values measured in the cross sectional area of the ascending aorta was between 3 and 15 N/m2 (Table 2 ). Thus, all valves produced levels of turbulence clearly below the stated critical threshold for blood cell damage. In the middle cardiac output range the Carbomedics valve exhibited statistically significant higher maximum RNS values than the other two valves (p = 0.02) and the St. Jude Medical valve statistically significant lower mean turbulence values than the Medtronic and Carbomedics valves (p = 0.007).


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  		Table 1. Maximum Reynolds normal stress values for the investigated mechanical heart valves
 

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  		Table 2. Mean Reynolds normal stress values for the investigated mechanical heart valve prostheses
 
Also in the high cardiac output range the St. Jude Medical valve exhibited statistically significant lower turbulence values than the other two valves (maximum turbulence, p = 0.03 and mean turbulence, p = 0.016). At low cardiac output there was no statistically significant difference between the three valves at neither mean nor maximum values (p > 0.05).

There was a general tendency towards higher RNS values with increasing cardiac output. This tendency was statistically significant and was seen at both maximum (p = 0.0033) and mean (p = 0.00037) values of RNS.

Since the formation of turbulence depends on stroke volume rather than cardiac output, this was calculated for all groups. There was no statistically significant difference in mean pulse or mean stroke volume between the three valve types at any of the cardiac output groups (p > 0.05).


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
5. Conclusion
 References
 
Measurement of turbulent stresses has been established as an important part of evaluation of new valve type designs. While the St. Jude Medical and the Carbomedics valves have been tested widely through the past years [9,13,14,22] turbulent stresses have so far not been measured in the newer Medtronic Advantage valve.

In this study we measured turbulent stresses over a wide physiologic range and found that none of the three valve designs exceeded the lowest critical threshold for thrombocyte and erythrocyte damage or activation. We did find a statistical significant difference in turbulence formation between the three valves especially in the high CO ranges. It was not possible to increase CO further than 7 L/min and therefore information on whether the turbulence curves of the three valves would converge at higher COs is not available. In the tested ranges of CO it is obvious that though statistically significant different there is no clinically relevant difference between the three valves in terms of turbulence formation.

Two main onsets of thromboembolic complications associated with mechanical heart valves are known. Firstly, turbulent shear stress above a critical level that causes damage to and direct activation of the formed elements of the blood. Secondly, the presence of foreign non-biological material in the blood stream induces activation of the platelets and causes them to aggregate. Some studies suggest that the presence of non-biological materials play the primary role in activation while other investigators believe that turbulence is the most important factor in the activation of platelets [3].

However, both turbulence and non-biological material is present at all times after implantation of a mechanical heart valve whereby both factors influence the elements of the blood at all times. Nygaard et al. [13] has suggested that the two factors actually intensify each other. Alteration of the influence of both non-biological material and turbulent shear stresses in addition to increased exposure times due to the vortex phenomenon and continuous passage through the valve suggests that the critical limit for damage or activation of platelets and RBCs may be lower than the value needed for damage from turbulence alone.

The relation between exposure time and formation of turbulence has been investigated by Brown et al. who found a linear correlation between exposure time and damage to the platelets. Acid phosphatase release doubled after one passage through the shear stress area. This indicates that the damage and activation of the thrombocytes accumulates by every passage of the valve [23]. The fact, that there is a cumulative damage and activation caused by shear stresses could mean that the thrombocytes are altered even though the critical lower threshold for damage is not reached.

Furthermore, a vortex is created downstream of the valve due to its obstruction of the blood flow. Some of the blood re-enters into this vortex and into the area of high TSS values. In this way blood that has been exposed to TSS once and is containing already activated and damaged platelets and RBCs, re-enters the area where they are affected by high levels of TSS several times [10,24]. The concept of a vortex distal to the valve implies that the exposure times and cumulative stress affections might be increased [10]. This means that even though turbulent shear stress values are lower than the critical threshold level alteration may still occur.

RNS values measured preoperatively in human beings by Nygaard et al. [9] were below 4 N/m2. The mean RNS values for all three valve types in this study are similar to the mean RNS values measured in native valves in 17 pigs by Hasenkam et al. [14]. Hasenkam et al. also measured RNS values in six pigs after cardioplegia but without implantation of a valve. Here the means of mean RNS values were 18 N/m2 (SD 12.9) with maximum values reaching as high as 57 N/m2. The mean cardiac output was 5 L/min (SD 1.8). Comparing the RNS values of the present study to those for native valves before and after cardioplegia in the study by Hasenkam et al. show that the RNS values in the three valve types in our study is within normal physiological ranges in pigs.

Nygaard et al. tested the St. Jude Medical valve in nine human beings and measured spatial mean RNS values between 4 and 13 N/m2. They furthermore tested the Carbomedics valve in six human beings and found spatial mean RNS values between 4 and 18 N/m2 [14]. In comparison we found RNS values for the St. Jude Medical valve to be between 6 and 8 N/m2 and Carbomedics values to be between 6 and 13 N/m2 depending on cardiac output. Other pig studies also show values that are similar to those found in our study [19].

4.1 Study limitations
In vitro studies have shown higher turbulent stresses downstream of mechanical heart valves than in vivo [13]. This can be due to difference in distance between the measuring points and the valve. When measurements of velocity are performed in vivo it is not possible to keep the transducers as close to the valve as it is in vitro. RNS values decrease dramatically with distance from the valve which suggests that values measured in vivo are underestimated [13]. Also, turbulence measurements in vitro are performed by measuring TSS directly instead of estimating them from RNS values which could result in TSS values that are more inaccurate than those measured in vitro. Furthermore, keeping the animals hemodynamically stable for the time required to perform the measurements was difficult. Reperforming measurements every time CO was outside the set ranges, even though only for a very short period of time, led to long hours post CPB. The stress on the hearts was in some cases too much and not all measurements were performed. Another limit of the animal studies was that the highest possible cardiac output to reach immediately after heart surgery was approximately 7 L/min. However, a porcine model was chosen in this project to mirror the anatomic and physiologic conditions of the human heart as close as possible; especially during increasing work loads on the heart mimicking exercise.


   5. Conclusion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusion
References
 
In this study we found that at low cardiac output all three valve types had low mean RNS values comparable to those seen in pigs with native valves. When we increased cardiac output we observed that the mean RNS values of all three valve types increased. Although statistically significant different, none of the three valves exhibited RNS values exceeding the critical limit for immediate blood cell damage at any of the cardiac outputs measured. In conclusion, all three valve types have low turbulent shear stress values that do not theoretically cause any direct or immediate alteration of the formed elements of the blood. Therefore, the difference in the turbulent stresses between the three valves has no clinically relevance.


   Acknowledgments
 
The authors wish to thank Tanja Thomsen for her time and expertise in performing these experiments and Niels Trolle Andersen for statistical consult. The authors also wish to thank The Danish Research Agency, The OTICON Foundation, Helga and Peter Kornings Foundation and Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Foundation for their generous financial support. Medtronic Inc. kindly supported the project by providing the Medtronic Advantage valve and by partial payment of the experimental costs.


   Footnotes
 
{star} Poster presentation of the 54th Annual Meeting of Scandinavian Association for Thoracic Surgery, Bergen, Norway, 2005.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 

  1. Edmunds Jr. LH. Thrombotic and bleeding complications of prosthetic heart valves. Ann Thorac Surg 1987;44(4):430-445.[Abstract]
  2. Edmunds Jr. LH, Mckinlay S, Anderson JM, Callahan TH, Chesebro JH, Geiser EA, Makanani DM, McIntire LV, Meeker WQ, Naughton GK, Panza JA, Schoen FJ, Didisheim P. Directions for improvement of substitute heart valves: National Heart, Lung, and Blood Institute's Working Group report on heart valves. J Biomed Mater Res 1997;38(3):263-266.[CrossRef][Medline]
  3. Hung TC, Hochmuth RM, Joist JH, Sutera SP. Shear-induced aggregation and lysis of platelets. Trans Am Soc Artif Intern Organs 1976;22:285-291.[Medline]
  4. Schmid-Schonbein H, Born GV, Richardson PD, Cusack N, Rieger H, Forst R, Rohling-Winkel I, Blasberg P, Wehmeyer A. Rheology of thrombotic processes in flow: the interaction of erythrocytes and thrombocytes subjected to high flow forces. Biorheology 1981;18(3–6):415-444.[Medline]
  5. Anderson GH, Hellums JD, Moake JL, Alfrey Jr. CP. Platelet lysis and aggregation in shear fields. Blood Cells 1978;4(3):499-511.[Medline]
  6. Anderson GH, Hellums JD, Moake J, Alfrey Jr. CP. Platelet response to shear stress: changes in serotonin uptake, serotonin release, and ADP induced aggregation. Thromb Res 1978;13(6):1039-1047.[CrossRef][Medline]
  7. Grigioni M, Daniele C, D’Avenio G, Barbaro V. Evaluation of the surface-averaged load exerted on a blood element by the Reynolds shear stress field provided by artificial cardiovascular devices. J Biomech 2002;35(12):1613-1622.[Medline]
  8. Mohandas N, Hochmuth RM, Spaeth EE. Adhesion of red cells to foreign surfaces in the presence of flow. J Biomed Mater Res 1974;8(2):119-136.[CrossRef][Medline]
  9. Nygaard H, Paulsen PK, Hasenkam JM, Kromann-Hansen O, Pedersen EM, Rovsing PE. Quantitation of the turbulent stress distribution downstream of normal, diseased and artificial aortic valves in humans. Eur J Cardiothorac Surg 1992;6(11):609-617.[Abstract]
  10. Wurzinger LJ, Schmid-Schonbein H. The role of fluid dynamics in triggering and amplifying hemostatic reactions in thrombogenesis. Monogr Atheroscler 1990;15:215-226.[Medline]
  11. Grigioni M, Daniele C, D’Avenio G, Barbaro V. A discussion on the threshold limit for hemolysis related to Reynolds shear stress. J Biomech 1999;32(10):1107-1112.[Medline]
  12. Lu PC, Lai HC, Liu JS. A reevaluation and discussion on the threshold limit for hemolysis in a turbulent shear flow. J Biomech 2001;34(10):1361-1364.[Medline]
  13. Nygaard H, Paulsen PK, Hasenkam JM, Pedersen EM, Rovsing PE. Turbulent stresses downstream of three mechanical aortic valve prostheses in human beings. J Thorac Cardiovasc Surg 1994;107(2):438-446.[Abstract/Free Full Text]
  14. Hasenkam JM, Pedersen EM, Østergaard JH, Nygaard H, Paulsen PK, Johannsen G, Schurizek BA. Velocity fields and turbulent stresses downstream of biological and mechanical aortic valve prostheses implanted in pigs. Cardiovasc Res 1988;22(7):472-483.[Medline]
  15. Nygaard H, Giersiepen M, Hasenkam JM, Reul H, Paulsen PK, Rovsing PE, Westphal D. Two-dimensional color-mapping of turbulent shear stress distribution downstream of two aortic bioprosthetic valves in vitro. J Biomech 1992;25(4):429-440.[Medline]
  16. Giersiepen M, Krause U, Knott E, Reul H, Rau G. Velocity and shear stress distribution downstream of mechanical heart valves in pulsatile flow. Int J Artif Organs 1989;12(4):261-269.[Medline]
  17. Hasenkam JM, Ostergaard JH, Pedersen EM, Paulsen PK, Nygaard H, Schurizek BA, Johannsen G. A model for acute haemodynamic studies in the ascending aorta in pigs. Cardiovasc Res 1988;22(7):464-471.[Medline]
  18. Kleine P, Kleisus AA, Scherer M, Abdel-Rahman U, Moritz A. Initial in vivo results of the new Medtronic Advantage(TM) bileaflet valve in aortic position and comparison to the SJM. Cardiovasc Surg 2002;10(5):494-499.[CrossRef][Medline]
  19. Kleine P, Perthel M, Nygaard H, Hansen SB, Paulsen PK, Riis C, Laas J. Medtronic Hall versus St. Jude Medical mechanical aortic valve: downstream turbulences with respect to rotation in pigs. J Heart Valve Dis 1998;7(5):548-555.[Medline]
  20. Hinze JO. Turbulence. New York, NY: McGraw-Hill; 1975p. 2.
  21. Nygaard H, Giersiepen M, Hasenkam JM, Westphal D, Paulsen PK, Reul H. Estimation of turbulent shear stresses in pulsatile flow immediately downstream of two artificial aortic valves in vitro. J Biomech 1990;23(12):1231-1238.[Medline]
  22. Kleine P, Perthel M, Hasenkam JM, Nygaard H, Hansen SB, Laas J. Downstream turbulence and high intensity transient signals (HITS) following aortic valve replacement with Medtronic Hall or St. Jude Medical valve substitutes. Eur J Cardiothorac Surg 2000;17(1):20-24.[Abstract/Free Full Text]
  23. Brown III CH, Lemuth RF, Hellums JD, Leverett LB, Alfrey CP. Response of human platelets to sheer stress. Trans Am Soc Artif Intern Organs 1975;21:35-39.[Medline]
  24. Bluestein D, Li YM, Krukenkamp IB. Free emboli formation in the wake of bi-leaflet mechanical heart valves and the effects of implantation techniques. J Biomech 2002;35(12):1533-1540.[Medline]




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