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Eur J Cardiothorac Surg 2008;33:600-606. doi:10.1016/j.ejcts.2008.01.011
Copyright © 2008, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.
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Michele De Bonis
Elisabetta Lapenna
Francesco Maisano
Lucia Torracca
Ottavio Alfieri
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Right arrow Congestive Heart Failure
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Evolution of tricuspid regurgitation after mitral valve repair for functional mitral regurgitation in dilated cardiomyopathy

Michele De Bonis*, Elisabetta Lapenna, Flavia Sorrentino, Giovanni La Canna, Antonio Grimaldi, Francesco Maisano, Lucia Torracca, Ottavio Alfieri

Department of Cardiac Surgery, San Raffaele University Hospital, Via Olgettina 60, 20132 Milan, Italy

Received 3 September 2007; received in revised form 3 January 2008; accepted 8 January 2008.

* Corresponding author. Tel.: +39 0226437102; fax: +39 0226437125. (Email: michele.debonis{at}hsr.it).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Objective: To assess the evolution of tricuspid regurgitation (TR) in dilated cardiomyopathy (DCM) patients submitted to mitral repair for functional mitral regurgitation (MR). Methods: Ninety-one DCM patients (mean age 61 ± 11.3) submitted to MV repair (±tricuspid repair) for functional MR were included. Preoperative EF was 30.9 ± 6.5%, left ventricular (LV) end-diastolic volume 113 ± 31.5 ml/m2, LV end-systolic volume 81.8 ± 26.7 ml/m2, functional MR ≥3+/4+. TR was classified as ≤1+/4+ in 57 patients (62.6%), 2+/4+ in 21 (23%) and ≥3+/4+ in 13 (14.2%). Most of the patients were in NYHA class III or IV. A tricuspid annuloplasty was associated to mitral repair whenever preoperative TR was ≥3+. Therefore 13 patients (14.2%) underwent concomitant tricuspid annuloplasty whereas the remaining 78 (with preoperative TR ≤2+) did not. Results: At follow-up (mean 1.8 ± 1.2 years), 12% of the patients (11/91) had still 3–4+ TR due to failure of the tricuspid repair or progression of untreated ≤2+ TR. Freedom from TR ≥3+ was 78 ± 8.8% at 3.5 years. Among the 78 patients not submitted to tricuspid repair, 14 (18%) showed a progression of TR severity equal or greater than two grades. The multivariate analysis identified grade of TR at discharge (OR 5.4, p = 0.01) and preoperative RV dysfunction (OR 19.6, p = 0.02) as the only independent predictors of TR ≥3+/4+ at follow-up. Conclusions: A significant number of patients submitted to mitral repair for functional MR present ≥3+ TR at follow-up as consequence of progression of untreated TR or failure of tricuspid repair. A more aggressive and effective treatment of functional TR in this setting should be pursued.

Key Words: Functional tricuspid regurgitation • Functional mitral regurgitation • Dilated cardiomyopathy


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Functional tricuspid regurgitation (TR) is often associated with mitral valve disease and is thought to be caused by dilatation of the tricuspid annulus and tethering of the tricuspid leaflets due to right ventricular (RV) dilatation [1–3]. With increasing prevalence of heart failure, functional TR is now encountered regularly in patients with severe left ventricular (LV) dysfunction submitted to cardiac operations. Surgical treatment of this condition remains a challenging problem since optimal techniques and timing of correction are still objects of debate. For many years the concept that secondary TR decreases after mitral valve surgery alone has been largely accepted [4,5] and, in common surgical practice this has led to functional TR being often ignored or undertreated [6]. More recently, compelling data have shown that surgically untreated functional TR can persist or even worsen despite correction of the associated left-sided lesion [7–10] suggesting that a more aggressive approach towards this disease should be advocated. Tricuspid annuloplasty represents the common surgical strategy employed although the rate of residual and recurrent regurgitation remains high [11–15]. Moreover most of the data available on the outcome of functional TR after mitral valve surgery come from series of patients affected by degenerative [13] or rheumatic mitral disease [10] with only a few reports dealing with regurgitation of the tricuspid valve in the context of dilated cardiomyopathy (DCM) [15]. The purpose of this study, therefore, was to assess the evolution of functional TR in patients with congestive heart failure who underwent surgical repair of functional mitral regurgitation (MR) with or without concomitant tricuspid annuloplasty.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 Appendix A
 References
 
2.1 Study population
A computerized database was prospectively constructed with the preoperative, postoperative and follow-up data of all the patients who underwent mitral repair (±tricuspid repair) for functional MR in our institution. Patients with unstable angina or recent myocardial infarction (<6 months), acute MR due to papillary muscle rupture, multiple organ failure or concomitant LV reconstruction were not included. For the purpose of this study the records of the first 121 consecutive patients included from 1998 to December 2005 were retrospectively reviewed. Thirty patients were excluded because of one or more of the following reasons: residual MR ≥1+ at discharge (15 pts), preoperative pacemaker wires across the tricuspid valve (6 pts), ICD and/or pacemaker implantation before discharge or within 6 months after surgery (5 pts), death in the hospital or before the first 6 months follow-up (7 pts). The final population comprised 91 patients with severe (4+/4+) or moderately severe (3+/4+) MR secondary to ischemic or idiopathic dilated cardiomyopathy. Most of them were in NYHA class III or IV and underwent mitral repair. A tricuspid annuloplasty was associated whenever preoperative TR was ≥3+/4+. All patients had a follow-up length of at least 6 months with the clinical visit and the echocardiographic assessment performed in our dedicate heart failure outpatient clinic. The institutional ethic committee approved this study and waived individual consent for this retrospective analysis.

2.2 Echocardiographic measurements
Preoperatively a transthoracic (TTE) followed by a transesophageal echocardiography (TEE) was performed. Tricuspid regurgitation grade was measured by TTE in the apical 4-chamber view, the parasternal short-axis view at the level of the aortic valve and the RV inflow view. The maximal ratio of color Doppler regurgitant jet area to right atrial area was calculated in the view in which the spatial distribution of the jet was maximal. The severity of TR was graded as mild, 1+/4+ (jet area/right atrial area <10%); moderate, 2+/4+ (jet area/right atrial area 10–20%); moderately severe, 3+/4+ (jet area/right atrial area 20–33%); and severe, 4+/4+ (jet area/right atrial area >33%) [15]. The vena contracta width at the narrowest portion of the regurgitant jet was also measured. Supportive signs of severity of TR were dilatation and respiratory variation of the inferior vena cava as well as reduction or reversal of systolic flow in the hepatic veins. Tricuspid regurgitation was considered significant when the regurgitant jet occupied >20% of the right atrial area (≥3+/4+) and/or when the vena contract width was ≥7 mm. In the apical 4-chamber view the tricuspid annulus was assessed in late diastole at the time of maximal tricuspid opening [16,17]. The presence of tethering of the tricuspid leaflets was evaluated at the time of maximal systolic closure by measuring the coaptation depth, which was defined as the distance between the tricuspid annular plane and the coaptation point of the tricuspid leaflets. A coaptation depth >5 mm defined significant tricuspid leaflet tethering and was usually described in the echocardiographic report. In the absence of significant tethering, the defect of leaflet coaptation responsible for functional TR was ascribed to annular dilatation alone. Enlargement of the tricuspid annulus was qualitatively reported by the operator although detailed dimensions were only occasionally measured. Right ventricular function was assessed by the percent RV area change [18]. Moreover, tissue Doppler imaging (TDI) was used to measure the peak systolic velocity of the tricuspid annulus (S-TDI) as an index of global RV function by placing the sample volume of the pulse-wave TDI on the tricuspid annulus at the site of attachment of the anterior leaflet in the 2D 4-chamber view. According to the measured S-TDI value, RV function was classified as normal (S-DTI ≥10 cm/s), moderately depressed (S-TDI ≤10 cm/s and ≥3 cm/s) and severely depressed (S-TDI <3 cm/s). Right ventricular dilatation was usually assessed qualitatively. Peak right ventricular systolic pressure (RVSP) as an estimate of pulmonary pressure was calculated by measuring peak tricuspid regurgitant velocity and using the modified Bernoulli equation, with 10 mmHg added for the estimated right atrial pressure [18–20]. Pulmonary hypertension was defined as a RVSP >40 mmHg. The severity of MR was graded as: mild, 1+ (jet area/left atrial area <10%); moderate, 2+ (jet area/left atrial area 10–20%); moderately severe, 3+ (jet area/left atrial area 20–45%); and severe, 4+ (jet area/left atrial area >45%). The vena contracta width of the MV was also measured. TEE was repeated in the operating room after surgery and serial TTEs were then performed at hospital discharge and every 6 months thereafter.

2.3 Surgery
All patients were operated through median sternotomy with standard cardiopulmonary bypass on moderate hypothermia. Myocardial protection consisted of antegrade and retrograde cold blood cardioplegia. The mitral valve was approached through a left atriotomy and repaired by means of an undersized annuloplasty. An edge-to-edge technique was associated to the annuloplasty when the tethering of the leaflets was more pronounced as defined by a coaptation depth >1 cm. The right atrium was not routinely opened to explore the tricuspid valve. Surgical correction of functional TR was performed only when the preoperative echocardiographic degree of TR was moderately severe or severe (TR ≥3+/4+ and/or vena contracta with ≥7 mm). The choice of the repair technique was at the discretion of the surgeon although, in general, we tended to use a ring in patients with more severe tricuspid annular dilatation or pulmonary hypertension. Tricuspid annuloplasty was usually performed under cardioplegic arrest.

2.4 Follow-up
After hospital discharge all patients had at least one 6-month clinical and echocardiographic (TTE) follow-up in a dedicated outpatient clinic at our institution. For the patients who underwent ICD/cardiac resynchronization therapy after surgery, the last echocardiogram considered was the one performed just before the device implantation. Follow-up was 100% complete (mean time 1.8 ± 1.2 years, range 0.5–5.7 years, median 1.8 years).

2.5 Statistical analysis
Calculations were performed using SPSS version 11.5 (SPSS Inc., Chicago, IL, USA) for Windows (Microsoft Corp, Redmond, WA) software package. Continuous data were expressed as mean ± SD. If they were normally distributed, comparison between two groups was performed with Student's t-test for (un)paired samples, as indicated. If continuous data were not normally distributed, the Mann–Whitney U test or the Wilcoxon signed-rank test were employed for independent or related samples, respectively. Comparison of categorical variables was performed using {chi} 2 and Fisher's exact test. NYHA functional class, grade of MR and TR were treated as ordinal variables and compared with the Wilcoxon signed-rank test (related samples) or with the Mann–Whitney U test (independent samples). Linear or logistic regression analysis was used for correlation of variables of interest as appropriate. Freedom from TR ≥3+ was evaluated by Kaplan–Meier analysis. Univariate analysis of predictors of significant TR (≥3+/4+ and/or vena contracta width >7 mm) at follow-up was performed with logistic regression and variables with a p value <0.1 were entered in a multivariable model. All data are presented as mean ± standard deviation (for actuarial estimates, standard error is reported instead).


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 Appendix A
 References
 
3.1 Patient characteristics and clinical results
Most of the patients had severe LV dilatation and dysfunction with a mean EF of 30 ± 6.5% and all of them had 3+ or 4+ functional MR. Concomitant TR was classified as ≤1+/4+ in 57 patients (62.6%), 2+/4+ in 21 (23%) and ≥3+/4+ in 13 (14.2%). Mitral regurgitation was treated by means of an isolated undersized annuloplasty in 45 patients (49.4%) while the edge-to-edge technique was associated in the remaining 46 (50.5%). The baseline characteristics of the patients and the operative data are presented in Table 1 . All the 13 patients (14.2%) with moderately severe (3+/4+) or greater preoperative TR underwent concomitant tricuspid annuloplasty (tricuspid annuloplasty group, TA group) whereas the remaining 78 (with preoperative TR ≤2+) did not (no tricuspid annuloplasty group, no-TA group). Table 2 reports the preoperative characteristics of the 13 patients (13/91, 14.2%) of the tricuspid annuloplasty group compared with the 78 who did not undergo tricuspid repair. Annuloplasty type depended on surgeon preference. Seven patients received a De Vega suture annuloplasty. In five patients a remodeling annuloplasty was preferred. The rings used were a Carpentier-Edwards semirigid ring (Edwards Lifesciences) in two cases (sizes 32 and 34) and an Edwards MCIII system (Edwards Lifesciences) in the remaining three (sizes 28, 30 and 34, respectively). Finally a reduction annuloplasty with a flexible St. Jude Medical Tailor ring n. 31 was chosen in the last patients. Concomitant procedures were CABG (41/91 pts, 45%) and ablation of permanent atrial fibrillation (14/91 pts, 15.3%). There were eight deaths (8/91, 8.7%) more than 6 months after surgery, all in the no-TA group (p = 0.4 compared to the TA group). The causes of death were congestive heart failure (4 pts), acute myocardial infarction (1 pt), liver cancer (1 pt) and unknown (1 pt). One patient had to be reoperated 7 months after mitral repair for endocarditis of the prosthetic ring. She underwent mitral valve replacement with a mechanical prosthesis and died of septic shock in the intensive care unit. At follow-up significant improvements in LV dimensions, LV function and systolic pulmonary artery pressure were documented (Table 3 ). From a clinical point of view most of the patients experienced an improvement of their heart failure symptoms after surgery: NYHA class III or IV was present in 69 patients (75.8%) before operation and in only 7 cases (7.7%) at the last outpatient visit (p < 0.0001).


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  		Table 1 Preoperative and operative data
 

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  		Table 2 Preoperative data in the TA and no-TA groups
 

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  		Table 3 Preoperative and follow-up echocardiographic data
 
3.2 Evolution of functional TR
At the last echocardiographic assessment functional TR was absent or mild in 52 patients (57.1%), moderate in 28 (30.7%), moderately severe in 9 (9.8%) and severe in 2 (2.2%). Significant TR (3+ or 4+) was therefore identified in 12% of the patients (11/91) due to failure of tricuspid repair (1 pt) or progression of surgically ignored preoperative TR (10 pts). In 14 of the 78 patients not submitted to tricuspid repair (14/78, 17.9%) functional TR worsened at least two grades (from 0 to 2+ in 6 cases and from 0–1+ to 3+ or 4+ in other 8 patients) (Fig. 1 ). Usually the mechanism of TR described at follow-up was annular dilatation, although leaflet tethering (coaptation depth >0.5 cm) was reported as an associate finding in six patients (three with moderate and three with moderately severe TR). The actuarial freedom from TR ≥3+ was 78 ± 8.8% at 3.5 years (Fig. 2 ). When the presence of significant (≥3+) TR at follow-up and the worsening of at least two grades of preoperative TR were considered together, this combined end-point was reached at follow-up by 17 of the 91 patients of the study (18.6%). Freedom from this combined end-point was 61 ± 10% at 3.5 years.


Figure 1
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  		Fig. 1. Patients with progression of at least two grades of untreated preoperative TR ≤2+ (14/78 pts, 18%).

 

Figure 2
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  		Fig. 2. Freedom from tricuspid regurgitation ≥3+ at last follow-up.

 
3.3 Predictors of significant (≥3+/4+) TR at follow-up
Predictors of significant (≥3+/4+) TR at follow-up are listed in Table 4 . At univariate analysis preoperative RV dilatation (OR 8.3, p = 0.009), preoperative RV dysfunction (OR 13.7, p = 0.0001) and TR grade at discharge (OR 3, p = 0.01) were significant risk factors. The multivariate analysis identified grade of TR at discharge (OR 5.4, p = 0.01) and preoperative RV dysfunction (OR 19.6, p = 0.02) as the only independent predictors of TR ≥3+/4+. As far as RV dysfunction is concerned, before surgery this condition was reported in 21 cases (23%) (moderate in 19 and severe in 2). During follow-up, RV dysfunction improved in 7 of these 21 patients and did not significantly change in the remaining 14. Ten more patients developed new RV dysfunction late after surgery for an overall prevalence of this condition at the last echocardiogram of 26.3% (24/91 pts) (p = 0.7 vs preoperative).


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  		Table 4 Predictors of tricuspid regurgitation ≥3+
 
3.4 Pulmonary hypertension and functional TR at follow-up
Pulmonary hypertension was still present at follow-up in 24 (26.3%) of the patients and was significantly correlated to the severity of LV dysfunction. Indeed, linear regression analysis demonstrated a statistically significant correlation between lower postoperative LV ejection fraction and higher SPAP at follow-up (r = 0.35, p = 0.001). The incidence of significant (≥3+) TR at follow-up was 37% (9/24) among the patients with pulmonary hypertension and 3% (2/67) among those with SPAP <40 mmHg at the last echocardiogram (p < 0.0001).

3.5 Patterns of LV remodeling and influence on functional TR
The pattern of LV remodeling after surgery influenced the evolution of functional TR. ‘Reverse LV remodeling’, defined as a decrease ≥15% in the LVESVI or in both LVESVI and LVEDVI at the last echocardiographic follow-up compared to the preoperative values, was demonstrated in 49 patients (53.8%) of the study population (reverse LV remodeling group). Significant (≥3+) TR occurred in only 1 patient of this group (1/49, 2%) whereas it was documented in 10 patients of the no reverse LV remodeling group (10/42, 23.8%) (p = 0.04).

3.6 Influence of recurrence of MR on functional TR at follow-up
At the last echocardiogram MR was absent or mild (1+) in 67 patients (73.6%), moderate (2+) in 15 (16.4%) and moderately severe (3+) or severe (4+) in 9 (9.8%). The incidence of TR ≥3+ at follow-up was comparable in patients with and without recurrence of moderately severe or severe mitral regurgitation after surgery (22% vs 11%, respectively, p = 0.6).


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
Appendix A
 References
 
Functional TR is thought to be caused by tricuspid annulus dilatation and tethering of the tricuspid leaflets after RV dilatation [1–3]. Repair of functional TR is a challenging problem. The decision to perform tricuspid annuloplasty is still often dictated by institutional or surgeon bias, with little data to guide decision-making. It is well accepted that significant TR (3+ to 4+) should be treated at the time of surgical correction of left-sided valvular disease [21,22]. However surgical indication for the correction of mild (1+) and moderate (2+) TR remains controversial with many surgeons still favoring a conservative approach in this context [15]. Until recently this policy has also been followed in our institution. However, an increasing number of studies are showing that such a conservative TR management may lead to a progressive worsening of tricuspid insufficiency particularly in patients with DCM, in whom progression of TR could be influenced by the natural history of the cardiomyopathy more than it could be in other pathologic conditions. In addition, the presence in congestive heart failure of LV and RV dysfunction, pulmonary hypertension, possible recurrence of functional MR after repair, and the need for ICD/biventricular pacing substantially increases the risk of progression of initially apparent but not significant TR or the possibility of its recurrence after tricuspid annuloplasty. Recently Matsunaga and Duran [15] reported that in their experience, among patients with functional MR submitted to mitral repair, the presence of significant (≥3+) functional TR was 30% before surgery. In more than half (57%), the regurgitation was ignored by the surgeon and, at follow-up, close to 50% of the patients showed significant TR despite successful revascularization and mitral repair. Matsuyama and associates [23] reported that 16% of the patients who underwent non-ischemic mitral valve surgery without concomitant tricuspid valve surgery developed 3+ to 4+ TR at an 8-year follow-up. Finally, Dreyfus and associates [7] clearly demonstrated that tricuspid annular dilatation is an ongoing process that will lead to severe TR with time. In their series, patients with severe annular dilatation and minimal TR who did not undergo a prosthetic ring annuloplasty, presented with a significant worsening of TR after a mean follow-up of 5 years. On the basis of these results they advocated that any patient with substantial annular dilatation should undergo repair regardless of TR grade or even no TR. Our study was specifically undertaken to assess the evolution of TR in patients with DCM submitted to mitral valve repair in whom the decision to perform tricuspid annuloplasty was traditionally based on the severity of regurgitation rather than on the degree of annular dilatation. Our findings confirm previous observations that uncorrected moderate or less TR in patients submitted to mitral repair for functional MR does not invariably improve after surgical correction of MR, but often persists and can even worsen after operation [15,23]. The mechanism responsible for the persistence, progression or recurrence of TR was not extensively studied at follow-up TTE in our series. Annular dilatation was described as the main mechanism in most of the cases whereas associated tethering of the leaflets (coaptation depth >0.5 cm) was reported overall in only six cases. It is likely that leaflet tethering due to RV dilatation and dysfunction was involved in the mechanism of functional TR more frequently than we have been able to document and report. Preoperative RV dysfunction and grade of TR at hospital discharge appeared to be strongly associated with TR progression. They might induce or increase annular dilatation and leaflet tethering leading to recurrence of significant TR after tricuspid annuloplasty [14]. RV function therefore needs to be carefully assessed to predict the likelihood of repair being a success and the possible progression of apparently non-significant degree of preoperative TR. Moreover, if tethering is present, besides annuloplasty, surgical techniques aiming at overcoming leaflet tethering should be considered for a more durable repair. In our series, most of the cases of progression or recurrence of significant TR occurred in patients with pulmonary hypertension at follow-up. It seems likely that the increased afterload caused on the right heart by persistent or new onset pulmonary hypertension led to worsening of functional TR. Previous studies have reported an association between increased SPAP and worse TR or higher rate of tricuspid repair failure [24,25]. Finally, in this study, functional TR at follow-up was influenced by the pattern of postoperative LV remodeling. Indeed all the cases of progression/recurrence of significant TR (but one) occurred among the patients who did not show signs of reverse LV remodeling. The findings of this study, together with other recent data showing the rate of progression of untreated functional TR, prompted a change in surgical practice in our institution leading to a more aggressive approach to tricuspid valve repair in dilated cardiomyopathy patients based on annular dilatation rather than on severity of TR.

4.1 Study limitations
This study is a retrospective analysis of routine clinical and echocardiographic data, which were entered into a computerized database. Several limitations need to be underlined. No consistent, accurate data were available preoperatively and at follow-up regarding right atrial dimension, tricuspid annular size and degree of leaflet tethering. Therefore a systematic comparison of those parameters before and after surgery to define the precise mechanism of TR at follow-up could not be performed. Moreover we cannot exclude that a certain number of patients had some degree of leaflet tethering, which was unreported or significant annular dilatation despite the presence of only mild functional TR before surgery. Indeed intraoperative inspection of the tricuspid valve was usually not performed in the patients who did not undergo tricuspid repair. In addition, we did not investigate in detail changes occurring in RV shape and dimensions. The jet area/right atrial area method used to quantify TR has limitations, because physiological conditions, machine settings and eccentric jets can influence the size of the distal TR jet. Although we used the vena contracta width to better assess TR severity, this method also has limitations in discriminating intermediate grades of regurgitation. Finally, in the present study, the number of patients is relatively small, particularly the number of those who underwent tricuspid repair.


   Appendix A
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
References
 
Conference discussion

Dr G. Dreyfus (Middlesex, United Kingdom): I think no one really in the audience agrees with all these conclusions, however, I do, and I do support completely the concept you have presented. However, a few questions arise.

Secondary severe tricuspid regurgitation occurs in only 18% of your patient population, whereas it takes place in up to 50% in some publications such as Carlos Duran in a similar group of patients. Do you believe that a longer follow-up would show a trend to increase even further your rate of ongoing TR?

Secondly, you have performed many echo studies to quantify TR jets, to assess tethering through coaptation depth, and to analyze RV dysfunction with tricuspid annulus systolic velocity by tissue Doppler imaging, however, you never tell us whether these parameters correlate well or not with the incidence of secondary TR. Perhaps they did not. If there would be one parameter, could you tell us which one you would choose to determine tethering?

Thirdly, you mentioned pulmonary hypertension as a risk factor, unlike Duran or even in our study, however, Table 2 of your manuscript does show that there was no difference at follow-up between the tricuspid annular group and the non-tricuspid annular group with regard to pulmonary hypertension, remodeling, recurrence of MR. Could you explain these discrepancies?

Fourthly, surgically, you have used seven De Vega and five rings. Do you believe that the De Vega technique has room for these very dilated and sick patients?

Fifth, you have mentioned that tethering could be a major pathophysiological component. Which surgical technique would you advocate to overcome the tethering?

And finally, do you believe that tethering is only a step further in the evolution of the disease and annular dilatation an earlier stage, or do you believe that tethering can occur without annular dilatation?

In conclusion, your presentation is very important and shows again that TR grading, even with sophisticated methods, is not reliable and that annular dilatation and tethering should be considered more carefully to guide appropriate surgery.

Dr De Bonis: I will try to recall all the questions starting from the first one. Yes, I do believe that probably with a longer follow-up the rate of recurrence or worsening of tricuspid regurgitation is going to increase. Indeed, one of the problems when dealing with TR assessed by the severity of the regurgitant jet is also the definition of the severity of tricuspid regurgitation. So when you read the manuscript with respect to moderate TR, you have to go further and look to what percentage of regurgitation or ratio in terms of regurgitant jet was assessed, because this can be misleading when comparing different studies. So, as far as the first question is concerned, we are changing our strategy in terms of being more aggressive basically because we believe that going on with the follow-up, we are going to get a worsening grade of preoperatively untreated 2+ or less TR.

The other question was about how we did assess right ventricular dysfunction. That, of course, is very difficult. We tried to use two parameters, which were right ventricular area changes and DTI measurement of the maximum systolic velocity of the tricuspid annulus excursion, longitudinal excursion, and we used as a cut-off a velocity more than 10 cm/s as an index of normal function, between 3 and 10 as moderate dysfunction, and below 3 as an index of severe right ventricular dysfunction. Of course this is just one way to try to learn more about right ventricular dysfunction, which still remains difficult to assess and unpredictable in terms of evolution.

How did we treat patients with tethering was another of your questions. Well, in the last one and a half years, we realized that we should do something more in presence of tethering. I would like to stress that among the patients who were submitted to tricuspid repair, three of them, submitted to ring annuloplasty, had tethering before surgery, and all three of them, despite being discharged with mild TR, had moderate TR at follow-up. So this is to underscore that tethering is important.

What we are doing now is to stitch the leaflets together, applying the edge-to-edge technique to the tricuspid side. So when the tethering of the leaflet is higher than 5 mm, besides annuloplasty, we stitch the central part of the three leaflets together, trying to force the coaptation at this level. That might decrease the rate of recurrence, or if recurrence of TR is going to happen, probably make it happening at a later stage.

Could you please remind me of some of the other questions?

Dr Dreyfus: I think you did cover most of it and that is fine.


   Footnotes
 
{star} Presented at the 21st Annual Meeting of the European Association for Cardio-thoracic Surgery, Geneva, Switzerland, September 16–19, 2007.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 

  1. Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H. Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two-dimensional echocardiography. Am J Cardiol 1984;53:160-163.[CrossRef][Medline]
  2. Come PC, Riley MF. Tricuspid annular dilatation and failure of tricuspid leaflet coaptation in tricuspid regurgitation. Am J Cardiol 1985;55:599-601.[CrossRef][Medline]
  3. Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA. 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]
  4. Braunwald NS, Ross Jr. J, Morrow AG. Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation 1967:I63-I69.
  5. Duran CM, Pomar JL, Colman T, Figueroa A, Revuelta JM, Ubago JL. Is tricuspid valve repair necessary?. J Thorac Cardiovasc Surg 1980;80:849-860.[Abstract]
  6. King RM, Schaff HV, Danielson GK, Gersh BJ, Orszulak TA, Piehler JM, Puga FJ, Pluth JR. Surgery for tricuspid regurgitation late after mitral valve replacement. Circulation 1984;70:I193-I197.[Medline]
  7. Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair?. Ann Thorac Surg 2005;79:127-132.[Abstract/Free Full Text]
  8. Colombo T, Russo C, Giliberto GR, Lanfranconi M, Bruschi G, Agati S, Vitali E. Tricuspid regurgitation secondary to mitral valve disease: tricuspid annulus function as guide to tricuspid valve repair. Cardiovasc Surg 2001;9:369-377.[CrossRef][Medline]
  9. Porter A, Shapira Y, Wurzel M, Sulkes J, Vaturi M, Adler Y, Sahar G, Sagie A. Tricuspid regurgitation late after mitral valve replacement: clinical and echocardiographic evaluation. J Heart Valve Dis 1999;8:57-62.[Medline]
  10. Izumi C, Iga K, Konishi T. Progression of isolated tricuspid regurgitation late after mitral valve surgery for rheumatic mitral valve disease. J Heart Valve Dis 2002;11:353-356.[Medline]
  11. 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]
  12. Onoda K, Yasuda F, Takao M, Shimono T, Tanaka K, Shimpo H, Yada I. Long-term follow-up after Carpentier-Edwards ring annuloplasty for tricuspid regurgitation. Ann Thorac Surg 2000;70:796-799.[Abstract/Free Full Text]
  13. McCarthy PM, Bhudia SK, Rajeswaran J, Hoercher KJ, Lytle BW, Cosgrove DM, Blackstone EH. Tricuspid valve repair: durability and risk factors for failure. J Thorac Cardiovasc Surg 2004;127:674-685.[Abstract/Free Full Text]
  14. Fukuda S, Song JM, Gillinov AM, McCarthy PM, Daimon M, Kongsaerepong V, Thomas JD, Shiota T. Tricuspid valve tethering predicts residual tricuspid regurgitation after tricuspid annuloplasty. Circulation 2005;111:975-979.[Abstract/Free Full Text]
  15. Matsunaga A, Duran CM. Progression of tricuspid regurgitation after repaired functional ischemic mitral regurgitation. Circulation 2005;112:453-457.[Free Full Text]
  16. Chopra HK, Nanda NC, Fan P, Kapur KK, Goyal R, Daruwalla D, Pacifico A. Can two-dimensional echocardiography and Doppler color flow mapping identify the need for tricuspid valve repair?. J Am Coll Cardiol 1989;14:1266-1274.[Abstract]
  17. Tei C, Pilgrim JP, Shah PM, Ormiston JA, Wong M. 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]
  18. Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J 1984;107:526-531.[CrossRef][Medline]
  19. Ubago JL, Figueroa A, Ochoteco A, Colman T, Duran RM, Duran CG. Analysis of the amount of tricuspid valve annular dilatation required to produce functional tricuspid regurgitation. Am J Cardiol 1983;52:155-158.[CrossRef][Medline]
  20. Currie PJ, Seward JB, Chan KL, Fyfe DA, Hagler DJ, Mair DD, Reeder GS, Nishimura RA, Tajik AJ. Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750-756.[Abstract]
  21. Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL, Lehman B, Benjamin EJ. Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study). Am J Cardiol 1999;83:897-902.[CrossRef][Medline]
  22. 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]
  23. Matsuyama K, Matsumoto M, Sugita T, Nishizawa J, Tokuda Y, Matsuo T. Predictors of residual tricuspid regurgitation after mitral valve surgery. Ann Thorac Surg 2003;75:1826-1828.[Abstract/Free Full Text]
  24. Fukuda S, Gillinov AM, McCarthy PM, Stewart WJ, Song JM, Kihara T, Daimon M, Shin MS, Thomas JD, Shiota T. Determinants of recurrent or residual functional tricuspid regurgitation after tricuspid annuloplasty. Circulation 2006;114(July (1 Suppl.)):I582-I587.[Medline]
  25. Ghanta RK, Chen R, Narayanasamy N, McGurk S, Lipsitz S, Chen FY, Cohn LH. Suture bicuspidization of the tricuspid valve versus ring annuloplasty for repair of functional tricuspid regurgitation: midterm results of 237 consecutive patients. J Thorac Cardiovasc Surg 2007;133(January (1)):117-126.[Abstract/Free Full Text]



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