Ann Thorac Surg 1998;65:1120-1126
© 1998 The Society of Thoracic Surgeons
Left Pulmonary Artery Kinking Caused by Outflow Tract Dilatation After Transannular Patch Repair of Tetralogy of Fallot
Doff B. McElhinney, MSaa,
Andrew J. Parry, MDaa,
V. Mohan Reddy, MDaa,
Frank L. Hanley, MDaa,
Paul Stanger, MDbb
a Division of Cardiothoracic Surgery, University of California, San Francisco, San Francisco, California, USA
b Division of Pediatric Cardiology, University of California, San Francisco, San Francisco, California, USA
Accepted for publication November 24, 1997.
Address reprint requests to Dr Hanley, 505 Parnassus Ave, M593, San Francisco, CA 94143-0118
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Abstract
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Background. Stenosis of the branch pulmonary arteries after tetralogy of Fallot repair can result from several mechanisms. In patients with free pulmonary regurgitation and right ventricular dilatation after transannular patch repair, we have observed that the pulmonary outflow tract can dilate and elongate craniad and rotate to the left, resulting in kinking and obstruction of the previously normal left pulmonary artery.
Methods. Ten patients referred for reoperation after tetralogy repair with severe pulmonary regurgitation and right ventricular outflow tract dilatation were found to have left pulmonary artery kinking. In 8 of these patients kinking was the sole or partial cause of left pulmonary artery obstruction, whereas there was no documented obstruction in the other 2. All patients underwent right ventricular outflow tract reconstruction and left pulmonary artery repair with removal of the redundancy at the kink point. Patching alone is not an effective method of repair in this condition, because the mechanism of obstruction is not corrected and the patch material can become redundant and lead to recurrent obstruction.
Results. All patients underwent successful pulmonary outflow tract reconstruction. Left pulmonary artery kinking was corrected in all patients, and relief of obstruction was attained in the 8 patients with stenosis. At follow-up ranging from 9 to 58 months, no patient has evidence of recurrent left pulmonary artery stenosis.
Conclusions. Left pulmonary artery kinking should be suspected at long-term follow-up after tetralogy repair in patients with significant pulmonary regurgitation and right-sided dilatation, even if previous evaluations showed no evidence of left pulmonary arterial abnormality. Because unilateral obstruction caused by kinking may lead to asymmetric pulmonary flow, it can exacerbate pulmonary regurgitation and right ventricular dilatation, in effect accelerating the processes that led to kinking in the first place. Kinking can be relieved successfully with the techniques described in this report.
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Introduction
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Branch pulmonary arterial obstruction is a common finding in both repaired and unrepaired tetralogy of Fallot (TOF). It is one of the most frequent indications for reoperation in patients undergoing early TOF repair [1], and it is encountered in many patients with TOF undergoing reoperation for other reasons [2, 3]. Pulmonary arterial obstruction after TOF repair may be residual, caused by hypoplastic native branch pulmonary arteries [4] or a coarctation resulting from the extension of ductal tissue into the left pulmonary artery (LPA) in the presence of a left-to-right ductal shunt [5]. In other cases, the obstruction may be iatrogenic, resulting from distortion at the location of a previously placed systemic–pulmonary arterial shunt [6, 7], discrete stenosis at the site of right ventricle–pulmonary arterial conduit anastomosis, or stenosis at the site of LPA anastomosis in patients who underwent repair of nonconfluent central pulmonary arteries.
We have observed that yet another mechanism is frequently responsible for LPA obstruction in patients with pulmonary regurgitation and a dilated right ventricular outflow tract after transannular patching. As the right ventricle and pulmonary trunk dilate and elongate secondary to severe pulmonary regurgitation, the right ventricular outflow tract, which is restricted on the right side by the dextraposed aorta and anteriorly by the chest wall, is shifted craniad and rotated to the left. This is a chronic, progressive process in which the normally obtuse angle created by the pulmonary trunk and LPA becomes acute, and the normally acute angle at the origin of the right pulmonary artery from the pulmonary trunk becomes obtuse (Fig 1). This causes the LPA to kink at its origin from the pulmonary trunk, which may be compounded by tethering of the LPA by the ligamentum arteriosum.
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Fig 1. Mechanism of left pulmonary artery (LPA) kinking after repair of tetralogy of Fallot, with pulmonary regurgitation and right heart dilatation. The right ventricular outflow tract (RVOT) dilates, elongates, and rotates craniad and leftward. The normally acute angle between the main pulmonary artery (PA) and the right pulmonary artery (RPA) becomes obtuse, while the normally obtuse angle between the main PA and LPA becomes acute. The resulting redundancy of the LPA enables it to kink, especially if it is tethered to the undersurface of the arch by an intact ligamentum arteriosum.
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Kinking of the LPA may occur with or without obstruction, and may be found as either an isolated form of obstruction or in combination with other mechanisms. For example, intrinsic pulmonary arterial hypoplasia or coarctation is not uncommon in TOF, so LPA kinking may be superimposed on one of these processes. Alternatively, the obstructed orifice may secondarily remodel over time, producing another mixed form of stenosis. Thus, the correction of LPA kinking will vary according to the composite picture.
Since July 1992, 10 patients undergoing reoperation at our institution 0.7 to 29.4 years after transannular patch repair of TOF were found to have LPA kinking. In this report, we describe our experience with these patients.
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Patients and methods
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Patients
Between July 1992 and November 1996, 30 patients who had previously undergone complete transannular patch repair of TOF were referred for reoperation on the right ventricular outflow tract. On preoperative angiography or at operation, it was determined that the LPA was kinked in 10 of these patients, 8 of whom had LPA obstruction caused entirely or partially by the kinking. In the other 2 patients, the LPA was redundant and kinked, but there was no evidence of obstruction at the kink point. These 10 patients constitute the study group for the present report (Table 1).
Age at reoperation ranged from 1.4 to 35 years (median, 12.7 years). Nine patients had undergone primary complete repair with transannular patching, whereas the other patient had a classic Blalock-Taussig shunt performed in infancy and later underwent complete repair with a transannular patch. Transannular patch repair was performed at a median age of 11.4 months (range, 11 days to 6.2 years), between 0.7 and 29.4 years before reoperation at our institution. The original repair was not performed by us in any patient. In all patients the transannular patch extended from the right ventricle to the pulmonary trunk; in 2 patients the patch had been carried up to the pulmonary arterial bifurcation. In no patient was the patch extended into either branch pulmonary artery. The original transannular patch material was pericardium in 8 patients and Dacron in 2. In 4 patients, all of the thickened pulmonary valvar tissue was removed at the time of transannular patch repair. Previous reoperations had been performed for residual ventricular septal defect in patients 2 and 3 (10 and 2 years previously), and for patch augmentation of left pulmonary artery stenosis in patient 5 (4 years previously).
Before reoperation at our institution, all patients underwent preoperative evaluation with cardiac catheterization and echocardiography, and all had evidence of severe pulmonary regurgitation along with secondary right ventricular and pulmonary outflow tract dilatation (see Table 1). Three patients had magnetic resonance scans performed (Fig 2), and 4 underwent preoperative perfusion studies, including 3 who had electrocardiogram-gated magnetic resonance imaging flow studies and 1 who underwent a preoperative technetium-99m scan. There was obstruction of flow into one or both branch pulmonary arteries in 9 patients, including 8 in whom obstruction of the LPA was present, as determined by either a pressure gradient at catheterization or a perfusion study (see Table 1). Kinking or tortuosity of the LPA was recognized on preoperative angiography in 7 patients (Fig 3), all except for patients 3, 7, and 9, in whom kinking was observed in the operating room. Preoperative cardiac catheterization and perfusion study data are summarized in Table 1. Additional findings were mild tricuspid regurgitation in 4 patients, small (n = 2) or moderate (n = 1) residual ventricular septal defect in 3, moderate aortic regurgitation with left ventricular dilatation in 2, inducible nonsustained ventricular tachycardia in 2, and residual secundum atrial septal defect in 1. Most of the older patients had mild exercise intolerance. Specific indications for operation varied and were based on the clinical judgment of the referring cardiologist and the surgeon.
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Fig 2. Preoperative magnetic resonance imaging study performed 3 months preoperatively in patient 5, who had left pulmonary artery obstruction caused by both kinking and focal stenosis. (A) Transverse T1-weighted image showing severe rotation of the pulmonary trunk (M), resulting in kinking of the left pulmonary artery (L) at its origin, which is shifted to the rightward-posterior aspect of the pulmonary trunk. (B) A transverse image 10 mm caudal to the scan depicted in part A, showing the obtuse transverse angle between the pulmonary trunk and the right pulmonary artery (R) (A = ascending aorta; D = descending aorta.)
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Fig 3. Angiograms of patient 5 6 years after repair, just before right ventricular outflow tract revision and repair of left pulmonary artery obstruction with kinking. (A) Anteroposterior and (B) lateral projections of a right ventriculogram performed 1 month before pulmonary outflow tract revision demonstrate an enlarged right ventricle, a massively dilated and leftward-rotated right ventricular outflow tract, and kinking of the left pulmonary artery at its origin (now posterior to the pulmonary trunk). Note that the left lung vasculature is substantially less opacified by contrast than the right. (C) Selective left pulmonary artery injection in a left anterior oblique projection highlights the kinked origin of the left pulmonary artery from an unusually posterior and rightward point.
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Operative techniques
After exposure of the inferior and superior venae cavae and the branch pulmonary arteries, patients were placed on cardiopulmonary bypass with bicaval and ascending aortic cannulation. Patients were cooled to 25°C and cardioplegia was administered in 4 patients with intra cardiac shunts or who required left-sided procedures. In the 2 patients with aortic regurgitation and left ventricular dilatation, aortic valvuloplasty was performed (Table 2). In 2 other patients, residual ventricular septal defects were closed; 1 of these patients also had closure of an atrial septal defect. After these procedures, and after cooling in the other patients, attention was turned to the right ventricular outflow tract.
The primary principle governing revision of the right ventricular outflow tract and correction of LPA kinking was removal of redundancy at the kink point. In patients with no mechanism of LPA stenosis other than kinking, this was accomplished by effectively shortening the dilated and elongated pulmonary trunk (see Table 2). Most often, the pulmonary trunk was shortened by replacing it with an allograft conduit tailored to be shorter than the elongated native pulmonary trunk, thus allowing the LPA to be pulled down to complete the distal anastomosis and eliminating the redundancy at the point of kinking (Fig 4). In 2 patients, the native pulmonary trunk was not excised entirely, but shortened by resection of a circumferential segment of tissue or wedges on each side, along with aneurysmectomy. In 3 patients (patients 7, 8, and 9), the ligamentum arteriosum was clearly tethering the LPA and contributing to the kinking. In all patients with an intact ligamentum arteriosum, this structure was clipped and divided.
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Fig 4. (A) Dilated right ventricular outflow tract with previous transannular patch (TP), showing kinked left pulmonary artery. (B) Correction of left pulmonary artery kinking after allograft (H) conduit reconstruction of the right ventricular outflow tract. (C) Alternative technique for correction of left pulmonary artery when another form of stenosis is present and a segment of stenotic left pulmonary artery is resected. The shortened left pulmonary artery is reimplanted into the side of the allograft (H) conduit.
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In cases of LPA stenosis due to kinking plus another mechanism, repair incorporated the basic concept of removing the redundancy at the kink but included other techniques as well (see Table 2). For example, the LPA obstruction in patient 4 was caused by a combination of kinking and juxtaductal coarctation. Along with conduit reconstruction of the right ventricular outflow tract, the LPA was transected distal to the ring of ductal tissue and anastomosed end-to-side into the conduit (Fig 4C). This accomplished both removal of the coarct segment and obliteration of LPA redundancy. In patients 3 and 5, LPA obstruction was a function of kinking along with secondary ostial stenosis. In addition to conduit reconstruction of the pulmonary outflow tract, the conduit was fashioned with a narrow extension of allograft tissue laterally, which was used to perform a patch augmentation of the LPA in the plane of the former kink angle, effectively smoothing off the kink. The conduit may be anastomosed to the pulmonary arterial confluence slightly toward the right pulmonary artery to provide a more favorable angle from which to perform the LPA arterioplasty. In patient 10, who had a combination of kinking and hypoplastic branch pulmonary arteries, removal of LPA redundancy was combined with augmentation of the hypoplastic pulmonary arteries along their superior aspect.
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Results
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On direct observation in the operating room after repair, the kinking of the LPA appeared to be corrected in all patients. Intraoperative multiplane transesophageal echocardiography showed the LPA stenosis to be completely relieved in all 8 patients with preoperative obstruction. There were no early deaths or complications. Discharge echocardiograms showed no residual LPA stenosis in any patient, and pulmonary regurgitation ranging from none to mild in the 8 patients who had conduits placed.
At follow-up ranging from 9 to 58 months (median, 39 months), there had been no deaths and no reinterventions. All patients had undergone follow-up echocardiography, with careful evaluation of the branch pulmonary arteries. There was no evidence of recurrent LPA obstruction in any patient, and no evidence of increased right pulmonary artery flow or acceleration anywhere in the pulmonary arteries. Three patients, all of whom underwent preoperative magnetic resonance imaging flow studies (patients 1, 2, and 5), had undergone postoperative technetium-99m perfusion scans between 9 and 15 months postoperatively. All had significantly improved left lung perfusion relative to the preoperative value, with left lung flow ranging from 42% to 44%. One patient (patient 6), who had moderate aortic regurgitation before pulmonary outflow tract revision, had no residual left pulmonary artery obstruction but progressive aortic regurgitation and supravalvar aortic stenosis on postoperative cardiac catheterization. Two years after right ventricular outflow tract revision, this patient underwent aortic valve replacement. No other patients required subsequent reoperation.
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Comment
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Mechanism of left pulmonary artery kinking after tetralogy of fallot repair
The present study does not allow for an estimation of the incidence of LPA kinking after transannular patch repair, as it draws only from the cohort of patients presenting for reoperation after TOF repair. Nevertheless, it does tell us that kinking is a common mechanism of LPA stenosis in this group of patients. Therefore, in patients with severe pulmonary regurgitation, right ventricular dilatation, and LPA obstruction after transannular patch repair of TOF, kinking of the LPA should be considered as a cause of obstruction. Furthermore, routine follow-up of all patients with transannular patch repair of TOF who exhibit significant pulmonary regurgitation and right heart dilatation should include evaluation of the LPA to rule out kinking. On angiography, this pattern appears as a dilated, leftward-rotated pulmonary outflow tract, with origination of the LPA from the pulmonary trunk more posteriorly than usual and sometimes with an obviously angled proximal course. There may be a superiorly directed component to the kink as well, especially if tethering by the ligamentum is present.
Because LPA kinking according to this mechanism is generally a secondary lesion, it will not often be found in isolation and will not constitute the sole indication for operation. Thus, patients may come to operation for right ventricular outflow tract revision without preoperative recognition of LPA kinking. The surgeon should be aware of this constellation of findings after transannular patch repair of TOF. On visual inspection of the pulmonary artery in situ (before the initiation of bypass), kinking is readily apparent. Kinking may be less evident once bypass has been instituted, because the dilated right heart is decompressed and the leftward and craniad forces on the right ventricular outflow tract are reduced. Although LPA kinking may be of little or no hemodynamic significance at the time of diagnosis, an effort should be made to identify the cause of any LPA obstruction that is present and carry out the appropriate repair. Branch pulmonary arterial stenosis (whether due to kinking or another mechanism) increases right ventricular afterload and contributes to the acceleration of pulmonary regurgitation and its deleterious effects on the right ventricle [8]. When the mechanism of obstruction is LPA kinking, which results from right ventricular dilatation secondary to pulmonary regurgitation in the first place, a positive feedback loop may be created. Pulmonary regurgitation leads to right ventricular dilatation and LPA kinking, which increases right ventricular afterload and may exacerbate pulmonary regurgitation, causing further ventricular enlargement and LPA kinking. Even if the pulmonary regurgitation is corrected with conduit placement, residual branch pulmonary arterial obstruction from uncorrected kinking may contribute eventually to an acceleration of right-sided compromise if pulmonary regurgitation recurs [9].
Approaches to management
Branch pulmonary arterial stenosis is a common finding after TOF repair [1–3], for which there are various therapeutic approaches, including percutaneous and surgical methods. When LPA obstruction is caused entirely or in part by the mechanism of kinking described in the present report, balloon dilatation is unlikely to be effective, although it may have some beneficial effect in a setting of obstruction due to kinking plus focal stenosis. Placing a stent transvascularly may be effective in certain cases if the stent is expanded in precisely the right position and the kink is mild. However, stenting is likely to be a suboptimal choice that will provide only temporary relief [10], especially considering that LPA kinking results from progressive right ventricular outflow tract dilatation secondary to pulmonary regurgitation, which is not addressed by placing a stent.
Before right ventricular outflow tract revision, 1 of our patients had undergone a previous reoperation for LPA stenosis, which was addressed with patch arterioplasty alone. However, this procedure produced only temporary relief, and LPA obstruction persisted until the patient was referred to us 4 years after the first reoperation. This illustrates a very important point regarding this condition. Namely, surgical treatment is likely to prove inadequate if patch arterioplasty is performed without removing the redundancy at the kink point. In fact, additional patch material in the context of a redundant outflow tract may provide substrate for recurrent kinking in patients who do not require augmentation of hypoplastic pulmonary arteries or discrete stenosis.
To correct LPA obstruction caused by kinking, it is usually necessary to perform a surgical pulmonary arterioplasty that includes the removal of redundancy at the kink. This can be achieved simply by decreasing the length of either the LPA or the pulmonary trunk, which has effectively been elongated in the process of dilatation. The most straightforward approach is to decrease the length of the pulmonary trunk, given that the right ventricular outflow tract is dilated and elongated in these patients and must be revised. This can be carried out either by excising a segment (or bilateral wedges) of the pulmonary trunk, along with reduction arterioplasty, or by replacing it with a conduit of shorter length than the pulmonary trunk itself. Because pulmonary regurgitation is the primary phenomenon responsible for right ventricular outflow tract dilatation and leftward-craniad rotation, it may be preferable to reestablish pulmonary valvar function by implanting a valved conduit, especially in older patients. This approach is supported by the mounting evidence that free pulmonary regurgitation after TOF repair is not well tolerated chronically [9, 11]. In most cases, the patients we have encountered with this lesion are old enough to receive an adult-sized conduit, so conduit reconstruction of the pulmonary outflow tract in these circumstances may not necessitate subsequent reoperation for conduit replacement, which is one of the primary drawbacks of this approach in younger children [12]. In patients with combined kinking and coarctation, it is usually necessary to remove the segment of ductal tissue in the LPA. After the coarct segment is excised, reimplantation of the LPA into the pulmonary trunk or the side of the conduit also removes the redundancy at the LPA kink point. Whatever technique is applied, the ligamentum should be divided if it is still intact, as it can serve as a fulcrum for the torsion exerted by the dilated pulmonary outflow tract. In addition, we recommend division (rather than simple ligation) of the ductus/ligamentum at the time of primary TOF repair.
Pulmonary arterial kinking in patients who have not been operated on
In addition to the 10 patients presented in this report, we have operated on 2 other patients with TOF and branch pulmonary arterial kinking caused by a mechanism similar to that described above. Both of these patients presented for primary TOF repair (at 3 and 10 months of age) and were found to have mild kinking of the LPA primarily due to a tethering effect exerted by a patent ductus (n = 1) or ligamentum arteriosum (n = 1). Division of the ligamentum and the arterial duct revealed no evidence of coarctation and nonstenotic branch pulmonary arterial orifices in both patients, and served to relieve the kinking completely. Although the focus of the present report is on LPA obstruction caused by kinking late after transannular patch repair of TOF, it is important to recognize that LPA kinking by similar mechanisms may occur in patients who have undergone repair recently (such as patient 10) and in patients who have not undergone operation as well, in whom it is equally simple to correct. It may also occur in lesions other than TOF [13].
Conclusions
Kinking of the LPA has been a common finding among patients undergoing reoperation at our institution after transannular patch repair of TOF. As we have described, this abnormality can be repaired by adhering to the principles outlined in this report, which should fit with any strategy for right ventricular outflow tract revision in patients with severe pulmonary regurgitation after repair of TOF. It is important to reiterate that simple patch arterioplasty should not be used to treat this condition. With respect to patients undergoing primary TOF repair, the likelihood of development of late pulmonary outflow tract dilatation and LPA kinking may be minimized by limiting the frequency of transannular patching and the size of the transannular patch when one is placed, as well as by dividing the ductus arteriosus or ligamentum arteriosum. As we have previously proposed, repair in neonates and young infants is often possible with minimal or no disruption of the pulmonary valve annulus [14]. When it is necessary to extend a patch across the annulus, every effort should be made to minimize the likelihood of pulmonary regurgitation and stenosis. Techniques to aid in this effort include incising across the annulus through a valve commissure rather than through a leaflet, minimizing the size of the patch, and extending the patch into the left or both branch pulmonary arteries [14].
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References
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Abstract
Introduction
