ATS
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):
Steve K. Singh
Gilbert H.L. Tang
William G. Williams
Tirone E. David
Michael A. Borger
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 Singh, S. K.
Right arrow Articles by Borger, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Singh, S. K.
Right arrow Articles by Borger, M. A.
Related Collections
Right arrow Valve disease

Ann Thorac Surg 2006;82:1735-1741
© 2006 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Midterm Outcomes of Tricuspid Valve Repair Versus Replacement for Organic Tricuspid Disease

Steve K. Singh, MDa, Gilbert H.L. Tang, MDa, Manjula D. Maganti, MSb, Susan Armstrong, MSb, William G. Williams, MDa,c, Tirone E. David, MDa,b, Michael A. Borger, MD, PhDa,b,*

a Divisions of Cardiac Surgery of the University of Toronto, Toronto, Ontario, Canada
b Toronto General Hospital, Toronto, Ontario, Canada
c The Hospital for Sick Children, Toronto, Ontario, Canada

Accepted for publication June 2, 2006.

* Address correspondence to Dr Borger, Toronto General Hospital, Room 4N-451, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4 (Email: michael.borger{at}uhn.on.ca).

Presented at the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
BACKGROUND: Organic tricuspid valve (TV) disease is uncommon. Few studies have compared TV repair with replacement in these patients. The current study compared midterm outcomes of TV repair versus replacement in a large group of patients with organic tricuspid disease.

METHODS: Two-hundred and fifty patients underwent surgery for organic TV disease at our institution from 1979 to 2003. Clinical and echocardiographic follow-up were obtained, were 99% complete, and were 5.2 ± 4.1 years long (mean ± standard deviation).

RESULTS: One hundred and seventy-eight patients (71%) underwent TV repair and 72 (29%) received TV replacement (54 bioprosthetic, 18 mechanical). Repair patients were more likely to have hypertension, rheumatic pathology, or elective surgery. Concomitant procedures included mitral (50% of patients), aortic (26%), and coronary bypass (6%) operations. Perioperative and midterm mortality were higher in the replacement group (both p < 0.001). Cox regression analysis revealed TV replacement as an independent predictor of midterm mortality (hazard ratio: 5.1, 95% confidence interval: 2.9 to 9.1, p < 0.001) and decreased event-free survival (hazard ratio: 2.0, 95% confidence interval: 1.1 to 3.6, p = 0.02). Follow-up echocardiography revealed more moderate to severe tricuspid regurgitation in repair patients (38% vs 5%, p < 0.001), but no difference in New York Heart Association functional class or reoperation rates.

CONCLUSIONS: Tricuspid valve repair is associated with better perioperative, midterm, and event-free survival than TV replacement in patients with organic tricuspid disease. Despite more tricuspid regurgitation in the repair group during follow-up, reoperation rates and functional class were similar. Repair should be performed whenever possible in patients with organic tricuspid disease.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
Tricuspid valve (TV) dysfunction can occur with structurally normal valves or with organic valvular disease. Tricuspid regurgitation (TR) in patients with normal leaflets is usually secondary to left heart pathology (ie, functional or secondary TR). It is the predominant cause of TV disease in North America, and readily managed with simple TV repair techniques [1]. In contrast, organic TV disease is rare and comprises less than 1% of all valve operations [2]. The etiologies of organic TV disease include rheumatic valvulopathies, endocarditis, myxomatous disease, carcinoid syndrome, rheumatoid arthritis, radiation therapy, Marfan disease, congenital anomalies (eg, Ebstein's anomaly, atrioventricular septal defect), systemic lupus, antiphospholipid syndrome, and other rarer causes [3]. Outcomes after surgery for organic TV disease are significantly worse than after repair of secondary TR [4].

The optimal choice of surgical procedure for organic TV disease is not well-studied. The decision of whether to repair or replace the TV is based on several factors, including extent of the disease process, amount of salvageable leaflet tissue, concomitant procedures (repair or replacement) on other heart valves, patient age and comorbidities, and surgical expertise. Previous studies have revealed a high perioperative mortality rate associated with TV replacement, usually in the range of 20% [2, 4]. However, it is unclear whether the increased mortality is a consequence of associated patient comorbidities or of the procedure itself. Although TV repair is associated with better perioperative survival, it has relatively high recurrent rates of late TR [2]. Residual TR can lead to biventricular heart failure, death, or reoperation [2, 3]. The latter is associated with high mortality rates, approaching 40% [2, 3].

There is a lack of contemporary study in the literature to guide the choice of surgical management for organic TV disease. The aim of the current study was, therefore, to compare midterm survival, echocardiographic, and clinical outcomes in patients undergoing TV repair versus replacement for organic TV disease.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
Approval was attained from our institution's research ethics board to review our prospective database and attain follow-up clinical notes and echocardiograms (waiving the need for individual consent of each patient or relative).

We performed a retrospective review of 250 patients who underwent surgery for organic TV disease between 1979 and 2003 at the Toronto General Hospital. Table 1 lists their pathologies, which included rheumatic, congenital (eg, Ebstein's, atrioventricular septal defect), prosthetic dysfunction, endocarditis, leaflet tears-prolapse, papillary muscle rupture, tumor, and myxomatous or degenerative disease. All patients with a diagnosis of secondary (functional) tricuspid disease were excluded from our analysis. Preoperative, operative, and postoperative data were entered into a database for analysis.


View this table:
[in this window]
[in a new window]
 
Table 1. Preoperative and Operative Characteristics of Patients With Organic Tricuspid Valve (TV) Disease Undergoing TV Surgery (n = 250)
 
Of the 250 patients who underwent TV surgery for organic pathology, 178 patients (71%) had TV repair. The other 72 patients (29%) received TV replacement (54 bioprosthetic, 18 mechanical). The choice of surgical therapy was at the discretion of the attending surgeon. Concomitant procedures included mitral valve surgery (50% of patients), aortic valve surgery (26%), and coronary bypass grafting (6%). Forty-eight percent of patients had a previous cardiac operation.

Cardiopulmonary bypass was instituted with venous cannulation of the superior and inferior vena cava. Tricuspid valve surgery was performed after concomitant cardiac procedures were completed, usually with the aortic cross-clamp in place. The TV repair techniques varied according to the specific valve pathology and included suture annuloplasty (n = 119), band annuloplasty (n = 59), and other techniques as required.

Follow-Up
Research personnel performed a cross-sectional follow-up, contacting all patients and(or) family members through mailed questionnaire and(or) telephone calls between February and September 2004. Clinical data on New York Heart Association (NYHA) functional status, postoperative morbidity, and mortality were tabulated. Patient clinical status and most recent transthoracic or transesophageal echocardiographic results were also obtained from the patients' cardiologists. Postoperative events were compiled and analyzed according to the American Association for Thoracic Surgery/Society of Thoracic Surgeons guidelines for reporting morbidity and mortality after cardiac valvular operations [5]. Follow-up was 99% complete with a mean (± standard deviation) follow-up time of 5.2 ± 4.1 years (range, 0 to 16 years).

Statistical Analyses
Categoric patient variables were compared using the {chi}2 test or the Fisher exact test where appropriate, and are reported as percentages. The means ± standard deviation of continuous variables were compared using the Student t test for normally distributed variables and the Wilcoxon rank sum test was used for variables that had nonparametric distribution.

The propensity for valve replacement versus repair was performed using logistic regression with all preoperative characteristics as the independent variables, and TV replacements as the dependent outcome. Midterm survival and freedom from morbid events were compared using the Kaplan-Meier method; independent predictors were determined by means of Cox regression analysis. Backward elimination of nonsignificant determinants was employed in analyses. Significance was assumed for p less than 0.05. The SAS version 8.2 statistical software (SAS, Cary, NC) was used.

The variables entered in the multivariable model to determine the significant independent predictors of survival and event-free survival included the following: tricuspid surgery (replacement versus repair), age, male gender, diabetes, hypertension, cholesterol, left ventricular dysfunction, previous stroke, peripheral vascular disease, preoperative renal dysfunction, concomitant coronary artery bypass graft surgery, concomitant mitral valve surgery, concomitant aortic valve surgery, any redo-operation, and active endocarditis.


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
Preoperative and Operative Characteristics
Table 1 shows the preoperative and intraoperative characteristics of the 250 patients who underwent either repair (n = 178) or replacement (n = 72) surgery for documented organic (nonsecondary) disease. The two groups were similar in most aspects, including era of operation. However, the repair group was more likely to have systemic hypertension, more likely to have rheumatic TV pathology, and less likely to undergo isolated TV surgery. The repair group was also less likely to be in preoperative shock or undergoing urgent surgery. There was a trend toward more regurgitant lesions in the repair group (p = 0.053). Cardiopulmonary bypass time was longer in the TV replacement group, but aortic cross-clamp times were similar.

Logistic regression analysis looked at the preoperative factors that increased the propensity for valve replacement versus repair. Significant, independent factors for replacement included urgent surgery, previous syncope or heart failure, hypertension, active endocarditis, and concomitant mitral valve surgery.

In-Hospital Outcomes
Both morbidity and in-hospital mortality were higher in the replacement patients (Table 2). Specifically, postoperative renal failure, duration of ventilatory support, and lengths of intensive care unit and hospital stays were significantly worse in the TV replacement group. There was a trend toward increased low cardiac output syndrome in the replacement group, but no differences were found for perioperative stroke, chest reopening, or insertion of permanent pacemaker.


View this table:
[in this window]
[in a new window]
 
Table 2. In-Hospital Outcomes of Patients With Organic Tricuspid Valve (TV) Disease Undergoing TV Surgery (n = 250)
 
Long-Term Outcomes
Figure 1 displays the midterm survival for the two groups of patients. Tricuspid valve repair was associated with a significantly better midterm survival than TV replacement, predominantly because of the markedly increased perioperative mortality in the replacement group. The multivariable predictors of survival, by Cox regression analysis, included TV replacement as a significant predictor of mortality with a hazard ratio (HR) of 5.1 (95% confidence interval [CI] 2.9 to 9.1, p < 0.0001). Age, male gender, poor left ventricular function, active endocarditis at the time of surgery, preoperative renal failure, preoperative stroke history, and concomitant mitral valve surgery were also significant predictors of death in our model (Table 3). Late deaths unrelated to the tricuspid operation occurred in 12 patients in the repair group and 8 persons in the replacement group. These included deaths from heart failure, myocardial infarction, cancer, other medical conditions, or accidental.


Figure 1
View larger version (12K):
[in this window]
[in a new window]
 
Fig 1. Kaplan-Meier curve comparing survival in patients with organic tricuspid disease who receive tricuspid valve (TV) repair versus replacement surgery.

 

View this table:
[in this window]
[in a new window]
 
Table 3. Independent Predictors of Long-Term Outcomes After Tricuspid Valve Surgery for Organic Disease, as Determined by Cox Proportional Hazards Models
 
Valve-related mortality was defined as any death due to structural and nonstructural valve dysfunction, valve thrombosis, major bleeding event, or valvular endocarditis requiring an operation. Deaths due to TV reoperation and sudden, unexpected or unexplained death were also included in this outcome. There were no significant differences in valve-related mortality between the two groups of patients (Fig 2).


Figure 2
View larger version (12K):
[in this window]
[in a new window]
 
Fig 2. Kaplan-Meier curve comparing freedom from valve-related mortality (VRM) in patients with organic tricuspid disease who receive tricuspid valve repair versus replacement surgery.

 
There was no significant difference in TV reoperation rates for the two groups of patients (Fig 3). Indications for reoperation in the replacement group were for structural valve deterioration (SVD) (2 patients) or valve thrombosis (1 patient). In the repair group, reoperations in the follow-up period were for recurrent TR (7 patients), endocarditis (1 patient), congestive heart failure (1 patient) or heart transplant (1 patient). As the replacement groups had significantly more perioperative deaths, cumulative incidence analysis of TV reoperation was performed. Once again, there were no significant differences between the two groups.


Figure 3
View larger version (12K):
[in this window]
[in a new window]
 
Fig 3. Kaplan-Meier curve comparing freedom from tricuspid valve (TV) reoperation in patients with organic tricuspid disease who receive tricuspid valve repair versus replacement surgery.

 
Event-free survival was defined as the freedom from thromboembolism, valve thrombosis, structural valve dysfunction, major bleeding event, endocarditis, recurrent severe TR, TV reoperation, and death. The 10-year event-free survival was 61 ± 6% in the repair group versus 54 ± 10% in the replacement group. Tricuspid valve replacement was found to be an independent predictor of lower event-free survival after Cox regression analysis (HR: 2.0, 95% CI 1.1 to 3.6, p = 0.02). Male gender, concomitant mitral valve surgery, and age were other independent predictors of lower event-free survival (Table 3).

Our results revealed no difference between the TV repair and replacement groups 10 years postoperatively with regard to freedom from valve thrombosis (99 ± 6% vs 98 ± 2%, p = 0.4) or bleeding rates (95 ± 2% vs 98 ± 2%, p = 0.5). Actuarial freedom from thromboembolic events at 10 years was also similar between groups (95 ± 2% vs 91 ± 7% for repair versus replacement, p = 0.5 by log rank). The use of anticoagulation at midterm follow-up was no different between the repair and replacement cohorts (55% vs 65%, p = 0.3).

Most recent echocardiographic follow-up showed that 95% of patients in the TV replacement group had mild or less TR, 2.5% had moderate TR, and 2.5% had severe TR. In comparison, 62% of those who had TV repair had mild or less TR, 26% had moderate TR, and 12% had severe TR. However, moderate to severe RV dysfunction on most recent echo was significantly higher in the replacement group (28% vs 9%, p = 0.003). Nonetheless, there was no difference in the functional status of patients in either group, as similar proportions were in NYHA class III–IV on follow-up (repair: 17% vs replacement: 16%, p = 0.9).


    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
Organic TV disease is valvular dysfunction due to a primary structural pathology of the tricuspid valve, and not secondary to other valvular or cardiac disease. It is an uncommon clinical entity and therefore there is limited experience from any one center and a paucity of studies to elucidate the optimal surgical technique. To the best of our knowledge, there have not been any series comparing TV repair versus replacement for organic TV disease since the 1970s [6].

Tricuspid valve repair techniques can be divided into those that are suture-based and those that utilize an annuloplasty ring. They are well-described in the literature in the setting of secondary (functional) TR. Such repair techniques usually do not add significantly to the operative time and can be performed with low rates of morbidity and mortality. Tricuspid valve repair is associated with improved long-term survival and event-free survival in patients with functional TR [7]. However, their long-term durability is questionable with relatively high published recurrence rates for TR [7, 8]. Tricuspid valve replacement operations, in contrast, are associated with marginally longer operative times and higher in-hospital mortality rates [2, 9, 10]. However, residual TR is not as frequent as in patients undergoing TV repair [2, 10]. Published TV replacement series contain a higher proportion of patients with organic pathology than published TV repair studies, making comparison of outcomes for the two surgical techniques difficult. For this reason, we chose to focus only on patients with organic TV pathology to compare repair with replacement.

Our results showed that TV repair for organic pathology resulted in significantly improved survival and event-free survival when compared with the TV replacement cohort, predominantly because of a higher early (perioperative) mortality rate in the TV replacement group. The survival curves for the two groups did not cross, nor were they parallel. The worsened mortality is possibly due to progressive RV dysfunction in the TV replacement group caused by a large, rigid object (the prosthetic valve) in a deformable, low-pressure cavity. Our results support this theory by the findings of increased perioperative low output syndrome and higher rate of RV dysfunction on follow-up echo in the TV replacement group. The association of acute RV failure post-cardiac surgery with increased mortality is well-supported in the literature [4].

Despite improved survival, midterm follow-up echocardiography revealed that the repair group had significantly more patients with recurrent moderate to severe TR. However, symptom severity and functional NYHA class were no different between the two groups. As noted above, RV function during follow-up was better in the repair group, despite the increased prevalence of recurrent TR. In addition, the incidence of overall TV reoperation rate, which is associated with significant risk of mortality, was not different between the two groups.

There is some related evidence in the echocardiography literature to compare with our findings. A study from the Cleveland Clinic examined 401 patients with TV dysfunction (etiology not stated) and followed them for 10 years post-surgery with serial echocardiography [11]. These investigators showed that early survival was worse in those that had TV replacement versus repair (relative risk 2.9). Late echocardiographic TV failure (moderate to severe TR) was associated with use of a TV repair-annuloplasty strategy, similar to our own results.

Our result of relatively high TR recurrence in the repair group is supported by other investigators, with reported recurrence rates up to 45% during long-term follow-up [12–15]. The recurrence rate varies according to the type of repair performed, with higher recurrences for suture annuloplasty, particularly the De Vega repair [7, 8].

Tricuspid valve replacement results from the literature are also similar to those reported in our study. Filsoufi and colleagues [9] reported 81 consecutive cases from the Brigham and Women's hospital over 15 years, 52 (64%) with organic TV dysfunction. Overall operative mortality was 22%, the same as in our study. The largest and longest series on TV replacement is from the UK Heart Valve Registry [2], which looked at 425 patients who underwent TV replacement for all etiologies. They reported no significant survival benefit based on choice of prosthesis (bioprosthetic versus mechanical). Overall 30-day mortality was 17%. Survival rates at one, five, and 10 years postoperative were 72%, 60%, and 43%, respectively, similar to our reported rates of 76%, 63%, and 55%. However, a small proportion of the UK Heart Valve Registry patients (4.5%) were undergoing redo-cardiac surgery, and patients with organic and functional disease were included. Half of the patients in our study underwent redo-cardiac surgery and all had organic TV disease, which is associated with a worse long-term prognosis than functional disease.

Thromboembolism is well-described in the literature as a complication of TV replacement surgery, particularly for mechanical prostheses [10, 15, 16]. A meta-analysis reported rates of 1.28% patient/year (range, 0.1 to 4.6% patient/year) [10]. Our results revealed no difference between the TV repair and replacement groups fifteen years postoperatively with regard to freedom from thromboembolic events, valve thrombosis, or bleeding rates. This is likely due to the fact that our study population included only 18 mechanical TV replacements.

Study Limitations
Our study is limited by its retrospective nature with all of the inherent limitations of such investigations. However, the current study is the largest series to date comparing TV repair to replacement for organic TV pathology. In addition, our follow-up was nearly complete. Therefore we feel our results are important for cardiac surgeons to consider when making the difficult decision of whether to repair or replace a TV with structural leaflet pathology.

Conclusion
Tricuspid valve repair is associated with better early and midterm survival than TV replacement in patients with organic tricuspid disease. The increased mortality is possibly due to low output syndrome and RV dysfunction secondary to a rigid prosthesis in the tricuspid position. Despite more recurrent TR in TV repair patients during follow-up, NYHA functional class and reoperation rates are similar. Tricuspid valve repair should be performed whenever possible in patients with organic tricuspid disease.


    Discussion
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 
DR HAROLD G. ROBERTS (Lauderdale Lakes, FL): I enjoyed your presentation very much. I have a couple of questions and observations. One is that I noted that your repair technique in two thirds of the cases was a De Vega. I wonder if your results with one third of the patients having moderate or worse tricuspid regurgitation might be improved if you used an annuloplasty ring, a rigid ring, rather than a De Vega? I and others have had the unfortunate experience of seeing De Vegas that are semi ripped out, "bowstringing" some years later.

In addition, was there any preop assessment of the right ventricular function? A counterhypothesis could be that very poor right ventricular function requires tricuspid replacement, rather than repair. Most surgeons don't go into the operating room thinking they are going to replace a tricuspid valve. The valve was replaced for a reason, and it was probably because the right ventricle was very dilated and poorly contractile, and an attempt to repair was done initially. One of the reasons not to have a good outcome in tricuspid repair is the right ventricle is so massively dilated and the leaflets so severely tethered, that no matter how small a ring you put in, the leaflets will not reach the annulus.

DR SINGH: Those are excellent observations. Firstly, two-thirds of the repairs were non-ring annuloplasties, including De Vega and non-De Vega repair techniques. We did not specifically look at the incidence of late tricuspid regurgitation (TR) within the different types of repair techniques. However, we have another paper in press, in Circulation, that compares late TR rates for ring versus no-ring repair for functional TR, and patients who received a ring had less recurrent TR and improved event-free survival. Therefore, as you point out, the choice of repair approach may be related to the rate of late recurrent TR. However, what we observed in the current analysis was that despite the repair group having more TR at long-term follow-up, the incidence of reoperation or patient NYHA (New York Heart Association) functional class was no different compared with the replacement group, who had minimal late recurrent TR.

Regarding your second comment, unfortunately we did not have any preoperative assessment of RV (right ventricular) function. As you mention, a massively dilated RV may not allow for a perfect repair outcome. As such, surgeons may replace the valve, particularly if they have already replaced one of the other valves. However, our findings would suggest that it may be better to accept a less than ideal repair, rather than replace the tricuspid valve. This is because replacement, as we and others have shown, is a very risky operation with high perioperative mortality. Doing a repair avoids this high mortality risk. As we have shown, even if the repair was not ideal and residual TR or late TR developed, this does not significantly affect the need for a future reoperation, or worsen patient function class in the long term. So, surgeons should repair the valve if at all possible, and even if not ideal with some residual TR, subsequent replacement should be avoided during the operation.

DR FRANK W. SELLKE (Boston, MA): Your death rate and renal failure rate and rate of prolonged ventilation was much higher in the replacement group. Doesn't that suggest that the groups were not equal? The mortality in the replacement group was 20%. That seems pretty high.

DR SINGH: Tricuspid valve replacement does carry a high mortality rate. Our data revealed perioperative mortality to be 22%. However, this is comparable to other series in the literature, such as the UK Heart Valve Registry.

There certainly were differences in the preoperative and operative characteristics of the replacement patients versus the repair group. Many in-hospital outcomes were worse in the replacement group, which, as you comment, may suggest that the two groups were not equal. However, we did our best to account for these differences by performing multivariable regression analysis. From this analysis we determined independent risk factors for poor outcomes, and TV replacement was a poor independent predictor of short- and long-term outcomes.

DR JAMES W. FREDERIKSEN (Chicago, IL): Were you able to determine why patients who had tricuspid valve replacement had that procedure instead of repair?

DR SINGH: That is a good question. Unfortunately we weren't able to determine why repair versus replacement was chosen at the time of surgery in most cases. I am sure that the surgeon preference and patient comorbidities were taken into account. Likewise, the extent of the disease, whether there was sufficient salvageable tissue for a repair, and concomitant valvular operations were factored in to whether a repair or replacement was performed. As stated above, however, our take-home message is that an imperfect repair is probably preferable to a tricuspid valve replacement procedure.


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 References
 

  1. Cohn LH. Tricuspid regurgitation secondary to mitral valve disease: when and how to repair J Card Surg 1994;9:237-241.[Medline]
  2. Ratnatunga CP, Edwards M, Dore CJ, Taylor KM. Tricuspid valve replacement: UK heart valve registry mid-term results comparing mechanical and biological prostheses Ann Thorac Surg 1998;66:1940-1947.[Abstract/Free Full Text]
  3. Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival J Am Coll Cardiol 2004;43:405-409.[Abstract/Free Full Text]
  4. Allard M, Boutin C, Burwash IG, et al. Canadian Cardiovascular Consensus 2004: surgical management of valvular heart disease Can J Cardiol 2004;20(Suppl E):50E-53E.
  5. Edmunds Jr LH, Clark RE, Cohn LH, Grunkemeier GL, Miller DC, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations J Thorac Cardiovasc Surg 1996;112:708-711.[Free Full Text]
  6. Breyer RH, McClenathan JH, Michaelis LL, McIntosh CL, Morrow AG. Tricuspid regurgitation: a comparison of nonoperative management, tricuspid annuloplasty, and tricuspid valve replacement J Thorac Cardiovasc Surg 1976;72:867-874.[Abstract]
  7. Rivera R, Duran E, Ajuria M. Carpentier's flexible ring versus De Vega's annuloplasty: a prospective randomized study J Thorac Cardiovasc Surg 1985;89:196-203.[Abstract]
  8. McCarthy PM, Bhudia SK, Rajeswaran J, et al. Tricuspid valve repair: durability and risk factors for failure J Thorac Cardiovasc Surg 2004;127:674-685.[Abstract/Free Full Text]
  9. Filsoufi F, Anyanwu A, Salzberg SP, Frankel T, Cohn LH, Adams DH. Long-term outcomes of tricuspid valve replacement in the current era Ann Thorac Surg 2005;80:845-850.[Abstract/Free Full Text]
  10. Rizzoli G, Vendramin I, Nesseris G, Bottio T, Guglielmi C, Schiavon L. Biological or mechanical prostheses in tricuspid position?a meta-analysis of intra-institutional results. Ann Thorac Surg 2004;77:1607-1614.[Abstract/Free Full Text]
  11. Bajzer CT, Steward WJ, Cosgrove DM, Azzam SJ, Arheart KL, Klein AL. Tricuspid valve surgery and intraoperative echocardiography: factors affecting survival, clinical outcome, and echocardiographic success J Am Coll Cardiol 1998;321023–21.
  12. Chidambaram M, Abdulali SA, Baliga BG, Ionescu MI. Long-term results of DeVega's tricuspid annuloplasty Ann Thorac Surg 1987;43:185-195.[Abstract/Free Full Text]
  13. Yada I, Tani K, Shimono T, Shikano K, Okabe M, Kusagawa M. Preoperative evaluation and surgical treatment for tricuspid regurgitation associated with acquired valvular heart diseaseThe Kay-Boyd method vs the Carpentier-Edwards ring method. J Cardiovasc Surg (Torino) 1990;31:771-777.[Medline]
  14. Konishi Y, Tatsuta N, Minami K, et al. Comparative study of Kay-Boyd's, DeVega's and Carpentier's annuloplasty in the management of functional tricuspid regurgitation Jpn Circ J 1983;47:1167-1172.[Medline]
  15. Scully HE, Armstrong S. Tricuspid valve replacement: fifteen years of experience with mechanical prostheses and bioprostheses J Thorac Cardiovasc Surg 1995;109:1035-1041.[Abstract/Free Full Text]
  16. Van Nooten GJ, Caes F, Taeymans Y, et al. Tricuspid valve replacement: postoperative and long-term results J Thorac Cardiovasc Surg 1995;110:672-679.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
Ann. Thorac. Surg.Home page
M. B. Izzat
Spring Retractor: A New Adjunct for Aortic Valve Surgery
Ann. Thorac. Surg., July 1, 2011; 92(1): 364 - 365.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
A. Lauten, M. Ferrari, K. Hekmat, R. Pfeifer, G. Dannberg, A. Ragoschke-Schumm, and H. R. Figulla
Heterotopic transcatheter tricuspid valve implantation: first-in-man application of a novel approach to tricuspid regurgitation
Eur. Heart J., May 2, 2011; 32(10): 1207 - 1213.
[Abstract] [Full Text] [PDF]


Home page
Postgrad. Med. J.Home page
R. B. Irwin, M. Luckie, and R. S. Khattar
Tricuspid regurgitation: contemporary management of a neglected valvular lesion
Postgrad. Med. J., November 1, 2010; 86(1021): 648 - 655.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
J. A. Sarralde, J. M. Bernal, J. Llorca, A. Ponton, L. Diez-Solorzano, J. R. Gimenez-Rico, and J. M. Revuelta
Repair of Rheumatic Tricuspid Valve Disease: Predictors of Very Long-Term Mortality and Reoperation
Ann. Thorac. Surg., August 1, 2010; 90(2): 503 - 508.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. M. Bernal, A. Ponton, B. Diaz, J. Llorca, I. Garcia, J. A. Sarralde, J. Gutierrez-Morlote, C. Perez-Negueruela, and J. M. Revuelta
Combined Mitral and Tricuspid Valve Repair in Rheumatic Valve Disease: Fewer Reoperations With Prosthetic Ring Annuloplasty
Circulation, May 4, 2010; 121(17): 1934 - 1940.
[Abstract] [Full Text] [PDF]


Home page
Interact CardioVasc Thorac SurgHome page
G. Vigano, A. Guidotti, M. Taramasso, A. Giacomini, and O. Alfieri
Clinical mid-term results after tricuspid valve replacement
Interact CardioVasc Thorac Surg, May 1, 2010; 10(5): 709 - 713.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
B. M.S. Shrestha, S. Fukushima, M. Vrtik, I. H. Chong, L. Sparks, H. Jalali, and P. G. Pohlner
Partial Replacement of Tricuspid Valve Using Cryopreserved Homograft
Ann. Thorac. Surg., April 1, 2010; 89(4): 1187 - 1194.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
T. C. Lee, B. Desai, and D. D. Glower
Results of 141 Consecutive Minimally Invasive Tricuspid Valve Operations: An 11-Year Experience
Ann. Thorac. Surg., December 1, 2009; 88(6): 1845 - 1850.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
C. K. Park, P. W. Park, K. Sung, Y. T. Lee, W. S. Kim, and T.-G. Jun
Early and Midterm Outcomes for Tricuspid Valve Surgery After Left-Sided Valve Surgery
Ann. Thorac. Surg., October 1, 2009; 88(4): 1216 - 1223.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. H. Rogers and S. F. Bolling
The Tricuspid Valve: Current Perspective and Evolving Management of Tricuspid Regurgitation
Circulation, May 26, 2009; 119(20): 2718 - 2725.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
C. J. Bruce and H. M. Connolly
Right-Sided Valve Disease Deserves a Little More Respect
Circulation, May 26, 2009; 119(20): 2726 - 2734.
[Full Text] [PDF]


Home page
J Am Coll CardiolHome page
A. Shiran and A. Sagie
Tricuspid Regurgitation in Mitral Valve Disease: Incidence, Prognostic Implications, Mechanism, and Management
J. Am. Coll. Cardiol., February 3, 2009; 53(5): 401 - 408.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
R. J. Moraca, M. R. Moon, J. S. Lawton, T. J. Guthrie, K. A. Aubuchon, N. Moazami, M. K. Pasque, and R. J. Damiano Jr
Outcomes of Tricuspid Valve Repair and Replacement: A Propensity Analysis
Ann. Thorac. Surg., January 1, 2009; 87(1): 83 - 89.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
J. M. Bernal, A. Ponton, B. Diaz, J. Llorca, I. Garcia, A. Sarralde, C. Diago, and J. M. Revuelta
Surgery for rheumatic tricuspid valve disease: a 30-year experience.
J. Thorac. Cardiovasc. Surg., August 1, 2008; 136(2): 476 - 481.
[Abstract] [Full Text] [PDF]


Home page
Eur J Cardiothorac SurgHome page
T. Guenther, C. Noebauer, D. Mazzitelli, R. Busch, P. Tassani-Prell, and R. Lange
Tricuspid valve surgery: a thirty-year assessment of early and late outcome
Eur J Cardiothorac Surg, August 1, 2008; 34(2): 402 - 409.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
R. H. Jones
The Year in Cardiovascular Surgery
J. Am. Coll. Cardiol., May 8, 2007; 49(18): 1887 - 1898.
[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):
Steve K. Singh
Gilbert H.L. Tang
William G. Williams
Tirone E. David
Michael A. Borger
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 Singh, S. K.
Right arrow Articles by Borger, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Singh, S. K.
Right arrow Articles by Borger, M. 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