Asian Cardiovasc Thorac Ann 1998;6:45-48
© 1998 Asia Publishing EXchange Pte Ltd
Chordal Replacement in Tricuspid Valve Repair in Children
Jacques AM van Son, MD, PhD,
Jörg Hambsch, MD,
Michael D Black, MD,
Friedrich W Mohr, MD, PhD
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Departments of Cardiac Surgery and Pediatric Cardiology Herzzentrum University of Leipzig Leipzig, Germany
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For reprint information contact: Jacques AM van Son, MD, PhD Herzzentrum, University of Leipzig Russenstrasse 19 Leipzig D-04289, Germany Tel:49 341 865 1445 Fax:49 341 865 1452
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ABSTRACT
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Congenital or traumatic tricuspid regurgitation in the pediatric population, although generally well tolerated initially, may lead ultimately to right atrial and ventricular dilation and dysfunction with dysrhythmias. In order to preserve right atrial and ventricular function and maintain sinus rhythm, it is our objective to repair the regurgitant tricuspid valve at an early stage. In 5 children (mean age 8.8 years) with congenital tricuspid regurgitation (2 with Ebstein's anomaly, 1 each with ventricular septal defect, tetralogy of Fallot, and partial agenesis of chordae), and in 1 child with traumatic tricuspid regurgitation, the shortened (n = 4), congenitally absent (n = 1), and ruptured (n = 1) chordae tendineae of the anterior or septal leaflets or both, were repaired with polytetrafluoroethylene artificial chordae. The tricuspid valve was successfully reconstructed in all 6 patients. De Vega's (n = 3) or Danielson's (n = 2) plication of the tricuspid valve annulus was performed in 5 patients. At a mean follow-up time of 15.7 months, tricuspid valve function was normal in 2 patients and the other 4 had mild residual tricuspid regurgitation. The mean diameter of the tricuspid annulus decreased from 36.7 mm preoperatively to 30.0 mm postoperatively, which is in the range for children with a normal tricuspid valve. In congenital or traumatic tricuspid regurgitation, chordal replacement using polytetrafluoroethylene artificial chordae is a useful adjunct to the armamentarium of tricuspid valve repair. Early repair avoids deterioration of right atrial and ventricular function and promotes maintenance of sinus rhythm.
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INTRODUCTION
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Important tricuspid regurgitation (TR) in children, if not secondary to associated regurgitation or stenosis of other cardiac valves or abnormal function of a structurally normal valve, is usually caused by prolapse or retraction of one or more leaflets as a consequence of elongation, rupture, agenesis, or shortening of the chordae tendineae. Secondary dilation of the tricuspid annulus leads to a vicious circle of increasing TR. While in cases of chordal elongation we have applied the technique of chordal plication, in cases of ruptured, shortened, or congenitally absent chordae of the tricuspid valve, we have recently used expanded polytetrafluoroethylene (PTFE) sutures to replace chordae, in analogy to the technique reported for mitral valve reconstruction.1 This report reviews our experience using artificial chordae for tricuspid valve reconstruction in pediatric patients.
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MATERIAL AND METHODS
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From July 1995 to December 1997, chordal replacement with PTFE sutures was performed in 6 pediatric patients (4 boys and 2 girls) with a mean age of 8.8 years (range 4.2 to 15.1 years). All 6 patients had sinus rhythm and their preoperative Doppler echocardiographic studies showed severe TR with a regurgitant jet to the back wall of the right atrium in all cases. In 5 patients, TR was secondary to a congenital cardiac anomaly. Two of these 5 patients had been operated on before, one for closure of a conoventricular ventricular septal defect and the other for correction of tetralogy of Fallot. Two patients had Ebstein's anomaly with a partially tethered, sail-like anterior leaflet and one patient had partial agenesis of chordae to the anterior leaflet. The remaining patient had TR with a flail anterior leaflet that was attributed to blunt chest trauma that had occurred in an automobile accident. The mean diameter of the tricuspid valve measured at end diastole was 36.7 mm (range 32 to 43 mm), which (with exception of the patient with tetralogy of Fallot) exceeded the range of tricuspid valve diameters in normal children.2 Table 1
summarizes the clinical data.
OPERATIVE TECHNIQUE
Generally, in young children primary chordae tendineae were replaced with 5/0 PTFE sutures. In older children or adolescents, 4/0 PTFE sutures might be preferred. Shortened or ruptured chordae were removed (Figure 1A). The optimal length of the PTFE suture was judged by measuring the distance between the apex of the papillary muscle or (in the case of agenesis of the papillary muscle) the right ventricular wall and the estimated level of the rim of the tricuspid valve leaflet during systole. A double-armed PTFE suture was passed twice through the papillary muscle, preferentially through the fibrous portion if present (Figure 1B). The suture was reinforced on both sides of the papillary muscle with autologous pericardial pledgets. The two arms of the suture were then brought up to the free margin of the leaflet, passed through the edge of the leaflet where the original chorda was attached, reinforced with an autologous pericardial pledget, and tied together on the ventricular side of the leaflet once the length of the suture was adjusted. Multiple knots were needed for this suture material. If a wider leaflet segment had prolapsed, the two arms of the PTFE suture were passed through the leaflet at a greater distance so that each arm of the suture replaced the function of one chorda. Subsequently, both ends of the suture were passed again through the free margin of the leaflet toward each other, the length of the sutures was adjusted and the ends were tied on the ventricular side of the leaflet.
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Figure 1. Chordal replacement of shortened or ruptured tricuspid valve chordae. A. Ruptured or shortened (arrows) chordae are resected. B. A double-armed polytetrafluoroethylene suture, reinforced on each side with pericardial pledgets, is passed twice through the papillary muscle and attached to the leaflet.
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In the case of leaflet prolapse secondary to agenesis of papillary muscle(s) and chordae, a double-armed pletgetted 5/0 PTFE suture was passed through the right ventricular wall at the anticipated position of the papillary muscle (Figure 2). The suture was then passed through the leaflet and tied on the ventricular side using double-pledget reinforcement. To reduce annular dilation, a De Vega annuloplasty was generally indicated. In Ebstein's anomaly of the tricuspid valve, prior to replacement of the anterior leaflet chordae, the tricuspid valve annulus size was reduced and the atrialized portion of the right ventricle was plicated. Tricuspid valve function was assessed by injection of cold normal saline solution into the right ventricle and by transesophageal echocardiography after termination of cardiopulmonary bypass.
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Figure 2. Chordal replacement for chordal agenesis. A. Preoperative situation with free-floating anterior leaflet. B. A double-armed polytetrafluoroethylene suture, reinforced with pericardial pledgets, is passed through the right ventricular free wall (at anticipated position of papillary muscle) [lower insert], and attached to the leaflet [upper insert].
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OPERATIONS PERFORMED
At operation, TR was found to be due to prolapse of the anterior leaflet in 4 patients, prolapse of the septal leaflet in 1 patient, and prolapse of both the anterior and septal leaflets in 1 patient (see Table 1
). Shortened (n = 4) or ruptured (n = 1) chordae were resected in 5 patients. The prolapse was corrected with one double-armed 5/0 PTFE suture in 2 patients, two double-armed 5/0 PTFE sutures in 2 patients, and two double-armed 4/0 PTFE sutures in the 2 oldest patients (12.7 and 15.1 years old). To reduce annular dilation, a De Vega annuloplasty was performed in 3 patients. In the 2 patients with Ebstein's anomaly, the atrialized portion of the right ventricle was plicated and a posterior annuloplasty was performed to reduce the annular width, thus allowing the anterior leaflet to function as a monocusp valve. In the patient with tetralogy of Fallot, besides repair of the tricuspid valve, the right ventricular outflow tract was reconstructed with a pulmonary homograft.
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RESULTS
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Intraoperative transesophageal echocardiography demonstrated an absence of TR in 2 patients, mild TR in 3 patients, and moderate central TR in the remaining patient. The median early postoperative right atrial pressure was 9 mm Hg (range 7 to 12 mm Hg). All patients remained in sinus rhythm. There was no early or late mortality.
The mean intensive care unit stay was 1.2 days and mean hospital stay was 7.6 days. At a mean follow-up period of 15.7 months (range 8 to 25 months), which included echocardiographic assessment, 2 patients had an absence of TR while in the other 4 there was mild central TR. The mean diameter of the tricuspid valve annulus had decreased from 36.7 mm preoperatively to 30.0 mm after surgery, which is within the normal range for children.2
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DISCUSSION
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TR is the result of failure of systolic leaflet coaptation. This failure may be multifactorial in origin and can be caused by structural alterations in one or all of the components of the tricuspid valve apparatus or by abnormal function of a structurally normal valve. Severe TR, although initially clinically benign, ultimately results in dilation of the tricuspid annulus and right atrial and right ventricular dysfunction with the potential for dysrhythmias. If surgery is delayed, as known from our experience with traumatic TR, the involved papillary muscle(s), chordae, and leaflet(s) are frequently found in a contracted and atrophic state that precludes valve repair.3,4 Therefore, early operation for congenital or traumatic TR may be advantageous in terms of feasibility of tricuspid valve repair and increased likelihood of maintaining or restoring sinus rhythm.
Indications for chordal replacement using expanded PTFE sutures in tricuspid valve repair are the presence of flail portions of the anterior or septal leaflets secondary to chordal rupture, congenital absence of chordae to the anterior or septal leaflets, or the presence of chordal shortening. In selected cases of Ebstein's anomaly with a well-developed and tethered anterior leaflet with shortened chordae, replacement of the chordae with PTFE sutures may avoid valve replacement.
Regarding the technique of chordal replacement with PTFE sutures, we believe that it is important to reinforce the proximal (papillary muscles or right ventricular free wall) and distal (tricuspid leaflet) anchoring points of the PTFE sutures with pledgets, preferably with autologous pericardium. This avoids tearing of the sutures through these delicate structures. In children, unlike the situation in adults, fibrous tissue is usually absent in the papillary muscles. Generally, in the presence of dilation of the tricuspid annulus, additional annuloplasty is required to reduce the diameter of the annulus and to enlarge the zone of coaptation between the tricuspid leaflets.
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CONCLUSION
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In conclusion, chordal replacement is a useful adjunct to the armamentarium of tricuspid valve repair. The technique is relatively simple to perform, appears reproducible, and has the advantage of avoiding many of the reported complications of prosthetic valve replacement. Good results require careful functional assessment of the tricuspid valve and the use of multiple techniques to address all components of the valve lesion.
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REFERENCES
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David TE, Bos J, Rakowski H. Mitral valve repair by replacement of chordae tendineae with polytetrafluoroethylene sutures. J Thorac Cardiovasc Surg
1991;101:495–501.[Abstract]
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King DH, Smith EO, Huhta JC, Gutgesell HP. Mitral and tricuspid valve annular diameter in normal children determined by two-dimensional echocardiography. Am J Cardiol
1985;55:787–93.[Medline]
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van Son JAM, Danielson GK, Schaff HV, Miller FA Jr. Traumatic tricuspid valve insufficiency. Experience in thirteen patients. J Thorac Cardiovasc Surg
1994;108:893–8.[Abstract/Free Full Text]
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van Son JAM, Starr A. Repair of traumatic tricuspid valve insufficiency by trabecular muscle elevation. Ann Thorac Surg
1995;59:740–2.[Abstract/Free Full Text]
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ABSTRACT
INTRODUCTION
