(Circulation. 1995;92:3282-3288.)
© 1995 American Heart Association, Inc.
Articles |
From the Departments of Cardiology (J.E.L., J.F.K., S.B.P.) and Medicine (A.J.P.), Children's Hospital, Harvard Medical School, Boston, Mass.
| Abstract |
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Methods and Results A retrospective review identified 44 patients
who underwent placement of 48 stents in obstructed RV-PA conduits.
Median patient age was 6.9 years (range, 7 months to 30 years), and
median follow-up time was 14.2 months (range, 0 to 48 months).
Stent implantation initially decreased the RV-PA pressure gradient from
61.0±16.9 to 29.7±11.9 mm Hg (P
.001) and the right
ventriculartosystemic arterial
pressure ratio from 0.92±0.17 to 0.63±0.20 (P
.001).
The
diameter of the stenotic region expanded from 9.3±3.5 to
12.3±3.3 mm in the anteroposterior view (P
.001) and from
6.6±2.9 to 10.9±2.5 mm in the lateral view (P
.001).
During the follow-up period, 2 patients had their stents redilated,
7 had additional conduit stents deployed, and 14 underwent surgical
replacement of their conduits. Actuarial freedom from conduit
reoperation was 65% at 30 months postprocedure. Seven patients were
found to have fractured stents on follow-up, suggesting an
important role for external compressive forces in conduit failure.
Recatheterization in 16 patients a median of 11.8
months (3 to 48 months) postprocedure demonstrated
hemodynamic evidence of recurrent obstruction despite
sustained enlargement at the previously stented sites. Complications
included stent displacement (n=1), bacterial endocarditis (n=1),
and
false aneurysm formation (n=1). One patient died awaiting
conduit replacement surgery.
Conclusions Stent implantation in obstructed RV-PA conduits results in significant immediate hemodynamic and angiographic improvement. In a subgroup of patients, the procedure prolongs conduit life span by several years and increases the interval between conduit reoperations. Recurrent obstruction is caused by external compression and progressive stenosis outside the stented region.
Key Words: stents catheterization heart defects, congenital angioplasty prosthesis
| Introduction |
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Surgical replacement of obstructed conduits incurs the morbidity associated with repeat sternotomy and cardiotomy and, in some patients, is technically difficult because of multiple prior operations. Percutaneous balloon angioplasty of stenosed conduits has shown marginal efficacy in diminishing pressure gradients and avoiding surgical intervention.10 11 12 Recently, balloon-expandable intravascular stents have been used to relieve stenotic lesions in various forms of congenital heart disease.13 14 15 By supporting the conduit wall after balloon dilation, stent implantation may relieve obstruction and delay surgical replacement. This article reports our experience implanting RV-PA conduit stents in 44 patients along with intermediate-term follow-up data.
| Methods |
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Stenting Technique
In general, patients were selected for
RV-PA conduit stent
placement if they failed balloon dilation and their RV pressure was
>80% of the systemic pressure or if there was evidence of RV
dysfunction. Patients whose nominal conduit diameter was deemed
inadequate because of somatic growth after surgery were not candidates
for the procedure.
The nonarticulated Palmaz stent (Johnson & Johnson Interventional Systems) constructed from stainless steel was used in all patients. The stent sizes used were (lengthxdiameter) 30x3.4 mm (n=20), 18x3.4 mm (n=14), 12x3.4 mm (n=1), 20x2.5 mm (n=6), and 15x2.5 mm (n=7). Three patients required placement of two or three overlapping stents in their RV-PA conduits.
The technique of percutaneous stent implantation was described previously.13 14 Briefly, patients were given heparin intravenously to maintain an activated clotting time >200 seconds. The stenotic region of the RV-PA conduit was predilated with a balloon angioplasty catheter in the usual fashion. Balloon size, in most cases, was arbitrarily limited to 10% larger than the nominal conduit diameter to minimize the risk of false aneurysm formation. High-pressure inflations up to 21 atm were used when a residual waist was present. In some patients, the conduit was dilated by simultaneous inflation of two balloons placed side by side. A long sheath (7F to 12F according to balloon and stent size) was then advanced over a SuperStiff (MediTech) or Rosen (Cook) guide wire. The stent was mounted on a balloon catheter, and together they were advanced over the wire through the sheath and positioned at the stenotic region. The sheath was withdrawn, and angiographic confirmation of stent position was obtained. The balloon was inflated by hand, and the stent was expanded and anchored to the vessel wall. If the stent was not fully expanded, a larger-diameter balloon was used to further dilate the stent. Postimplantation pressure measurements and angiography were performed when possible. When the angiograms were reviewed, the extent of conduit calcification was qualitatively assessed and categorized as absent, mild, or severe.
Intravenous antibiotic, usually cefazolin (12.5 mg/kg), was administered at the time of stent placement and every 6 hours for a total of three doses. After catheterization, patients were placed on a continuous heparin infusion to maintain a partial thromboplastin time twofold control for a minimum of 12 hours. At discharge, most patients were prescribed either aspirin 40 to 80 mg/d (n=25) or aspirin 40 to 80 mg/d and dipyridamole 1 to 2 mg·kg-1·d-1 (n=16) for 6 to 12 months to inhibit thrombus formation. Two patients were anticoagulated with warfarin because they had a mechanical prosthetic valve or a stent in the systemic venous circulation. One patient with chronic thrombocytopenia was not placed on any anticoagulation medication.
Other Procedures Performed
In addition to RV-PA conduit stent
implantation, 18 patients
underwent other interventions during the same
catheterization. These procedures included PA stent
placement (n=7), PA balloon angioplasty (n=8), pulmonary valve
balloon angioplasty (n=2), coil embolization of collateral vessels
(n=1), and residual VSD closure with a clamshell device (n=1).
Statistical Analysis
Preplacement and postplacement data were
compared by a paired
two-tailed Student's t test. The univariate
relations between patient parameters and outcome were
evaluated by a one-way ANOVA, a two-sample t test,
or a linear regression model when appropriate. In the analysis
of reoperation and stent fracture, time to failure was the response
variable of interest. Patients who did not fail were considered to
be censored at the time of last follow-up. Survival estimates were
obtained by the Kaplan-Meier method. Risk factor subgroups were
compared by the log-rank test; a Cox proportional-hazards model
was used to assess multivariate associations. Results
were considered significant if P
.05. Values are expressed
as mean±SD. The STATA statistical package (Computing
Resource Center) supported the analysis.
| Results |
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One patient was lost to follow-up after the immediate postcatheterization period. The remaining patients have been followed from 1 to 48 months (median, 14.2 months) since conduit stent implantation, a total of 59.9 patient-years.
Initial Stent Implantation
A single stent was placed in the
stenotic RV-PA conduit of
41 patients, two overlapping stents in 2 patients, and three
overlapping stents in 1 patient. The mean
catheterization time was 233±73 minutes (range, 85 to
531 minutes). The average hospital stay for patients admitted
electively and not undergoing surgery was 1.9±1.2 days (n=37).
Figs 1 through 3![]()
![]()
illustrate
examples of stent placement in RV-PA conduits.
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Table 1
reports the prestent and poststent mean values
of the RV-PA peak-to-peak pressure gradient, the RVp/Sp ratio,
and the stenosis diameter in the AP and lateral views. Stent
implantation resulted in significant improvements in all of these
parameters (Fig 4
). The
number of patients with pressure gradients
50 mm Hg declined from 34
prestent to 3 poststent. In 5 patients, stent implantation failed to
reduce the pressure gradient by >25%. The number of patients with an
RVp/Sp ratio
0.75 fell from 38 prestent to 8 poststent. Seven
patients had a <10% reduction in their RVp/Sp ratio. For those
patients in whom angiographic measurements were available both before
and after stent placement, the diameter of the stenotic region
expanded by a mean of 2.9±2.0 mm in the AP view (n=35) and by a
mean
of 4.4±1.8 mm in the lateral view (n=37).
|
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In univariate analyses, the following parameters were not significantly associated with the reduction in RV-PA pressure gradient or RVp/Sp ratio: patient age, weight, sex, cardiac diagnosis, patient age at conduit placement, conduit age, homograft versus bioprosthetic conduit, pulmonary versus aortic homograft, nominal conduit diameter, conduit calcification, and utilization of simultaneous side-by-side balloon dilation. Conduit dilation with a high-pressure balloon before or after stent placement resulted in a slightly greater reduction in the RVp/Sp ratio (P=.043) but had no significant effect on gradient relief (P=.17). Angiographic improvement in the AP view was most strongly associated with the absence of calcification (P=.032) and younger conduit age (P=.029) in a multivariate model. None of the parameters were significantly associated with enlargement in the lateral view. Finally, no "learning curve" effect on immediate efficacy was detected with later procedures.
Follow-up Catheterization
In general, follow-up
catheterization was
recommended when noninvasive assessments of RV pressures suggested
progressive restenosis. Sixteen of the initial 44 patients
were referred for recatheterization at our center 3
to 48 months (median, 11.8 months) after stent implantation. Table
2
reports the prestent, immediate poststent, and
follow-up mean values of the RV-PA pressure gradient, the RVp/Sp
ratio, and the stenosis diameters. Although stent implantation
resulted in immediate improvement in all these measurements
(P
.001), there was a return to prestent values for the
mean pressure gradient and mean RVp/Sp ratio in this subgroup (Fig
5
). Nevertheless, the AP and
lateral-view diameters at the stent site demonstrated a significant
sustained improvement compared with their prestent values. Careful
examination of the angiograms revealed conduit stent fractures in 5 of
the patients as described in further detail below. Even among the
remaining 11 patients with intact stents, the follow-up RV-PA
gradient and RVp/Sp ratio demonstrated reobstruction to prestent levels
despite persistent angiographic enlargement at the stent site (data not
shown).
|
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Repeat Stent Implantation and Redilation
Seven of the 16
patients who underwent follow-up
catheterization at our center had additional conduit
stents placed during the procedure (Fig 5
). The repeat
stent implantations occurred from 7 to 27 months (median, 9.7 months)
after the initial placement. All 5 of the patients with fractured
stents had a second stent positioned to partially overlap the original
one. The other patients had either one or two additional overlapping
stents deployed. As a result, the RV-PA pressure gradient decreased
from 59.6±16.3 to 40.9±13.9 mm Hg (P=.002,
n=7) and the
RVp/Sp ratio declined from 0.98±0.14 to 0.70±0.10
(P=.006,
n=7). Significant diameter enlargement was noted in the lateral view
(P=.045, n=5) but not in the AP view
(P=.59,
n=5).
Two patients underwent balloon dilation of their intact
conduit stents
without implantation of additional stents 9 and 14 months after initial
placement, respectively. In both patients, the RV-PA pressure gradient
was decreased by <10 mm Hg. The RVp/Sp ratio declined from 0.9 to 0.7
in 1 patient and was unchanged in the other. The stent diameter in each
case increased by
1 mm in both the AP and lateral views.
Conduit Replacement
Fourteen (32%) of the 44 patients
underwent surgical replacement
of their RV-PA conduits from 1 to 33 months (median, 11.0 months) after
stent placement. No major technical difficulties with the operations
related to the stents were reported. Actuarial freedom from conduit
reoperation was 65% (Greenwood 95% CI, 48% to 82%) at 30 months
after stent placement (Fig 6
). None of
the following prestent parameters had a significant effect
on reoperation-free survival: patient age, weight, sex, cardiac
diagnosis, patient age at conduit placement, conduit age, homograft
versus bioprosthetic conduit, pulmonary versus
aortic homograft, nominal conduit diameter, conduit calcification, use
of simultaneous side-by-side balloon dilation, use
of high-pressure balloons, RV-PA gradient, RVp/Sp ratio, and
stenosis diameter. In a multivariate
analysis, the strongest predictors of early surgical
replacement were a greater poststent RVp/Sp ratio (P=.010)
and a narrower poststent diameter in either view
(P=.044).
|
Nine of the 16 patients who had follow-up catheterization later underwent conduit replacement (five patients within 1 week of catheterization). Among the 7 patients who had a second conduit stent implanted, 4 had surgical revision. Two of these patients had replacement performed within 3 days of the second stent placement, while the other 2 remained free of surgery for 12 and 23 months, respectively. Both patients who had only balloon dilation of their stents underwent conduit replacement within 5 months.
Echocardiographic Follow-up
At the completion of the
follow-up period, 22 patients had not
been referred for recatheterization or conduit
reoperation. Echocardiography data were available
for 19 of these patients (86%), with the most recent studies performed
from 1 to 32 months (median, 16.2 months) after stent implantation. One
patient had evidence of an RV pressure >80% of systemic pressure, and
2 other patients had Doppler gradients >60 mm Hg across their
conduits. No fractured or displaced stents were detected in this
subgroup.
Stent Fracture
Seven patients (16%) were found to have
fractures of their
conduit stents during the follow-up period. All were
asymptomatic events identified on chest radiograph,
echocardiogram, or catheterization from 5 to 27 months
(median, 8.4 months) after implantation. In 3 of these patients, stent
fragments embolized to the pulmonary circulation. No
evidence of significant pulmonary blood flow obstruction was
seen in the 2 patients who had angiography, and all embolized
fragments were left in place. Five patients in the fracture group had a
second conduit stent placed, and no subsequent fractures were observed.
Four patients in the fracture group, including 3 who had a second stent
implantation, underwent surgical replacement of their conduits. No
significant risk factors for stent fracture were identified with a Cox
proportional-hazards model. It is noteworthy, however, that for 2
patients in the fracture group, stent expansion was asymmetric, thereby
creating a shorter posterior length on initial implantation. This
condition may have led to the development of unusually high stress on
the supporting struts of the stent and eventual fracture.
Procedural Complications
Catheterization complications
included a
hemothorax (secondary to difficult vascular access into an internal
jugular vein) that was percutaneously drained without
reaccumulation, an episode of atrial flutter that was successfully
treated by esophageal pacing, and a brachial plexus injury that
self-resolved. Bacterial endocarditis developed in 1 patient 5
weeks after stent implantation. He was effectively treated with
intravenous antibiotics and has not required conduit
replacement. One patient developed a pseudoaneurysm and
arteriovenous fistula in the subclavian vein, which had been used for
venous access during catheterization. The fistula was
closed by coil embolization. Balloon rupture occurred frequently, and
in most instances there were no sequelae; however, in 3 patients, the
balloon ruptured along the transverse axis, creating a distal fragment.
In one case, the fragment was successfully withdrawn after a large
sheath was placed over it; in another, the balloon became lodged in the
femoral vein and was retrieved via cutdown. The third instance occurred
during stent dilation and required withdrawal of the partially expanded
stent to the iliac vein, in which it was deployed.
Late Complications
One patient, a 17-month-old boy with
transposition of the
great arteries, VSD, and pulmonary stenosis status post
Rastelli repair with an RV-PA aortic homograft, died unexpectedly at
home 5 months after conduit stent implantation. At a
cardiology outpatient visit 2 weeks before his death,
his physical examination and chest radiograph had been unchanged, and
his ECG showed a right bundle-branch pattern with no ectopy. An
echocardiogram demonstrated severe proximal conduit obstruction and a
dilated RV with approximately systemic pressure and poor function.
Accordingly, surgery to replace his homograft was scheduled. The
patient's death occurred at night in the setting of an acute febrile
illness with vomiting. No specific cause of death was found, and at the
parents' request, no autopsy was performed.
Proximal displacement of a stent into the RV cavity was discovered in 1 patient 2 months after implantation. Because the patient had phrenic nerve paralysis, the stent had intentionally been placed just proximal to the homograft valve to avoid creating free pulmonary regurgitation and decreased systemic venous return. The patient remained clinically well and successfully underwent surgical removal of the stent and homograft replacement.
In 1 patient, a false aneurysm in the RVOT was identified 18 months after stent placement. At surgery, it appeared that the homograft had dehisced from the RV just proximal to the homograft stent. The patient underwent homograft excision and replacement and has subsequently done well. For this stent implantation, a low-pressure balloon 10 mm in diameter was used for dilation and placement into a homograft with a nominal diameter of 7 mm. Although there was no angiographic evidence of vascular injury during the procedure, the oversized balloon may have excessively dilated the homograft and weakened the vessel wall.
| Discussion |
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This report, with a cohort of 44 patients and almost 60 patient-years of follow-up, provides important data on a technique designed to delay conduit reoperation. Stent implantation in obstructed RV-PA conduits resulted in immediate hemodynamic and angiographic improvement that was both physiologically and statistically significant. During the follow-up period, 2 patients had their stents redilated, 7 had additional conduit stents deployed, and 14 underwent surgical replacement of their conduits. Actuarial freedom from conduit reoperation was 65% at 30 months postprocedure. On the basis of their initial hemodynamic measurements, almost all of the patients in this study would have been candidates for conduit replacement at the time of stent implantation. Thus, for a subgroup of our patients, stent implantation appears to postpone reoperation by at least several years.
Further efforts to prolong RV-PA conduit life span will require an improved understanding of their mechanisms of obstruction. Two insights into this process are suggested by our follow-up catheterization data in 16 patients with hemodynamic evidence of reobstruction. The occurrence of stent fractures in 5 of these patients supports an important role for external compressive forces in conduit failure. Stents implanted in RV-PA conduits may be predisposed to fracture because of compression between the sternum and heart, proximity to beating ventricular myocardium, or extensive calcification of the homograft vessel wall. When placing stents in pulmonary arteries, we have observed stent fracture at the time of balloon dilation but not spontaneously on follow-up evaluation. Strategies to delay conduit reobstruction must therefore take into account compressive forces that are apparently unique to the RVOT. A second important observation in the recatheterization subgroup is that we found hemodynamic evidence of recurrent obstruction despite sustained enlargement at the previously stented sites. This finding implies that reobstruction occurs all along the conduit and is multifactorial. Notably, we did not observe exuberant pseudointimal growth within the stents.
While most observed complications of stent placement could be expected
in a complex interventional procedure, one deserves special comment. A
false aneurysm was identified in the RVOT of 1 patient 18
months after stent implantation. The balloon size used for dilation was
40% larger than the nominal conduit diameter. Although other
conditions may have contributed to aneurysm formation, we
recommend in most cases limiting balloon size to 10% larger than the
nominal conduit diameter to minimize the risk of this complication.
This study has several important limitations. Because of its retrospective design and the lack of standardized follow-up, the reported prevalence of complications and conduit reoperation should be considered lower bounds. In particular, since the stent fractures were all asymptomatic events and not all patients have had a recent radiological evaluation, additional patients may have as yet undetected fractures. Moreover, several stents that appeared intact on plain radiographs and echocardiography were found to be fractured on fluoroscopy. Our reported frequency of conduit reoperation after stent placement also merits scrutiny, since the indications for replacement were not uniform. We cannot completely exclude the possibility that stent placement raised the threshold for surgical referral during the follow-up period. Recurrent conduit obstruction warranting surgery may also have gone undetected. Ideally, all of our patients would have undergone recatheterization within the follow-up period, thereby permitting the most accurate assessment of the durability of hemodynamic and angiographic improvement. Since this was not clinically indicated, we have depended, in part, on noninvasive assessments to detect recurrent conduit obstruction. Several reports have documented the reliability of Doppler echocardiography in assessing RV-PA conduit dysfunction.16 17 18 Because no prestent parameters were significantly associated with reoperation-free survival, we were unable to refine our patient selection criteria for conduit stent placement. This failure may be attributable to the relatively small number of patients and the limited power of the study. Finally, we acknowledge that the additional procedures performed during stent placement might confound the comparison between prestent and poststent parameters. Such effects, however, would not have altered the angiographic analysis.
Patient selection for RV-PA conduit stent placement must be individualized. The most prevalent adverse effect associated with the procedure was stent fracture requiring either repeat stent placement or conduit replacement. Although we have not detected any obstruction to pulmonary blood flow by the embolized stent fragments, this risk remains. The principal benefit of stent implantation lies in prolonging conduit life span and increasing the interval between the almost inevitable reoperations. Accordingly, we would consider children whose conduits develop obstruction before being outgrown as candidates for this intervention. In this scenario, stent implantation may decrease the expected number of conduit reoperations as the patient ages from a neonate to an adult. Patients who develop significant conduit obstruction and are poor surgical candidates, typically because of multiple prior operations, may also be appropriate subjects for stent placement. After the procedure, radiological assessment for stent fractures, either with plain radiographs or preferably with fluoroscopy in multiple views, should be performed on a regular basis.
Conclusions
Stent implantation in obstructed RV-PA conduits
results in
significant immediate hemodynamic and angiographic
improvement. In a subgroup of patients, the procedure prolongs conduit
life span by at least several years and provides an effective means of
increasing the interval between conduit reoperations. Recurrent
obstruction is caused by progressive stenosis along the entire
RVOT and stent fracture from external compression. Goals for further
study include (1) refining patient selection, (2) proper timing of
stent placement, (3) long-term follow-up to better determine
outcomes and risk, (4) developing stents more resistant to
fracture, and (5) further clarifying causes of conduit
restenosis.
| Selected Abbreviations and Acronyms |
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| Acknowledgments |
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| Footnotes |
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Received May 9, 1995; revision received July 12, 1995; accepted July 23, 1995.
| References |
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C. Ovaert, C. A. Caldarone, B. W. McCrindle, D. Nykanen, R. M. Freedom, J. G. Coles, W. G. Williams, and L. N. Benson ENDOVASCULAR STENT IMPLANTATION FOR THE MANAGEMENT OF POSTOPERATIVE RIGHT VENTRICULAR OUTFLOW TRACT OBSTRUCTION: CLINICAL EFFICACY J. Thorac. Cardiovasc. Surg., November 1, 1999; 118(5): 886 - 893. [Abstract] [Full Text] [PDF] |
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S. Nemoto, A. Sakai, Y. Miyoshi, K. Yasuhara, and M. Seguchi Pathologic finding of restenosis in stent-implanted right ventricle-pulmonary artery extracardiac conduit Ann. Thorac. Surg., October 1, 1999; 68(4): 1411 - 1413. [Abstract] [Full Text] [PDF] |
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