Ann Thorac Surg 1998;66:172-176
© 1998 The Society of Thoracic Surgeons
Original articles: cardiovascular
Repair of congenital tricuspid valve abnormalities with artificial chordae tendineae
V. Mohan Reddy, MDa,
Doff B. McElhinney, MDa,
Michael M. Brook, MDb,
Norman H. Silverman, MDb,
Paul Stanger, MDb,
Frank L. Hanley, MDa
a Division of Cardiothoracic Surgery, University of California at San Francisco, San Francisco, California, USA
b Division of Pediatric Cardiology, University of California at San Francisco, San Francisco, California, USA
Accepted for publication February 12, 1998.
Address reprint requests to Dr Reddy, 505 Parnassus Ave, M593, San Francisco, CA 94143-0118
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Abstract
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Background. Congenital abnormalities of the tricuspid valve, including Ebstein’s malformation, dysplasia, straddling, and those found in pulmonary atresia with intact septum and congenitally corrected transposition, are an uncommon cause of tricuspid regurgitation. Congenital tricuspid valve anomalies are found as a spectrum of disease in which both the leaflets and the subvalvar apparatus are often involved. Tricuspid valve repair is complicated in such patients because the chordae tendineae are often abnormally short and thick. Replacement or augmentation of chordae tendineae has proved to be a useful component of mitral valve repair. In the present report, we describe the techniques and results of chordal augmentation in the repair of congenital tricuspid valve abnormalities.
Methods. Since July 1992, tricuspid valve repair has been performed in 5 children with severe tricuspid regurgitation secondary to congenital abnormalities of the tricuspid valve with significant chordal pathology. As a component of the repair, chordal replacement or augmentation was performed using expanded polytetrafluoroethylene suture.
Results. Intraoperative and postoperative echocardiographic assessment showed good mobility of the tricuspid valve leaflets and trivial to mild tricuspid regurgitation. There were no complications and no early or late mortality. At follow-up of 34 to 60 months (median, 49 months), tricuspid valve function has remained excellent in 4 of the 5 patients. In the remaining patient, progressive regurgitation of the right ventricle to pulmonary artery allograft conduit has led to right ventricular dilatation, with a secondary increase in tricuspid regurgitation from trivial to moderate.
Conclusions. Chordal replacement or augmentation with expanded polytetrafluoroethylene suture is a useful technique in the repair of congenitally dysplastic tricuspid valves with abnormal chordal structures.
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Introduction
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In their description of the spectrum of dysplasia of the tricuspid valve, Becker and colleagues [1] defined tricuspid valve dysplasia as "faulty development of chordae and papillary muscles and thickening or focal agenesis of valvular tissue" in congenitally malformed tricuspid valves. Tricuspid regurgitation due to congenital valve dysplasia is an uncommon but well-recognized phenomenon [1–4], and similar valve pathology has been described in patients with pulmonary atresia and intact ventricular septum as well [5]. In recent years, fetal echocardiography has demonstrated that congenital anomalies of the tricuspid valve have a high mortality in utero, which is consistent with the significance of the right heart in the fetal circulation [4]. Substantial mortality has also been observed in patients with severe tricuspid regurgitation manifesting in the neonatal period [1–4]. Over time, progressive regurgitation can lead to right heart failure and arrhythmias, and tricuspid valve repair may be an important means of improving cardiovascular performance in such patients. However, standard techniques of valvuloplasty may not result in optimal tricuspid valve function, especially when the leaflets are tethered by abnormally short chordae tendineae or when chordae are absent altogether. Avoidance of prosthetic replacement of the tricuspid valve is desirable, especially in children, because of both the complications of anticoagulation and the poor long-term function of prosthetic valves in the right heart [6–9].
Chordal replacement as a component of mitral valve repair has been reported by several investigators since the 1960s [10–14]. However, only recently has expanded polytetrafluoroethylene (ePTFE) used for chordal replacement been shown to heal well to the leaflet and papillary muscle and to retain the length it had at implantation [13–15]. In contrast to experience with mitral valve repair, there have been few reports of tricuspid valve chordal augmentation with ePTFE [16]. Recently, we have used ePTFE for chordal augmentation in the repair of congenitally abnormal tricuspid valves in 5 patients. In the present report, we describe the techniques and results of this approach.
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Patients and methods
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Patients
Between July 1992 and October 1994, 5 patients underwent operation for severe tricuspid valve regurgitation secondary to congenital tricuspid valve anomalies with significant chordal abnormalities at our institution. Age at repair ranged from 3.3 to 16.5 years (median, 9 years). All patients were in New York Heart Association functional class II or III, and 3 were receiving digoxin and furosemide for signs of heart failure. Previous operations included outflow tract patch repair of pulmonary atresia with intact ventricular septum in 2 patients. The diagnosis of tricuspid regurgitation with right atrial and ventricular dilatation was made by echocardiography in all patients.
Surgical techniques
The heart and great vessels were exposed through a standard median sternotomy, and cardiopulmonary bypass was instituted with aortic and bicaval cannulation and moderate hypothermia. After cardioplegic arrest was established, the right atrium was opened and the tricuspid valve exposed. Tricuspid valve competence was tested by loading the right ventricle with saline solution from a bulb syringe. The decision to use artificial chordae was made intraoperatively after examining the valve thoroughly. Chordal abnormalities were repaired by either chordal replacement or chordal augmentation.
Chordal replacement was performed by attaching a single 2-0 or 4-0 ePTFE suture to the free edge of the tricuspid valve leaflet with two Teflon pledgets. Both ends of the ePTFE suture were then passed through the free wall of the right ventricle at the level corresponding approximately to the location of the papillary muscle origin, and tied over a Teflon felt pledget on the epicardial surface of the ventricle (Fig 1).
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Fig 1. Technique of chordal replacement. A single 4-0 expanded polytetrafluoroethylene suture is attached to the rim of the valve leaflet and the ventricular wall at the level corresponding approximately to the location of the papillary muscle origin, and reinforced at both points with Teflon felt pledgets. The insets indicated by arrows show the detail of leaflet and ventricular wall attachment.
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Chordal augmentation was performed by transecting the abnormally short chordae tendineae and elongating them with a segment of 2-0 ePTFE suture. A double-armed 2-0 ePTFE suture was passed through the valvar aspect of the transected chordae and sewn to the corresponding papillary muscle with Teflon pledgets for reinforcement (Fig 2). Both proximal and distal attachments of the ePTFE suture were secured with interrupted 4-0 polypropylene stitches.
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Fig 2. Technique of chordal augmentation. The unrepaired valve, with short chordae, is shown at left. The short chordae are transected and augmented, as indicated by the arrows, with one 2-0 expanded polytetrafluoroethylene suture, which is reinforced at its proximal and distal attachments with 4-0 polypropylene sutures.
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With both techniques, the proper length of the artificial chordae was determined by filling the right ventricle with saline solution and allowing the leaflets to float to the level of the annulus. In addition, anteroposterior and posteroseptal commissural annuloplasty procedures with interrupted horizontal mattress sutures were performed in all patients. After repair, the tricuspid valve was again tested for regurgitation. The right atriotomy was closed once a satisfactory result was obtained. The patient was weaned from bypass and transesophageal echocardiography was performed to evaluate tricuspid valve function.
Postoperative evaluation and follow-up
Postoperatively, all patients underwent echocardiographic evaluation at the time of discharge. During follow-up, all patients were evaluated clinically and by echocardiography at regular intervals by the referring cardiologist.
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Results
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Echocardiographic and operative findings
All patients had severe tricuspid regurgitation, with moderate or severe right atrial and ventricular dilatation. In 2 patients (patients 2 and 4), the regurgitation was attributable to isolated failure of leaflet coaptation, which appeared to be the result of tethering of the leaflets, particularly the septal leaflet, by abnormally short chordae. The regurgitant jet was wide based and directed centrally or toward the septal wall of the atrium. On direct inspection, the chordae tendineae of the septal leaflet were thick and foreshortened, with poor mobility. In 1 of these patients, the valve leaflets proper were also mildly thickened, whereas in the other patient they were normal in appearance. Both of these patients underwent lengthening of the affected chordae with ePTFE suture. The 2 patients who had undergone previous outflow tract patching for pulmonary atresia with intact ventricular septum had free pulmonary regurgitation and no pulmonary outflow obstruction. In both patients, the tricuspid valve appeared to be tethered by short septal leaflet chordae, and the regurgitant jet was directed along the atrial surface of the anterior leaflet and into the right atrial free wall. On operative inspection, these 2 patients had similar valve pathology, with a moderately thickened and rolled septal leaflet, and septal leaflet chordae that were thick and extremely short. In 1 patient, the thickened and short chordae were excised and replaced with ePTFE suture chordae, whereas in the other patient the chordae were transected and lengthened. In addition, a valved right ventricle to pulmonary artery allograft conduit was placed in both patients. The remaining patient (patient 1) was found on preoperative transesophageal echocardiography to have isolated flail and prolapse of the anterior tricuspid valve leaflet (Fig 3). The regurgitant jet was directed along the atrial surface of the septal and posterior leaflets and into the atrium septum (Fig 3). On direct visual inspection, the tricuspid valve leaflets were normally attached to the annulus, but the anterior leaflet did not have any free edge chordae and was flail and prolapsing. There was no evidence of chordal rupture, and it appeared that there was congenital absence of the chordae. The other tricuspid valve leaflets and chordae appeared normal. Artificial chordae were placed from the free edge of the septal leaflet and brought out through the right ventricular free wall and tied over a pledget, as depicted in Figure 1.
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Fig 3. Transesophageal echocardiograms performed in the operating room before and after tricuspid valve repair in patient 1. (A) Anterior leaflet of the tricuspid valve (arrow) can be seen prolapsing into the right atrium (RA) during systole. (B) Doppler color flow imaging in the same projection, demonstrating severe tricuspid regurgitation, with the jet directed along the course of the septal leaflet toward the atrial septum. (C) After repair, the tricuspid valve leaflets coapt without prolapse of the anterior leaflet. Doppler color flow imaging demonstrated trivial regurgitation (not shown). (LA = left atrium; LV = left ventricle; RV = right ventricle.)
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Early results
In all patients, early postoperative tricuspid valve function was excellent or good (Table 1). There were no early deaths and the postoperative course was uncomplicated in all patients. All patients were extubated on the first postoperative day and discharged from the hospital 4 to 6 days after the operation.
Follow-up
Cross-sectional follow-up was obtained in all patients and was complete as of July 1997. There were no late deaths or reoperations at follow-up ranging from 34 to 60 months (median, 49 months). Patients 1, 2, 4, and 5 were not receiving any cardiac medications and were in New York Heart Association functional class I. Tricuspid valve function in these patients was unchanged from the early postoperative period, with only trivial or mild regurgitation (see Table 1). In patient 3, who also underwent reconstruction of the pulmonary outflow tract with a valved allograft conduit at the time of tricuspid valve repair, moderate conduit regurgitation developed, which led to dilatation of the right ventricle and tricuspid annulus. As a result, tricuspid regurgitation increased from trivial at hospital discharge to moderate on follow-up echocardiography 60 months after the operation.
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Comment
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Long-term follow-up reports show that tricuspid valve replacement is a poor solution for tricuspid regurgitation [5–7], and is particularly undesirable in children [8] because of concerns about the complications and inconvenience of long-term anticoagulation, as well as the poor long-term function of prosthetic valves in the right heart. Tricuspid valve repair is a preferred alternative, especially if the valve leaflets are not grossly thickened and calcified. Severe tricuspid regurgitation secondary to congenital tricuspid valve dysplasia with chordal abnormalities is extremely rare. Nevertheless, salvaging the valve should be the primary goal in patients with this problem.
For regurgitation secondary to a congenitally dysplastic atrioventricular valve with abnormal chordae that are too short, too thick, too long, or ruptured, chordal replacement is a potentially ideal solution. Follow-up of more than 4 years has been reported after ePTFE chordal replacement in the mitral position, and suggests that thinner grades of ePTFE retain a natural level of flexibility after complete tissue incorporation [11, 12]. However, in a recent experimental study, a 5-0 ePTFE suture used to reinforce the leaflets of a mitral valve homograft was found to be ruptured [17]. Thus, it may be advisable to use 4-0 or 2-0 sutures, and to reinforce the leaflet with multiple artificial chordae if a large tensile stress is anticipated. It has also been shown recently that ePTFE suture used for mitral valve chordal replacement is covered in part or completely with collagen and endothelial cells within 5 months of implantation [15], a finding that correlates with earlier experimental work in sheep [18]. Although inflammatory cells have been found in the interstices of ePTFE sutures used for replacement of mitral valve chordae 21 days after operation [19], Minatoya and colleagues [15] reported complete absence of cellular infiltration of ePTFE sutures 5 months after chordal replacement.
In our experience, replacement or augmentation of the tricuspid valve chordae has resulted in markedly improved mobility of the leaflet in all patients with short septal chordae (patients 2 to 5). In these cases, tricuspid valve orifice size was maintained while the tricuspid regurgitation was relieved. In patient 1, the unusual finding of absent chordae along the entire free edge of the anterior leaflet was corrected by creating new chordae to support the leaflet. In all patients, the length of the chordae was adjusted such that, when the right ventricle was filled with saline solution, the valve leaflets billowed up normally to the level of the annulus without any prolapse. However, because the annulus was dilated, a conservative annuloplasty was necessary to ensure adequate coaptation of the leaflets, thereby minimizing any residual leak. Tricuspid annuloplasty rings were not used in any patient. The mechanism of tricuspid regurgitation secondary to short chordae should not be confused with failure of leaflet coaptation due simply to a dilated annulus. In patients whose tricuspid regurgitation is the result of both abnormal chordae and a dilated right ventricle and tricuspid annulus, it is important to perform an adequate annuloplasty along with chordal lengthening.
Midterm follow-up indicates that the functional integrity of the valve does not deteriorate. In patient 3, increasing pulmonary regurgitation was probably a causative factor for the relative decline in tricuspid valve function. In patients who underwent chordal replacement, there may be a need for further operation as the child grows, although it is also possible that compensatory growth of the leaflet will be sufficient to maintain adequate valve function. In patients who underwent chordal augmentation, we speculate that growth of the native tensor apparatus may preserve valve function in the long term.
On the basis of our limited experience, we conclude that chordal replacement or augmentation with ePTFE suture is a useful approach to tricuspid valve repair in patients with regurgitation due to congenital tricuspid valve anomalies with absent or abnormal chordae. Although midterm results appear promising, further follow-up is necessary to ascertain the long-term durability of ePTFE sutures in this position.
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References
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Abstract
Introduction
