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Ann Thorac Surg 1996;62:136-142
© 1996 The Society of Thoracic Surgeons
Department of Pediatric Cardiac Surgery, "Marie Lannelongue" Hospital, Paris Sud University, Le Plessis Robinson, France
Accepted for publication February 29, 1996.
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Abstract |
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Methods. Between May 1977 and May 1995, 37 consecutive patients underwent repair of absent pulmonary valve syndrome. Patients were divided into two groups according to age at operation: group A (10 infants less than 1 year old) and group B (27 patients older than 1 year). Mean age at operation was 5 ± 4 months in group A and 72 ± 42 months in group B. Initially, repair consisted of ventricular septal defect closure and relief of right ventricular outflow tract obstruction combined with pulmonary valve implantation. More recently, the concept of treatment has evolved with pulmonary arterioplasty without pulmonary valve insertion, except in patients with elevated pulmonary artery pressure.
Results. Of the 37 patients, 34 had successful repair. The overall in-hospital mortality rate was 8% (two deaths in group A and one in group B). No hemodynamic data were correlated with operative death. Death was associated with longer extracorporeal circulation time (p= 0.005) and longer aortic cross-clamping time (p = 0.019). In fact, these were clearly related to more complex anatomy (p = 0.001): multiple ventricular septal defects in 1, left pulmonary artery arising from the ductus in another, and left pulmonary artery arising from the aorta in the remainder. Follow-up was available in 22 of the 34 survivors. Mean follow-up time was 30 ± 47 months in group A and 38 ± 33 months in group B. All but 1 had no restriction of exercise, and most of them had pulmonary incompetence on Doppler echocardiography. One developed severe exercise intolerance because of pulmonary valve stenosis (xenograft), leading to uneventful reoperation 123 months after initial repair. One infant died suddenly of complete atrioventricular block 3 months after repair. The late mortality rate was 5%.
Conclusions. Surgical treatment of absent pulmonary valve syndrome should include pulmonary arterioplasty to reduce bronchial obstruction, with no need for pulmonary valve insertion. This procedure is feasible and is recommended especially in markedly symptomatic infants.
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Introduction |
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Material and Methods |
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There were 20 girls and 17 boys. Age at operation ranged from 1 to 180 months, with an average of 54 months. Ten of these patients were infants. At operation, body weight ranged from 2.7 to 42 kg (mean, 14.7 kg), and body surface area ranged from 0.19 to 1.35 m2 (mean, 0.61 m2).
A large spectrum in the severity of symptoms was observed among patients. Patients could be classified into two groups according to their age at operation. Group A consisted of 10 infants less than 1 year old. Nine of these infants were markedly symptomatic with severe respiratory distress, episodes of respiratory obstruction, and bronchopulmonary infection requiring prolonged and repeated hospital admissions. Three of them required mechanical ventilation just before repair. One infant had moderate cardiac failure and poor weight gain. Age at operation ranged from 1 to 11 months (mean, 5 ± 4 months), and weight ranged from 2.7 to 6.6 kg (mean, 4.7 ± 1.4 kg). Group B included 27 patients older than 1 year at operation. Eight patients were markedly symptomatic. Partial or complete bronchial obstruction was confirmed at bronchoscopy in 4 of them; 1 required right bilobectomy because of lobar emphysema secondary to bronchial obstruction before repair. Another underwent complete repair in another center at 3 months of age with VSD closure, right infundibulectomy, and right ventricular outflow tract (RVOT) enlargement with a monocusp patch. At 8 years of age, complete left bronchial obstruction developed because of aneurysmal dilatation of the pulmonary artery. Bronchial stent implantation was attempted twice, without success. She was then referred to our unit for operative remodeling of the pulmonary arteries. Eleven additional patients had a progressive decrease in exercise tolerance. Six other patients were cyanotic, 2 of them requiring modified Blalock-Taussig shunts before complete intracardiac repair because of severe cyanosis with hypoxic spells. Finally, 2 patients were completely asymptomatic. Age at operation ranged from 13 to 180 months (mean, 72 ± 49 months), and weight ranged from 5.6 to 42 kg (mean, 18.1 ± 10.1 kg).
Physical findings were similar in both groups. Auscultation revealed a systolic murmur at the left upper sternal border associated with an early diastolic murmur at the left sternal border, resulting in the characteristic "to-and-fro" murmur. Chest roentgenogram usually showed cardiomegaly (mean cardiothoracic ratio 0.57 ± 0.05) and prominence of the right or left hilar region caused by massively dilated proximal major pulmonary artery branches. Four patients had extracardiac anomalies, including hemophilia (n = 1), aplastic anemia (Fanconi) (n = 1), and DiGeorge syndrome (n = 2).
All patients but 1 had complete cardiac catheterization and angiography before repair (Fig 1
). Angiography results confirmed the diagnosis, showing absent pulmonary leaflets with pulmonary regurgitation, subaortic VSD with overriding aorta, small pulmonary annulus, and gross dilatation of either the pulmonary trunk or one or both pulmonary arteries. In group A, all patients had a predominant left-to-right shunt ranging from 1.3 to 2.3 (mean, 1.8 ± 0.5). The systolic right ventricle (RV) pressure was 98 ± 19 mm Hg (range, 60 to 114 mm Hg), the systolic pulmonary artery (PA) pressure was 30 ± 5 mm Hg (range, 23 to 38 mm Hg), and the peak systolic RV-PA pressure gradient was 67 ± 17 mm Hg (range, 35 to 85 mm Hg). The systemic arterial oxygen saturation was 81% ± 7% (range, 75% to 88%). Within group B, the predominant shunt was left to right, ranging from 1.2 to 3.9 (mean, 2.2 ± 0.9). The systolic RV pressure was 97 ± 11 mm Hg (range, 77 to 115 mm Hg), the systolic PA pressure was 25 ± 10 mm Hg (range, 11 to 54 mm Hg), and the peak systolic RV-PA pressure gradient was 72 ± 11 mm Hg (range, 51 to 86 mm Hg). The systemic arterial oxygen saturation was 83% ± 13% (range, 53% to 94%).
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Surgical Technique
All 37 patients were operated on through a median sternotomy using cardiopulmonary bypass, hypothermia to 28°C, and cold potassium cardioplegia (crystalloid with patient blood). Extracorporeal circulation time ranged from 63 to 173 minutes (mean, 110 ± 25 minutes), and aortic cross-clamping time ranged from 22 to 107 minutes (mean, 58 ± 21 minutes). The right atrium was opened and atrial septal defect was closed (n = 7).
A vertical infundibulotomy was then performed, and the intracardiac anatomy was defined. All but 5 patients had transannular incision of the RVOT. All patients, except for the patient with previous complete repair, had patch closure of the subaortic outlet VSD performed through either a transventricular (n = 32) or a transatrial (n = 4) approach. To close the VSD, a Dacron patch was used in 22 patients, a Weavnit patch in 8, a Teflon patch in 5, and a Gore-Tex (W.L. Gore & Assoc, Flagstaff, AZ) patch in 1. The right infundibulum was found to be thickened in 26 patients (3 in group A and 23 in group B), requiring hypertrophied muscle band resection, although the obstruction was mostly at the annular level.
Remodeling of the pulmonary arteries has been performed systematically since 1989 (21 patients, including 9 infants). After aortic transection to obtain good exposure of the pulmonary arteries, two triangular segments were resected on the anterior wall of both branches. Resection was extended beyond the hilum of both lungs close to the origin of the lower lobe arteries. In some cases, anterior resection was combined with plication by direct suture of the posterior wall. Pulmonary arterioplasty was performed on both pulmonary arteries (n = 15), on the right pulmonary artery (n = 4), and on the pulmonary trunk (n = 2). The final diameter of the pulmonary arteries was adjusted to a size slightly larger than normal according to the child's body surface area, and special care was taken to obtain an unobstructed pulmonary bifurcation. The aorta was reconstructed then by direct anastomoses. In 17 of these patients, pulmonary artery plication was performed without pulmonary valve insertion. In the remaining 4, pulmonary arterioplasty was associated with pulmonary valve insertion because of elevated pulmonary artery pressure (1 in group A and 3 in group B).
The RVOT was reconstructed with a patch alone in 21 patients (2 in group A and 19 in group B), in conjunction with pulmonary valve insertion in 11 patients. Infundibular-pulmonary patch was performed with autogenous pericardium in 13 patients, Gore-Tex in 5, autologous pulmonary artery tissue in 2, and Dacron in 1. In the remaining 11 patients, reconstruction included implantation of a homograft monocusp patch (n = 5), a xenograft valve (n = 3), a cryopreserved valved pulmonary artery homograft (n = 2), and a pericardial valved homograft (n = 1).
The 3 patients with associated left pulmonary artery arising from either the aorta or the ductus arteriosus had detachment of the left pulmonary artery with reimplantation to the pulmonary trunk.
Histologic study of the aneurysmal pulmonary artery was performed in 1 patient. Examination revealed necrosis of the media with mucoid accumulation.
Statistical Methods
Statistical analysis was done using the Mann-Whitney test for evaluating nonparametric data and contingency table analysis for categoric data. A p value less than 0.05 was considered significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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In group B, the duration of mechanical ventilation after repair varied from 1 to 33 days (mean, 3 ± 6 days), and intensive care unit stay varied from 2 to 54 days (mean, 5 ± 10 days). The postoperative course was completely uneventful in 10 patients. Fourteen patients had transient right ventricular failure, with pleural effusion in 6. One patient required early postoperative reoperation because of mediastinal bleeding. Recovery from respiratory distress was delayed in 1 patient who had inhalation pneumonia requiring mechanical ventilation for 33 days. Finally, another patient died in the immediate postoperative period.
Overall postoperative mortality for both groups was 3 of 37. Age at death was 1, 9, and 17 months, respectively. Statistical analysis was performed to determine risk factors for hospital death. Operative death was associated with a longer extracorporeal circulation time, 163 ± 12 minutes versus 105 ± 22 minutes (p = 0.005); and a longer aortic cross-clamping time, 91 ± 22 versus 52 ± 20 minutes (p = 0.019). Age at operation, residual systolic RV-PA gradient, or the postoperative ratio of RV to left ventricular systolic pressure had no influence on operative death. In fact, death was clearly related to more complex anatomy (p = 0.001): 1 patient had multiple VSDs, another patient had the left pulmonary artery arising from the ductus arteriosus, and the remaining patient had the left pulmonary artery arising from the ascending aorta associated with abnormal partial pulmonary venous return and coronary–right ventricular fistula. Two of them had undergone associated pulmonary arterioplasty. Postmortem examination was performed in each of these patients and revealed satisfactory intracardiac repair (Fig 2).
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In group B, follow-up was available for 16 patients of the 26 survivors after operation. The follow-up interval ranged from 1 to 99 months (mean, 38 ± 33 months). No late death was observed. No patients had restriction of exercise. On Doppler echocardiography, most of them had pulmonary incompetence, and the systolic RV-PA systolic gradient ranged from 3 to 65 mm Hg (mean, 34 ± 20 mm Hg). Two patients, who had undergone complete repair with plasty of both pulmonary arteries at 17 and 103 months of age, respectively, subsequently experienced branch pulmonary artery stenosis with a systolic gradient of 60 mm Hg. Both are completely asymptomatic. Two additional patients, who had had homograft monocusp patch implantation for RVOT reconstruction, had severe pulmonary incompetence at late follow-up, with no exercise intolerance. At the closing date of the study, the late mortality rate after repair of absent pulmonary valve syndrome was 5%.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The clinical course of this syndrome was well described by Miller and associates [3] in 1962, who emphasized the major role of the markedly dilated pulmonary arteries, leading in some cases to compression of the bronchial tree with severe respiratory distress in the first months of life, as observed in 9 of the 10 infants requiring repair before 1 year of age in our series. The clinical course varies, and there are usually two common presentations: the first, in infants presenting with respiratory distress due to bronchial obstruction; and the second, in older children presenting with a bidirectional shunt at the ventricular level with prominent left-to-right shunt. Classically, the former group is considered to have a poor prognosis, and medical treatment usually fails to control the symptoms.
The pathogenesis of this syndrome is still controversial. In the past, some authors suggested that agenesis of the ductus arteriosus may be responsible for the intrauterine pulmonary artery dilatation [6]. The occasional association with patent ductus arteriosus in this syndrome, as observed in 1 of our patients and by other authors [1, 5], does not support this theory. In 1989, Fouron and colleagues [7] reported prenatal diagnosis of this syndrome using echocardiography and showed that intrauterine closure of the ductus arteriosus led to a massive right-to-left shunt through the associated unrestrictive VSD both in systole and in diastole. The role of "decompression" of the right-sided circulation, achieved in utero by the ductus, might then be accomplished by the associated unrestrictive VSD. In fact, it is clear that absence or premature closure of the ductus arteriosus cannot explain the pulmonary artery dilatation by overflow to the lung.
On the other hand, orientation of the infundibulum and the degree of pulmonary valvular stenosis with poststenotic turbulence have been held responsible for pulmonary artery dilatation [6, 8]. In 1990, Momma and associates [9] created an experimental model of tetralogy of Fallot with absent pulmonary valve in rats treated by bis-diamine, a teratogen interfering with neural crest cells. These authors found that enlargement of the pulmonary arteries was already present in utero and was correlated with a lesser degree of pulmonary annulus stenosis. Moreover, they noticed compression and deformity of the bronchial tree already during fetal life.
The possibility of primary structural anomaly of the pulmonary artery also has been raised. Hiraishi and co-workers [10] found on cardiac catheterization an increase in pulmonary artery compliance, leading to the aneurysmally dilated pulmonary arteries. Histologic abnormalities of the pulmonary arteries have been described. Different authors [3, 11] have reported degenerative changes in the intima and media of the proximal pulmonary arteries. Childers and McCrea [12] described 1 case with the combination of absence of the pulmonary valve and Marfan syndrome. Similar findings were observed in the only case in whom we performed histologic study. Such observations raise the possibility that a common defect in vascular wall structure may be present in both syndromes [13]. Other investigators [14, 15] encountered abnormalities of arborization, with tufts of arteries encircling and compressing the intrapulmonary bronchi. Karl and associates [14] and Stellin and colleagues [16] found irregularities of the bronchial cartilage ranging from dysplasia to complete absence, explaining the loss of bronchial wall support and the severe respiratory distress observed in infants. It is clear that the true etiology of absent pulmonary valve syndrome remains speculative, but all of these reports suggest a multifactorial cause.
Many operative treatments have been proposed, with various results. Classically, closure of the VSD associated with relief of the RVOT obstruction is considered the treatment of choice.
However, much controversy exists regarding the management of symptomatic patients, usually infants, with progressive pulmonary insufficiency and right ventricular failure. The aim of operative procedures is to relieve respiratory symptoms.
Initially, Pinsky and co-workers [17] believed that most of these patients should be managed without operation and recommended vigorous, continuous respiratory therapy. If this failed, operation was advocated without pulmonary valve insertion. In fact, differences in symptoms have led surgeons to try various palliative procedures.
Byrne and associates [18] successfully performed complete ligation of the main pulmonary artery and construction of a central aortopulmonary shunt in 1 infant. These authors related the pathophysiology of this syndrome to the severity of the pulmonary insufficiency. Similarly, Ilbawi and colleagues [19] performed a combination of pulmonary artery ligation and modified Blalock-Taussig shunt. Two of the 4 patients died soon after the procedure. Few authors have advocated a similar technique [20, 21]. The main drawbacks of this technique are the need for further complete repair as the child grows older and the absence of relief of bronchial obstruction.
In fact, there is no worldwide consensus with regard to pulmonary valve insertion and the need for pulmonary arterioplasty. Some authors, relating symptoms to the pulmonary insufficiency, have emphasized pulmonary valve insertion as the treatment of choice. In their first report, Ilbawi and colleagues [22] recommended that valve insertion be performed in all patients at the time of intracardiac repair. Similarly, Layton and associates [23] considered that the procedure should include correction of the pulmonary regurgitation and advocated the use of an aortic valvular homograft to reconstruct the RVOT. In our earlier experience, a similar approach was realized with the use of xenograft valve or homograft monocusp patch. Retrospectively, it appears clear that the monocusp implantation used in 5 of our patients could not prevent severe pulmonary incompetence at late follow-up. Moreover, there are concerns about the midterm complications of valve insertion, with development of calcification and stenosis. Some of these patients will thus require further operations [1, 24], as observed in 1 patient in our series, and probably in some others in whom follow-up was not available. As pointed out previously, compression of the tracheobronchial tree by the aneurysmal pulmonary arteries is not obviated with any of these techniques.
Therefore, because of respiratory distress, which remains the major problem for some patients, different authors have suggested another approach with remodeling of the aneurysmal pulmonary arteries to reduce the bronchial obstruction. Miller and associates [3] recommended suspension of the aortic arch anteriorly and pulmonary artery aneurysmorrhaphy on the side of the arch to relieve bronchial obstruction. Similarly, Bove and colleagues [25] reported successful pulmonary artery aneurysmectomy combined with anterior suspension of the pulmonary arteries to the retrosternal fascia in an infant. Dunningan and co-workers [26] performed the first plication of a right pulmonary artery in a 3-week-old patient using a dilator as a sizing stent. Cardiac catheterization 14 months later confirmed the good result, with no persistent aneurysmal pulmonary artery dilatation. In 1985, the Mayo Clinic group recommended insertion of a valve or a valved conduit combined with reduction of pulmonary artery size [1]. A similar approach has been advocated by many authors [14,24,27–29].
Based on these latter reports, our approach to the absent pulmonary valve syndrome has evolved recently from classic pulmonary valve insertion with no pulmonary artery remodeling to pulmonary arterioplasty without pulmonary valve insertion. In our most recent experience, reduction of aneurysmal pulmonary arteries was essential to treat severely ill infants. In 1983, Stellin and colleagues [16] reported a new technique of arterioplasty. Resection of the anterior wall associated with plication of the posterior wall of both pulmonary arteries was performed. Moreover, shortening of the main pulmonary artery by plication was performed to draw the orifice of the right pulmonary artery inferiorly and the bifurcation area away from the trachea. This procedure was successful in 1 infant [16]. A similar remodeling procedure was performed successfully in 21 of our patients (including 9 infants), and became the rule since 1989. We strongly believe that any infant with severe respiratory distress requires such an early operative repair. Reconstruction of the pulmonary arteries should be carried out as distally as possible. In addition, plication of the posterior wall may provide support and reduce the compression of adjacent bronchi. Development of secondary pulmonary branch stenosis, as observed on Doppler echocardiography in 2 of our patients, appears to be rare and does not compromise this technique [28].
Pulmonary arterioplasty without pulmonary valve insertion will leave patients with pulmonary insufficiency. We do not share the view that a large number of patients may later require a valved pulmonary conduit. In addition, the experience with patients operated on for tetralogy of Fallot suggests that pulmonary insufficiency after reconstruction of the RVOT does not usually result in adverse sequelae, although close follow-up of these patients is necessary [30]. On the other hand, we strongly agree with Pinsky and associates [17], who recommended pulmonary valve insertion in patients with pulmonic branch stenosis or other defects causing elevated pulmonary artery pressure, as performed in 4 of our most recent patients with associated pulmonary arterioplasty.
In conclusion, 37 consecutive patients, aged 1 to 180 months and including 10 infants, underwent total correction of absent pulmonary valve syndrome from 1977 to 1995. Repair consisted initially of closure of VSD and relief of RVOT obstruction, usually associated with pulmonary valve implantation. More recently, remodeling of aneurysmal pulmonary arteries to reduce bronchial obstruction and VSD closure have become the rule, without the need for pulmonary valve implantation. This latter procedure was performed in 21 patients (including 9 infants) and was successful in 19 of them. Such a procedure is thus recommended especially in symptomatic patients, and can be performed with good results even in infants.
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Acknowledgments |
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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