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Eur J Cardiothorac Surg 2007;32:296-300. doi:10.1016/j.ejcts.2007.05.003
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

What to expect after tricuspid valve replacement? Long-term results

Department of Cardiovascular Surgery, Yuksek Ihtisas Hospital of Turkey, Ankara, Turkey

Received 14 March 2007; received in revised form 13 April 2007; accepted 7 May 2007.

^_* Corresponding author. Address: N. Tandogan cad. 5/6 Kavaklidere, 06540 Ankara, Turkey. Tel.: +90 312 426 7574; fax: +90 312 426 6181. (Email: kvural{at}tr.net).

	Abstract

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

 
Objective: Current knowledge in long-term results of tricuspid valve replacement is limited. Present study reviews our experience from a consecutive series. Methods: Forty-two patients (16 male, 26 female; mean age: 33 ± 15) underwent tricuspid valve replacement between March 1987 and December 2004. The etiology was rheumatic in 64%, Ebstein's anomaly in 31%, and endocarditis in 5%. Nineteen patients were in New York Heart Association (NYHA) Class III functional capacity (45%), and 13 in class IV (31%). Twenty patients (48%) underwent isolated tricuspid valve replacement. The remaining underwent combined (mitral and/or aortic) valve replacements. Tricuspid replacement device was mechanical in 31% and bioimplant in 69%. Results: Hospital mortality was 26%. Rheumatic etiology, reoperation and elevated pulmonary artery pressure were associated with higher early mortality. The patients with decreased functional capacity (NYHA Class III/IV), congestive symptoms and rheumatic origin were more prone to low cardiac output development. The Kaplan–Meier survivals were 37% at 10 years and 30% at 15 years. The 10-year event-free survival was 31%. Elevated pulmonary artery pressure and rheumatic etiology unfavorably affected the long-term results. The average functional capacity in survivors improved significantly after operation. Conclusions: Any tricuspid disease not amenable to repair thus necessitating replacement is an unfortunate situation since both the short and long-term results of valve replacement are suboptimal in regard to those of left-sided valve replacements, probably due to different structural and geometrical characteristics of right ventricle and the low-pressure venous system hemodynamics. Etiology, clinical presentation and pulmonary vascular hemodynamics are major determinants of the outcome.

Key Words: Tricuspid valve replacement • Heart valve • Endocarditis • Rheumatic

	1. Introduction

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

 
Surgeons encountering an organic tricuspid lesion in daily practice often try to avoid a valve replacement as much as possible, and generally prefer some sort of repair with or without using annuloplasty rings. Indeed, the results of valve replacements on the right side of the heart are usually not so satisfactory as those of the ‘left-side’ replacements. Still, there are instances in which a tricuspid valve replacement is unavoidable. Interestingly, although the technique for tricuspid valve replacement is pretty straightforward when compared to various repair options which necessitates considerable skill and experience, there is continuing debate on some aspects of the valve replacement, such as the choice of the prosthesis type according to age and risk groups. This is partly due to our limited knowledge on the long-term results of the procedure.

The following study is an analysis of our experience in tricuspid valve replacement and may provide insight for the reader about its possible applications in daily practice.

	2. Material and methods

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

 
2.1 Demographics
Forty-two patients, 16 male (38%) and 26 female (62%); with a mean age of 33 ± 15 (range: 7–70 years) underwent 45 tricuspid valve replacements between March 1987 and December 2004. The etiology of tricuspid valve disease was rheumatic in 27 (64%), Ebstein's anomaly in 13 (31%), and endocarditis in 2 (5%). Among them, 16 patients (38%) had undergone previous cardiac surgery (mitral valve replacement in 9, mitral + aortic valve replacement in 2, aortic valve replacement in 1, pericardiectomy in 1 and mitral valve replacement + tricuspid annuloplasty in 3). During the same period, 739 patients underwent tricuspid valve repair (annuloplasty and/or valvotomy) and these 42 tricuspid valve replacements represented 5.4% of all tricuspid procedures.

2.2 Clinical presentation
Ten patients were in New York Heart Association Class-II functional capacity (24%), 19 were in Class III (45%), and 13 were in class IV (31%). Dyspnea was present in 26 patients (62%), tachyarrhythmia in 25 (60%), congestive symptoms and signs in 25 (60%), cyanosis in 8 (19%) and fever in 2 (5%).

2.3 Procedure
Twenty patients (48%) underwent isolated tricuspid valve replacement. The remaining patients underwent combined mitral and tricuspid (17 patients; 40%), or aortic, mitral and tricuspid (5 patients; 12%) valve replacements. Tricuspid replacement device was mechanical (St. Jude or Carbomedics) in 15 patients (36%) and bioimplant (Carpentier-Edwards or St. Jude) in 27 (64%). A bioimplant was preferred in patients undergoing isolated tricuspid valve replacement with no previously implanted mitral or aortic mechanical valves, especially in the old age group, and for those in whom the anticoagulant therapy would be problematic. Tricuspid valve was replaced either on cardiopulmonary bypass with the heart beating (in 12 isolated tricuspid valve replacements and 7 combined valve procedures), or under cardiac arrest with the aorta cross-clamped (in 12 isolated tricuspid valve replacements and 11 combined valve procedures). Our technique involved the preservation of tricuspid valvular and subvalvular apparatus when possible, and largely incorporating these tissues in the bite when taking stitches. We think that this reduces the need for taking deeper bites from the ring, therefore minimizes damage risk to the adjacent structures, such as the conduction tissue. The preservation of the subvalvular apparatus may also be beneficial for postoperative right ventricular functions. We prefer to use teflon pledget-reinforced, separate polyester sutures instead of continuous suturing technique.

2.4 Follow-up
Follow-up was obtained in all patients. The mean follow-up time was 5.6 years (up to 18.3 years, a total of 175 patient years). Three patients underwent reoperation for repeat tricuspid replacement during the follow-up, two for prosthetic valve thrombosis and one for bioprosthesis degeneration 2 years after the primary operation.

2.5 Statistical analysis
Means are presented ± standard deviation. Determinants of mortality or complications were analyzed by Chi-square or Fisher's exact tests when applicable. Comparisons of means were performed using t-test. Survival and complication-free survival estimates were expressed as Kaplan–Meier curves, using Log rank test for any comparison. A p-value equal or smaller than 0.05 was considered statistically significant.

	3. Results

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

 
3.1 Early outcome
Hospital mortality was 26% (11 patients, 8 females and 3 males, p = 0.48; mean age: 39.5 ± 14.9; range 21–70 years). The major cause for early mortality was right heart failure and low cardiac output syndrome. Among the mortalities, five patients had undergone tricuspid valve replacement under cardioplegic arrest and six on cardiopulmonary bypass with the heart beating (p = 0.45). Bioprosthetic tricuspid valves were implanted in seven patients and mechanical prostheses in four patients. Eight of them were combined valve procedures and three were isolated tricuspid valve replacements.

The risk factors associated with perioperative mortality were, (1) Rheumatic etiology, (10 of 27; 37% vs only 1 of 13 patients of Ebstein's anomaly group; p = 0.05), (2) Reoperation (50 vs 11%; p = 0.01) and (3) Elevated pulmonary artery pressure (exceeding 30 mmHg; 50 vs 5.9%; p = 0.004). The mean pulmonary artery pressure was 26.7 ± 11.8 mmHg in survivors versus 36.2 ± 10.2 mmHg in those died perioperatively. Pulmonary hypertension was also a determinant of postoperative survival (see below).

Early complications were seen in 25 patients (59.5%), namely, transient bradyarrhythmia in 8 patients (19%), low cardiac output requiring inotropic support in 21 (50%), transient renal function impairment in 1 (2.4%), respiratory complications necessitating prolonged mechanical ventilatory support in 2 patients (4.8%), sepsis in 1 (2.4%), and cardiac tamponade in 4 (9.5%).

Perioperative low cardiac output development was strongly associated with poor preoperative functional class, as it developed in 9 of the 19 patients in NYHA Class-III and 10 of the 13 patients in Class-IV, in contrast to only 2 of the 10 patients in Class-II (p = 0.007). Similarly, low cardiac output was more frequent in those presented with preoperative congestive heart failure symptoms and signs (hepatomegaly, lower extremity edema, ascites). Sixteen of 25 such patients developed low cardiac output in contrast to only 5 of 17 patients admitted with no congestive signs (p = 0.02). Also, low cardiac output developed more frequently among those of rheumatic origin (17 of 27 patients of rheumatic origin in comparison to only 2 of 13 patients Ebstein's anomaly). No difference in outcome, in terms of early mortality or low cardiac output development, was observed between those undergoing tricuspid valve replacement on cardiopulmonary bypass with the heart beating and those operated on under cardioplegic arrest (p = 0.45 and p = 0.32, respectively).

3.2 Long-term outcome
Survivors were followed up for an average postoperative period of 5.6 ± 5.5 years (up to 18.3 years, a total of 175 patient years). Nine patients died during postoperative follow-up. Three patients underwent repeat tricuspid valve replacements (see below). The Kaplan–Meier survival estimates were 37 ± 11% at 10 years (Fig. 1 ) and 30 ± 11% at 15 years with an average survival was 8.5 ± 1.41 years (all including operative mortality), and longest postoperative follow-up was 18 years.

View larger version (8K): [in this window] [in a new window]   Fig. 1. Postoperative survival after tricuspid valve replacement. The Kaplan–Meier survival estimates were 37 ± 11% at 10 years and, 30 ± 11% at 15 years.

3.3 Risk factors influencing long-term outcome
For the patients with elevated pulmonary artery pressure (exceeding 30 mmHg) the long-term survival was less favorable with a 10-year Kaplan–Meier survival rate of 21%, in contrast to 54% in those with normal pulmonary artery pressures (p = 0.01) (Fig. 2 ).

View larger version (10K): [in this window] [in a new window]   Fig. 2. The impact of elevated pulmonary artery pressure on postoperative survival after tricuspid valve replacement. The Kaplan–Meier survival was 21% in patients with elevated pulmonary artery pressures in contrast to 54% in those with normal pulmonary artery pressures (p = 0.01; Log rank) at 10 years.

Another factor influencing the long-time survival was the underlying disease, as 10-year Kaplan–Meier survival was 53% in patients of congenital origin (Ebstein) versus 41% in those of rheumatic origin (p = 0.01; Log rank) (Fig. 3 ).

View larger version (10K): [in this window] [in a new window]   Fig. 3. The impact of underlying disease on postoperative survival after tricuspid valve replacement. The Kaplan–Meier survival was 53% in patients of congenital origin (Ebstein) versus 41% in those of rheumatic origin (p = 0.01; Log rank) at 10 years.

Ten-year ‘event-free survival’ was 31% for the whole group, including perioperative and long-term mortality, hospitalizations and repeat valve operations. No statistically significant difference was detected between mechanical or bioprosthetic valves in regard to perioperative mortality, low cardiac output, long-term survival or event-free survival.

3.5 Functional capacity improvement
The average functional capacity in survivors improved from NYHA Class-III to NYHA-IV postoperatively (p < 0.0001). A comparison between preoperative and postoperative functional capacity based on NYHA Classification is represented in Fig. 4 .

View larger version (15K): [in this window] [in a new window]   Fig. 4. Postoperative functional capacity improvement among survivors was evident in terms of New York Heart Association Class (p < 0.0001).

	4. Discussion

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

Many previous studies reported considerably high mortality and morbidity after tricuspid valve replacement in both early and late postoperative period [1–3]. Our results are in accordance with this observation, with a relatively high operative mortality, and a 10-year survival of only 37% (including operative mortality). Ten-year event-free survival was 31% for the whole group, with no statistically significant difference between mechanical or bioprosthetic valves. One positive observation is that the average functional capacity improved significantly after the tricuspid valve replacement in survivors.

The risk factors for early mortality were rheumatic etiology, reoperation and elevated pulmonary artery pressure. Low cardiac output developed more frequently in those with decreased functional capacity (NYHA Class III an IV), congestive symptoms and those of rheumatic origin. Among the survivors, elevated pulmonary artery pressure and rheumatic etiology affect the long-term survival unfavorably. Rheumatic (or rather, organic) etiology was perhaps the most important predictor for poor outcome. This is understandable, because rheumatic disease is a destructive and ongoing process causing extensive and sometimes irreparable damage not only to tricuspid valve but also to myocardium. There is frequently a tri-layer involvement, albeit with variable severity from one layer to another, called ‘pancarditis’. Rheumatic involvement of tricuspid valve often indicates that the other valves are already attacked by the inflammatory process. The elevated pulmonary pressure may simply reflect the left-sided valvular involvement with all its implications on pulmonary vasculature and left ventricular myocardium. Most of these prognostic determinants are absent in Ebstein's anomaly. Moreover, rheumatic etiology more frequently necessitates valve replacement instead of repair.

Another issue to point out here is the fact that our series included both Ebstein's and rheumatic cases. There are similar examples reported previously. Our goal was not to analyze a group of patients of a specific ‘etiology’ (be it Ebstein's or rheumatic) but to review the results of a certain ‘procedure’ (i.e. tricuspid valve replacement). This made it possible to point out to the differences between those of diverse etiologies undergoing the same treatment. Furthermore, although the presented Ebstein's cases are of congenital origin, the disease became manifested during adulthood or adolescence, a fact that makes them differ substantially from the classical Ebstein's cases presenting early in infancy. On the other hand, with respect to surgical approach and operative techniques, the adult Ebstein's cases have similarities with those of other etiologies undergoing tricuspid valve replacement. We believe that they carry a good deal of information about the fate of tricuspid valve replacement, justifying their presence in the current study group.

Going back to the causes responsible for the suboptimal outcome, another factor may be the prolonged overloading of right ventricle by pulmonary hypertension, a condition known to cause sometimes irreversible structural and functional deterioration. Sometimes the tricuspid regurgitation may serve as a compensatory mechanism against pressure and/or volume-overloading of the right ventricle (afterload mismatch). Abrupt restoration of valve competence (by valve replacement) may result in right ventricular decompensation by redirecting the entire stroke volume against a high-pressure system.

Therefore, the suboptimal results of tricuspid valve replacement may partly be due to the very nature of the disease, i.e. the etiology, which dictates clinical presentation and pulmonary vascular pathophysiology. However, there must be other factors causing unsatisfactory results after valve replacement when done on tricuspid valve. For example, the different structural and geometrical characteristics of right ventricle and the low-pressure venous system hemodynamics may also play a role. At least in theory, the rigid circular frames of prosthetic valves may distort the normally crescent-shaped tricuspid annulus and right ventricular myocardial fiber arrangements in a way that rendering them ‘less effective’. This may unfavorably affect the right ventricular contraction dynamics and may also compromise left ventricular contraction by septal distortion. The characteristic bulging appearance of the rigid prosthetic frame during right ventricular systole is visible to naked eye at the operation, before coming off bypass.

In addition to all these mentioned above, the currently available prosthetic valves are rather far from being ideal, and this is more so for the right-sided implantations. The inherited disadvantages of both bioprostheses and mechanical prostheses seem to be accentuated when implanted into the low-pressured right-side system. Some authors advocate using bioprostheses in tricuspid position due to high thromboembolic complications following mechanical valve implants [4]. Our results did not support this argument, probably because of the relatively low incidence of valve-related events in our series. Nevertheless, others do not accept this theory proposing that the cardiac output is the same for both right and left heart and therefore the flows, and consequently their washing effect, should be equal. They propose a prostacyclin-based explanation in which the prostacyclin-rich content of the blood returning from the lungs to the left atrium is held responsible for lower rates of thromboembolism at this side of the heart [5].

Therefore, the choice between the mechanical and biological prostheses is a subject of ongoing debate. Some authors advocate the use of biologic prostheses even in young patients because of limited life expectancy unrelated to the type of tricuspid prostheses at long-term follow-up [6]. Others suggest that even greater care is needed to prevent valve thrombosis in mechanical valves, there is still a greater chance for reoperation in bioprosthetic valves [7]. Bioprostheses are more prone to tissue degeneration and destruction, and their low durability precludes their universal recommendation, especially in destructive processes such as carcinoid. Patients with tricuspid valve endocarditis secondary to long-term intravenous drug addiction pose a significant problem because they often lack peripheral venous access, which renders anticoagulation monitoring almost impossible. The strongest argument against the use of biological valves in the tricuspid position is that the rate of reoperation escalates after 10–15 years. However, bioprostheses may outlast patients with drug addiction and previous endocarditis, thus negating the benefit of a mechanical valve. Nevertheless, there are those advocating the use of bioprosthetic valves [4,8], those supporting the use of mechanical valves [3] and those, including us, failed to show any superiority of one on the other in terms of survival, event free survival, freedom from reoperation or quality of life [2,9].

All these arguments above need to be more elucidated to go beyond being simple speculations. Nevertheless, the fact is that the short and long-term results after tricuspid valve replacement are poorer than those of left-sided replacements. Most survivors, however, will have a better quality of life, as the improvement in their NYHA class is evident.

	References

Top Abstract 1. Introduction 2. Material and methods 3. Results 4. Discussion References

 

1. Filsoufi F, Anyanwu AC, 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]
2. Ratnatunga CP, Edwards MB, 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. Kaplan M, Kut MS, Demirtas MM, Cimen S, Ozler A. Prosthetic replacement of tricuspid valve: bioprosthetic or mechanical. Ann Thorac Surg 2002;73:467-473.[Abstract/Free Full Text]
4. Kawano H, Oda T, Fukunaga S, Tayama E, Kawara T, Oryoji A, Aoyagi S. Tricuspid valve replacement with the St. Jude Medical valve: 19 years of experience. Eur J Cardiothorac Surg 2000;18:565-569.[Abstract/Free Full Text]
5. Péterffy Á, Szentkirályi I. Mechanical valves in tricuspid position: cause of thrombosis and prevention. Eur J Cardiothorac Surg 2001;19:735.[Free Full Text]
6. Carrier M, Hebert Y, Pellerin M, Bouchard D, Perrault LP, Cartier R, Basmajian A, Page P, Poirier NC. Tricuspid valve replacement: an analysis of 25 years of experience at a single center. Ann Thorac Surg 2003;75:47-50.[Abstract/Free Full Text]
7. Chang BC, Lim SH, Yi G, Hong YS, Lee S, Yoo KJ, Kang MS, Cho BK. Long-term clinical results of tricuspid valve replacement. Ann Thorac Surg 2006;81:1317-1323.[Abstract/Free Full Text]
8. Dalrymple-Hay MJ, Leung Y, Ohri SK, Haw MP, Ross JK, Livesey SA, Monro JL. Tricuspid valve replacement: bioprostheses are preferable. J Heart Valve Dis 1999;8:644-648.[Medline]
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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Kerem M. Vural Ilknur Bahar Levent Mavioglu Ahmet Saritas Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Iscan, Z. H. Articles by Saritas, A. Search for Related Content PubMed PubMed Citation Articles by Iscan, Z. H. Articles by Saritas, A. Related Collections Valve disease