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Ann Thorac Surg 2005;79:127-132
© 2005 The Society of Thoracic Surgeons


Original article: Cardiovascular

Secondary Tricuspid Regurgitation or Dilatation: Which Should Be the Criteria for Surgical Repair?

Gilles D. Dreyfus, MD*, Pierre J. Corbi, MD, K.M. John Chan, AFRCS, Toufan Bahrami, MD

Department of Cardiothoracic Surgery, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Harefield, Middlesex, United Kingdom

Accepted for publication June 4, 2004.

* Address reprint requests to Dr Dreyfus, Department of Cardiothoracic Surgery, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Hill End Rd, Harefield, Middlesex UB9 6JH, UK (E-mail: g.dreyfus{at}rbh.nthames.nhs.uk).


    Abstract
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Secondary tricuspid dilatation may or not be accompanied by tricuspid regurgitation (TR). Tricuspid dilatation can be objectively measured whereas TR can vary according to the preload, afterload, and right ventricular function. The purpose of this prospective study was to determine whether surgical repair of the tricuspid valve based on tricuspid dilatation rather than TR could lead to potential benefits.

METHODS: Between 1989 and 2001, 311 patients underwent mitral valve repair (MVR). The tricuspid valve was examined in each patient. Tricuspid annuloplasty was performed only if the tricuspid annular diameter was greater than twice the normal size (≥ 70 mm) regardless of the grade of regurgitation. Patients in group 1 (163 patients; 52.4%) received MVR alone. Patients in group 2 (148 patients; 47.6%) received MVR plus tricuspid annuloplasty.

RESULTS: Although not significant there was a difference with regard to hospital mortality (group 1 = 1.8%, group 2 = 0.7%) and actuarial survival rate (Kaplan–Meier: group 1 = 97.3%, 96.2%, and 85.5%; group 2 = 98.5%, 98.5%, and 90.3% at 3, 5, and 10 years, respectively). The New York Heart Association (NYHA) functional class was significantly improved in group 2 (group 1 = 1.59 ± 0.84; group 2 = 1.11 ± 0.31; p1). TR increased by more than two grades in 48% of the patients in group 1 and in only 2% of the patients in group 2 (p < 0.001).

CONCLUSIONS: Remodeling annuloplasty of the tricuspid valve based on tricuspid dilation improves functional status irrespective of the grade of regurgitation. Considerable tricuspid dilatation can be present even in the absence of substantial TR. Tricuspid dilatation is an ongoing disease process that will, with time, lead to severe TR.


    Introduction
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Tricuspid common pathology affecting the tricuspid valve. However the relevance of tricuspid regurgitation (TR) is often not appreciated until it is moderate or severe. It is thought that secondary TR decreases or even disappears after surgical correction of mitral valve disease. This concept has been widely supported [1, 2] and has influenced current practice regarding the management of secondary TR.

An understanding of the pathological process of functional TR is necessary to determine the optimal management strategy for this condition. The tricuspid annulus is a component of both the tricuspid valve and the right ventricle. For the tricuspid valve to leak, the tricuspid annulus and hence the right ventricle has to be dilated [3–6]. If the tricuspid annulus and the right ventricle are not dilated, there is a very low probability that TR can occur [4, 5]. Dilatation of the tricuspid annulus is only possibility with regard to its anterior and posterior aspects. These correspond to the free wall of the right ventricle (Fig 1). In addition to tricuspid dilatation, three important factors determine whether TR occurs: the preload, the afterload, and the right ventricular function. This may explain why TR is difficult to accurately assess because these factors can interfere with regard to the severity of TR under different conditions. Significant TR may not be detected echocardiographically despite considerable pathology in the tricuspid valve and yet this may exhibit an influence on the functional capacity of patients and subsequent progression of TR [6].



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Fig 1. Pathological process of tricuspid annular dilatation. Arrows designate the intercommissural distance that increases with dilatation and that is measured intraoperatively. (Ant. = anterior; Post. = posterior; Sept. = septal.)

 
An understanding of these important fundamental concepts would seem to contradict current practice regarding the management of secondary TR which focuses on the assessment of the severity of TR and which advocates treatment of the primary lesion alone (ie, mitral valve disease). Treatment of the mitral lesion alone only decreases the afterload. It does not correct tricuspid dilatation nor does it affect preload or right ventricular function. Once the tricuspid annulus is dilated, its size cannot spontaneously return to normal and may, in fact, continue to dilate further. This may explain why some patients require a second operation for TR years after the initial mitral valve surgery [7].

As tricuspid annular dilatation seems to be the underlying mechanism regarding nonorganic TR, it may be a more reliable indicator of tricuspid valve pathology compared with TR. Moreover successful treatment of secondary tricuspid valve pathology may necessitate the correction of tricuspid annular dilatation in addition to mitral valve surgery. This has been our practice during the past 12 years. We have prospectively recorded all the patient data to determine if tricuspid valve repair (TVR) for secondary tricuspid valve dilatation irrespective of the severity of TR improves outcome.


    Material and Methods
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Three-hundred eleven patients with chronic severe mitral regurgitation (MR) received mitral valve repairs (MVR) between April 1989 and February 2001. After approval by the local ethics committee, all patients were operated on by one surgeon in the same institution. Concomitant TVR was performed in 148 patients. All patients were operated through median sternotomy under cardiopulmonary bypass at normothermia. Double venous cannulation was used. Myocardial protection consisted of antegrade cold blood cardioplegia.

As a first stage the mitral valve was approached through a left atriotomy in the atrial-ventricular groove. The mitral valve was repaired using standard techniques. Ring annuloplasty was used in all cases. As a second stage the right atrium was opened vertically in all patients irrespective of the grading of preoperative TR. The tricuspid annular diameter was measured from the anteroseptal commissure to the anteroposterior commissure using a supple ruler (Fig 2). Patients with a tricuspid annular dimension greater than or equal to 70 mm underwent a remodeling tricuspid annuloplasty: 144 patients were operated on using a semirigid Carpentier-Edwards ring that was inserted using a series of 3-0 ethibond mattress sutures and 4 patients were operated on using a De Vega annuloplasty. The ring was manually distorted to fit the geometry of the tricuspid annulus that is deeper in the septal area than it is in the anterior area. A size 34 mm ring was routinely used for males and a size 32 mm ring was routinely used for females. Patients were divided into two groups according to the presence or absence of tricuspid dilatation: group 1 patients did not exhibit tricuspid dilatation (ie, tricuspid annular dimension was < 70 mm) and received isolated MVR (n = 163). Group 2 patients underwent tricuspid dilatation (ie, tricuspid annular dimension was ≥ 70 mm) and received MVR and TVR (n = 148).



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Fig 2. Measurement of the tricuspid annular diameter from the anteroseptal commissure to the anteroposterior commissure using a sterile supple ruler.

 
All data were collected at the time of surgery and prospectively entered into the study database. All patients were reviewed at yearly intervals by their local cardiologists who completed a questionnaire containing the following information: New York Heart Association (NYHA) functional class, medications, electrocardiogram (ECG) data, echo data, and cardiac events. Cardiac events were defined as thromboembolic or hemorrhagic events and reoperations.

The two-sample t test was used when the data in each sample exhibited approximately normal distributions; the means ± standard deviations are given. The Mann–Whitney (nonparametric) test was used when the data was not normally distributed. The {chi}2 test was used for binary data; in these instances, we have provided the percentages and the frequencies. The survival rate was estimated using the Kaplan–Meier method and the log-rank test was used to compare survival curves. Computations were carried out using Minitab Release 12 (Minitab Inc., State College, PA) and S-Plus (Insightful Corp., Seattle, WA). Values of p less than 0.05 indicate significant evidence of a difference in the two groups.


    Results
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The preoperative patient demographics are listed in Table 1. There was no statistical evidence of a difference between the two groups with regard to age, sex, incidence of atrial fibrillation, ejection fraction, and NYHA functional class. The etiology of MR was similar in both groups with the predominant etiology being degenerative (Table 2).


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Table 1. Comparison of Preoperative Demographics in Patients
 

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Table 2. Etiology of Mitral Valve Disease
 
Preoperative TR grading was performed using transthoracic echocardiography. The results are given in Table 3. The mean TR grade was 0.7 ± 0.5 in group 1 and 0.9 ± 0.6 in group 2 (p = 0.027).


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Table 3. Tricuspid Regurgitation Grade Measured by Transthoracic Echocardiography
 
Hospital mortality was 1.8% in group 1 (3 out of 163 patients) and 0.6% in group 2 (1 out of 148 patients) (NS). In group 1, one of the deaths was cardiac related, secondary to heart failure 3 days after surgery, and the two other deaths were secondary to multiorgan failure. The only death in group 2 was caused by a cerebral vascular accident 8 days after surgery.

Postoperative in-hospital morbidity comparisons are listed in Table 4. There was no statistical evidence of a difference regarding postoperative morbidity in the two groups. No systolic anterior motion occurred among the 311 patients who underwent MVR. In group 2 there was 1 patient who required reoperation for a failed DeVega annuloplasty 4 days after the initial operation.


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Table 4. Comparison of In-Hospital Morbidity
 
All patients were reviewed at yearly intervals by the referring cardiologist. Follow-up was completed for all 307 surviving patients and ranged from 2–12 years (mean 4.8 ± 2.9 years). Follow-up data is given in Table 5.


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Table 5. Comparison of Late Follow-Up Data (Mean Follow-Up 4.8 ± 2.9 Years)
 
At the last follow-up, 63.2% of the patients in group 1 were assessed as NYHA class I and 22.5% of the patients were assessed as NYHA class II. In group 2, 89.6% of the patients were categorized in NYHA class I and 11% of the patients were categorized in class II. Of the patients in group 1, 12.2% were graded as NYHA class III and 1.9% were graded as NYHA class IV. No patients in group 2 were sorted in either NYHA class III or IV. The mean NYHA class was 1.6 ± 0.8 in group 1 and 1.1 ± 0.3 in group 2 (p < 0.0001).

Echocardiographic data are given in Table 5. The mean MR grade was 0.4 ± 0.5 in group 1 and 0.6 ± 0.7 in group 2 (p = 0.015). The TR grade was significantly improved for group 2 (0.4 ± 0.6) compared with group 1 (2.1 ± 1.0) (p = 0.0001). Postoperative TR grading is provided in Table 3. The TR grade increased by 1.4 ± 1.1 in group 1 and decreased by 0.5 ± 0.9 in group 2 (p < 0.001). More late TR (p = 0.085) did not significantly develop in patients with Barlow's disease.

Five late deaths occurred in group 1 and two late deaths occurred in group 2. The causes of deaths were cardiac related for 2 patients in group 1 (1 patient died post-TVR 7 years after undergoing the first operation and 1 patient died at 83 years of age 8 years after the initial operation attributable to a subsequent cardiac arrest). The actuarial survival rate was 97.3% (confidence interval [CI] 94.7%–99.9%), 94.5% (90%–99.1%), and 85.4% (72.5%–98.4%) at 3.3, 6.5, and 9.5 years, respectively, in group 1 and 98.5% (96.5%–100%) and 90.3% (74.8%–100%) at 1.2 and 8 years, respectively, in group 2 (Fig 3). There was no evidence that the survival curves differed (p = 0.45).



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Fig 3. Comparison of actuarial survival rates for the two groups using the Kaplan–Meier method (p = 0.45). Group 1 = mitral regurgitation (MR) (dashed lines); group 2 = MR (solid line) and tricuspid regurgitation (TR).

 
Cardiac events were defined as thromboembolic or hemorrhagic complications or reoperations. The event free survival rate at 10 years was 90.5% ± 4.7% in group 1 and 92.8% ± 5.0% in group 2 (p = 0.20) (Fig 4). Two patients in group 1 experienced a cerebral vascular accident (one was thromboembolic, one was hemorrhagic). Both underwent isolated MVRs. No patients in group 2 exhibited thromboembolic or hemorrhagic complications.



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Fig 4. Comparison of cardiac-related event free survival rates between the two groups. Group 1 = mitral valve repair (MR) (dashed lines); group 2 = MR (solid line) and tricuspid valve repair (TR).

 
Five patients underwent mitral valve replacement at 4, 5, 6, and 7 years after the initial operation. One patient in each group underwent reoperation for hemolysis. One patient underwent TVR 7 years after the initial operation. There were three reoperations in each group.


    Comment
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The presence of secondary tricuspid pathology is often not appreciated especially if severe TR is not present. Although there is no question that considerable tricuspid pathology is present when there is severe TR, considerable tricuspid pathology may also be present when the severity of TR is only mild or moderate [8]. This is because the assessment of the tricuspid valve at a given time by echocardiography is dependent upon the preload and afterload conditions of the patient and these conditions may vary from time to time. The absence of TR or the presence of only mild TR does not mean that the tricuspid orifice is free of any abnormality such as tricuspid annular dilatation. Considerable tricuspid dilatation may not always result in pronounced TR at a given time [9].

The converse, however, is not true and considerable functional TR can only occur when there is considerable tricuspid annular dilatation, however little is known regarding the normal and pathological size of the tricuspid valve. As tricuspid dilatation is the only constant feature with regard to secondary tricuspid pathology, we have prospectively analyzed all tricuspid orifices in patients undergoing MVR. All patients whose tricuspid annular dimension was dilated to greater than twice the normal size (ie, > 70 mm) underwent TVR in addition to MVR. Although this threshold size for tricuspid annuloplasty was not correlated to patient size, the body surface area was the same in both groups as is indicated in Table 4. Significant TR was not detected for the majority of these patients during preoperative assessment even though the tricuspid annular diameter was dilated to greater than twice the normal size. Most of the patients with tricuspid dilatation (88%) indicated grade 0 or 1 TR at preoperative echocardiographic assessment. There is thus no correlation between TR and tricuspid dilatation. We therefore believe that tricuspid dilatation is a more reliable indicator of tricuspid pathology as, unlike TR, it is a constant measurement and not related to any other factors.

Our method of assessing the tricuspid annular dimension in the arrested heart measures the maximal diastolic size of the tricuspid annulus between the anteroseptal and anteroposterior commissure (ie, the part of the annulus that dilates [Fig 1 and 2]). This measurement is reliable, reproducible, and allows comparison with regard to different tricuspid orifices. We do not measure the total circumference of the tricuspid orifice, which would give the true diameter, for two reasons: (1) echocardiographic data validating the assessment of tricuspid circumference has not been indicated and (2) commercially available sizers for such large orifices are not currently available.

This method has indicated reliability (ie, free of preload and afterload). The importance of measuring the tricuspid annular diameter is supported by many authors [10] and echocardiographic studies have indicated that tricuspid annular dilatation is the most consistent and most important predictor of TR [6, 11]. However preoperative assessment of tricuspid annular diameter using echocardiography or even using cardiac magnetic resonance scans is problematic because it is still dependent upon the preload and afterload conditions of the patient at the time of measurement. We are aware that this intraoperative sizing does not reflect reality as in systole. Even in diastole the size of the tricuspid orifice cannot be as wide. However tricuspid annular dilatation (similar to mitral annular dilatation) is associated with a decrease of systolic contraction of the annulus and the tricuspid annulus remains in a more or less permanent diastolic position. Just as in mitral annuloplasty, tricuspid annuloplasty changes an orifice that remains permanently in a diastolic position into a permanent systolic position.

Because we did not possess reliable preoperative sizing of the tricuspid annulus, we have systematically examined all tricuspid orifices irrespective of the preoperative grading of TR. Two important points can be stated with regard to our practice. First we have been very conservative as we decided not to correct annular dilatation that did not reach greater than twice the normal size. Therefore all orifices measuring less than 70 mm were left untreated. An increase in tricuspid annular diameter to twice the normal size would, in fact, correspond to and cross-sectionally increase to four times its normal size. Some authors have suggested treating dilatation at an earlier stage. This might be correct however the necessity exists to perform further studies to determine the threshold size for tricuspid annular dilatation beyond which it should be repaired. Second the incidence of tricuspid valve treatment approaches 48% for all patients undergoing mitral valve surgery at our practice. This is extremely high [12, 13] and specifies an incidence rate approaching 30%.

For many decades it has been thought that functional tricuspid valve disease was strictly related to left-sided lesions such as mitral stenosis or MR. It was thought that once the left-sided lesions were treated, functional tricuspid pathology would regress spontaneously. The term "functional" is probably misleading in this instance as it is now well-established that the main factor causing TR is tricuspid dilatation indicating that anatomical abnormalities do exist. This suggests the notion that once the annulus is dilated, perhaps it can return to normal. This, however, seems very unlikely [11]. The annulus is partly a component of the valve, but it is also a ventricular component. Therefore if the annulus is dilated, the right ventricle is also dilated. Our study demonstrates that secondary TR is an ongoing process, as during follow-up an increase in the TR by at least two grades subsequently developed in 45% of the patients who received isolated MVR. Eleven patients graded 0 preoperatively were assessed as grade IV at follow-up and 38 patients graded I preoperatively were assessed as grade III at follow-up. We have analyzed whether other factors could have influenced this outcome. Residual pulmonary pressures were not substantially different in both groups. Even pulmonary hypertension greater than 50 mm Hg systolic preoperatively did not play any role in the postoperative assessment. We have also analyzed the residual MR. Surprisingly the residual MR was significantly greater at 0.60 in group 2 as opposed to 0.41 in group 1 (although not significantly so). This clearly demonstrates that without considerable MR, TR can worsen. Contrary to current beliefs, TR does not spontaneously disappear once the left lesion has been corrected. The data demonstrates that once the annulus is dilated and, consequently, the right ventricular function mildly impaired, the process of TR is progressive and will subsequently become clinically relevant.

The slightly longer cross-clamp time and the addition of a new prosthetic ring did not seem to influence morbidity as indicated by similar inotropic requirements and the intensive care duration of the two groups. Although the patients in group 2 were slightly more debilitated when the surgery was performed, their functional capacity at late follow-up was markedly improved compared with those in group 1.

Functional class and echocardiographic data were obtained during follow-up by local cardiologists and not by the team who had treated the patients. We, therefore, believe these results to be unbiased. Although actuarial survival rates were not significantly different for both groups, it seems quite favorable that extremely ill patients with larger right ventricles manifest the same late survival rate as those without annular dilatation. One could speculate that treating tricuspid dilatation impacts right ventricular function and subsequently aids in preventing deaths related to such a condition. Only 1 patient in group 1 required repeat surgery 8 years after the initial operation and subsequently died in the postoperative period. However it is well-known that hospital mortality is extremely high with regard to redo surgery of isolated secondary severe TR [10] and that medical treatment for such patients is rather limited and inefficient.

This study was apportioned with more than 300 patients, some of whom have also been followed-up for more than 10 years. Follow-up analysis has revealed that tricuspid annuloplasty performed at the time of mitral valve surgery improves functional capacity. A precise method used for sizing the tricuspid orifice has been defined. It is simple, expedient, and reproducible. However the threshold size to correct tricuspid dilatation requires further study and perhaps lesser degrees of tricuspid dilatation should also be corrected. Finally this study demonstrates that there is little or no correlation between tricuspid dilatation and regurgitation and that tricuspid dilatation is more reliable than TR when assessing secondary tricuspid valve disease. The aim of treating tricuspid annular dilatation at the same time that mitral valve surgery is performed is to prevent future treatment of symptomatic TR. This approach, which is based on tricuspid dilatation and not TR, allows more adequate treatment with regard to tricuspid pathology&mdasha condition that typically remains indiscriminate for extended periods of time, but becomes a considerable challenge when clinically relevant.


    Acknowledgments
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
We gratefully acknowledge the contribution of Dr Derek Robinson (Senior Lecturer at the Centre for Statistics and Stochastic Modeling, School of Mathematical Sciences, University of Sussex, Brighton, UK) for all the statistical analysis performed for this study.


    References
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Braunwald NS, Ross J, Morrow AG. Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement Circulation 1967;35:I-63-69.
  2. Duran CMG, Pomar JL, Colman T, et al. Is tricuspid valve repair necessary? J Thorac Cardiovasc Surg 1980;80:849-860.[Abstract]
  3. Tei Chuwa, Pilgrim JP, Shah PM, et al. The tricuspid valve annulus: study of size and motion in normal subjects and in patients with tricuspid regurgitation Circulation 1982;66:665-671.[Abstract/Free Full Text]
  4. Sagie A, Schwammenthal E, Padial LR, et al. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients J Am Coll Cardiol 1994;24:446-453.[Abstract]
  5. Ubago JL, Figueroa A, Ochoteco A, et al. Analysis of the amount of tricuspid valve annular dilatation required to produce functional tricuspid regurgitation Am J Cardiol 1983;52:155-158.[Medline]
  6. Groves PH, Lewis NP, Ikram S. Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral replacement for rheumatic mitral valve disease Br Heart J 1991;66:295-301.[Abstract/Free Full Text]
  7. King RM, Schaff HV, Danielson GK, et al. Surgery for tricuspid regurgitation late after mitral valve replacement Circulation 1984;70:I-193-197.
  8. Porter A, Shapira Y, Wurzel M, et al. Tricuspid regurgitation late after mitral valve replacement: clinical and echocardiographic evaluation J Heart Valve Dis 1999;8:57-62.[Medline]
  9. Fukuda N, Oki T, Iuchi A, et al. Tricuspid inflow and regurgitant flow dynamics after mitral valve replacement: differences relating to surgical repair of the tricuspid valve J Heart Valve Dis 1997;6:184-188.[Medline]
  10. Sugimoto T, Okada M, Ozaki N, et al. Long term evaluation of treatment for functional tricuspid regurgitation with regurgitant volume: characteristic differences based on primary cardiac lesion J Thorac Cardiovasc Surg 1999;117:463-471.[Abstract/Free Full Text]
  11. Colombo T, Russo C, Ciliberto G, et al. Tricuspid regurgitation secondary to mitral valve disease: tricuspid annulus function as guide to tricuspid valve repair Cardiovasc Surg 2001;9:369-377.[Medline]
  12. Carpentier A, Chauvaud S, Fabiani JN, et al. Reconstructive surgery of mitral valve incompetence: ten-year appraisal J Thorac Cardiovasc Surg 1980;79:338-348.[Abstract]
  13. Duran CM. Tricuspid valve surgery revisited J Card Surg 1994;9:242-247.[Medline]



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J. Thorac. Cardiovasc. Surg.Home page
R. K. Ghanta, R. Chen, N. Narayanasamy, S. McGurk, S. Lipsitz, F. Y. Chen, and L. H. Cohn
Suture bicuspidization of the tricuspid valve versus ring annuloplasty for repair of functional tricuspid regurgitation: Midterm results of 237 consecutive patients
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A. M. Anwar, M. L. Geleijnse, F. J. ten Cate, and F. J. Meijboom
Assessment of tricuspid valve annulus size, shape and function using real-time three-dimensional echocardiography
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G. D. Dreyfus, O. S. Neto, and S. Aubert
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J Am Coll CardiolHome page
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R. O. Bonow, B. A. Carabello, K. Chatterjee, A. C. de Leon Jr, D. P. Faxon, M. D. Freed, W. H. Gaasch, B. W. Lytle, R. A. Nishimura, P. T. O'Gara, et al.
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T.-T. Ton-Nu, R. A. Levine, M. D. Handschumacher, D. J. Dorer, C. Yosefy, D. Fan, L. Hua, L. Jiang, and J. Hung
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B. Alsoufi, V. Rao, M. A. Borger, M. Maganti, S. Armstrong, C. M. Feindel, H. E. Scully, and T. E. David
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