Ann Thorac Surg 2004;78:1486-1488
© 2004 The Society of Thoracic Surgeons
How to do it
Tricuspid Valve Repair with Papillary Muscle Shortening for Severe Tricuspid Regurgitation in Children
Yoshio Ootaki, MD, PhD*,a,
Masahiro Yamaguchi, MD, PhDa,
Naoki Yoshimura, MD, PhDa,
Shigeteru Oka, MD, PhDa,
Masahiro Yoshida, MDa,
Tomomi Hasegawa, MDa
a Department of Cardiothoracic Surgery, Kobe Children's Hospital, Kobe, Hyogo, Japan
Accepted for publication April 28, 2003.
* Address reprint requests to Dr Ootaki, 1-1-1 Takakuradai, Suma-ku, Kobe, Hyogo 654-0081, Japan
y.ootaki{at}nifty.ne.jp
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Abstract
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We describe tricuspid valve repair using papillary muscle shortening for severe tricuspid regurgitation due to leaflet prolapse in children combined with De Vega annuloplasty. The papillary muscle was shortened until the prolapsed leaflet was at the same height as the other nonprolapsed leaflets. Although echocardiographic tricuspid regurgitation tends to increase over time, it rarely requires long-term intervention.
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Introduction
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Congenital abnormalities of the tricuspid valve without downward displacement of the septal and posterior tricuspid leaflets are very uncommon causes of tricuspid regurgitation (TR). If the patient can tolerate the TR, then the patient should be treated medically without surgery during infancy and childhood. However, progressive regurgitation can lead to right heart failure, arrhythmias, and irreversible deterioration of right ventricular function [1]. Tricuspid valve repair may be an important method to improve cardiovascular performance in these patients because tricuspid valve replacement has poor short-term and long-term outcomes and a high rate of postoperative complications.
Recently, chordal replacement using expanded polytetrafluoroethylene and papillary muscle repair surgery [2, 3] as components of mitral valve repair in adults have been reported by several investigators. These techniques were also used for pediatric patients with congenital mitral valve disease [4, 5]. In contrast to experience with mitral valve repair, there have only been a few reports of tricuspid valve repair surgery for severe TR in children. Furthermore, the prognosis for children remains unknown with this approach. We report the use of papillary muscle shortening for treating severe tricuspid regurgitation in children.
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Technique
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From March 1993 to February 1999, papillary muscle shortening was performed in 3 children with severe TR as assessed by a preoperative echocardiogram (Table 1). From the echocardiographic data, TR was classified as trivial, mild, moderate, or severe. After a median sternotomy, total cardiopulmonary bypass was established between the ascending aorta and both venae cavae. Myocardial protection was achieved using moderate systemic hypothermia and antegrade cold blood cardioplegia, repeated every 20 minutes. The right atrium was opened parallel to the atrioventricular groove. Structural abnormalities of the tricuspid valve were found in all patients. Prolapse of the anterior tricuspid leaflet was observed in 2 patients and the posterior tricuspid leaflet in 1 patient. Although the anatomy of the papillary muscle was normal, elongation of the chordae of the tricuspid valve was observed in all patients.
A felt pledget-reinforced suture was placed through the base of the papillary muscle on one side, such that it exited at the midpoint of the papillary muscle on the same side as the pledget. Then the suture was brought through the fibrous tip, exiting on the side opposite to the pledget on the base, in order to shorten the elongated chordae and thus achieve a correction of the length with a subsequent correction of the leaflet prolapse (Fig 1). The papillary muscle was shortened until the prolapsed leaflet was at the same height as the other nonprolapsed leaflets. In patient 3, the redundant central portion of the anterior leaflet was partially resected in a triangular fashion and was sutured using intermittent 7-0 Prolene sutures (Ethicon, Somerville, NJ). The annulus of the tricuspid valve was dilated in 2 patients, and a De Vega tricuspid annuloplasty was performed using 4-0 Prolene (Ethicon) and 3-0 Nespolen (Azwell lnc, Osaka, Japan). Confirmation of valve competence at this time showed trivial or no regurgitation in all patients. The atrial septal defect and the ventricular septal defect, if any, were closed with a Dacron patch (Bard Impra, Tempe, AZ) through the right atriotomy.

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Fig 1. Surgical techniques of papillary muscle shortening consist of moving the papillary muscle attached to the prolapsed valve down into the right ventricle. To achieve this, we place a stitch in the fibrous tip of the papillary muscle (left) and tie it to its base (right).
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The postoperative course was uneventful in each patient. No patient had significant tricuspid stenosis or heart block develop that was attributable to the surgery. Postoperative catheterization performed 1 month after the surgery revealed that the TR decreased and the right ventricular end-diastolic volume was reduced in all patients. Tricuspid regurgitation at the time of discharge was trivial in 2 patients and mild in 1. There were no late deaths or reoperations during the time of follow-up, which ranged from 39 to 109 months. Tricuspid regurgitation increased from trivial or mild at the time of hospital discharge to moderate at follow-up echocardiography in patients 2 and 3.
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Comment
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Although acquired TR occurs in children with other congenital heart defects, especially after the repair of right-sided obstructive heart disease [1], congenital abnormalities of the tricuspid valve are very uncommon. For these patients, tricuspid valve replacement is one therapeutic option to treat the diseased valve. However, the prognosis of tricuspid valve replacement is poor, particularly in children, because of the necessity for long-term anticoagulation and poor long-term function of the prosthetic valve in the right-side of the heart. Therefore, the valve should be salvaged and repaired in children with severe TR whenever possible.
Tricuspid valve repair surgery using papillary muscle shortening was successfully performed on all of our patients with severe TR. This technique was used to treat leaflet prolapse in adults [2, 3] and children [4, 5] during mitral valve repair surgery. However, our literature search did not reveal previous use of this technique to treat TR in children. Carpentier [6] has advocated chordal shortening and chordal transposition techniques to treat leaflet prolapse. Each technique has some advantages and shortcomings. Technically, chordal shortening is not a direct method to shorten elongated chordae. An effective chordal shortening represents half of the length of chordae buried into a trench of papillary muscle. This technique requires great care to prevent the chordae from rupturing over time, especially in the small hearts of children. The effect of several sutures placed in the papillary muscle of a developing child remains unknown. On the contrary, papillary muscle shortening is a direct method to shorten the elongated chordae and reposition them. In our 3 patients, this technique required only one suture to treat leaflet prolapse, resulting in a shorter procedure time. Therefore papillary muscle shortening is a simpler and faster technique when compared with chordal shortening.
De Vega tricuspid annuloplasty was performed in 2 patients with a dilated tricuspid annulus. Kanter and associates [7] reported the effectiveness of De Vega's tricuspid annuloplasty for children with tricuspid valve regurgitation and right-sided obstructive disease. Early postrepair echocardiography quantified TR as absent or mild in 81% of patients [7]. Morishita and associates [8] reported that the actuarial survival rate at 15 years after operation was 74.0% of patients, the 15-year freedom from reoperation was 91.6%, and the 15-year freedom from all events was 58.7%. Although these data were for patients with secondary TR with annular dilatation, this technique was also effective in patients with primary TR with annular dilatation. 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. However, tricuspid stenosis was not suspected on the echocardiographic findings of our patients.
De Vega annuloplasty and closure of the atrial septal defect may decrease TR. However, the main anomaly of the valve or the cause of TR was due to the prolapse of the leaflet itself. We believe that papillary muscle shortening played the most important role in repairing severe TR, especially in the early postoperative period.
Tricuspid regurgitation increased during follow-up in 2 patients. Annuloplasty with a prosthetic ring is one of the choices for treating TR with a dilated annulus, as with our third patient. This technique should not be used on a growing child. However, in the case of the postpubescent patient, we should have implanted a prosthetic annuloplasty ring to prevent further dilatation of the annulus. On the contrary, TR of the patient who did not receive De Vega annuloplasty increased over time. Generally, the ideal time to repair severe TR is after puberty. However, we had to perform the repair surgery in 1 infant because of his severe illness. As we were concerned about impairing the development of the valve, we did not perform an annuloplasty for the infant. He may require annuloplasty to prevent further dilatation of the annulus. Long-term follow-up is needed to clarify the effect of annuloplasty in children.
In conclusion, tricuspid valve repair utilizing papillary muscle shortening for severe TR in children was successfully performed. Although echocardiographic TR tends to increase with time, it rarely requires long-term intervention.
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Acknowledgments
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We thank Michael Kopcak for his editorial advice.
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References
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