Circulation. 2000;102:III-130-III-135
(Circulation. 2000;102:III-130.)
© 2000 American Heart Association, Inc.
Surgery for Congenital Heart Disease |
Factors Affecting Longevity of Homograft Valves Used in Right Ventricular Outflow Tract Reconstruction for Congenital Heart Disease
James S. Tweddell, MD;
Andrew N. Pelech, MD;
Peter C. Frommelt, MD;
Kathleen A. Mussatto, RN;
John D. Wyman, BA;
Raymond T. Fedderly, MD;
Stuart Berger, MD;
Michele A. Frommelt, MD;
David A. Lewis, MD;
David Z. Friedberg, MD;
John P. Thomas, Jr, MD;
Ramesh Sachdeva, MD;
S. Bert Litwin, MD
From the Department of Surgery (Cardiothoracic Surgery), Pediatrics
(Cardiology), and the Center for Outcomes Research and Quality Management,
Children’s Hospital of Wisconsin, Medical College of Wisconsin,
Milwaukee, Wis.
Correspondence to James S. Tweddell, MD, Cardiothoracic Surgery, Children’s Hospital of Wisconsin, 9000 W Wisconsin Ave, MS 715, Milwaukee, WI 53226. E-mail jstwedde{at}mcw.edu
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Abstract
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Background—Few studies have
explored the long-term function
of cryopreserved homograft valves used
for reconstruction of
the right ventricular tract (RVOT) in
patients with congenital
heart disease.
Methods and Results—Among 205 patients receiving cryopreserved
homografts for reconstruction of the RVOT between November 1985 and
April 1999, the outcome of 220 homografts in 183 operative survivors
was analyzed. There were 150 pulmonary and 70 aortic
homografts used. Median age at implantation was 4.4 years (mean
6.9±7.6 years, range 3 days to 48 years). End points included (1)
patient survival, (2) homograft failure (valve explant or late death),
and (3) homograft dysfunction (homograft insufficiency or
homograft stenosis). Survival was 88% at 10 years. Freedom
from homograft failure was 74±4% at 5 years and 54±7% at 10 years.
Univariable analysis identified younger age, longer donor
warm ischemic time, valve Z value <2, and
previous procedure as risk factors for homograft failure and
dysfunction. Aortic homograft type and extracardiac operative technique
predicted homograft failure but not dysfunction. For patients 
1 year
of age, valve type did not predict failure or dysfunction.
Multivariable analysis identified younger age and longer
donor warm ischemic time as risk factors for homograft failure
and dysfunction, whereas, Z value <2 and aortic valve
type predicted homograft valve failure.
Conclusions—Homograft valves used for RVOT reconstruction provide
effective intermediate palliation with excellent late survival. Factors
that adversely affect graft longevity include younger age, longer donor
warm ischemic time, smaller homograft size, use of aortic
homograft in the older patient, and extracardiac operative
technique.
Key Words: valves • heart defect, congenital • surgery
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Introduction
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Valved conduits are commonly used in cardiac
reconstruction
for lesions in which there is hypoplasia of the right
ventricular
outflow tract (RVOT) or pulmonary
arteries and/or in which the
postoperative right heart pressures may be
elevated, such as
truncus arteriosus and pulmonary atresia with
ventricular septal
defect.
1 2 3 4 5 Valved conduits
are also used for management
of right ventricular failure
caused by pulmonary insufficiency
and ventricular
arrhythmias after initial nonvalved
repair.
6 7 8 Valved homografts, initially introduced in
1966 by Ross
and Somerville,
2 have become the most
commonly used valved
conduit for reconstruction of the
RVOT.
2 9 10 11 12 Among the
advantages of homografts are the
technical ease of implantation
and improved
hemostasis.
12 13 14 Early results with cryopreserved
homografts
for reconstruction of the RVOT in congenital heart disease
have
been good, but there are few studies reporting late outcomes.
The
purpose of this study was to evaluate factors affecting
the durability
of homografts used in the reconstruction of the
RVOT in congenital
heart disease.
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Methods
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From November 1985 through April 30, 1999, 205 patients with
congenital
heart disease underwent RVOT reconstruction, with a total of
242
cryopreserved homograft valves at Children’s Hospital
of
Wisconsin, Milwaukee. There were 22 (11%) early deaths in
the group
(within 30 days of operation or same hospitalization).
The purpose of
this study was to determine factors affecting
the durability of
homografts used in RVOT reconstruction; therefore,
perioperative
deaths not attributable to homograft
failure or dysfunction
were excluded from risk factor analysis.
The remaining 183 patients
who received a total of 220 homograft valves
during this time
period constitute the population for this review and
analysis.
Of these 183 patients, 178 underwent initial
homograft placement
at the Children’s Hospital of Wisconsin and an
additional
5 were seen for homograft replacement after initial
homograft
placement at another hospital. Medical records and clinic
charts
were reviewed for all valve recipients. Data collected from
the
operative admission included diagnosis, previous operative
procedures,
age, sex, height, and weight at operation. Previous
operative
procedures were defined as palliative or corrective,
for example,
repair of tetralogy of Fallot with a transannular
patch was considered
a corrective procedure, whereas a systemic–to–pulmonary
artery
shunt was considered palliative. Patient follow-up was obtained
from
hospital and clinic visit records as well as direct recipient
contact
when necessary. Follow-up information was available within the
past
calendar year for 98% of the 183 patients; mean follow-up
duration
was 3.6 years. Patient characteristics including
diagnostic
category, previous procedure, age at initial
homograft placement,
and subsequent operations are summarized in Table 1
.
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Table 1. Diagnostic Categories of RVOT Homograft
Recipients, Previous Procedures, and Initial and Replacement Homograft
Operative Characteristics
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Each valve implant was analyzed as a separate event. Valve
information included valve type, size (mm), donor warm ischemic
time (asystole to complete dissection), duration of cryopreservation,
and donor age and sex. Seventy aortic valves and 150 pulmonary
valves were used. Valves were obtained primarily from Cryolife, Inc. A
Z value for each implanted valve was calculated, with the
valve diameter compared with normal values for the patient’s body
surface area.15 Normal valve dimensions and standard
deviations were obtained from 1999 Human Heart Valve Diameters chart
(Cryolife Inc).
Implant techniques varied, based on the recipient’s anatomy,
and were categorized into 3 groups. For extracardiac placement, the
posterior one third of the homograft annulus was sutured directly to
the superior edge of a ventriculotomy in the pulmonary
ventricle. A hood was used to complete the connection to the right
ventricle. A variety of materials were used for the hood including the
attached anterior mitral leaflet of an aortic homograft, an additional
piece of homograft, pericardium, or synthetic material, such as Dacron
(Du Pont Co) or Gore-Tex (W.L. Gore and Associates). In situ placement
described operations in which the homograft annulus was sutured to the
infundibular septum, placing the homograft within the RVOT in a near
anatomic position. When necessary, completion of the in situ
implantation also involved placement of a hood. Finally, valve
replacement was used to describe procedures in which a subsequent
homograft was being placed in a patient who had previously undergone
homograft RVOT reconstruction by either the in situ or extracardiac
technique. Table 2 summarizes the
operative techniques and homograft type by primary
diagnostic category.
Homograft failure was defined as explant of the valve for any reason or
late death (occurring >30 days after surgery) as the result of any
cause. Homograft dysfunction was defined as any one of the following:
moderate or severe stenosis or insufficiency as well as explant
or late death. Homograft insufficiency was defined
echocardiographically as moderate when there was a
broad regurgitant jet of less than the annulus width associated with
diastolic color Doppler flow reversal from the distal
main pulmonary artery. A regurgitant jet that encompassed the
entire annulus width associated with diastolic flow
reversal in the branch pulmonary arteries was graded as severe.
Homograft stenosis was defined as a transvalvular peak
instantaneous pressure gradient >40 mm Hg. The follow-up echo in
which the patient first met one or both of these dysfunction criteria
was recorded as the duration of functional valve life.
Descriptive data are presented as mean values±1 SD. For
continuous variables, ANOVA techniques were used to analyze
between-group differences; 
2 was used for
categoric variables. Survival curves for freedom from valve failure
and valve dysfunction were obtained by use of the Kaplan-Meier method,
and comparisons were performed with the log-rank test. To evaluate the
impact of younger age on homograft durability, age was entered into
multivariable analysis as both a continuous variable
and dichotomized into 2 categories: 1 year and >1 year. Additional
survival analyses for the separate end points of homograft
failure or dysfunction were performed by means of a Cox proportional
hazards, multiple regression model.16 The selection of
independent variables for the model was based on statistical
significance in univariable testing. A value of P<0.05
was considered significant. All analyses were performed with
SPSS® Version 9.0 software (SPSS Inc).
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Results
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There were 22 early deaths among 205 patients undergoing placement
of
a homograft in the RVOT. There were 6 late deaths. Two patients
died
of complications of bacterial endocarditis and 1 patient
died from
cardiogenic shock and congestive heart failure 2 months
after repair of
truncus arteriosus. These 3 deaths are considered
to be valve related.
The remaining 3 late deaths were not related
to the homograft valve.
One late death occurred as a consequence
of mitral stenosis and
insufficiency after a Ross-Konno procedure
for aortic stenosis.
One patient with tetralogy of Fallot and
absent pulmonary valve
syndrome with severe bronchomalacia died
of pulmonary
complications. One patient died of pneumonia after
aspiration. For the
entire group of 205 valve recipients, late
survival was 88% at 10
years (Figure 1
).
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Figure 1. Kaplan-Meier survival curve for 205 patients
undergoing homograft reconstruction of RVOT. There were 28 deaths: 22
early and 6 late; 10-year survival was 88%.
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Mean age at implantation was 6.9±7.6 years, with a median age of 4.4
years and a range of 3 days to 48 years. There were 44 (24%) patients
12 months of age. Earliest conduit replacement was performed 10 days
after initial homograft placement, as part of a revision of
pulmonary artery reconstruction in a patient with
pulmonary atresia /ventricular septal defect and
major aortopulmonary collaterals. One conduit is in place 13
years after implantation. There have been 42 valves explanted. In this
group, 32 patients have undergone 1 homograft replacement, and of these
32 patients, 5 patients have undergone a second homograft replacement.
Five patients had their homograft explanted and replaced with an RVOT
outflow patch or other nonhomograft valved conduit. Among late
survivors, 135 (74%) patients have their original homograft in place
and 98 (54%) have valves that are free from dysfunction. Freedom from
homograft failure was 95±2% at 1 year, 74±4% at 5 years, and
54±7% at 10 years (Figure 2). Freedom
from dysfunction was 84±3% at 1 year, 47±5% at 5 years, and 22±5%
at 10 years.
The results of the univariable and multivariable
analyses are summarized in Table 3. Univariable analysis
identified younger age (Figure 3), longer
warm ischemic time (Figure 4),
implanted valve Z value <2 (Figure 5), and previous operative procedure as
predictive of homograft failure and dysfunction. The use of an aortic
homograft (Figure 6) and extracardiac
operative technique were predictive of homograft failure but not
dysfunction. Duration of cryopreservation, date of operation, homograft
replacement, and sex were not significant. To further delineate the
impact of valve size on homograft failure, Z values were
determined at the time of homograft implantation and last follow-up.
Failed homografts had smaller Z values compared with
functioning homografts at the time of surgery (1.1±1.0 versus
1.9±1.4, P=0.001) and at the time of last follow-up
(0.77±1.5 versus -0.3±1.4, P<0.001). To rule out the
possibility of different growth rates between patients who received
small and large homografts, we also determined the net change in
Z value from implantation to last follow-up. There was no
difference in the net change in Z value between the failure
and nonfailure groups (-1.2±1.3 versus -1.4±1.1, P=NS)
or between the dysfunction and no dysfunction groups (-1.4±1.2 versus
-1.1±1.3, P=NS).
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Table 3. Risk Factors for Homograft Failure (Explantation or
Late Death) and Dysfunction (Explantation, Late Death, Moderate or
Severe Stenosis or Insufficiency): Results of Univariable
and Multivariable Analysis
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Figure 3. Kaplan-Meier freedom from homograft valve failure
(explantation or late death) stratified according to age (<1 year or
 1 year) at operation. Younger age was a risk factor for homograft
valve failure (P<0.001).
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Figure 4. Cox proportional hazards regression model for
freedom from homograft valve failure (explantation or late death)
stratified according to duration of donor warm ischemic time
(time from donor asystole to organ procurement). Mean warm
ischemic time was 5.5 hours. Longer donor warm ischemic
time was a risk factor for homograft valve failure
(P=0.04).
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Figure 5. Kaplan-Meier freedom from homograft valve failure
(explantation or late death) stratified according to Z
value (<2 or 2) at time of operation. Use of a smaller homograft was
a risk factor for homograft valve failure
(P<0.001).
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Figure 6. Kaplan-Meier freedom from homograft valve failure
(explantation or late death) stratified according to type of homograft
(aortic vs pulmonary). Use of aortic homograft was a risk
factor for homograft valve failure (P<0.001).
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Multivariable analysis identified younger age, longer warm
ischemic time, and Z value <2 as independent risk
factors for homograft failure and dysfunction. The use of an aortic
homograft was identified as an independent risk factor for failure but
not dysfunction, whereas extracardiac operative technique was
identified as an independent risk factor for dysfunction but not
failure. Multivariable analysis did not identify previous
procedure as a risk factor for either failure or dysfunction. The
multivariable analysis reported in Table 3
was
performed with age as a continuous variable. Multivariable
analysis was also performed with age used as a dichotomous
variable, 1 year, and >1 year. Although for patients >1 year of
age, the use of an aortic homograft still predicted homograft failure;
for patients 1 year, homograft type did not have an impact on failure
or dysfunction.
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Discussion
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Homografts were the initial valved conduit used for reconstruction
of
the RVOT; however, early preservation techniques involving
antibiotic
preservation were associated with early valve
failure.
2 Porcine
heterografts mounted in Dacron conduits
became available in
a variety of sizes and were widely used for complex
reconstructions.
Heterografts, however, were more difficult to implant.
In particular,
they did not conform to the anatomy as easily as
homografts,
and hemostasis was more difficult to
achieve.
13 14 Furthermore,
the porcine conduits became
calcified rapidly, and the Dacron
graft developed a pseudointimal peel
that could result in stenosis
of small-diameter conduits. The
development of cryopreservation
techniques combined with improved
availability has resulted
in the widespread use of homografts for
reconstruction of the
RVOT in congenital heart disease. Although early
results with
homograft reconstruction of the RVOT have been good,
relatively
few data are available on the mid- and long-term results.
The
purpose of this study was to determine the mid-term result of
homograft
reconstruction of the RVOT and to identify risk factors for
homograft
failure and dysfunction.
This series of patients includes a broad spectrum of congenital heart
defects involving hypoplasia or atresia of the pulmonary valve
and RVOT. For the period of time included in this review, only 6% of
patients had RVOT homografts placed as part of surgery for aortic
stenosis or insufficiency. Therefore, this study is
representative of the outcomes that can be expected for
homograft reconstruction of the RVOT in congenital heart disease. Our
data are consistent with the overall results of other
contemporary series reviewing the outcome of homograft reconstruction
of the RVOT. Gradual deterioration over time can be expected for
homograft valves.9 10 11 12 The 14-year period of this study
spanned significant changes in the timing of surgery, role of
palliative procedures, and improvements in
perioperative management. To remove confounding
variables caused by operative mortality and isolate those factors
affecting durability of the homografts themselves, we analyzed
risk factors for freedom from failure and dysfunction among operative
survivors only. Freedom from failure was 74% at 5 years and freedom
from dysfunction was 47% at 5 years (Figure 2). These data
would suggest that valve dysfunction is likely to occur by 10 years and
that homograft replacement may be required in many patients having a
homograft placed in the RVOT during childhood. However, late survival
is excellent, with only 6 late deaths among 183 patients (Figure 1).
Younger age was identified as a risk factor for homograft failure and
dysfunction (Figure 3). Primary repairs in the newborn period or
infancy were frequent in this series (n=44) and included 28 patients
undergoing repair of truncus arteriosus. Limitations of the size of
homografts that can be implanted in neonates, infants, and small
children will predictably result in the need for homograft replacement
as the child grows.9 10 12 The data support the concept of
outgrowth as a mode of failure of the homograft. Z values
were used to normalize homograft size to the patients’ body surface
area. Multivariable analysis identified smaller
Z value at implantation (<2) as a risk factor for homograft
failure (Figure 5). To further explore the role of growth as a
factor in homograft failure, the Z value of patients at the
time of homograft implantation was compared between the failure and
nonfailure groups. The Z value at implantation was
significantly higher among patients whose homografts had not failed:
1.9±1.4, compared with 1.1±1.0 for failed homografts
(P<0.001). The Z value at last follow-up,
determined by normalizing the homograft size (assuming no change in
valve diameter since implantation) to the patient’s size at last
follow-up, was also evaluated. Again, homografts that had not failed
had a significantly higher Z value, 0.77±1.5, compared with
failed homografts, -0.3±1.4 (P<0.001). The net change in
Z value from implantation to last follow-up was not
significantly different in either comparison (failure versus
nonfailure, dysfunction versus no dysfunction) identifying similar
growth in all patients. These data suggest that whenever possible,
larger homografts should be used.
The use of aortic homografts was associated with more rapid homograft
failure and was significant in the multivariable analysis
(Figure 6). To more completely evaluate the interaction of age
and homograft type, the impact of homograft type (aortic versus
pulmonary) on freedom from failure and dysfunction was
evaluated in patients >1 and <1 year of age. In patients <1 year of
age, homograft type alone was not predictive of homograft failure.
These findings are consistent with data reported by Perron and
associates17 that in small patients, size and outgrowth
overwhelm homograft type as a predictor of failure. This suggests that
aortic homografts can be used for complex reconstruction in newborns
and infants without the need for earlier reoperation. Given the
relative shortage of small pulmonary homografts, the
determination that aortic homografts can be used in infants and
neonates without compromising long-term results may allow better
utilization of the available homograft supply.
Recent reports suggest that the durability of homografts has decreased
in the current era. Niwaya et al12 identified later year
of operation as a risk factor for homograft failure. Stark and
associates11 noted that homograft replacement was
associated with a higher risk of failure than the original homograft.
Possible explanations for this observation include a broadening of the
indications for homograft placement including younger patients with
more complex lesions as well as a decreased threshold for replacement
of a dysfunctional homograft. Another possible explanation for these
observations is a change in the homograft donor supply. In this study,
increased duration of warm ischemic time was identified as a
risk factor for homograft failure (Figure 4). The overall
pressure on the scarce resource of heart donors for transplantation and
homograft valves may have resulted in a broadening of donor criteria
for homografts. In particular, given the increase in pediatric heart
transplantation, homografts are more commonly obtained from
asystolic donors. Homografts with longer donor warm
ischemic time may have more injury, resulting in an exaggerated
reparative and immune response in the host that results in more rapid
dysfunction and failure.18 19 The overall increase in the
warm ischemic time among more recently procured homografts may
result in decreased performance compared with historic
controls.
Limitations of This Study
This is a retrospective analysis of patients with diverse
anatomy operated on over a 14-year period. Undoubtedly,
indications for homograft use, timing of surgery, and indications for
homograft replacement changed during this time period. Variables
analyzed such as homograft type were determined by surgeon
preference and graft availability and were not randomized or
standardized. It is possible, because of the relations between
variables, such as operative technique and diagnosis, that the
influence of some factors have been underestimated and others have been
given more importance. Only operative survivors were analyzed
to remove the influence of perioperative factors on
long-term outcome. Nevertheless, this series looks at factors affecting
the durability of homografts in a large number of patients undergoing
RVOT reconstruction for congenital heart disease. The long-term outcome
of cryopreserved homografts is not completely established, and
therefore the contribution of these data is important. Continued
follow-up studies will be necessary to identify risk factors for
homograft failure.
Conclusions
Among 183 patients undergoing reconstruction of the RVOT with
cryopreserved homografts, durability of the homografts was adversely
affected by younger age, longer donor warm ischemic time,
smaller homograft size at implantation, the use of aortic homografts in
older patients, and extracardiac operative technique. Outgrowth of the
homograft valves appears to be an important cause of homograft failure.
Despite a gradual deterioration, homograft function over time and
patient survival were excellent.
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Acknowledgments
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The authors wish to thank Cryolife Inc for graciously providing
data
concerning homograft donors. We are indebted to Stephanie Frisbee
from
the Center for Outcomes Research and Quality Management at the
Children’s
Hospital of Wisconsin. We also wish to thank Susan Laudon
for
her help with preparation of the manuscript.
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Top
Abstract
Introduction
