(Circulation. 2001;103:2165.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Balloon Dilation Angioplasty of Peripheral Pulmonary Stenosis Associated With Williams Syndrome
From the Department of Cardiology, Children’s Hospital, and the Department of Pediatrics, Harvard Medical School, Boston, Mass.
Correspondence to Robert L. Geggel, MD, Department of Cardiology, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail geggel{at}cardio.tch.harvard.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Experience of balloon dilation of peripheral pulmonary stenosis (PPS) in Williams syndrome (WS) is limited.
Methods and Results—Catheterizations in all patients with WS undergoing therapy for PPS from 1984 to 1999 were reviewed. Criteria for successful dilation included an increase >50% in predilation diameter and a decrease >20% in ratio of right ventricular (RV) to aortic (Ao) systolic pressure. Median age and weight were 1.5 years and 9.5 kg. There were 134 dilations during 39 procedures in 25 patients. The success rate for initial dilations was 51%. In multivariate analysis, successful dilation was more likely (1) in distal than in central pulmonary arteries (P=0.02), (2) if the balloon waist resolved with inflation (P=0.001), and (3) with larger balloon/stenosis ratio (P<0.001). RV pressure was unchanged after dilation (96±30 versus 97±31 mm Hg), primarily because of failure to enlarge central pulmonary arteries. The Ao pressure increased (102±14 versus 109±19 mm Hg, P=0.03), and the RV/Ao pressure ratio decreased (0.97±0.34 versus 0.91±0.30, P=0.05). Aneurysms developed after 24 dilations (18%) and were not related to balloon/stenosis ratio. Balloon rupture in 12 dilations produced an aneurysm in all 7 cases when rupture was in a hypoplastic segment. Three patients died, none from pulmonary artery trauma, and all before 1994.
Conclusions—Mortality occurred early in our experience. Despite successful dilation of distal pulmonary arteries, there was modest initial hemodynamic improvement, mainly because of persistent central pulmonary artery obstruction. A serial approach of distal dilations followed by surgical repair of proximal obstruction may be a rational and successful therapy.
Key Words: Williams syndrome • catheterization • balloon • pediatrics • stenosis
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Williams syndrome is a multisystem disorder affecting 1 in 20 000 live births and is associated with congenital cardiovascular malformations in 60% to 80% of patients.1 2 Supravalvar aortic stenosis is the most common cardiac defect, and peripheral pulmonary stenosis (PPS) is the second most commonly identified lesion.3 PPS can be multiple and bilateral and can be associated with hypoplasia of the pulmonary arterial bed.
Experience of balloon dilation of PPS associated with
Williams syndrome has been limited. Previous series have either
considered patients with isolated congenital PPS as a group without
distinguishing those with Williams
syndrome4 5 6 7 8 9
or included results from 
4 vessels in patients with Williams
syndrome.10 11 12 13 14
To more fully assess the effect of balloon dilation of PPS associated with Williams syndrome, we reviewed our experience with this patient group. We evaluated the change in vessel diameter as well as hemodynamic effects and complications.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Group
From 1984 to 1999, 25 patients with Williams syndrome underwent balloon dilation of PPS and had cineangiograms available for review. The diagnosis of Williams syndrome was based on clinical features1 or genetic analysis.15 Thirty-nine catheterizations involved balloon dilation of PPS, and 5 were follow-up studies. No patient had >3 procedures involving balloon dilation of PPS. For patients having >1 dilation procedure, the median time interval between the first and second catheterization was 3.8 months (range 0.2 to 30 months, n=9) and between the second and third intervention, 3.9 months (range 2.3 to 55 months, n=5).
The study group included 12 female and 13 male patients. Patient age ranged from 1 month to 26 years (median 1.5 year). Patient weight ranged from 2.8 to 57 kg (median 9.5 kg). Coexisting heart defects were present in 23 patients. Seven patients had valvar and supravalvar main pulmonary artery stenosis, 18 had supravalvar aortic stenosis, 4 had coarctation, 2 had large membranous ventricular septal defect, 6 had atrial septal defect, and 1 had severe right ventricular (RV) dysfunction.
Indications
In general, the indications for balloon angioplasty
were more restrictive for patients with Williams syndrome than for
those with isolated or postoperative
PPS.8 For the 39
interventional procedures, 32 were performed because of near systemic
or suprasystemic RV pressure. One of these patients had markedly
reduced flow to 1 lung, and another had syncope. The other 7 procedures
were performed because of markedly reduced flow to 1
lung.
Procedure
Venous access was obtained from the femoral vein
(n=38) or the subclavian vein (n=1). Beginning in 1991, if there was
either RV pressure >90% of systemic level or left-sided obstruction
of >30 mm Hg, and if a septal communication was not present,
an atrial septal defect was created by transseptal puncture followed by
balloon dilation with a 6- or 8-mm
balloon.16 For
pulmonary artery dilations, balloon dilation catheters were
manufactured by Medi-tech, ACS, or B. Braun. The angioplasty technique
has been described
previously.17 Predilation
and postdilation arterial diameters were determined from
biplane cineangiograms. Magnification errors were corrected
by relating vessel size to the known diameter of a fully inflated
balloon on the dilation catheter. An aneurysm was defined
according to previous criteria as a sacular formation that tapered
abruptly and measured at least twice the diameter of the adjacent
pulmonary artery.17
Pulmonary perfusion scans were performed by established
techniques.18
Criteria for Success
A successful dilation was defined by
parameters proposed
previously.17 These included
an increase of >50% of predilation diameter, a decrease of >20% in
the ratio of systolic RV to aortic pressure (RV/Ao), or an
increase of >20% in flow to a lung.
Statistical Analysis
Arterial diameters and
hemodynamic parameters were compared before
and after dilation by the paired
t test. Fisher’s exact test
was used for the comparison of proportions. Generalized estimating
equation (GEE) models were used to evaluate factors associated with
successful vessel
dilation.19 Unlike logistic
regression, the GEE technique adjusts for the correlation among
multiple vessels within the same patient. To examine the
simultaneous effects of all factors on outcome status,
variables significant at the 0.20 level in univariate
analysis were considered for inclusion in a
multivariate GEE model. A significance level of 0.05
was required for retention in the final
model.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Procedure
In the 39 interventional procedures, initial management involved intravenous sedation in 22 procedures and general anesthesia in 17 procedures. Three patients receiving sedation required subsequent intubation, 1 for management of hemoptysis and 2 for cardiopulmonary resuscitation. After 1992, all patients with RV systolic pressure >90% of systemic level alone (5 patients) or in combination with left-sided obstruction of >30 mm Hg (7 patients) had general anesthesia at the start of the case. From 1984 through 1992, only 2 of 14 patients fulfilling these criteria had general anesthesia (14% versus 100%, P<0.001).
A total of 134 dilations were performed. The median number of arteries dilated in each procedure was 3, ranging from 0 to 9. There was no effect of year of procedure on the number of vessels dilated (P=0.62). One patient had 2 vessels that were not imaged after dilation because of hemodynamic instability. Stents were dilated in 3 mediastinal arteries. Of the remaining 129 dilations, 111 were initial, 14 were second, and 4 were third attempts. Twenty-nine dilations involved the mediastinal portion of the pulmonary artery, and 100 involved the intraparenchymal segments. Fluoroscopy time ranged from 29 to 264 minutes (median 71 minutes, n=29). The contrast used ranged from 1.7 to 8.9 mL/kg (median 4.1 mL/kg). The balloon inflating pressure was recorded in 42 dilations (31%) and ranged from 5 to 28 atm (median 14 atm).
Atrial Septal Defect Creation
An atrial septoplasty was performed in 7 procedures. In
6 procedures, left-sided obstruction of >30 mm Hg alone (1
patient) or in combination with RV systolic pressure >90% of
systemic level (5 patients) was present. In 1 patient, antegrade
entry into the left ventricle was required for angiography. Twenty-one
other procedures were performed in which RV systolic pressure
was >90% of systemic level alone (n=7) or in combination with
left-sided obstruction of >30 mm Hg (n=14). In 2 of these
procedures, no septal defect was present or created; 1 of these
patients had a catheterization-related
death.
Arterial Diameter
Biplane pulmonary angiography was mandatory to
adequately define pulmonary artery anatomy and direct
wire and catheter placement
(Figure 1
). Because multiple dilations of the same vessel are
unlikely to be independent, the change in arterial diameter
was analyzed for initial dilations only. For the 111 initial
dilations, the average increase in diameter was 68±67%. The mean
arterial diameter increased from 2.4±1.2 to 3.6±1.7
mm (P<0.001). In 51% of
vessels, the angiographic diameter increased by 
50%. For successful
dilations, the diameter increased 112±65%, with the mean diameter
increasing from 2.0±1.0 to 4.0±1.9 mm
(P<0.001). For failed
dilations, the diameter increased 20±20%, with the mean diameter
changing from 2.7±1.3 to 3.3±1.4 mm
(P<0.001).
|
Successful dilation was more likely to occur in
intraparenchymal than mediastinal arteries, in arteries in which an
aneurysm developed, in arteries with a smaller initial
diameter, and with use of a larger balloon/stenosis ratio
(Table 1). For a balloon/stenosis ratio 3,
66% of dilations were successful, whereas for a ratio <3, 32% were
successful (P=0.001).
Successful dilations were also somewhat more likely to occur in
procedures performed in 1992 or later and with disappearance of the
balloon waist. In multivariate analysis
(Table 2), successful dilations were more likely to occur in
distal rather than central pulmonary arteries, when the balloon
waist resolved with inflation, and with use of larger
balloon/stenosis ratios.
|
|
Serial Angiography
Follow-up angiograms were available for 49 arteries.
Ten of these vessels were dilated a second time and 4 a third
time. Twenty-eight of these initial dilations were successful (7 of 13
mediastinal and 21 of 36 intraparenchymal arteries). Of these
dilations, restenosis to a diameter similar to the baseline
value occurred in 9 arteries (32%), 1 mediastinal (14%) and 8
intraparenchymal (38%)
(P=0.37). Two distal vessels
that restenosed were redilated, 1 of which was successful and
maintained its diameter when imaged 4 months later. Redilations in 8
arteries that had been failures were successful in 1. Redilations in 4
arteries that were successful increased the diameter by >50% from the
new baseline in 1.
Hemodynamics
For initial dilations, baseline and postdilation values
for systolic pulmonary artery pressure distal to a
stenosis were measured in 20 vessels (18%) and a
systolic pressure gradient across the segment was measured in
12 vessels (11%). For 8 successful dilations, the initial distal
pressure was 20±10 mm Hg, postdilation pressure 47±29
mm Hg (P=0.03), initial
gradient (available for 5 dilations) 76±37 mm Hg, and
postdilation gradient 56±37 mm Hg
(P=0.09). For 12 failed
dilations, baseline pulmonary pressure was 22±7 mm Hg,
postdilation pressure 29±12 mm Hg
(P=0.02), initial gradient
(available for 7 dilations) 42±18 mm Hg, and postdilation
gradient 39±18 mm Hg
(P=0.25).
Baseline and postdilation measurements of RV and aortic systolic pressures were available for 25 interventional procedures. Comparisons were not made in 14 procedures because of death (3 patients), presence of a nonrestrictive ventricular septal defect (2 patients), or an unavailable pressure value (9 procedures). Mean RV pressure was unchanged (96±30 versus 97±31 mm Hg, P=0.72), aortic pressure increased (102±14 versus 109±19 mm Hg, P=0.03), and the RV/Ao ratio decreased (0.97±0.34 versus 0.91±0.30, P=0.05).
The RV/Ao ratio decreased 20% in 4 procedures. Three
procedures included dilations of the pulmonary valve or main
pulmonary artery; in 1 procedure without dilation in this
region, the RV pressure did not change (80 mm Hg). Four patients
with serial catheterizations had reduction in RV
systolic pressure from systemic or suprasystemic values at the
initial catheterization to <80% of systemic levels at
the second study. Three of these patients had intervening surgery,
including closure of a large ventricular septal defect (1
patient), repair of central pulmonary artery stenosis
by pericardial patch augmentation (1 patient)
(Figure 2), or placement of a RV–pulmonary artery
homograft (1 patient). The fourth patient had unchanged RV pressure
(90 mm Hg).
|
Endovascular Stents
Three stents were dilated in the proximal portion of
mediastinal vessels. The diameter increased in each artery (3.3 to 5.7,
3.9 to 7.5, and 2.3 to 5.9 mm). Because of
hemodynamic instability, reliable pressures were not
available in 1 patient. In the other 2 patients, RV pressure remained
suprasystemic.
Pulmonary Perfusion Scans
Baseline and postdilation scans were obtained for 7 of
the 39 dilation procedures. In 5 of these, the percentage change in
percent perfusion to a lung was <20%. Two procedures included
dilations of intraparenchymal arteries that were equally distributed
between the 2 lungs. Three procedures had dilations of only the
proximal right pulmonary artery, 2 of which were unsuccessful.
These 5 patients also had distal obstructions that masked the effects
of proximal dilations. In 2 procedures, the percent change in perfusion
was >20%. The percent perfusion to the right lung in 1 patient
increased from 17% to 33% (94% increase) and in the other from 32%
to 45% (41% increase).
Aneurysms
Twenty-five aneurysms developed after 24
dilations (18%). Twelve occurred distal to the stenosis
(Figure 3), 9 at the stenotic site, and 4 proximal to
the stenosis. The balloon/stenosis ratio for first
dilations associated with aneurysm formation was 3.5±1.2 and
without this complication, 3.4±1.3
(P=0.81). Serial measurements
were available for 13 aneurysms. Eight aneurysms
increased in size
(Figure 2
), 4 persisted with similar size, and 1 resolved.
One distal aneurysm produced occlusion of its proximal
arterial segment.
|
Balloon Rupture
The balloon ruptured in 12 dilations (9%). An
aneurysm formed in all 7 procedures in which the balloon
ruptured in a hypoplastic portion of the pulmonary artery. An
aneurysm did not form in the 5 procedures in which the balloon
ruptured in an enlarged segment
(P=0.001). In 1 instance,
balloon rupture produced a transmural tear that required placement of
Gianturco coils to achieve hemostasis
(Figure 4).
|
Complications
Complications occurred in 19 of 39 interventional
procedures (49%). Hypotension occurred in 11 procedures (28%) and was
treated with transfusion alone (2 procedures) or in combination with
inotropic agents (9 procedures). Transient pulmonary edema
developed after 6 procedures (15%). Arrhythmia occurred in 5
procedures (13%) and consisted of ventricular premature
beats, ventricular tachycardia, or
supraventricular tachycardia. Pulmonary
artery perforation occurred in 3 vessels in 2 procedures because of
overdilation of segments distal to the stenosis. Each vessel
was occluded with Gianturco coils
(Figure 4). One of these patients developed hemoptysis that
was treated with intubation, and the other required pleurocentesis.
Transient hemoptysis occurred in another patient who developed
aneurysmal dilation.
There were 3 deaths, each occurring before 1994, and none associated with pulmonary artery trauma. The first occurred in the initial patient and has been reported previously.17 The patient had suprasystemic RV pressure, had an intact atrial septum, and developed hypotension as the dilating catheter was being passed into the left pulmonary artery. The second death occurred when hypotension developed after a pigtail catheter was placed retrogradely into the left ventricle, documenting a 60 mm Hg gradient. An autopsy demonstrated preostial obstruction to coronary flow created by a thickened shelf of aortic wall at the sinotubular junction and dysplastic aortic valve leaflets. In addition, there was severe biventricular hypertrophy. The third death occurred in a child with severe RV dysfunction and suprasystemic RV pressure. He was hemodynamically unstable during multiple dilations. An autopsy showed moderate left main coronary ostial stenosis and severe RV hypertrophy.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Vessel Diameter
Balloon dilation of PPS has been the subject of numerous reports, principally of postoperative conditions. The success rate with low-pressure balloons has ranged from 34% to 71%4 5 6 7 9 12 17 20 21 22 and with high-pressure balloons, from 56% to 72%.8 11 Published experience of dilation of PPS associated with Williams syndrome has been limited.10 11 12 13 14 Structurally, there is diffuse wall thickening consisting of intimal proliferation and medial dysplasia with hypertrophy, fibrosis, and nonparallel mosaic arrangement of smooth muscle cells.3 23 24 This structure has been considered the basis for less success of dilation in this group.10
The success rate in our study was similar to that reported in patients with PPS associated with other conditions. Disappearance of the waist on the inflated balloon has been considered the sine qua non of successful dilation8 9 17 and was a predictive feature in our experience. Vessels in which dilation attempts failed generally were unsuccessfully dilated at later catheterizations, indicating that balloon dilation in subsequent interventions should be directed to different arteries.
Hemodynamic Changes
Despite the success in improving vessel diameter, there
was no change in RV pressure and only a modest decrease in the RV/Ao
ratio. The persistently elevated RV pressure was produced by
stenoses distal to the dilated region and hypoplasia of the
pulmonary vascular
bed20 ; these issues
contributed to doubling of distal pressure after successful dilations.
An additional factor was the difficulty in dilating the proximal
portions of pulmonary arteries. Reduction of the RV/Ao ratio of
>20% occurred principally in procedures involving successful dilation
of the pulmonary valve and main pulmonary artery or in
serial studies with intervening surgical enlargement of the proximal
pulmonary arteries.
Restenosis
Successfully dilated pulmonary arteries have
been reported to restenose to near their baseline diameter in 10% to
44% of
cases.6 8 11 13 17
These vessels may represent instances in which dilation
produced transient stretching rather than tearing of the vessel wall,
or healing of a tear with
fibrosis.17 The
restenosis rate in our patients was 32%. We had limited
experience in redilation of such arteries.
Aneurysms
Aneurysms occurred after 18% of dilations in
our patients, a value 2 to 4.5 times higher than in previous series of
PPS associated with other
conditions.6 8 11 17
The aneurysms in our series occurred most often distal to the
obstruction, a pattern reported in other
studies.6 8 11 17
The presence of elevated pulmonary pressure and overdistension
of small distal segments contributed to the higher incidence.
Aneurysms can resolve, become smaller, persist without change
in dimension, or increase in
size.6 8 11 13 17
Effect of Balloon Rupture
The relative sizes of the balloon and vessel determine
the degree of vessel wall injury after balloon rupture. In vitro
studies of infant aortas have demonstrated that balloon rupture
produces vessel rupture if the balloon is oversized, intimal-medial
tears if the aortic and balloon sizes are similar, and no injury if the
balloon is undersized.25 If
the balloon size is similar to or larger than that of the vessel,
rupture of the balloon can concentrate pressure release at 1 adherent
site and produce injury.26
Our experience was consistent with these experimental results
and documented that balloon rupture in hypoplastic segments produces
aneurysms. The thickened vessel wall present in Williams
syndrome23 may provide a
"cushioning" effect, because only 1 of 7 balloon ruptures in a
hypoplastic segment was complicated by vessel
rupture.
Complications
Unilateral pulmonary
edema,17 27
arrhythmias,6 7 8 9
and hypotension17 were more
common than, whereas the incidence of vessel perforation was
similar17 to, that reported
in other series of PPS. Our mortality rate of 7.7% (3 of 39
procedures) was more than twice that of other
series.7 9 17
Patients with Williams syndrome have increased mortality associated
with cardiac catheterization caused by coronary
artery
stenosis2 3
or subendocardial ischemia arising from
hemodynamic perturbations in the setting of
ventricular
hypertrophy.28
Both of these factors accounted for the 3 deaths in our series. There
were no deaths after 1993 in the final 14 patients. During this period,
there was greater use of general anesthesia as well as
creation of an atrial communication if no septal defect was present
in patients with severe obstruction. Statistical analysis of
the effects of these 2 procedural issues was not
possible.
Intervention Versus Observation
In Williams syndrome, the obstruction associated with
PPS may improve spontaneously, especially in patients with milder, more
proximal
obstructions.3 29
Although mortality improved in the second half of this series, the
incidence of complications remains significant. This finding, coupled
with the possibility of spontaneous improvement has caused us to
recommend frequent noninvasive observation in the
asymptomatic infant or young patient with subsystemic RV
pressure who does not have significant left-sided involvement. In the
patient with persistent systemic levels of RV pressure or significant
biventricular obstruction, balloon dilation is effective in
the majority of distal vessels. Because of a lower success rate in
proximal vessels, however, the hemodynamic benefit is
modest in most patients. Because patients having surgical enlargement
of central pulmonary artery obstruction resistant to
balloon dilation had reduction in RV pressure, a serial approach of
distal dilation followed by proximal surgical repair may be a rational
and successful therapy for this difficult group of
patients.
Received October 30, 2000; revision received January 24, 2001; accepted February 5, 2001.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Joyce CA, Zorich B, Pike SJ, et al. Williams-Beuren syndrome: phenotypic variability and deletions of chromosomes 7, 11, and 22 in a series of 52 patients. J Med Genet. 1996;33:986–992.
2. Conway EE, Noonan J, Marion RW, et al. Myocardial infarction leading to sudden death in the Williams syndrome: report of three cases. J Pediatr. 1990;117:593–595.[Medline] [Order article via Infotrieve]
3. Zalzstein E, Moes CAF, Musewe NN, et al. Spectrum of cardiovascular anomalies in Williams-Beuren syndrome. Pediatr Cardiol. 1991;12:219–223.[Medline] [Order article via Infotrieve]
4. Trant CA Jr, O’Laughlin MP, Ungerleider RM, et al. Cost-effectiveness analysis of stents, balloon angioplasty, and surgery for the treatment of branch pulmonary artery stenosis. Pediatr Cardiol. 1997;18:339–344.[Medline] [Order article via Infotrieve]
5. Zeevi B, Berant M, Blieden LC. Midterm clinical impact versus procedural success of balloon angioplasty for pulmonary artery stenosis. Pediatr Cardiol. 1997;18:101–106.[Medline] [Order article via Infotrieve]
6. Hosking MCK, Thomaidis C, Hamilton R, et al. Clinical impact of balloon angioplasty for branch pulmonary arterial stenosis. Am J Cardiol. 1992;69:1467–1470.[Medline] [Order article via Infotrieve]
7. Kan JS, Marvin WJ Jr, Bass JL, et al. Balloon angioplasty-branch pulmonary artery stenosis: results from the valvuloplasty and angioplasty of congenital anomalies registry. Am J Cardiol. 1990;65:798–801.[Medline] [Order article via Infotrieve]
8. Gentles TL, Lock JE, Perry SB. High pressure balloon angioplasty for branch pulmonary artery stenosis: early experience. J Am Coll Cardiol. 1993;22:867–872.[Abstract]
9. Ring JC, Bass JL, Marvin W, et al. Management of congenital stenosis of a branch pulmonary artery with balloon dilation angioplasty. J Thorac Cardiovasc Surg. 1985;90:35–44.[Abstract]
10. D’Orsogna L, Sandor GGS, Culham JAG, et al. Successful balloon angioplasty of peripheral pulmonary stenosis in Williams syndrome. Am Heart J. 1987;114:647–648.[Medline] [Order article via Infotrieve]
11. Ettinger LM, Hijazi ZM, Geggel RL, et al. Peripheral pulmonary artery stenosis: acute and mid-term results of high pressure balloon angioplasty. J Intervent Cardiol. 1998;11:337–344.
12. Rocchini AP, Kveselis D, Dick M, et al. Use of balloon angioplasty to treat peripheral pulmonary stenosis. Am J Cardiol. 1984;54:1069–1073.[Medline] [Order article via Infotrieve]
13. Beekman RH, Rocchini AP, Rosenthal A. Therapeutic cardiac catheterization for pulmonary valve and pulmonary artery stenosis. Cardiol Clin. 1989;7:331–340.[Medline] [Order article via Infotrieve]
14. Hijazi ZM, Al-Fadley F, Geggel RL, et al. Stent implantation for relief of pulmonary artery stenosis: immediate and short-term results. Cathet Cardiovasc Diagn. 1996;38:16–23.[Medline] [Order article via Infotrieve]
15. Ewart AK, Morris CA, Atkinson D, et al. Hemizygosity at the elastin locus in a developmental disorder, Williams syndrome. Nat Genet. 1993;5:11–16.[Medline] [Order article via Infotrieve]
16. Lang P. Other catheterization laboratory techniques and interventions: atrial septal defect creation, transseptal puncture, pericardial drainage, foreign body retrieval, exercise and drug testing. In: Lock JE, Keane JF, Perry SB, eds. Diagnostic and Interventional Catheterization in Congenital Heart Disease. Boston, Mass: Kluwer Academic Publishers; 1999:245–268.
17. Rothman A, Perry SB, Keane JF, et al. Early results and follow-up of balloon angioplasty for branch pulmonary artery stenosis. J Am Coll Cardiol. 1990;15:1109–1117.[Abstract]
18. Treves ST, Harris GBC. Lung. In: Treves ST, ed. Pediatric Nuclear Medicine. New York, NY: Springer; 1985:289–330.
19.
Liang KY, Zeger
SL. Longitudinal data analysis using generalized linear models.
Biometrika. 1986;73:13–22.
20.
Lock JE,
Castaneda-Zuniga WR, Fuhrman BP, et al. Balloon dilation angioplasty of
hypoplastic and stenotic pulmonary arteries.
Circulation. 1983;67:962–967.
21. Bass JL. Percutaneous balloon dilation angioplasty of pulmonary artery branch stenosis. Cardiovasc Intervent Radiol. 1986;9:299–302.[Medline] [Order article via Infotrieve]
22. Chau AKT, Leung MP. Management of branch pulmonary stenosis: balloon angioplasty or endovascular stenting. Clin Exp Pharmacol Physiol. 1997;24:960–962.[Medline] [Order article via Infotrieve]
23.
van Son JAM,
Edwards WD, Danielson GK. Pathology of coronary arteries,
myocardium, and great arteries in supravalvular
aortic stenosis. J Thorac
Cardiovasc Surg. 1994;108:21–28.
24. Zeevi B, Berant M, Blieden LC. Late death from aneurysm rupture following balloon angioplasty for branch pulmonary artery stenosis. Cathet Cardiovasc Diagn. 1996;39:284–286.[Medline] [Order article via Infotrieve]
25. Waller BF, Girod DA, Dillon JC. Transverse aortic wall tears in infants after balloon angioplasty for aortic valve stenosis: relation of aortic wall damage to diameter of inflated angioplasty balloon and aortic lumen in seven necropsy cases. J Am Coll Cardiol. 1984;4:1235–1241.[Abstract]
26.
Edwards BS, Lucas
RV Jr, Lock JE, et al. Morphologic changes in the pulmonary
arteries after percutaneous balloon angioplasty for
pulmonary arterial stenosis.
Circulation. 1985;71:195–201.
27. Arnold LW, Keane JF, Kan JS, et al. Transient unilateral pulmonary edema after successful balloon dilation of peripheral pulmonary artery stenosis. Am J Cardiol. 1988;62:327–330.[Medline] [Order article via Infotrieve]
28.
Vincent WR,
Buckberg GD, Hoffman JIE. Left ventricular subendocardial
ischemia in severe valvar and supravalvar aortic
stenosis. Circulation. 1974;49:326–333.
29. Wren C, Oslizlok P, Bull C. Natural history of supravalvular aortic stenosis and pulmonary artery stenosis. J Am Coll Cardiol. 1990;15:1625–1630.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  R. Formigari, G. Michielon, M. C. Digilio, G. Piacentini, A. Carotti, A. Giardini, R. M. Di Donato, and B. Marino Genetic syndromes and congenital heart defects: how is surgical management affected? Eur. J. Cardiothorac. Surg., April 1, 2009; 35(4): 606 - 614. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. J. Hickey, G. Jung, W. G. Williams, C. Manlhiot, G. S. Van Arsdell, C. A. Caldarone, J. Coles, and B. W. McCrindle Congenital Supravalvular Aortic Stenosis: Defining Surgical and Nonsurgical Outcomes Ann. Thorac. Surg., December 1, 2008; 86(6): 1919 - 1927. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M. Burch, F. X. McGowan Jr, B. D. Kussman, A. J. Powell, and J. A. DiNardo Congenital Supravalvular Aortic Stenosis and Sudden Death Associated with Anesthesia: What's the Mystery? Anesth. Analg., December 1, 2008; 107(6): 1848 - 1854. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. F. Rhodes, Z. M. Hijazi, and R. J. Sommer Pathophysiology of Congenital Heart Disease in the Adult, Part II: Simple Obstructive Lesions Circulation, March 4, 2008; 117(9): 1228 - 1237. [Full Text] [PDF]
|
|
|
|
|
|
K. Gauvreau Hypothesis Testing: Proportions Circulation, October 3, 2006; 114(14): 1545 - 1548. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||