JTCS Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Friedhelm Beyersdorf
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Handke, M.
Right arrow Articles by Geibel, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Handke, M.
Right arrow Articles by Geibel, A.
Related Collections
Right arrow Valve disease

J Thorac Cardiovasc Surg 2003;125:1412-1419
© 2003 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

In vivo analysis of aortic valve dynamics by transesophageal 3-dimensional echocardiography with high temporal resolution

Michael Handke, MDa, Gudrun Heinrichs, Dipl-Inga, Friedhelm Beyersdorf, MDb, Manfred Olschewski, MScc, Christoph Bode, MDa, Annette Geibel, MDa

From the Departments of Cardiology and Angiology, Cardiovascular Surgery, and Medical Biometrics, Albert-Ludwigs-University, Freiburg, Germany.

Supported by the Deutsche Forschungsgemeinschaft (German Research Foundation) and the Center for Clinical Research II at the Albert-Ludwigs-University Freiburg.

Received for publication June 5, 2002. Revisions requested Aug 1, 2002; revisions received Sept. 18, 2002. Accepted for publication Sept. 24, 2002. Address for reprints: Dr Michael Handke, Department of Cardiology and Angiology, Albert-Ludwigs University, Hugstetter-Str 55, Freiburg 79106, Germany (E-mail: handke{at}mm31.ukl.uni-freiburg.de).


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 
Objectives: Knowledge of aortic valve function has been obtained from experimental studies. The aim of the present study was to investigate characteristics of aortic valve motion in humans.
Methods: Fifty-six patients were studied: 19 with normal valve and good systolic left ventricular function (Group NL), 12 with normal valve and reduced left ventricular function (Group CMP), and 25 with aortic stenosis and good left ventricular function (Group AS). The frame rate was doubled (50 Hz) compared with previous 3-dimensional systems. A mean of 38 ± 9 images were acquired per cardiac cycle, with 14 ± 4 images during the systole. The changes in shape and orifice area were analyzed over time.
Results: With normal valves, valve movement proceeded in 3 phases: rapid opening, slow closing, rapid closing. Stenotic valves showed a slower opening and closing movement. The times to maximum opening in Groups NL, CMP, AS were 76 ± 30, 88 ± 18 (P = .06), and 130 ± 29 (P < .01) ms, respectively. It was inversely correlated to the maximum orifice area (r = -0.59, P < .001). The opening velocities in Groups NL, CMP, AS were 42 ± 23, 28 ± 9 (P < .05), and 5 ± 2 (P < .001) cm2/s, respectively. There was a close correlation between the opening velocity and the maximum orifice area (r = 0.87, P < .001). Slow valve closings occurred at a velocity of 8.0 ± 5.2, 5.3 ± 2.0 (P = .21), 2.8 ± 1.1 (P < .01) cm2/s, respectively, and rapid closings in Groups NL and CMP at 50 ± 23, 29 ± 8 (P < .01) cm2/s. The results show good agreement with experimental data.
Conclusion: Rapid aortic valve movement can be recorded by 3-dimensional echocardiography and analyzed quantitatively. Time and velocity indices of valve dynamics are influenced by valvular and myocardial factors. A comparable in vivo analysis is not possible with any other imaging procedure.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 References
 



View larger version (158K):
[in this window]
[in a new window]
  		Dr Handke

 
Depiction of aortic valve movement in vivo is a challenge even to modern imaging procedures due to the rapid movement of the valvular structures. Our knowledge of the opening and closing behavior of the valve were thus obtained primarily by experimental studies. Initial studies have been performed with pulsatile models.Go Go 1-5 Studies leading further have been performed on the beating heart in animal models: use of contrast dyes or labeling the valve with radiopaque markers made X-ray depiction of the valve and its function possible.Go Go 6-11 Direct imaging of valve function in animal models was achieved in endoscopic cinematographic studies.Go Go 12-15 Recent experimental approaches are based on electromagnetic induction or stereo-photogrammetry.Go Go 16-18 In humans, the systolic movement pattern can be recorded by means of M-mode echocardiography.Go Go 19-21 Since, in this procedure, only two of three cusps are visible, no information can be obtained on the shape of the valve or area changes. The precision of 2D echocardiography is limited, as the valve opening can often not be exactly recorded during the entire systole, due to the axial movement of the valve apparatus and the movement of the cusps.Go 22

3-dimensional (3D) echocardiography has the potential for thorough analysis of cardiac anatomy and function in vivo.Go Go 23,24 Smaller cardiac structures do, however, set particularly high requirements for spatial and temporal resolution.Go Go 25-28 3D studies on the aortic valve thus far addressed the depiction of morphology and quantification of the maximum orifice area.Go Go Go 25,29-31 3D imaging of normal or pathological aortic valve movement has hardly been examined, as the low temporal resolution has been a limiting factor. The objectives of this study were (1) to examine the extent to which a new technique with higher frame rates would make it possible to record aortic valve movement; (2) to analyze physiological and pathological movement patterns in the aortic valve and compare our results with those of experimental studies.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 References
 
Study population
Fifty-six patients were examined (20 women, 36 men, mean age 62 ± 14 years). The study population consisted of 3 groups: 19 patients (Group NL) had normal systolic left ventricular (LV) function (mean ejection fraction = 59 ± 5%) and a morphologically unremarkable aortic valve. Transesophageal echocardiography (TEE) was indicated in the Group NL patients in search of a source of cardiac embolism. Group NL had the youngest patients, with a mean age of 48 ± 10 years. Twelve consecutive patients with cardiomyopathy (Group CMP) were examined prior to surgical reduction of the left ventricle. These patients had high-grade reduction of LV function (ejection fraction in 3D echocardiography 24 ± 6%Go 32) with underlying ischemic or dilatative cardiomyopathy. The mean age of the patients in Group CMP was 68 ± 11 years. Twenty-five consecutive patients with aortic stenosis (Group AS) underwent TEE as part of this study. These patients had moderate to severe aortic stenosis (orifice area determined by continuity equation 0.77 ± 0.18 cm2) and normal systolic LV function (mean ejection fraction = 57 ± 5%). The mean age of the patients in Group AS was 71 ± 9 years. None of the patients in Groups NL and CMP had aortic insufficiency > grade I. Two of the patients in Group AS had aortic insufficiency grade I-II, 1 patient grade II, and 1 patient grade II-III. The maximum orifice area determined by 3D echocardiography was 2.70 ± 0.63 cm2 (Group NL), 2.38 ± 0.77 cm2 (Group CMP, P = .09 vs NL), and 0.67 ± 0.24 cm2 (Group AS, P < .001 vs Group NL, P < .001 vs Group CMP). All patients were in sinus rhythm. The study was approved by the local ethics committee. The individual examinations were performed after the patient had granted informed consent.

Transesophageal 3D echocardiography
A 5-MHz multiplane probe (Toshiba SSA 380A) was used for TEE. Controlled by the 3D unit (TomTec EchoScanSystem, TomTec Inc, Unterschleißheim), 90 rotation levels were recorded at intervals of 2 degrees. Data acquisition was triggered by electro cardiogram and respiration. Acquisitions were performed at a frame rate of 50 Hz.

3D data reconstruction and analysis
3D data analysis was made with the TomTec EchoScan 4.1 Program. Within a 3D data set, an "en face" view from the aorta ascendens to the aortic valve was selected. Threshold and transparency values were adjusted based on the gray-value information of the 3D data set. Finally, by application of rendering algorithms, the volume-rendered image was reconstructed and the orifice area planimetered. The changes in the aortic valve during the systole was depicted in all image phases (Figure 1, A) and the orifice area planimetered in each phase. The change in orifice area was depicted graphically in an area-time diagram (Figure 1Go, B). The following time and velocity indices were calculated: time to maximum opening, opening velocity, time for slow valve closure, slow valve closure velocity, time for rapid valve closure, and rapid valve closure velocity (Figure 2).



View larger version (52K):
[in this window]
[in a new window]
  		Fig. 1. A, Dynamic changes in normal aortic valve. During the systole, the aortic orifice changes not only its size, but also its shape. In this example, the orifice takes an "intermediate" (between round and triangular) shape at the time of maximum opening. Later, there is a slow closing movement, and the form becomes clearly triangular. B, Corresponding area-time diagram. AOA, aortic orifice area.

 


View larger version (16K):
[in this window]
[in a new window]
  		Fig. 2. Determination of the time and velocity indices based on the area-time-diagram. AOA, aortic orifice area; A1, maximum orifice area; A2, difference between maximum orifice area and orifice area at the end of the slow closing movement; A3, orifice area at the end of the slow closing movement; T1, time to maximum valve opening; T2, time for the slow closing movement; T3, time for the rapid closing movement; V1, velocity of rapid valve opening; V2, velocity of slow closing movement; V3, velocity of rapid closing movement.

 
Statistical analysis
The SPSS 10.0 Software Package was used for statistical data analysis. Grouped values were recorded as mean ± standard deviation. Paired data were compared using the Wilcoxon signed-ranks test, unpaired data with the Kruskal-Wallis test, and the Mann-Whitney U test. Differences of P < .05 were considered statistically significant. Correlations between methods were determined by regression analysis. For determination of intra-/interobserver variabilities, the mean difference of the measurements was calculated.Go 33


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 References
 
Adequate imaging of the aortic valve could be achieved in all patients with normal aortic valve and good LV function (Group NL, n = 19) as well as in all patients with normal valve and cardiomyopathy (Group CMP, n = 12). Among the patients with aortic stenosis (Group AS, n = 25), 9 were excluded from further analysis because the valve orifice in the 3D data set could not be reliably imaged in all systolic phases. This affected especially valves with marked calcification.

Temporal resolution of valve movement
A mean of 38 ± 9 (21 to 62) images were recorded per cardiac cycle, and a mean of 14 ± 4 (6 to 22) images were recorded during the systole.

Systolic changes in the shape of the aortic orifice
During the systole, the aortic orifice changes not only in size but also in shape. It may be stellate, circular, triangular, or an intermediate form of these three variants (Figure 3). In normal valves (Group NL, Group CMP) at the time of maximum opening, 9 valves were round, 10 were triangular, and 12 took on an intermediate form.



View larger version (43K):
[in this window]
[in a new window]
  		Fig. 3. Typical forms of aortic orifice during systolic movement: stellate, round, intermediate, triangular. The drawings are based on recorded data.

 
After the initial rapid opening, the valve begins a slow closing movement in the early systole. The shape of the valve changes usually toward a triangular morphology. At the end systole, there is a rapid closure movement until the valve is completely closed.

In the presence of AS, the initial opening movement is slower; the maximum opening of the valve is attained later in the systole than in normal valves (Figure 4). In the closing movement of the valve, it is frequently not possible to clearly differentiate between slow and rapid phase.



View larger version (50K):
[in this window]
[in a new window]
  		Fig. 4. A, Dynamic changes in a stenosed aortic valve during the systole. The valve is functionally bicuspid; left- and right coronary cusps are fused. The opening movement of the valve is lethargic compared with a normal valve. B, Corresponding area-time diagram. AOA, aortic orifice area.

 
Figure 5 shows the area-time curves of three patients in Groups NL, CMP, and AS in comparison.



View larger version (18K):
[in this window]
[in a new window]
  		Fig. 5. Imaging of the systolic motion pattern of the aortic valve in 3 patients of the study groups NL, CMP, and AS. AOA, aortic orifice area; NL, normal; CMP, cardiomyopathy; AS, aortic stenosis.

 
Determination of time and velocity indices
1. Phase of valve opening
Time to maximum opening of the aortic valve. In Group NL, the time to attaining maximum opening was a mean 76 ± 30 (40 to 160) ms; in Group CMP, 88 ± 18 (60 to 120) ms, P = .06 (Figure 6, A). In Group AS, the time to maximum opening was significantly longer at 130 ± 29 (80 to 180) ms, P < .001 vs Group NL, P < .01 vs Group CMP. The time to reaching maximum valve opening showed a highly-significant inverse correlation to the opening area (r = -0.59, P < .001) (Figure 6Go, B).



View larger version (14K):
[in this window]
[in a new window]
  		Fig. 6. A, Time to maximum valve opening in the 3 patient groups. Stenosed valves required significantly more time to maximum opening of the valve. B, Relationship between maximum orifice area and time to maximum opening. There was a highly significantly inverse correlation between the two parameters. AOA, aortic orifice area; CMP, cardiomyopathy, AS, aortic stenosis. **P < .01.

 
Valve opening velocity. The opening velocity in Group NL was higher (42 ± 23 cm2/s) than in Group CMP (28 ± 9 cm2/s, P < .05). In Group AS, it was significantly lower than in the other 2 groups (5 ± 2 cm2/s, P < 0.001 vs Group NL, P < .001 vs Group CMP) (Figure 7, A). Figure 7Go, B shows the close relationship between the velocity of valve opening and the maximum orifice area (r = 0.87, P < .001). The smaller the orifice, the lower the velocity of valve opening. With an opening area >2 cm2 the mean opening velocity was 40 ± 20 cm2/s; in aortic stenosis with <1 cm2 the mean velocity was only 5 ± 2 cm2/s.



View larger version (12K):
[in this window]
[in a new window]
  		Fig. 7. A, Comparison of valve opening velocities in the 3 groups examined. In the patients with reduced left ventricular function, the valve opened more slowly. Stenosed aortic valves opened slowest. B, Relationship between maximum orifice area and opening velocity. A close and highly significant correlation is found between the two parameters. AOA, aortic orifice area; CMP, cardiomyopathy; AS, aortic stenosis. *P < .05; **P < .001.

 
Valve opening in aortic stenosis: Relationship to the transvalvular gradient. The maximum transvalvular gradient in Group AS was 40 to 130 mm Hg (mean 75 ± 23 mm Hg). Figure 8 shows the relationship between the transvalvular gradient and the time to maximum valve opening. There was a significant correlation with r = 0.62, P = .01. Stenoses with high gradients required more time to maximum structural opening.



View larger version (18K):
[in this window]
[in a new window]
  		Fig. 8. Relationship between the maximum Doppler gradient and the time to maximum structural opening of the valve in patients with aortic stenosis.

 
The gradient and the valve opening velocity showed an inverse correlation (r = -0.31, P = .25). Valves with a high gradient thus had a tendency to open with lower velocity.

2. Phase of valve closing
Slow valve closure. The velocity of slow valve closing in Group NL was 8.0 ± 5.2 cm2/s; in Group CMP 5.3 ± 2.0 cm2/s, P = 0.21. In Group AS, it was significantly lower than in the other two groups (2.8 ± 1.1 cm2/s, P < .001 vs Group NL, P < 0.01 vs Group CMP). In Group AS, the time from maximum opening to complete closure was used to calculate the time, as differentiation of slow and rapid phase could usually not be made in the presence of AS. At the end of the slow valve closure, the valve opening in Group NL was 68 ± 12%, in Group CMP 70 ± 7% (P = .89) of the maximum orifice area.

Rapid valve closure. The time for rapid valve closing in Group NL was 42 ± 16; in Group CMP 60 ± 12 ms, P < .01. The rapid closing velocity in Group NL was 50 ± 23 cm2/s; in Group CMP 29 ± 8 cm2/s, P < .01.

Variability of planimetric measurements. To determine intra- and interobserver variability, 15 patients were independently quantified by 2 examiners. Five patients were randomly selected from each subgroup for this purpose. The mean difference ± SD between the measurements was determined and tested for difference from 0. The intraobserver variability was -0.02 ± 0.32 cm2; the difference between the measurements was not significant (P = .65). The interobserver variability was 0.04 ± 0.34 cm2; the difference was statistically significant (P < .01). The correlation coefficients were r = 0.95, P < .01 for intraobserver variability and r = 0.94, P < .01 for interobserver variability.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 References
 
As the surgical treatment of aortic valve disease has become more sophisticated, the need has grown for a better understanding of the aortic valve's geometry and function. Valve-preserving surgery and the design of valve prostheses both require description and analysis of the dynamic changes the aortic valve undergoes during the cardiac cycle. Aortic valve function has been investigated in numerous experimental studies so far.Go Go 1-18 In addition, powerful computer systems now make possible theoretic analysis using finite element models.Go Go 34,35 On the other hand, there still is no imaging procedure that makes possible a thorough description of aortic valve dynamics for clinical application.

In this study, we undertook for the first time a thorough in vivo description and analysis of systolic aortic valve movement. 3D echocardiography enabled (1) spatial imaging of valve morphology, (2) quantitative determination of the orifice area, and (3) a relatively high-resolution recording of the changes over time. In addition to examination of normal valve motion, we were able to demonstrate that dynamics are influenced by both myocardial and valvular changes.

Temporal resolution of valve movement
Compared with previous 3D systems we were able to attain temporal imaging at 50 Hz, which is about double the usual imaging (25 to 30 Hz, Real-Time 3D Systems, about 20 Hz). Thus, up to 22 images were attained systolic. Arsenault and colleagues recorded up to 16 images in their 2D study of movement patterns in aortic stenosis (video frequency 33 Hz).Go 22 Other procedures like high-speed cineradiography with radiopaque markers,Go 11 endoscopy,Go Go 12-15 or stereo-photogrammetryGo 18 can only be applied in experimental studies.

Normal aortic valve dynamics: Comparison with experimental studies
Our results can be compared mainly to experimental studies to date. Good qualitative and quantitative agreement was found. The shape of the aortic orifice varies and changes during the systole. As described by several authors, the shape may be stellate, circular, or triangular or it may take on an intermediate form.Go Go Go Go 5,8,9,14 Experimental data indicate that the shape depends on the flow and the elasticity of the aortic root.Go Go 9,36

The present study shows that the movement of the normal aortic valve can be subdivided into 3 phases: (1) rapid opening with early attainment of maximum opening; (2) slow valve closure starting in the early systole; (3) rapid end-systolic valve closure. It is noteworthy that the increase and decrease in orifice area apparently occurs differently than the increase and decrease of the transvalvular blood flow: experimental studies have shown that (1) valve opening begins even before the onset of blood flow due to expansion of the aortic root; (2) the maximum opening is attained prior to maximum flow; (3) the (slow) valve closure begins while the flow is still increasing; (4) rapid valve closure begins at the end of the forward flow across the valve.Go Go Go 9,15,17

With respect to time and velocity indices of valve movement, we found good agreement with data of a dog model published recently.Go 17 Our measurements revealed a mean time of 76 ms to maximum valve opening, Higashidate and colleaguesGo 17 found a time of 57 ms. It must be noted that a slight systematic overestimation results in our calculation: a time of 20 ms (at 50-Hz imaging frequency) is assumed for the phase from the last 3D image with closed to the first image with opened valve, while it is actually only between 1 and 20 ms. For the opening velocity and slow and rapid closure velocity, we found values of 42, 8, and 50 cm2/s and thus also good agreement with the values reported by Higashidate and colleaguesGo 17 (34, 4, 29 cm2/s).

De Paulis and colleagues found shorter times for valve opening and closing in humans in a study published recently.Go 21 They did not examine the movement characteristics of the aortic valve on the basis of area changes, but 1-dimensionally using M-mode echocardiography.

Influence of reduced LV function and aortic stenosis on valve dynamics
The velocity of the valve opening is influenced by both valvular changes and by changes in LV contractility. Our data show that the valve opens more slowly and attains a smaller orifice area in the presence of reduced LV contractility. Experimental studies have shown that higher stroke volumes lead to more rapid opening velocities and that there is a correlation between the stroke volume and the maximum orifice area.Go Go 17,19

Stenosed valves show very low opening velocities, even in the presence of good LV contractility. The stroke volume is also reduced in high-grade stenosis, but the reduced mobility of the valve leaflets and reduced elasticity of the aortic root play the more decisive role here.Go 22 In the entire collective, there was a close relationship between valve opening velocity and maximum orifice area. With r = 0.87, we found the same correlation as Arsenault's group (r = 0.86) in their 2D echocardiographic study.Go 22

Stenosed valves not only open more slowly, they also attain their maximum orifice later than normal valves. The time to maximum opening was significantly longer in patients with aortic stenosis than in patients with normal valves, and there was an inverse correlation with the maximum orifice area (r = -0.59, P < .001). In patients with aortic stenosis, there was a significant positive correlation between the maximum transvalvular gradient and the time to maximum opening (r = 0.62, P = .01). Thus, the time to maximum opening seems to represent the rigidity of the valve. With increasing immobility of the cusps, the valve requires a longer time to structural opening, and stronger forces, as defined by the pressure gradient, are needed to make it open. Despite delayed opening, however, the maximum orifice was attained in most of the patients with aortic stenosis in the first half of the systole. Contrary to this, Badano and colleagues had reported that the maximum hemodynamically effective opening in aortic stenosis is not attained until the late systole.Go 37 These differences may possibly indicate that anatomically and hemodynamically effective opening in aortic stenosis have different temporal courses: the effective area is still increasing when the anatomical area has already begun to decrease.

Limitations
In spite of the encouraging results, the limitations of current 3D technology must be taken into account. Further improvement in temporal resolution is still needed for more detailed recording of movement patterns. This applies especially for valve opening, which is brief and occurs at high speed. It is also recorded in only a few images with the technique presented here. Use of ultrasound raw data will make image frequencies of more than 100 Hz possible in the future.Go 38 In the area of structural resolution, the current technique can also only be considered as preliminary. Reconstruction from multiple 2D slices has the basic problem of being susceptible to movement artefacts and variations in heart rate or respiratory patterns.

Perspectives for the future and clinical implications
3D echocardiography will enable more detailed studies of the physiology and pathology of cardiac valves. Detailed analysis of aortic valve motion has potential in several clinical conditions:

  1. As Lester and colleagues recently showed in their Doppler echocardiographic study, the rate of the area change is important in the prediction of aortic stenosis progression.Go 39 This could be more precisely visualized by 3D echocardiography.
  2. Geometry and dynamic changes of aortic bioprostheses have been studied for the most part experimentally.Go Go 40,41 3D echocardiography could make comparable studies in humans possible.
  3. In recent studies using M-mode echocardiography, Leyh and colleagues and De Paulis and coworkers showed the influence of various surgical techniques on the opening and closing movement after valve-preserving surgery.Go Go 20,21 With 3D echocardiography, more precise recording of geometry and function might be possible.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
References
 
3D echocardiography with high temporal resolution enables a detailed analysis of aortic valve dynamics. This is influenced by valvular and myocardial factors. Comparable in vivo analysis is not presently possible with any other imaging procedure.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 

  1. Kelley RR, Goodale F, Castleman B. The dynamics of rheumatic and calcific aortic valve disease. Circulation. 1960;22:365-75.[Free Full Text]
  2. Bellhouse BJ, Talbot L. The fluid mechanics of the aortic valve. J Fluid Mech. 1969;35:721-35.
  3. Bellhouse B, Bellhouse F. Fluid mechanics of model normal and stenosed aortic valves. Circ Res. 1969;25:693-704.
  4. Van Steenhoven AA, van Dongen MEH. Model studies of the closing behaviour of the aortic valve. J Fluid Mech. 1979;90:21-32.
  5. Stein PD, Munter WA. New functional concept of valvular mechanics in normal and diseased aortic valves. Circulation. 1971;44:101-8.[Abstract/Free Full Text]
  6. Von Bernuth G, Tsakiris AG, Wood EH. Effects of variations in the strength of left ventricular contraction on aortic valve closure in the dog. Circ Res. 1971;28:705-16.[Abstract/Free Full Text]
  7. Mercer JL. The movements of the dog's aortic valve studied by high speed cineangiography. Br J Radiol. 1973;46:344-49.[Abstract/Free Full Text]
  8. Thubrikar M, Harry R, Nolan SP. Normal aortic valve function in dogs. Am J Cardiol. 1977;40:563-8.[Medline]
  9. Thubrikar M, Bosher LP, Nolan SP. The mechanism of opening of the aortic valve. J Thorac Cardiovasc Surg. 1979;77:863-70.[Abstract]
  10. Thubrikar M, Piepgrass WC, Shaner TW, Nolan SP. The design of the normal aortic valve. Am J Physiol. 1981;241:H795-801.
  11. Thubrikar MJ, Heckman JL, Nolan SP. High speed cine-radiographic study of aortic valve leaflet motion. J Heart Valve Dis. 1993;2:653-61.[Medline]
  12. Hider CF, Taylor DEM, Wade JD. Action of the mitral and aortic valves in vivo studied by endoscopic cinephotography. Quart J Exper Physiol. 1966;51:372-9.
  13. Brooks DH, Whiteford J, Berk AD, Bahnson HT. Cinematographic studies of the interior of the actively contracting heart. Ann Surg. 1968;167:786-90.[Medline]
  14. Padula RT, Cowan GSM, Camishion RC. Photographic analysis of the active and passive components of cardiac valvular action. J Thorac Cardiovasc Surg. 1968;56:790-8.[Medline]
  15. Van Steenhoven AA, Verlaan CWJ, Veenstra PC, Reneman RS. In vivo cinematographic analysis of behavior of the aortic valve. Am J Physiol. 1981;240:286-92.
  16. Tamiya K, Higashidate M, Beppu T. An in vivo area meter for real-time measurement of cross-sectional area in the cardiovascular system. Clin Phys Physiol Meas. 1991;12:253-60.[Medline]
  17. Higashidate M, Tamiya K, Beppu T, Imai Y. Regulation of the aortic valve opening. In vivo dynamic measurement of aortic valve orifice area. J Thorac Cardiovasc Surg. 1995;110:496-503.[Abstract/Free Full Text]
  18. Gao ZB, Pandya S, Hosein N, Sacks MS, Hwang NHC. Bioprosthetic heart valve leaflet motion monitored by dual camera stereo photogrammetry. J Biomech. 2000;33:199-207.[Medline]
  19. Laniado S, Yellin E, Terdiman R, Meytes I, Stadler J. Hemodynamic correlates of the normal aortic valve echocardiogram. Circulation. 1978;54:729-37.
  20. Leyh RG, Schmidtke C, Sievers HH, Yacoub MH. Opening and closing characteristics of the aortic valve after different types of valve-preserving surgery. Circulation. 1999;100:2153-60.[Abstract/Free Full Text]
  21. De Paulis R, De Matteis GM, Nardi P, Scaffa R, Buratta MM, Chiariello L. Opening and closing characteristics of the aortic valve after valve-sparing procedures using a new aortic root conduit. Ann Thorac Surg. 2001;72:487-94.[Abstract/Free Full Text]
  22. Arsenault M, Masani N, Magni G, Yao J, Deras L, Pandian N. Variation of anatomic valve area during ejection in patients with valvular aortic stenosis evaluated by two-dimensional echocardiographic planimetry: comparison with traditional Doppler data. J Am Coll Cardiol. 1998;32:1931-7.[Abstract/Free Full Text]
  23. Wollschläger H, Zeiher AM, Geibel A, Kasper W, Just H. Transesophageal echo computer tomography. In: Roelandt JRTC, editor. Cardiac ultrasound. London: Churchill Livingstone, 1993. p. 181-6.
  24. Pandian NG, Roelandt JR, Nanda NC, et al. Dynamic three-dimensional echocardiography: methods and clinical potential. Echocardiography. 1994;11:237-59.
  25. Abraham TP, Warner JG Jr, Kon ND, et al. Feasibility, accuracy, and incremental value of intraoperative three-dimensional transesophageal echocardiography in valve surgery. Am J Cardiol. 1997;80:1577-82.[Medline]
  26. Handke M, Schöchlin A, Schäfer DM, Beyersdorf F, Geibel A. Myxoma of the mitral valve: diagnosis by two- and three-dimensional echocardiography. J Am Soc Echocardiogr. 1999;12:773-6.[Medline]
  27. Handke M, Schäfer DM, Müller G, Schöchlin A, Magosaki E, Geibel A. Dynamic changes of atrial septal defect area: new insights by three-dimensional volume-rendered echocardiography with high temporal resolution. Eur J Echocardiography. 2001;2:46-51.
  28. Handke M, Schäfer DM, Heinrichs G, et al. Improved 3D echocardiographic endocardial border delineation using the contrast agent FS069 (Optison®)—transesophageal studies in a porcine model. Ultrasound Med Biol. 2001;27:1185-90.[Medline]
  29. Handke M, Schäfer DM, Heinrichs G, Magosaki E, Geibel A. Quantitative assessment of aortic stenosis by three-dimensional anyplane and three-dimensional volume-rendered echocardiography. Echocardiography. 2002;19:45-53.[Medline]
  30. Nanda NC, Roychoudhury D, Chung S, Kim KS, Ostlund V, Klas B. Quantitative assessment of normal and stenotic aortic valve using transesophageal three-dimensional echocardiography. Echocardiography. 1994;11:617-25.[Medline]
  31. Kasprzak JD, Salustri A, Roelandt JRTC, Ten Cate FJ. Three-dimensional echocardiography of the aortic valve: feasibility, clinical potential and limitations. Echocardiography. 1998;15:127-38.[Medline]
  32. Nosir YF, Lequin MH, Kasprzak JD, et al. Measurements and day-to-day variabilities of left ventricular volumes and ejection fraction by three-dimensional echocardiography and comparison with magnetic resonance imaging. Am J Cardiol. 1998;82:209-14.[Medline]
  33. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1:307-10.[Medline]
  34. Gnyaneshwar R, Kumar RK, Balakrishnan KR. Dynamic analysis of the aortic valve using a finite element model. Ann Thorac Surg. 2002;73:1122-9.[Abstract/Free Full Text]
  35. Grande-Allen KJ, Cochran RP, Reinhall PG, Kunzelman KS. Recreation of sinuses is important for sparing the aortic valve: a finite element study. J Thorac Cardiovasc Surg. 2000;119:753-63.[Abstract/Free Full Text]
  36. Brewer RJ, Deck JD, Capiti B, Nolan SP. The dynamic aortic root. Its role in aortic valve function. J Thorac Cardiovasc Surg. 1976;72:413-7.[Abstract]
  37. Badano L, Cassottano P, Bertoli D, Carratino L, Lucatti A, Spirito P. Changes in effective aortic valve area during ejection in adults with aortic stenosis. Am J Cardiol. 1996;78:1023-8.[Medline]
  38. Berg S, Torp H, Martens D, et al. Dynamic three-dimensional freehand echocardiography using raw digital ultrasound data. Ultrasound Med Biol. 1999;25:745-53.[Medline]
  39. Lester SJ, McElhinney DB, Miller JP, Lutz JT, Otto CM, Redberg RF. Rate of change in aortic valve area during a cardiac cycle can predict the rate of hemodynamic progression in aortic stenosis. Circulation. 2000;101:1947-52.[Abstract/Free Full Text]
  40. Thubrikar M, Skinner JR, Aouad J, Finkelmeier BA, Nolan SP. Analysis of the design and dynamics of aortic bioprostheses in vivo. J Thorac Cardiovasc Surg. 1982;84:282-90.[Abstract]
  41. Thubrikar MJ, Konstantinov IE, Selim GA, Gong GG, Fowler B, Robicsek F. The influence of sizing on the dynamic function of the free-hand implanted porcine aortic homograft: an in vitro study. J Heart Valve Dis. 1999;8:242-53.[Medline]



This article has been cited by other articles:


Home page
 J Am Coll CardiolHome page
M. Handke, G. Heinrichs, U. Moser, F. Hirt, F. Margadant, F. Gattiker, C. Bode, and A. Geibel
Transesophageal Real-Time Three-Dimensional Echocardiography: Methods and Initial In Vitro and Human In Vivo Studies
J. Am. Coll. Cardiol., November 21, 2006; 48(10): 2070 - 2076.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
R. Fries, T. Graeter, D. Aicher, H. Reul, C. Schmitz, M. Bohm, and H.-J. Schafers
In vitro comparison of aortic valve movement after valve-preserving aortic replacement
J. Thorac. Cardiovasc. Surg., July 1, 2006; 132(1): 32 - 37.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Friedhelm Beyersdorf
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Handke, M.
Right arrow Articles by Geibel, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Handke, M.
Right arrow Articles by Geibel, A.
Related Collections
Right arrow Valve disease

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS