Asian Cardiovasc Thorac Ann 2004;12:239-245
© 2004 Asia Publishing EXchange Ltd
Evolution of Repaired and Non-repaired Tricuspid Regurgitation in Rheumatic Mitral Valve Surgery without Severe Pulmonary Hypertension
Kaan Kirali, MD,
Suat Nail Ömero
lu, MD,
Kemal Uzun, MD,
Vedat Erentu, MD,
Nilgün Bozbua, MD,
Ercan Eren, MD,
Mehmet Balkanay, MD,
Mete Alp, MD,
Cevat Yakut, MD
Department of Cardiovascular Surgery, Ko!uyolu Heart and Research Hospital, Istanbul, Turkey
For reprint information contact: Kaan Kirali, MD Tel: 90 216 326 6969 Fax: 90 216 339 0441 Email: imkkirali{at}yahoo.com Department of Cardiovascular Surgery, Ko#uyolu Heart and Research Hospital, Kadiköy 81020, Istanbul, Turkey.
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ABSTRACT
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The aim of this study was to evaluate the usefulness of repairing significant tricuspid regurgitation (
grade 2) without severe pulmonary hypertension (
50 mm Hg). Between 1993 and June 2001, 88 consecutive patients were operated on for rheumatic mitral valve disease associated with significant tricuspid regurgitation and without severe pulmonary hypertension. The severity of the tricuspid valve disease was assessed by echocardiography. Sixty-three patients had severe ( grade 3) tricuspid regurgitation (Group I), and 25 patients had moderate (grade 2) tricuspid regurgitation (Group II). There was no hospital mortality. six patients died during follow-up. The overall actuarial survival rate for 8 years was 92.1% ± 3.1%. Cox proportional hazard regression analysis showed that age ( p = 0.006) and pulmonary complication ( p = 0.01) were associated with increased late mortality. Freedom from death was similar in both groups at 8 years (93.1% ± 3.3% versus 88% ± 8%, p = 0.7). Severe postoperative tricuspid regurgitation ( grade 3), caused by the failure of tricuspid repair or leaving the valve untouched, impaired long-term survival after surgery, and actuarial survival was 96.1% ± 2.7% and 83% ± 7.8% at 7 years ( p = 0.048), respectively. Severe tricuspid regurgitation, functional or organic, should be corrected at the time of mitral valve surgery, whereas untouched functional moderate tricuspid regurgitation improves after mitral valve surgery.
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INTRODUCTION
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Significant tricuspid regurgitation ( grade 2) is not uncommon in patients with rheumatimitral valve disease and may be present in more than half of those requiring mitral valve replacements. In left-sided valvular heart disease, tricuspid regurgitation is usually functional and occurs secondary to pulmonary hypertension or right ventricular volume overload caused by long-standing chronic mitral valve disease. The decision to repair the tricuspid valve is particularly important in patients with severe pulmonary hypertension (> 50 mm Hg). The condition of mild tricuspid regurgitation (< grade 2) often regresses after the correction of mitral valve lesions. The strategy of treatment for moderate tricuspid regurgitation remains controversial, mainly because a choice must be made between repairing and not repairing. Failure to correct significant tricuspid regurgitation at the time of the mitral valve surgery may result in a poor prognosis.1 Leaving significant tricuspid regurgitation unattended adversely affects early and late outcomes.2 Continuance or worsening of moderate or severe tricuspid regurgitation likely worsens long-term outcomes.3–5
The aim of this study was to evaluate the usefulness of tricuspid valve repair in significant tricuspid regurgitation ( grade 2) without severe pulmonary hypertension ( 50 mm Hg) during isolated mitral valve surgery.
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PATIENTS AND METHODS
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Between 1993 and June 2001, 88 consecutive patients without severe pulmonary hypertension ( 50 mm Hg) underwent mitral valve replacement or repair for isolated rheumati mitral valve disease with significant tricuspid regurgitation ( grade 2). All patients were operated on electively, except one patient, who had received a mechanical valve in the first operation and underwent urgent reoperation because of the stuck valve. Seventeen (19.3%) patients had undergone previous mitral valve intervention without any surgical treatment to the tricuspid valve. Nine patients had been operated on with cardiopulmonary bypass, i.e. 2 open mitral commissurotomy, 1 ring annuloplasty, 5 biological and 1 mechanical prosthetic valve replacements. Percutaneous balloon mitral valvuloplasty had been performed in 2 patients, and 6 patients had undergone closed mitral valvotomy. All patients with mild tricuspid regurgitation (< grade 2), mixed tricuspid lesion (stenosis and insufficiency), severe pulmonary hypertension (> 50 mm Hg), all other etiologies except rheumatic fever (infective endocarditis, mitral valve prolapse, degenerative disease), and mitral valve disease associated with another cardiac pathology (aortic valve disease, coronary artery disease, congenital heart diseases) were excluded from this study. All patients underwent transthoracic echocardiography pre and postoperatively. Cardiac catheterization for hemodynamic study and coronary angiography were performed when patients were older than 40 years. Intraoperative transesophageal echocardiography was used only in patients receiving mitral valve repair.
Preoperative diagnosis of tricuspid regurgitation was made by the conventional 4-grade classification based on the distance reached by the tricuspid regurgitation jet in 2-dimensional Doppler echocardiography.6 Echocardiographic tricuspid regurgitation was graded as moderate or severe based on the occupancy of the right atrial area, regurgitation was considered moderate if the jet area occupied 20% to 33% and severe for > 33% occupancy.3 Systolic flow reversal in the inferior vena cava or hepatic veins was considered indicative of at least moderate tricuspid regurgitation. In the present study, 63 (71.6%) patients had severe ( grade 3) tricuspid regurgitation (Group I), and the other 25 (28.4%) had moderate (grade 2) tricuspid regurgitation (Group II). Preoperative characteristics of both groups are presented in Table 1
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The cause of the tricuspid regurgitation was functional in 60 (68.1%) patients and organic in 28 (31.9%) (Table 2). Tricuspid regurgitation is considered organic if rheumatic valvulitis, thickening of the tricuspid valve or annulus is diagnosed with preoperative echocardiography. Four patients were diagnosed as having functional tricuspid regurgitation preoperatively, but their tricuspid leaflets were found to be thickened in surgery and they were reclassified into the organic group.
All patients were operated on using standard cardiopulmonary bypass with aortic and bicaval cannulae with snares. Before cannulation, the tricuspid valve was investigated by digital palpation through the right atrial appendage. Moderate whole body hypothermia (28 to 30°C) and antegrade intermittent isothermic blood cardioplegia were used for myocardial protection. Seventy-nine (89.8%) patients received mitral valve replacement, 7 (7.9%) mitral valve commissurotomy and Kay annuloplasty, and 2 (2.3%) mitral valve commissurotomy and posterior leaflet pericardial enlargement. The coaptation of the repaired mitral valves was successful with intraoperative transesophageal echocardiography. After procedure was completed on the mitral valve, the right atrium was opened and the tricuspid valve investigated. We did not repair it and left the tricuspid valve untouched when the tricuspid valve had moderate regurgitation preoperatively, or if the tricuspid valve and annulus had normal morphology at visualization intraoperatively. In the opposite conditions we repaired the tricuspid valve with the DeVega annuloplasty technique using a double-armed 3-0 pledgeted suture through the annulus. We began the suture annuloplasty technique at the anteroseptal commissure and continued through the tricuspid annulus along anterior and posterior leaflets, before tying both ends at the posteroseptal commissure. After weaning the patient off cardiopulmonary bypass, the competence of the tricuspid valve was assessed digitally by passing a finger into the right atrium through its appendage before tying the appendage, and then by echocardiography postoperatively. The repaired tricuspid valves of the patients receiving mitral repair at the same time were checked by transesophageal echocardiography intraoperatively. All patients received a low dosage of angiotensin converting enzyme inhibitors, anticoagulant therapy, and a diuretic, if necessary.
Postoperative clinical evaluations and transthoracic echocardiography were conducted annually. The last echocardiographic data of the late deaths were added into the statistic analyses. No patient was excluded, and follow-up was 100% complete with a mean postoperative interval of 4.3 ± 2.45 years (range, 2 months to 8.5 years; total 378 years). A commercial statistical software package (SPSS for Windows, version 10.0, SPSS Inc. Chicago) was used for data analysis. Data are presented with a mean ± standard deviation. Differences between categorical variables were tested using the 
2 test; differences between continuous variables were tested using the Student’s t test. Wilcoxon-signed ranks were used to compare pre and postoperative changes on the hemodynamic parameters. Cox proportional hazard regression analysis was used to assess risk factors as independent predictors of patient survival. Forward stepwise logistic regression analysis was used to determine predictors of postoperative severe tricuspid regurgitation. Actuarial survival and event-free estimates were generated by the Kaplan-Meier method, and differences between curves were tested with a log-rank test. Event-free rates are presented with a mean ± standard error of the estimate. A p-value of less than 0.05 was considered statistically significant.
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RESULTS
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There was no early mortality. Sixty-eight (77.3%) patients were in NYHA functional class I and 20 (22.7%) patients in class II postoperatively. Postoperative improvement of functional capacity in the whole group was significant (p < 0.001). One patient underwent mitral valve reoperation during follow-up because of severe mitral restenosis. Another patient underwent reoperation for mitral restenosis and severe tricuspid regurgitation. This patient had a history of organic tricuspid disease. The reason of the reoperation was annular dilatation because of technically unsuccessful repair in the first operation. Actuarial freedom from tricuspid valve reoperation (n = 1) was 95% ± 4.9% at 8 years (0.26% per pt-yr).
Six (6.8%) patients died during the follow-up. Causes of death were biventricular failure in 2 patients, anticoagulant-related hemorrhage in 2 patients, and non-cardiac in 2 patients. Both patients with biventricular failure had grade 3 tricuspid regurgitation in spite of receiving DeVega annuloplasty, which had been successful in the early postoperative period. They also had impaired cardiac function before the operation. Univariate analysis showed that age, pulmonary complications and late neurologic events were significantly associated with late mortality. Only age and pulmonary complications were found by Cox proportional hazard regression analysis to be associated with increased late mortality in the presence of the other factors (Table 3). When we investigated pre and postoperative hemodynamic parameters on the late mortality, multivariate analysis did not show any significant predictor (Table 4).
The overall actuarial survival was 92.1% ± 3.1% at 3 and 8 years (1.6% per pt-yr). Long-term outcome was not affected by the severity of preoperative tricuspid regurgitation and actuarial survival was similar in Group I (93.1% ± 3.3%) and Group II (88% ± 8%) at 8 years ( p = 0.7) (Figure 1). When we compared patients according to the treatment procedures for the tricuspid valve, we observed that actuarial survival was similar in repair and non-repair groups ( p = 0.97): 92.6% ± 3.6% versus 90.8% ± 6.25% at 8 years, respectively. Actuarial survival was 92.4% ± 3.7% in functional regurgitation versus 91.1% ± 6.1% in organic regurgitation at 8 years ( p = 0.94). Postoperative continuance of severe tricuspid regurgitation ( grade 3) impaired long-term survival. Actuarial survival was 96.1% ± 2.7% and 83% ± 7.8% at 7 years ( p = 0.048), respectively. Univariate analysis showed that the degree ( p = 0.003) and etiology ( p = 0.008) of preoperative tricuspid regurgitation were significant risk factors for the late developed severe tricuspid regurgitation, but only the degree of preoperative tricuspid regurgitation ( p = 0.015; odds ratio 2.5, 90% CI 1.3–4.7) was found to be statistically significant in forward stepwise logistic regression analysis, whereas the etiology of preoperative tricuspid regurgitation ( p = 0.053; odds ratio 0.4, 90% CI 0.1–0.9) was significant in the limit.
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Figure 1. Freedom from death in both groups. The upper rows show the total number of patients in both groups. The lower rows show the total number of patients who died and postoperative death-time in both groups.
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When pre and postoperative echocardiographic parameters were compared, tricuspid regurgitation, pulmonary artery systolic pressure, and left atrial diameter showed a significant decrease (Table 5). The improvement of preoperatively severe tricuspid regurgitation was significant in patients with functional tricuspid regurgitation (Table 2
). However, severe tricuspid regurgitation improved only in 1 (25%) of 4 untouched patients reclassified in Group II during long-term follow-up.
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DISCUSSION
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Tricuspid regurgitation is usually functional and may be associated with approximately 50% of patients requiring mitral valve surgery.1 On the other hand, organic tricuspid regurgitation can develop after rheumatic fever,7 but it is not uncommon in our practice. It is perhaps wrong to classify tricuspid etiology as organic or functional because organic tricuspid disease is often present along with functional tricuspid regurgitation, and its incidence varies from 28% to 95%.8 Tricuspid insufficiency develops mostly because of dilatation of the right ventricle and the tricuspid ring, which are long-term results of left side valvular pathology. Furthermore, development of tricuspid regurgitation causes volume overload on the right ventricle by tricuspid regurgitation itself along with dilatation of the tricuspid annulus.5 Following mitral valve intervention with or without surgical correction of functional tricuspid regurgitation, right ventricular function can improve and postoperative tricuspid regurgitation can decrease. On the other hand, organic lesions can worsen and decrease the effectiveness of tricuspid annuloplasty during long-term follow-up. If functional or organic tricuspid regurgitation is left uncorrected it can affect the early and long-term outcomes. Decreasing tricuspid regurgitation is more important than the etiology of preoperative tricuspid regurgitation.
Surgical management of tricuspid regurgitation associated with rheumatic left-sided heart valve disease is disputatious. There are three treatment alternatives for tricuspid regurgitation to achieve better long-term outcome, namely non-operative management of the incompetent valve, and the repair or replacement of the valve. After Duran and colleagues9 pointed out that tricuspid lesions must be surgically corrected in two circumstances (when the functional insufficiency is moderate to severe, and when the lesion is organic), most surgeons accept that severe tricuspid regurgitation with abnormal valve pathology is the main indication for operative management. The main reason for untouched strategy is the significant improvement on the left atrial and pulmonary artery pressure after the mitral valve intervention, which decreases right ventricular overload and afterload, and tricuspid insufficiency. As shown in this study, significant improvement was observed more in patients with functional tricuspid regurgitation than in those with organic tricuspid lesion. Also, untouched tricuspid pathology improved poorly in organic disease. No difference was shown in the long-term survival between groups with or without preoperatively severe tricuspid regurgitation ( p = 0.7), and between patients with repaired or non-repaired tricuspid regurgitation ( p = 0.97). However, postoperatively severe tricuspid regurgitation impaired long-term survival ( p = 0.048). This means that survival after rheumatic mitral valve surgery must be affected by variables other than tricuspid annuloplasty. It could improve quality of life, but it is not effective alone in improving late outcomes. Our policy is to repair organic tricuspid regurgitation, but is not to touch the moderate functional tricuspid regurgitation. The other question is which strategy must be chosen for patients with moderate tricuspid regurgitation whether it is functional or organic. As our study showed, when moderate tricuspid regurgitation (Group II) was not repaired it did not worsen after successful mitral valve intervention and did not impair long-term outcomes. We usually do not prefer to repair moderate functional tricuspid regurgitation whenever a patient has severe pulmonary hypertension (> 50 mm Hg).
Most studies show that the right ventricular function is impaired irreversibly in patients with serious mitral valve disease because of a long-standing severe tricuspid regurgitation.5 Leaving significant tricuspid regurgitation after the first operation worsens late outcomes. Late tricuspid regurgitation is associated with a severe reduction in exercise capacity, and a poor surgical outcome.10 In this study, we observed that the severity of preoperative tricuspid regurgitation alone did not impair late outcomes. However, the healing of tricuspid insufficiency is more important than the severity of preoperative tricuspid regurgitation. Tricuspid annular dilatation regresses after mitral valve replacement because the right ventricular function will improve due to a decrease in volume and pressure overload. If severe tricuspid regurgitation continues after the operation or develops in the follow-up period, this pathology will impair long-term survival. Late severe tricuspid regurgitation was observed in 27 (30.7%) patients in the whole group, and this pathology increased right heart failure and late mortality.
The feasibility of repairing the tricuspid valve depends on multiple factors such as the experience of the surgical team and the involvement of the tricuspid leaflets. There are different suture annuloplasty techniques,1,11–13 but ring or suture annuloplasty techniques might result in a high incidence of residual incompetence. Suture annuloplasty techniques are preferred here in order to avoid tricuspid valve replacement because of the high hospital mortality rate.7 DeVega annuloplasty is one of the effective repair techniques for tricuspid regurgitation. It is a simple and quicker method with a lower cost than ring annuloplasty, and for these reasons this method is the most preferable technique in developing countries. When suture annuloplasty techniques are used in the treatment of patients with significant tricuspid regurgitation, outcomes might worsen because of the residual significant tricuspid incompetence. In this study, we observed that the ratio of the residual significant incompetence of this technique was 35.6%, whereas the continuance of significant tricuspid regurgitation was 31% among non-repaired patients ( p = 0.67). Organic tricuspid regurgitation had worse improvement after DeVega annuloplasty (42.9% versus 76.8%, p = 0.01). For this reason, significant and/or long-standing organic tricuspid regurgitation should be repaired without considering its degree, and may be it would be better to choose ring annuloplasty in these patients. Tricuspid valve replacement is an alternative.14
Coexistent high pulmonary artery pressure (> 50 mm Hg) and pre and postoperative pulmonary complications may further increase the risk of operation, especially in older patients. In the present study, age and pulmonary complications were also found to be significant risk factors for the late mortality in patients without severe pulmonary hypertension. Older age increases the severity of natural pathology, which causes irreversible pulmonary changes and biventricular failure despite the absence of severe pulmonary hypertension. A longer clinical course could impair pulmonary functions, where pulmonary complications after operating impair early and late outcomes. It is likely that the elapsed time from the onset of symptoms is the determining factor rather than age itself. We believe that earlier surgical intervention for mitral valve pathologies could prevent a greater degree of clinical and hemodynamic deterioration and greater surgical risk.15 This fact is valid for the tricuspid valve.
In conclusion, significant tricuspid regurgitation can improve after treatment of mitral valve disease, whereas postoperative severe tricuspid regurgitation is associated with high late mortality. Early correction of mitral valve pathology is therefore warranted. Mild-moderate (< grade 2) tricuspid regurgitation without severe pulmonary hypertension can be left uncorrected, but echocardiographic follow-up must be performed annually. Severe ( grade 3) functional and all significant ( grade 2) organic tricuspid regurgitation should be corrected at the time of mitral valve surgery, whereas moderate (grade 2) functional tricuspid regurgitation can be left non-repaired. Severe organic tricuspid regurgitation must be treated using ring annuloplasty or valve replacement, because suture annuloplasty might not be effective over a long time.
Presented at the 50th International Congress of the European Society for Cardiovascular Surgery, June 20th to 23nd, 2001, Budapest.
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REFERENCES
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ABSTRACT
INTRODUCTION
