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Ann Thorac Surg 2001;72:1344-1348
© 2001 The Society of Thoracic Surgeons


Original article: cardiovascular

De Vega tricuspid annuloplasty for tricuspid regurgitation in children

Kirk R. Kanter, MDa, Nancy R. Doelling, MDb, Derek A. Fyfe, MDa,b, Shiva Sharma, MDb, Vincent K.H. Tam, MDa

a Division of Cardio-Thoracic Surgery, Department of Surgery, Atlanta, Georgia, USA
b The Sibley Heart Center, Children’s Healthcare of Atlanta at Egleston, Division of Pediatric Cardiology, Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia, USA

Address reprint requests to Dr Kanter, Division of Cardio-Thoracic Surgery, Emory University School of Medicine, 1365 Clifton Rd, Atlanta, GA 30322
e-mail: kkanter{at}emory.org

Presented at the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
Background. Significant tricuspid valve regurgitation (TR) occurs with other congenital heart defects, typically after repair of right-sided obstructive lesions. Since 1991, we applied the De Vega tricuspid annuloplasty technique for TR in children.

Methods. Forty-one children, aged 5 months to 22.7 years (mean, 9.9 years) underwent 42 De Vega tricuspid annuloplasties for moderate or severe TR during correction of other heart defects. One child had a De Vega during primary ventricular septal defect repair. The remaining patients had prior repair of tetralogy of Fallot or pulmonary atresia, or both (19 patients), double-outlet right ventricle (6 patients), pulmonary stenosis (4 patients), pulmonary atresia and intact ventricular septum (3 patients), complete atrioventricular septal defect (3 patients), and other diagnoses (6 patients). At the time of the De Vega, 37 patients (88%) had pulmonary valve replacement or right ventricular to pulmonary artery conduit replacement. Other procedures included aortic or mitral repair or replacement (6 patients), atrial septal defect and ventricular septal defect closure (5 patients), pulmonary arterioplasty (6 patients), and tracheoplasty (1 patient).

Results. There were no deaths at follow-up of 3.4 ± 2.1 years; 1 child required cardiac transplantation 17 months postoperatively. Early postrepair echocardiography quantified TR as absent or mild (34 patients; 81%), mild-to-moderate (4 patients), moderate (3 patients), and severe (1 patient). The most recent echocardiogram showed moderate TR in 11 patients and severe TR in 2 patients (both with recurrent right ventricular hypertension). One child required tricuspid valve replacement 3 years later and 1 child had redo De Vega at the time of conduit re-replacement. No other child has symptomatic TR, significant tricuspid stenosis, or De Vega-related pacemaker implantation.

Conclusions. The De Vega tricuspid annuloplasty safely provides excellent relief of TR, usually in children undergoing pulmonary valve replacement or conduit replacement. Although echocardiographic TR tends to increase with time (especially with right ventricular hypertension), it rarely requires reintervention or causes symptoms.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
Although congenital tricuspid valve regurgitation is uncommon in children, acquired tricuspid regurgitation does occur in association with other congenital heart defects, typically after repair of right-sided obstructive lesions [1]. Invariably, these children have functional tricuspid regurgitation caused by right ventricular dilatation and resultant stretching of the tricuspid valve annulus. This situation is analogous to rheumatic mitral disease with secondary tricuspid regurgitation in the face of a structurally normal tricuspid valve [2]. Many of these regurgitant tricuspid valves can be made competent by simply reducing the annular size with the annuloplasty technique of De Vega [3]. We reasoned that this experience in adults could be extrapolated to children undergoing repair of other congenital heart defects who have secondary tricuspid valve regurgitation with an apparently structurally normal tricuspid valve. Since 1991, we have applied the De Vega tricuspid annuloplasty technique in 41 children with moderate to severe tricuspid regurgitation during correction of other heart defects. We believe the application of this technique in a series of children has not been reported previously.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
Patient population
Forty-one children aged 5 months to 22.7 years (mean, 9.9 ± 6.4 years) underwent 42 De Vega tricuspid annuloplasties for moderate or severe tricuspid regurgitation at the time of correction of other heart defects. Tricuspid regurgitation was assessed using preoperative transthoracic echocardiography or intraoperative transesophageal echocardiography, or both, measured by spectral Doppler analysis; the study with the greater degree of regurgitation was used for classification. Tricuspid regurgitation was semiquantitatively categorized as absent, mild, moderate, or severe [1]. Mild tricuspid regurgitation was defined as a narrow band jet of less than 1 mm at its base, which did not extend beyond an imaginary line one third of the distance from the tricuspid valve annulus to the posterior wall of the right atrium on a four-chamber echocardiographic view. Moderate tricuspid regurgitation was defined as a band jet between 1 to 2 mm in diameter extending to the middle third of the right atrium. Severe tricuspid regurgitation extended broadly in the distal right atrium with a width greater than 3 mm. Using this grading system, 22 children preoperatively had moderate tricuspid regurgitation, 4 children had moderate-to-severe tricuspid regurgitation, and 16 children had severe tricuspid regurgitation.

The underlying primary diagnosis is shown in Table 1. Thirty-five patients (85%) originally had obstructive lesions of the right ventricular outflow tract, such as tetralogy of Fallot, pulmonary atresia, or pulmonary stenosis. Only 1 child did not have a previous surgical repair. This 3-year-old girl had been treated for endocarditis of a restrictive ventricular septal defect. She had a significant shunt from her left ventricle to the right atrium through the ventricular septal defect with moderate tricuspid regurgitation caused by annular dilatation. The remaining patients had from one to five previous operations (mean, 1.9). The interval from original surgical repair to De Vega annuloplasty was 3 weeks to 21 years (mean, 8.4 years). During this time an additional 118 children with less than moderate tricuspid regurgitation underwent pulmonary valve replacement or replacement of a right ventricular to pulmonary artery conduit without an associated De Vega tricuspid annuloplasty.


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Table 1. Principal Diagnosis (n = 41)

 
Operative techniques
No child in this series underwent operation solely for tricuspid regurgitation. In 37 patients (88%), the primary indication for operation was replacement of the pulmonary valve replacement or a right ventricular to pulmonary artery conduit for significant pulmonary insufficiency or right ventricular outflow tract obstruction. Other procedures performed at the time of the De Vega annuloplasty are listed in Table 2.


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Table 2. Other Procedures With De Vega Annuloplasty

 
Operations were performed through a redo sternotomy (except for the 1 patient with endocarditis and a ventricular septal defect described above) on standard cardiopulmonary bypass with bicaval cannulation. Hypothermic cardioplegic arrest was used only in those patients undergoing repair of left-sided structures (eg, mitral valve repair or replacement, aortic valve replacement, etc.). In the majority who had pulmonary valve replacement or right ventricular to pulmonary artery conduit replacements, the heart was fibrillated or allowed to beat with the branch pulmonary arteries snared.

After performing the primary operation, a De Vega tricuspid annuloplasty was performed using a modification of De Vega’s technique [4]. The tricuspid valve was exposed through a right atriotomy and tested for incompetence by injecting saline into the right ventricle. A pledgetted annuloplasty suture of 3-0 or 4-0 polypropylene was started at the anteroseptal commissure and sewn intermittently to the junction of the annulus and the right ventricle along the anterior and posterior leaflets until just past the posteroseptal commissure (Fig 1A). Another pledget was placed and the suturing was reversed along the posterior and anterior leaflets 1 to 2 mm from the first row alternating the suture technique (ie, taking bites on the second row where the suture was out on the first row and vice versa) until the original pledget at the anteroseptal commissure was reached (Fig 1B). The suture was tied down snugly over a Hegar dilator calibrated to 2 to 3 mm larger than the predicted appropriate pulmonary annulus size derived from published nomograms [5] (Fig 1B).



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Fig 1. (A) Operative technique. The pledgetted annuloplasty suture is started at the anteroseptal commissure and sewn intermittently in clockwise direction in the junction between the annulus and the right ventricle along the anterior and posterior leaflets. (AVN = atrioventricular node; CS = coronary sinus). (B) Operative technique (continued). The annuloplasty suture finishes just beyond the posteroseptal commissure where a pledget is applied. The suture is then reversed in counterclockwise direction 1 to 2 mm external to the first row attempting to alternate suture technique ending at the original pledget. The suture is now tied over a Hegar dilator.

 
Follow-up
The tricuspid valve was evaluated in the operating room with transesophageal echocardiography and before hospital discharge with transthoracic echocardiography using the grading system outlined above. Patients were followed after discharge with periodic cardiologic evaluations and transthoracic echocardiograms. The result of the most recently available echocardiographic study was used for quantification of the degree of late tricuspid regurgitation.


    Results
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 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
There were no operative or late deaths at mean follow-up of 3.4 ± 2.1 years. On early postrepair echocardiography, tricuspid regurgitation was classified as absent or mild in 34 patients (81%), mild to moderate in 4 patients, moderate in 3 patients, and severe in 1 patient. No patient developed significant tricuspid stenosis or heart block related to the De Vega annuloplasty.

One patient underwent successful cardiac transplantation 17 months postoperatively for severe heart failure (an echocardiogram before transplantation showed only mild tricuspid regurgitation). Another patient with moderate tricuspid regurgitation on early postoperative echocardiography developed severe symptomatic tricuspid regurgitation and underwent tricuspid valve replacement 3 years postoperatively. A third patient born with pulmonary atresia with intact ventricular septum had undergone construction of a right ventricular to pulmonary artery conduit with a homograft valve at another institution at 3 years of age. He developed severe conduit stenosis with severe tricuspid regurgitation for which he underwent conduit replacement with a 22-mm pulmonary homograft and a De Vega tricuspid annuloplasty. Although the initial result was quite satisfactory, inexplicably he again developed severe stenosis of his homograft-valved conduit with resultant severe tricuspid regurgitation. Fourteen months postoperatively, he had yet another conduit replacement (this time using a porcine valve) and redo De Vega tricuspid annuloplasty with satisfactory results to date.

In the remaining patients, the most recent echocardiogram showed moderate tricuspid regurgitation in 11 patients and severe tricuspid regurgitation in 2 patients (both of whom had severe right ventricular systolic hypertension calculated by Doppler echocardiography of 65 mm Hg and 74 mm Hg). The 1 patient with severe tricuspid regurgitation on early postrepair examination has moderate tricuspid regurgitation on his latest study. The remaining patients have absent or mild tricuspid regurgitation. No patient had late tricuspid stenosis, symptomatic tricuspid regurgitation, or De Vega-related heart block.


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
Tricuspid regurgitation in children, although uncommon as a primary isolated lesion, occurs occasionally after repair of congenital heart defects, particularly after relief of right-sided obstructive lesions. Kobayashi reported a 48% incidence of tricuspid regurgitation in 133 patients after repair of tetralogy of Fallot with 19% being graded as moderate or severe by echocardiography [1]. Rocchini and colleagues [6] showed an 11% incidence of moderate or severe tricuspid regurgitation in 102 patients undergoing cardiac catheterization after tetralogy repair, although most of these patients had a residual ventricular septal defect. Similarly, Coles and colleagues [7] found a 19% incidence of tricuspid regurgitation at follow-up of children who had relief of critical pulmonary stenosis in infancy.

In this series, 35 of 41 children (85%) originally had obstructive lesions of the right ventricular outflow tract (Table 1). In 88% of our patients, the primary indication for operation included pulmonary valve replacement or replacement of a right ventricular to pulmonary artery conduit for pulmonary insufficiency or right ventricular outflow tract obstruction (Table 2). All of our patients had moderate or severe tricuspid regurgitation. In a series from San Francisco, 6 of the 12 patients undergoing pulmonary valve replacement for pulmonary regurgitation after tetralogy repair had tricuspid regurgitation [8]. Risk factors for tricuspid regurgitation after tetralogy repair in Kobayashi’s experience were increased right ventricular end-diastolic volume (> 200% predicted) or elevated right ventricular systolic pressure (greater than 60 mm Hg) [1]. These data support the hypothesis that tricuspid regurgitation in children after repair of right-sided obstructive lesions can be caused by chronic right ventricular volume or pressure overload with or without right ventricular dysfunction. This leads to dilatation of the tricuspid annulus with resultant regurgitation despite a structurally normal valve.

We reason that this situation is analogous to the setting of secondary functional tricuspid valve regurgitation seen with rheumatic valvular heart disease. At the time of mitral or aortic valve repair or replacement, the tricuspid valve is repaired or replaced [2, 9], postulating that with relief of tricuspid regurgitation these patients will have a smoother postoperative course and better long-term outcome. The De Vega tricuspid annuloplasty has the advantages of simplicity and effectiveness [4]. Follow-up reports of the De Vega tricuspid annuloplasty in patients with rheumatic heart disease have shown good late results. Freedom from recurrent tricuspid regurgitation was 91% at 3 years [10] and actuarial freedom from reoperation was 90% at 14 years [11].

In this series, we used the De Vega technique forty-two times in 41 children. The surgical procedure was quite simple, generally adding only 5 or 10 minutes to the operation. In almost all of the operations, the heart was perfused during this portion of the procedure. Early results were very gratifying, with only 4 patients (9.5%) that had persistent moderate or severe tricuspid regurgitation. Concerns about creation of heart block or tricuspid stenosis were unfounded in our experience.

The durability of the De Vega annuloplasty in children is unknown. On follow-up of 3.4 ± 2.1 years, only 2 patients have had reoperations on the tricuspid valve: one tricuspid valve replacement and one redo De Vega annuloplasty at the time of conduit re-replacement. A third patient underwent cardiac transplantation. None of the remaining children had symptomatic tricuspid regurgitation, although on the most recent echocardiogram, 11 patients had moderate tricuspid regurgitation and 2 patients had severe regurgitation. Both of these children with severe regurgitation had significant residual or recurrent right ventricular hypertension. Thus, one might infer that children at risk for recurrent or persistent right ventricular systolic hypertension are at risk for failure with a De Vega annuloplasty, particularly because the only other patient in our series with significant right ventricular hypertension (calculated right ventricular pressure > 50 mm Hg) was the one who required transplantation.

There is also the concern of fixing the size of the tricuspid valve annulus in a growing child for fear of creating long-term tricuspid stenosis. For this reason, we have avoided the use of annuloplasty rings in these patients. Duran and colleagues [12] proposed the use of absorbable sutures to prevent this complication in the growing child. However, our experience to date would indicate that concern of the De Vega annuloplasty creating tricuspid stenosis in a growing child is more theoretical than real.

Obviously, one could argue that the tricuspid regurgitation in these children would improve without direct surgical intervention simply by correcting the underlying primary problem (eg, pulmonary insufficiency or right ventricular outflow tract obstruction). The resultant decrease in right ventricular volume or pressure work would allow for improved tricuspid valve function as the tricuspid annulus decreases in size. However, our contention is that this procedure minimally increases operative time and risk with the advantage of immediate improvement of tricuspid regurgitation that can potentially have a salutary effect on postoperative hemodynamics and recovery. Furthermore, our results have not revealed any short-term or long-term disadvantages of this procedure. Certainly, however, the question of whether or not these children would have had a similar reduction in degree of tricuspid regurgitation and a similarly uneventful postoperative course can only be answered with a prospective randomized trial, which is beyond the scope of this current series.

In conclusion, the De Vega tricuspid annuloplasty safely provides excellent relief of tricuspid regurgitation in children undergoing repair of other heart problems. It is simple, reliable, inexpensive, and, in our experience, free of complications. Although echocardiographic tricuspid regurgitation tends to increase with time (particularly in patients with right ventricular hypertension), in the long term it rarely requires reintervention or causes symptoms. Therefore, this technique is a simple and useful adjunct in the surgical treatment of congenital heart disease.


    Discussion
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 
DR JOSEPH J. AMATO (Chicago, IL): Congratulations on an excellent presentation with excellent results.

I merely stand to give some historical perspective to the De Vega annuloplasty. In 1972, Dr De Vega presented his annuloplasty as a single row of suture annuloplasty. But in 1977, Dr Mathias Pandit from Brompton Clinic presented a double row of suture annuloplasty for the mitral valve repair. This was similar to the two row annuloplasty that Dr De Vega published in 1980. We have used this annuloplasty of Dr Pandit’s in about 12 patients, both with mitral valve repair or for tricuspid valve regurgitation.

I’m surprised at the use of the polypropylene because this may not promote growth of the annulus. We have used absorbable suture material, and I am wondering whether your follow-up material, as the children continue to grow, might show some distortion of the tricuspid valve.

DR KANTER: That certainly is a theoretical concern. Duran published a paper on the use of absorbable suture for De Vega tricuspid annuloplasty in an animal model. However, as on our follow-up, which admittedly averages only about 3 years, we have not seen tricuspid stenosis. I suspect that with the use of Prolene in growing children, as the child grows the Prolene itself breaks. The answer is still not in as to whether or not it will be a long-term problem, but certainly our experience thus far makes it a theoretical concern only.

DR MARSHALL JACOBS (Philadelphia, PA): Dr. Kanter, my compliments to you on a very fine series and a very fine presentation. My question is this:

It appears that these De Vega annuloplasties in approximately 80% of the patients were done in association with a primary procedure that had the goal of reducing either the pressure load or the volume load on the right ventricle, or both. Prior to undertaking the tricuspid annuloplasty, did you make an assessment, having completed the primary procedure, to see whether the accomplishment of the primary procedure had resulted in a reduction by one or more grades of the tricuspid regurgitation? And if, for example, replacement of a conduit or implantation of a pulmonic valve had resulted in less tricuspid regurgitation, did you still go ahead with the annuloplasty?

DR KANTER: As I mentioned in the presentation, the annuloplasty was performed during rewarming and not after coming off bypass. Again, I would like to emphasize that we extrapolated this series from the adult experience, and there was an argument, a decade ago or so, as to whether or not to address the tricuspid valve at the time of mitral valve repair or replacement, recognizing that a percentage of those patients would not need anything done to the tricuspid valve. I agree that the inference of your question in that there is a percentage of these patients without an annuloplasty who would have had improved tricuspid regurgitation without an annuloplasty.

However, without doing a randomized study, I have no way of knowing. Because it adds, at most, 5 or 10 minutes to the operation, and it does not add ischemic time. In our series there are no associated complications, so it seems like a simple thing to do with low risk. Since you can’t predict who is going to really need it, just do it to everybody with moderate to severe tricuspid regurgitation. Again, I have to emphasize that it was not the primary procedure in any of these operations.

DR ANDREW C. FIORE (St. Louis, MO): I enjoyed your paper. Great results. I have one question, Kirk. In the hypoplastic left heart syndrome group, when they come back for their hemi-Fontan or bidirectional Glenn, if they have severe tricuspid regurgitation with a structurally normal valve, would you use this technique for repair? And if not, what technique would you use?

DR KANTER: There are a handful of children where the right ventricle is a systemic ventricle with tricuspid regurgitation in whom we applied this technique. I purposely excluded them to not confound the analysis. In this series, we presented only pulmonary ventricles. In that subset of patients you mentioned, we have used it with good success if, and again, this is the entire precept upon which the De Vega is based: if the valve is structurally normal and the regurgitation is simply from annular dilatation. In the handful of patients in whom we have applied it, where the right ventricle is a systemic ventricle, we have seen good results.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Discussion
 References
 

  1. Kobayashi J., Kawashima Y., Matsuda H., et al. Prevalence and risk factors of tricuspid regurgitation after correction of tetralogy of Fallot. J Thorac Cardiovasc Surg 1991;102:611-616.[Abstract]
  2. McGrath L.B., Gonzalez-Lavin L., Bailey B.M., Grunkemeier G.L., Fernandez J., Laub G.W. Tricuspid valve operations in 530 patients. Twenty-five-year assessment of early and late phase events. J Thorac Cardiovasc Surg 1990;99:124-133.[Abstract]
  3. De Vega N.G. La anuloplastia selectiva, regulable y permanente. Una técnica original para el tratamiento de la insuficiencia tricuspide. Rev Esp Cardiol 1972;25:555-556.[Medline]
  4. Rabago G., De Vega N.G., Castillon L., et al. The new De Vega technique in tricuspid annuloplasty: results in 150 patients. J Cardiovasc Surg 1980;21:231-238.[Medline]
  5. Blackstone E.H., Kirklin J.W., Pacifico A.D. Surgical management of pulmonary stenosis in tetralogy of Fallot. J Thorac Cardiovasc Surg 1979;77:526-532.[Abstract]
  6. Rocchini A.P., Rosenthal A., Freed M., Castaneda A.R., Nadas A.S. Chronic congestive heart failure after repair of tetralogy of Fallot. Circulation 1977;56:305-310.[Abstract/Free Full Text]
  7. Coles J.G., Freedom R.M., Olley P.M., Coceani F., Williams W.G., Trusler G.A. Surgical management of critical pulmonary stenosis in the neonate. Ann Thorac Surg 1984;38:458-465.[Abstract]
  8. Misbach G.A., Turley K., Ebert P.A. Pulmonary valve replacement for regurgitation after repair of tetralogy of Fallot. Ann Thorac Surg 1983;36:684-691.[Abstract]
  9. Kratz J.M., Crawford F.A., Jr, Stroud M.R., Appleby D.C., Hanger K.H. Trends and results in tricuspid valve surgery. Chest 1985;88:837-840.[Abstract/Free Full Text]
  10. Hejnal J., Málek I., Frídl P., Formánek P., elízko M. Long-term results of tricuspid annuloplasty according to De Vega. Cor Vasa 1992;34:293-299.[Medline]
  11. Chidambaram M., Abdulali S.A., Baliga B.G., Ionescu M.I. Long-term results of De Vega tricuspid annuloplasty. Ann Thorac Surg 1987;43:185-188.[Abstract]
  12. Duran C.M.G., Balasundaram S.G., Bianchi S., Herdson P. The vanishing tricuspid annuloplasty: a new concept. J Thorac Cardiovasc Surg 1992;104:796-801.[Abstract]



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