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Ann Thorac Surg 2007;83:1458-1462
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Neonatal Mitral and Tricuspid Valve Repair for In Utero Papillary Muscle Rupture

Petros V. Anagnostopoulos, MD, Nelson Alphonso, MD, Lars Nölke, MD, Lisa K. Hornberger, MD, Gary W. Raff, MD, Anthony Azakie, MD, Tom R. Karl, MD*

Pediatric Heart Center, University of California San Francisco Children’s Hospital, San Francisco, California

Accepted for publication October 23, 2006.

* Address correspondence to Dr Karl, University of California, San Francisco Division of Pediatric Cardiothoracic Surgery, 513 Parnassus Ave, Suite S-549, Box 0117, San Francisco, CA 94143-0117 (Email: karlt{at}surgery.ucsf.edu).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: Papillary muscle rupture in the fetus and neonate is a rare event that leads to severe mitral or tricuspid insufficiency and is associated with high perinatal mortality. We undertook surgical repair of this lesion in the neonatal period and report on our midterm results.

Methods: Three neonates with tricuspid insufficiency and 1 infant with mitral insufficiency, all due to papillary muscle or chordal rupture, underwent surgical repair with artificial chordal replacement and a modification of the de Vega annuloplasty technique that allowed external adjustment of the annulus size under transesophageal echocardiographic guidance after separation from cardiopulmonary bypass.

Results: All patients recovered well from the operation. There have been no late deaths and no valve-related complications. On discharge, all 3 patients had evidence of trace to mild atrioventricular valve regurgitation. At a median follow-up of 33 months (range, 7 to 50; 123 patient-months), all 4 patients are growing normally. Three patients have had no change in the degree of tricuspid or mitral regurgitation. One patient required reoperation at 54 months postoperatively for acute mitral insufficiency secondary to separation of an artificial chorda from the ventricular wall.

Conclusions: Surgical repair of critical neonatal tricuspid and mitral insufficiency associated with papillary muscle or chordal rupture is feasible and can result in good early and midterm results. Our modification of the De Vega annuloplasty technique with the ability to externally adjust the size of the annulus under echocardiographic guidance may improve the accuracy of the repair in the neonate.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
There are few case reports in the literature regarding newborns with critical atrioventricular valve insufficiency secondary to a ruptured papillary muscle or chordae tendinae [1–4]. In adults, postischemic papillary muscle rupture frequently results in acute atrioventricular valve incompetence and life-threatening cardiac failure, often constituting a surgical emergency. The etiology and course in neonates are less well known. In this article, we summarize our experience with 4 neonates who presented with important tricuspid valve insufficiency (3 patients) and mitral valve insufficiency (1 patient) associated with papillary muscle or chordal rupture, and we describe an operative strategy for neonatal atrioventricular valve repair in such cases.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Consent for the study was obtained from our Institutional Review Board. Requirement for individual consent was waived.

Patient 1
A 3.2-kg term baby was born by forceps-assisted vaginal delivery and was transferred to University of California San Francisco because of persistent hemoglobin desaturation. Initial echocardiographic assessment revealed a closed ductus arteriosus, a 5.0-mm atrial septal defect, and evidence of right ventricular infarction during fetal life. There was severe tricuspid insufficiency due to rupture of chordae tendinae to the anterior leaflet of the tricuspid valve. The baby continued to deteriorate despite efforts to decrease the pulmonary vascular resistance and improve the right ventricular failure. She was placed on transcervical venoarterial extracorporeal life support at 21 hours of life. She remained on extracorporeal life support for 11 days and could not be weaned owing to a combination of pulmonary hypertension, right to left shunting through the atrial septal defect with severe hypoxemia, tricuspid valve insufficiency, and low cardiac output. The decision was made to proceed with operative repair.

Patient 2
A 3-kg newborn was transferred for the management of hydrops fetalis. The baby was delivered by urgent cesarean section at 33 weeks of gestation to a 33-year-old mother with good antenatal care. Four days before delivery, she had described decreased fetal movement. On the day of delivery, she underwent prenatal ultrasonography that showed fetal hydrops and oligohydramnios. The first echocardiogram after delivery showed a structurally normal heart with severe tricuspid insufficiency, evidence of rupture of chordae tendinae to the anterior leaflet, and a ductus arteriosus with right to left shunting. The baby initially required resuscitation with inotropic support. After 2 weeks of inotropic suppport, the baby’s circulation remained volume overloaded. The decision was made to proceed with operative intervention.

Patient 3
A 3.9-kg term baby presented with cyanosis immediately after delivery. An echocardiogram revealed severe tricuspid insufficiency due to anterior leaflet prolapse from papillary muscle rupture, and right to left shunting through a foramen ovale. After a short period of diuresis, the baby underwent surgical repair.

Patient 4
A 7-week-old infant presented with tachypnea, irritability, failure to thrive, and congestive heart failure. He was born at term by an uncomplicated spontaneous vaginal delivery. An echocardiogram on admission showed severe mitral insufficiency due to rupture of the posteromedial papillary muscle. In addition, the baby had a 5-mm perimembranous ventricular septal defect. After a short period of diuresis, the patient underwent surgical repair.

Operative Findings
In the first patient, the valve leaflets were structurally normal. The head of the papillary muscle was infarcted, and the chordal attachments of the anterior leaflet of the tricuspid valve had ruptured. The second patient had two clusters of chordae from the anterior leaflet that had separated from the papillary muscle. The etiology was unclear, as the papillary muscles did not appear to be infarcted. In the third patient, there was rupture of the papillary muscle that supported all the anterior leaflet chordae. The lesion appeared to have happened late during fetal life, as there was yellow discoloration and fibrosis of the papillary muscle. The right ventricular wall surrounding the papillary muscle appeared normal. The fourth patient had evidence of ischemia in the posteromedial papillary muscle of the left ventricle. The muscle had ruptured at its tip so that the free distal end of the muscle was still attached to the chordae tendinae of the posterior leaflet of the mitral valve.

Surgical Technique
The technique of surgical repair was similar in all 4 patients. Each was placed on cardiopulmonary bypass through the aorta with direct cannulation of the superior and inferior vene cavae. The aorta was clamped, and antegrade cold blood cardioplegia was administered every 20 minutes. A right atriotomy was used for all cases, and the mitral valve was repaired using the transseptal approach. The mechanism of insufficiency was determined by distending the ventricle with saline (Fig 1). A pledgeted double-stranded 6-0 expanded polytetrafluoroethylene (ePTFE) suture was placed in the base of the ruptured papillary muscle near its junction with the ventricle and then through the unsupported part of the valve leaflet (Fig 2). The artificial chorda was completed by tying the two ends over a pledget, matching its height to the length of the unruptured chordae tendinae. Then, using a 6-0 ePTFE suture, a de Vega type tricuspid annuloplasty was created (Fig 3) [5]. The two ends of the suture were brought through the wall of the atrium and passed through a pledget and then a tourniquet. In the mitral valve repair, the annuloplasty was extended along the posterior annulus. The atriotomies were closed, the heart deaired, and the aortic clamp was removed. After separation from cardiopulmonary bypass, the annuloplasty was tightened externally under transesophageal echocardiographic guidance to eliminate any remaining central valve insufficiency, without creating valve stenosis. The annuloplasty was fixed in the appropriate position by hemostatic clips applied to the shortened tourniquet. All patients had primary closure of the atrial septal defect. The third patient also had patch closure of the ventricular septal defect.


Figure 1
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  		Fig 1. Valve insufficiency secondary to a ruptured papillary muscle (arrow).

 

Figure 2
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  		Fig 2. The leaflet free edge is supported with neochordae of 6-0 expanded polytetrafluoroethylene, sutured to the base of a papillary muscle, but not in the infarcted area. The length is adjusted to neutralize the prolapse.

 

Figure 3
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  		Fig 3. The tricuspid valve annulus us stabilized using a modified de Vega technique with a 5-0 expanded polytetrafluoroethylene suture. The ends of the suture are passed through the wall of the right atrium and controlled with a tourniquet. The annulus can be adjusted after separation from cardiopulmonary bypass using transesophageal control. (SVC = superior vena cava.)

 

   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
All patients are alive. The first patient had postoperative seizures, and workup revealed a left frontal lobe infarct in the anterior cerebral artery distribution. She recovered well, and her seizure medications have been discontinued. She has mild residual right hemiparesis with normal cognitive skill development. She has no cardiac symptoms; her echocardiogram at 4 years of age showed normal biventricular function, without evidence of tricuspid stenosis and only trivial tricuspid insufficiency. The second patient was discharged home with no tricuspid insufficiency. Follow-up echocardiogram at 18 months showed good biventricular function with evidence of trace tricuspid insufficiency without evidence of tricuspid valve stenosis. The third patient was discharged home on postoperative day 8. Discharge echocardiogram showed trivial tricuspid insufficiency and no evidence of tricuspid stenosis. Seven months later, he remains well with no valve insufficiency.

The fourth patient was also discharged home in good condition. Discharge echocardiogram showed good biventricular function with no evidence of mitral insufficiency. A follow-up echocardiogram at 36 months showed good biventricular function with mild mitral insufficiency and no evidence of mitral stenosis. At 54 months, a change in the murmur associated with his mitral insufficiency was noted. An echocardiogram showed severe prolapse of the medial segment of the anterior mitral leaflet with moderate mitral insufficiency. At reoperation, separation of one of the previously placed ePTFE artificial chorda from the posteromedial papillary of the left ventricle was noted. Two ePTFE artificial chordae were interposed between the unsupported segments of the anterior mitral leaflet and the ventricular wall, and were further reinforced by transferring a secondary chorda from the posterior leaflet to the free edge of the adjacent anterior leaflet. The repair was completed with a semicircular modified de Vega type annuloplasty suture with ePTFE. The patient was discharged with mild mitral insufficiency and remains well 3 months after his operation.

In summary, all 4 patients are growing normally at a median follow-up of 33 months (range, 7 to 50; 123 patient-months). Three patients have had no change in the degree of tricuspid or mitral insufficiency. One patient required reoperation 54 months after repair.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
Neonatal left and right atrioventricular valve insufficiency frequently complicates other forms of congenital heart disease [6–9]. In contrast, isolated valve insufficiency in the presence of normal valve morphology and without displacement of the valve leaflets (as in Ebstein’s anomaly) is rare [10]. Hypoxia in the newborn can cause papillary muscle dysfunction, pulmonary hypertension, and tricuspid valve insufficiency. This insufficiency is benign and transient, however, and thus does not usually warrant operative correction. Myocardial ischemia and infarction in the fetus and the neonate may result in papillary muscle or chordal rupture and is frequently fatal [2–4]. Myocardial ischemia may result from ante partum or peripartum asphyxia, congenital heart disease, viral infections, Rhesus isoimmunization, thromboembolism, or other more obscure causes [2, 11, 12]. Two of our patients had gross evidence of papillary muscle ischemia. The etiology of the chordal rupture was not obvious in the third case. Severe tricuspid valve insufficiency is poorly tolerated in utero and is associated with a mortality rate as high as 83%, probably due to the dominant role of the right heart in the fetal circulation. In addition, recent data show that fetuses with tricuspid insufficiency have reduced left ventricular performance secondary to diastolic dysfunction [13–15]. The presence of isolated severe mitral insufficiency in the neonatal period can also lead to substantial mortality [3, 4, 14, 16, 17]. Systemic atrioventricular valve insufficiency has also been shown to influence outcome in children with other cardiac lesions [18, 19].

Patients with isolated tricuspid or mitral insufficiency due to ruptured papillary muscles or chordae tendinae constitute in some respects a very favorable group. Such patients generally have well-developed right and left ventricular cavities, no right ventricular outflow tract obstruction, and competent pulmonary and aortic valves without left-sided obstructive lesions. If recognized before the occurrence of irreversible end-organ damage, and with proper surgical repair, these children have an excellent chance for a good outcome. If in utero papillary muscle rupture is identified, the fetus should be carefully monitored until considered viable, and delivered at the first sign of fetal distress. The newborn should be similarly observed, and surgical intervention should be recommended before hemodynamic instability supervenes. Our first patient had to be resuscitated with the use of extracorporeal life support owing to hemodynamic compromise with progressive lactic acidosis, and she suffered a cerebrovascular accident from which she partially recovered. We hypothesize that earlier intervention could have prevented the occurrence of this cerebrovascular accident.

Atrioventricular valve repair rather than replacement should be the goal with every patient. Valve replacement remains undesirable in children even though data point to improved survival in the current surgical era in both single- and two-ventricle circulation patients [17, 20, 21]. Preservation of native atrioventricular tissue offers the advantage of avoiding thromboembolism and anticoagulation-related complications, potentially decreases the need for reoperation, and maintains the subvalvar apparatus that helps to preserve ventricular geometry and function.

Several different techniques for the repair of atrioventricular valve prolapse have been utilized in children with good immediate and midterm results [7–10, 17]. In our patients, the surgical options include resection of the unsupported part of the leaflet with sliding annuloplasty, chord translocation from the opposite leaflet, use of the Alfieri apposition suture [21], and creation of artificial chordae. We have also used artificial chordae as adjustable annuloplasty in larger patients for years, and we are pleased with the results. The advantages of artificial ePTFE chordae have been reviewed in the past, and include availability, ease of use, and good midterm reliability in children [17, 22] and adults [23]. Reddy and associates [17] suggest that a 5-0 ePTFE suture may not be adequate when a large tensile strength is required, and advise the use of 4-0 or 2-0 sutures. In our infants, we used 6-0 sutures without encountering any ruptures of the artificial chordae. It is known that the artificial material eventually will be covered with fibrous tissue [24]. The additional support and the inherent strength and elasticity of the ePTFE material may be responsible for the strength of the artificial chordae. At least for older (nonneonatal) children, the fate of the chordae as the patient grows has been well documented [25]. Whether the same longer term results can be achieved in neonates is yet to be determined. The good intermediate results in our patients and in previous reports have not validated the concerns of growth-related leaflet restriction. In the fourth patient, it is likely that we unestimated the extent of ischemic damage to the ruptured papillary muscle and attached the artificial chorda to the weakened tip of the ruptured papillary muscle. Why the dehiscence occurred at 54 months and not earlier remains unclear. In cases with clear evidence of ischemic damage to the papillary muscle, it is probably advisable to secure the artificial chorda to the base of the papillary muscle or directly to the adjacent left ventricular wall (Fig 2).

The use of annuloplasty ring techniques to remodel the dilated annulus and to support the valve repair, while standard in adults, is controversial in children. We believe that in most patients a supported annulus will decrease the chance of future failure of the leaflet and tensor repair techniques employed. Even with appropriate leaflet and tensor repair, central leaks from annular dilation and poor right ventricular function may persist. Reddy and associates [17] recommend the use of annuloplasty techniques in patients whose tricuspid insufficiency is the result of both abnormal chordae and dilated right ventricle, but do not recommend the use of an annuloplasty ring. Others have used commissural plication and semicircular strips of pericardium or prosthetic strips to reinforce the annulus, thus avoiding the use of prosthetic rings in small children for fear of development of valve stenosis [7, 8, 26].

The de Vega annuloplasty is a technically simple, fast, and effective technique to relieve tricuspid insufficiency, and has been used with success in pediatric patients. Kanter and associates [9] used this annuloplasty technique in 42 patients with moderate or severe tricuspid insufficiency and concluded that the children at risk for failure of this technique are those at risk for recurrent or persistent right ventricular systolic hypertension. None of our patients had a reason for or any evidence of persistent postoperative right ventricular hypertension. The principles of this annuloplasty technique can easily be transferred to the posterior annulus of the mitral valve as demonstrated in 1 of our patients. Techniques for externally adjustable tricuspid annuloplasty techniques have been described in prior publications [27–29]. The advantage of the use of an external tourniquet to adjust the annuloplasty under echocardiographic guidance is obvious: it helped us tailor the size of the annuloplasty in the beating heart to minimize valve insufficiency and avoid valve stenosis, a task that is very difficult in small children using other techniques. It also offers the theoretical advantage of the possibility of adjustment of the annuloplasty in the immediate postoperative period without the use of cardiopulmonary bypass. The long-term fate of this annuloplasty technique is not clear. None of our patients has clinical or echocardiographic evidence of mitral or tricuspid valve stenosis. It is not clear whether that is due to growth of the part of the annulus that was not included in the annuloplasty or fracture of the e PTFE suture. To date, we have not had to adjust the annuloplasty size late after patient discharge, and thus we do not know whether that is possible.

In summary, we conclude that surgical repair of critical neonatal tricuspid and mitral insufficiency associated with papillary muscle rupture is technically feasible and, if undertaken before the occurrence of irreversible end-organ damage, can result in good early and midterm results. The modification of the de Vega valvuloplasty technique and the ability to externally adjust the size of the annulus under direct echocardiographic guidance help improve the accuracy of the repair in the neonate.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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