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Ann Thorac Surg 2006;81:1802-1807
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

The Lecompte Maneuver for Relief of Airway Compression in Absent Pulmonary Valve Syndrome

Lars Nölke, FRCS C-Th, Anthony Azakie, MD, Petrous V. Anagnostopoulos, MD, Nelson Alphonso, FRCS C-Th, Tom R. Karl, MD *

Pediatric Heart Center, UCSF Children's Hospital, San Francisco, California

Accepted for publication December 1, 2005.

* Address correspondence to Dr Karl, 513 Parnassus Ave, S-549, San Francisco, CA 94143-0117 (Email: karlt{at}surgery.ucsf.edu).

Presented at the Poster Session of the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Congenital absence of the pulmonary valve syndrome (APVS) is a rare cardiac defect characterized by aneurysmal pulmonary arteries, hypoplastic pulmonary valve cusps, and tracheobronchial abnormalities. Absence of the pulmonary valve syndrome usually occurs in conjunction with ventricular septal defect (VSD) and right ventricular outflow tract obstruction (RVOTO). Surgical mortality rates as high as 16% to 56% have been reported. Here, we describe the surgical results using the Lecompte maneuver, reduction pulmonary arterioplasty, and a valved right ventricle to pulmonary artery (RV-PA) conduit.

METHODS: Medical records and operative and echocardiography reports for all surgical APVS cases were retrospectively examined for pertinent clinical variables. A patient with left bronchial compression due to enlarged pulmonary arteries associated with totally anomalous pulmonary venous drainage (TAPVD) is included to illustrate the value of the Lecompte maneuver.

RESULTS: From January 2002 to December 2004, 4 children with APVS had surgery at a median age of 5 months (range, 3 months to 3.5 years). Three had malalignment VSD and RVOTO. Four had respiratory signs (cough, wheeze, tachypnea, oxygen dependence, ventilator dependence), and all 5 had evidence of tracheobronchial compression by computed tomography or magnetic resonance imaging. Repair included a Lecompte maneuver, a valved conduit with reduction pulmonary arterioplasty, and VSD closure as necessary. The TAPVD patient had repair of the anomalous veins and a Lecompte maneuver. There have been no deaths, and all patients were discharged in good condition. Follow-up is complete at a median of 24 months (range, 9 to 35). Echocardiography has shown no progressive enlargement of the pulmonary arteries.

CONCLUSIONS: Use of the Lecompte maneuver, reduction arterioplasty, and a valved conduit for repair of APVS provides favorable early and midterm results.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Absent pulmonary valve syndrome (APVS) is a rare cardiac defect, characterized by the congenital absence or hypoplasia of the pulmonary valve cusps, annular stenosis with or without infundibular stenosis, dilatation of the pulmonary arteries, and tracheobronchomalacia. Absent pulmonary valve syndrome most commonly occurs in conjunction with a malalignment ventricular septal defect (VSD) and right ventricular outflow tract obstruction (RVOTO), with varying degrees of right ventricular hypertrophy; hence, it is considered by many to be a variant of tetralogy of Fallot. However, APVS is only seen in 3% to 6% of tetralogy of Fallot cases [1]. Absent pulmonary valve syndrome can also occur in isolation, with an intact ventricular septum (IVS) or may occur in conjunction with other cardiac anomalies such as ductus arteriosus, major aortopulmonary collateral arteries, atrioventricular septal defect, double outlet right ventricle, transposition of the great arteries, or atrial septal defect.

For the purpose of this paper, we have used the terms APVS-VSD-RVOTO and APVS-IVS rather than TOF-APVS. This is because, although the majority of APVS patients have a VSD, cases of APVS with IVS do occur, as in this series in which 1 of 4 cases had an IVS. Treatment of APVS, independent of the presence of a VSD or IVS, should be directed at the main components of the condition, namely, congenital absence or hypoplasia of the pulmonary valve cusps, annular stenosis with or without infundibular stenosis, dilatation of the pulmonary arteries, and tracheobronchomalacia.

Patients with APVS can generally be divided into two groups depending on their clinical status. Neonates and infants presenting for the first time at a young age often do so in respiratory failure that may necessitate ventilation, which negatively affects outcome, with operative mortality as high as 16% to 56% [2–7]. Older infants at first presentation tend to have less cardiorespiratory compromise and have risks similar to infants undergoing tetralogy of Fallot repair. Antenatal diagnosis and the routine insertion of a competent pulmonary valve as part of the repair of APVS may improve the outcome in the former group [2].

In this article, we describe our current technique for repair of APVS in infants and children with and without associated anomalies. The case of an infant with totally anomalous pulmonary venous drainage (TAPVD) and left bronchus compression is included to demonstrate the value of the Lecompte maneuver in relieving airway compression secondary to enlarged pulmonary arteries.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Between January 2002 and December 2004, 4 patients had surgical correction of APVS and 1 child had surgery for TAPVD associated with bronchomalacia secondary to enlarged pulmonary arteries (Table 1). The APVS patients show many of the characteristic features (Table 1). Younger patients at first presentation tended to have more respiratory compromise than older patients. Three APVS patients had an associated malalignment VSD and RVOTO, and 3 patients were symptomatic at the time of presentation.


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  		Table 1. Primary Diagnosis, Symptoms, and Diagnostic Tests Used to Confirm the Diagnosis of Absent Pulmonary Value Syndrome (APVS)
 
Diagnosis was made with echocardiography and airway compromise was confirmed with bronchoscopy, computed tomography, or magnetic resonance imaging of the thorax (Fig 1A–C). The Institutional Committee on Human Research at the University of California, San Francisco Children's Hospital, approved this retrospective study.


Figure 1
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  		Fig 1. Magnetic resonance image: (A) coronal, (B) sagittal, and (C) transverse sections of the thorax showing a massively enlarged pulmonary artery and compressed right bronchus.

 
Surgical Technique
All operations were performed through a median sternotomy with cardiopulmonary bypass, mild systemic hypothermia 28° to 30°C and cold blood cardioplegia. The aortic cannulation and aortic cross clamp were placed high on the ascending aorta to allow for subsequent aortic transection. The pulmonary arteries were extensively mobilized into the hila of both lungs, and the ductus arteriosus was ligated and divided if present. After aortic cross clamping and administration of blood cardioplegia, the aorta was transected. A 1- to 1.5-cm cuff of aorta was removed in 1 case to shorten the aorta. Subsequently, the main pulmonary artery was transected slightly above the pulmonary annulus. The Lecompte maneuver was performed, and the aortic anastamosis was completed.

Coexisting intracardiac defects were then repaired through a right atriotomy. The RVOTO was excised through the transatrial and transpulmonary route. When necessary, an infundibulotomy was performed to more clearly define the anatomy, and to allow resection of RVOTO and patching of the right ventricular outflow tract. A reduction pulmonary arterioplasty was then performed by cutting an anterior wedge out of the left and right pulmonary arteries as required (Fig 2A). The pulmonary arteries were repaired primarily so that their size was approximately 1 to 2 SD larger than predicted by a standard nomogram (Fig 2B). A Contegra (valved xenograft) conduit (Medtronic Inc, Minneapolis, MN) was used in the 3.5-year-old infant and a homograft in the remainder.


Figure 2
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  		Fig 2. (A) The enlarged pulmonary arteries and the closed ventricular septal defect. (B) The completed Lecompte maneuver and a reduction arterioplasty and right ventricle to pulmonary artery valved conduit.

 
In the case of the child with supracardiac TAPVD, the venous confluence was anastamosed to the roof of the left atrium in the transverse sinus, after dividing the vertical vein. The Lecompte maneuver was then completed by dividing the ascending aorta and transferring the widely mobilized pulmonary arteries anteriorly. A right atrial line and atrial and ventricular pacing wires were then placed; and after weaning from bypass, all patients had modified ultrafiltration.

Functional Outcome and Follow-Up
After hospital discharge, patients were regularly followed up by their primary physician and referring cardiologist with echocardiography. Follow-up is complete for a median of 24 months (range, 9 to 35).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
There have been no deaths to date. The patient with the preoperative tracheostomy and gastrostomy continued to require a tracheostomy owing to his subglottic stenosis. The other patients were extubated within 2 days of surgery and were discharged on days 5, 6, 8, and 13 postoperatively. Two patients required readmission for the treatment of pericardial effusions, which were treated with steroids. The patient with Klinefelter syndrome (XXY) and tracheostomy required readmission for the insertion of a permanent pacemaker for intermittent complete heart block 2 months after APVS repair. Eleven months postoperatively, he underwent an uncomplicated elective replacement of his right ventricle to pulmonary artery homograft conduit for progressive conduit insufficiency and stenosis, with a new homograft. The remaining patients are symptom free with satisfactory echocardiographic results, with no evidence of progressive enlargement of the pulmonary arteries and no clinical evidence of airway obstruction (Table 2).


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  		Table 2. Follow-Up and Results
 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Absent pulmonary valve syndrome is frequently associated with features of a malalignment VSD, annular or infundibular pulmonary stenosis, and right ventricular hypertrophy. Patients who have APVS with a VSD and RVOTO tend to have ductal agenesis with pronounced pulmonary artery enlargement, whereas the rarer variant of APVS with IVS tends to have less pulmonary artery dilatation and is usually associated with a ductus arteriosus [8, 9]. Furthermore, as many as 25% of APVS cases with a VSD and RVOTO, have a 22q11 chromosomal microdeletion typical of conotruncal lesions, unlike APVS with an IVS in which this microdeletion has not been identified [9, 10]. Antenatal diagnosis of APVS using ultrasound can be achieved with neither false positive nor incorrect diagnoses [9]. Survival in cases diagnosed antenatally is very poor (14.6%) owing to several factors, including in-utero death (14.6%), termination of pregnancy (36.5%), major chromosomal abnormalities (trisomy 13, trisomy 21, or triploidy), and severe cardiorespiratory failure at birth resulting in death before surgical intervention (14.6%) [9, 10]. In the series by Volpe and colleagues [9] and Razavi and associates [10], of 41 cases of APVS diagnosed antenatally (from a total of 20,578 pregnancies referred for ultrasound assessment of known or suspected congenital heart disease), 11 APVS patients survived to surgery, of whom 6 (54.4%) survived.

The cause of the pulmonary artery dilation in APVS remains speculative. The mechanism may differ depending on the constellation of features, for example, APVS with a VSD, RVOTO, and ductal agenesis versus an intact septum associated with a ductus arteriosus. The presence of a ductus arteriosus in utero in APVS patients with an IVS may explain the lesser dilation of the pulmonary arteries in this group, and why some of these patients develop respiratory symptoms at an older age as compared with APVS with VSD/RVOTO [8]. Absent pulmonary valve syndrome with VSD/RVOTO patients as previously mentioned tend not to have a ductus arteriosus in utero, causing an increased blood flow through an immature pulmonary artery. This may explain the larger pulmonary arteries in this group and high attrition rate in utero and early after birth in these neonates. The presence of a ductus arteriosus and VSD in association with APVS in utero may be incompatible with life as initially proposed by Zach and coworkers [11], due to the interference with diastolic filling of both ventricles. Free communication of the fetal aorta and the ventricular chambers as would exist in APVS/VSD and a ductus arteriosus, should result in markedly elevated diastolic ventricular pressures, and therefore limit atrial inflow, severely compromising cardiac output. In the absence of a VSD, these hemodynamic abnormalities would be limited to the right side of the heart, allowing relatively normal left ventricular function and survival of the fetus [8]. Furthermore, the presence of the 22q11 microdeletion in this group may make them more prone to major aortopulmonary collateral arteries formation and an intrinsic abnormality in the pulmonary arteries [2, 12, 13]. Some of the histologic and angiographic features suggestive of an intrinsic abnormality of the pulmonary arteries in APVS were previously presented and reviewed by Karl and associates [2].

The surgical management of APVS has changed over time. Initial palliation with a Glenn shunt was proposed by Waldhausen and colleagues [14] in 1969, for the relief of the bronchial compression. Pulmonary aneurysmorrhaphy with and without various additions such as retrosternal suspension of the pulmonary artery or replacement of the right pulmonary artery with a conduit anterior to the aorta were subsequently reported [15, 16]. Most repair techniques now involve pulmonary reduction arterioplasty or replacement of the central pulmonary arteries, and possibly, placement of a pulmonary valved conduit [3, 7, 17]. Patient age and symptoms at the time of surgery further influence the technique used [4, 5, 7].

Asymptomatic patients with APVS repaired with a transannular patch and aneurysmorrhaphy appear to do well in the long term, despite free pulmonary incompetence [18]. However, there is evidence from the experience in repaired tetralogy of Fallot patients with moderate to severe pulmonary incompetence that they have a poorer exercise capacity and that they may be at higher risk of sudden death [19, 20].

Symptomatic patients or those with elevated pulmonary pressures or reactive pulmonary artery pressures or pulmonary artery branch stenosis seem to benefit postoperatively in terms of ventricular function, exercise tolerance, and smaller pulmonary arteries from a valved pulmonary conduit [2, 3, 5, 17]. Furthermore chronic pulmonary incompetence may irreversibly damage the right ventricle, making it desirable to have a competent valve insitu from the outset. The use of a valved conduit, while beneficial in the neonatal or symptomatic group, has the distinct disadvantage of requiring reoperation, even if it is a relatively low risk reoperation. Choice of conduit is related to many factors, including surgeon and availability of type and size. Smaller homografts can be difficult to attain, and Contegra grafts are available on a named patient basis only at our institution. Downsizing of conduits homograft or Contegra has been described and is useful when appropriately sized grafts are not available. Another approach, advocated by Hew and coworkers [7], involves the use of a valved conduit in neonates to replace the main pulmonary artery and the left and right branch pulmonary arteries, whereas in older infants, they advocate a nonvalved transannular patch with or without aneurysmorrhaphy.

Our present technique, first described by Hraska [21] and Hraska and colleagaues [22] involves a reduction pulmonary arterioplasty, placement of a valved pulmonary conduit, and the Lecompte maneuver. Translocation of the right pulmonary artery anterior to the aorta with a reduction pulmonary arterioplasty reduces the compression of the tracheobronchial tree by the pulmonary arteries. Unlike Hraska, we have only shortened the ascending aorta in one case to date. Shortening of the aorta for aortic redundancy is usually not required in the younger patient. Extensive mobilization of the superior vena cava is required, as is mobilization of the pulmonary arteries into the hila of both lungs and the proximal aortic arch to make room and prevent compression or excessive stretching of vessels (superior vena cava, right pulmonary artery, and right coronary artery) during the Lecompte maneuver. The combination of a reduction arterioplasty and the Lecompte maneuver appears to make more space in the mediastinum and lifts the pulmonary arteries off the tracheobronchial tree. The Lecompte maneuver without a reduction arterioplasty (as in the TAPVD case) appears to relieve the airway compression, although some of this effect may be related to the reduction in the pulmonary artery pressures after repair of the TAPVD.

Arteriopexy operations of various types (suture pexy, pericardial flap pexy, aortopexy versus pulmonary arteriopexy) have been described to relieve the compression of the tracheobronchial tree [23]. Although effective in tracheomalacia, failure rates for aortopexy in tracheobronchial or bronchial involvement of as high as 80% have been reported [24]. Other authors have differentiated between aortopexy and pulmonary arteriopexy for the relief of tracheobronchial collapse versus distal left bronchial collapse when the later pexy was more useful [25]. However, this experience was gained in a different patient population of interrupted aortic arch and VSD. Pexy operations alone are usually not sufficient to relieve the airway compression in APVS. In contrast aneurysmorrhaphy/pulmonary artery plication relieves much of the compression [26]. The combination of a pulmonary reduction arterioplasty and anterior displacement of the pulmonary artery by the use of the Lecompte maneuver seems to achieve better results by combining the various techniques. Shortening of the aorta may be necessary in selected cases to prevent iatrogenic compression of the distal trachea and right main bronchus, as has been described after the arterial switch operation [27].

Stenting for relief of the tracheobronchial obstruction, whether by external stents as described by Hagl and colleagues [28] or internal airway stents, deals with the consequence of the enlarged pulmonary arteries compressing the tracheobronchial tree, but that does nothing to deal with the cause and they have no potential for growth.

In conclusion, consistent with the experience from tetralogy of Fallot repair, we advocate placement of a valved conduit to reduce the long-term risks associated with free pulmonary incompetence [19, 20]. The addition of the Lecompte maneuver and reduction arterioplasty appears to have good early to midterm results in the repair of absent pulmonary valve syndrome.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
Special thanks to Jun Edo Orlanes for his work on the surgical sketches.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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  17. Ilbawi MN, Idriss FS, Muster AJ, Wessel HU, Paul MH, DeLeon SY. Tetralogy of Fallot with absent pulmonary valve. Should valve insertion be part of the intracardiac repair? J Thorac Cardiovasc Surg 1981;81:906-915.[Abstract]
  18. McCaughan BC, Danielson GK, Driscoll DJ, McGoon DC. Tetralogy of Fallot with absent pulmonary valve. Early and late results of surgical treatment J Thorac Cardiovasc Surg 1985;89:280-287.[Abstract]
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