(Circulation. 1997;96:2206-2214.)
© 1997 American Heart Association, Inc.
Articles |
Pulmonary Autograft Procedure for Aortic Valve Disease
Long-term Results of the Pioneer Series
From Royal Brompton Hospital, London, England (incorporating the former National Heart Hospital, London).
Correspondence to Dr J. Somerville, Grown-Up Congenital Heart Unit, Royal Brompton Hospital, Sydney St, London SW3 6NP, England.
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Abstract |
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Background Pulmonary autograft replacement of the diseased aortic valve has not been widely practiced due to concerns regarding late autograft competence and the consequences of creating pulmonary valve disease. To investigate this, the fate of the pioneering series of patients has been determined.
Methods and Results The 131 hospital survivors of the pulmonary autograft operation at the National Heart Hospital from 1967 to 1984 were identified and their outcomes determined to 1994. Age at operation was 11 to 52 years, and 109 patients were male. Autograft implantation was orthotopic subcoronary (107), free-standing root (20), or Dacron mounted (2). In 113 patients, homografts replaced the native pulmonary valve. Ten and 20 years after operation, survival was 85% and 61%, freedom from autograft replacement was 88% and 75%, and freedom from replacement of pulmonary position homografts was 89% and 80%, respectively. Causes of deaths (53) included chronic heart failure (13), complications of reoperation (12), and endocarditis (7). Autograft regurgitation, the most common indication for reoperation, appeared primarily technical in nature, usually due to cusp prolapse. Degeneration was found in only 3 of 30 explanted autografts, and the young patients showed no increase in late valve failure. Homografts outperformed other valve replacements in the pulmonary position, but patients with orthotopic subcoronary and root autografts survived similarly.
Conclusions The pulmonary autograft offers low rates of degeneration, endocarditis, and thromboembolism for a period lasting >20 years, particularly in the young, with reoperation mainly required for malpositioning of the autograft cusps. The capacity of the autograft to maintain viability with minimal degeneration is not matched by any other biological valve replacement.
Key Words: grafting • valves • aorta
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Introduction |
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In 1967, Ross described the pulmonary autograft procedure for replacement of the diseased aortic valve.1 In this operation, the patient's own healthy pulmonary valve is transposed to the aortic position and forms the aortic valve replacement. The deficiency created in the right ventricular outflow tract is filled with a biological valve, usually an aortic homograft. It was hoped that owing to its close structural similarity to the normal aortic valve, its viability, and its autologous nature, the pulmonary valve would be an ideal aortic valve replacement, particularly for young patients. However, concerns were expressed about the ability of the pulmonary valve to withstand aortic pressure, the effects of creating pulmonary valve disease in addition to aortic valve disease, and the longer bypass time needed for this more complex procedure.2 Until 5 years ago, the operation had not been widely practiced.
Increasing appreciation of the failings of standard aortic valve replacements has rekindled interest in the autograft procedure.3 4 Recent reports have shown that with current cardiothoracic techniques, in particular the care that is taken to preserve the first septal artery and to maintain the correct alignment of autograft cusps, the pulmonary autograft operation can be performed with minimal perioperative complications and good results over short-term follow-up. For example, Kouchoukos et al,5 using the pulmonary autograft as a free-standing root replacement, reported no deaths and only 1 reoperation in 33 patients followed up for <48 months. Although this confirms surgical dexterity, concerns regarding the late outcome of the procedure persist. To address them, we have identified the 131 consecutive hospital survivors of the autograft operation at a single pioneering center, the National Heart Hospital, and determined their outcome at up to 26 years after surgery. (In 1990, the National Heart Hospital merged with the Royal Brompton Hospital, and it is now known by the latter name.)
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Methods |
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Study Population
Between 1967 and 1984, 151 patients underwent the pulmonary autograft procedure for replacement of the diseased aortic valve at the National Heart Hospital. During this period, it was the preferred operation for young patients with isolated aortic valve disease. The short-term outcome at this center, including the in-hospital deaths, has been described.6 7 8 To focus on the late outcome of the operation, the study population in this report comprised, by design, only the 131 consecutive hospital survivors. The series was stopped in 1984 (although the operation has continued to be practiced) to allow a minimum of 10 years' follow-up. The demographic and preoperative cardiac variables of these 131 hospital survivors are summarized in Table 1
. Patients were
aged 11 to 52 years (mean, 32 years) and showed the usual male
predominance and range of aortic valve pathology. No patient had known
coronary disease, and 13 had coexistent mitral
valve disease.
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Operative Procedures
Operative details are summarized in Table 1
. The surgical
methods used have been described.9 The operation is
performed in four stages: excision of the diseased aortic valve;
excision (after inspection) of the patient's own healthy
pulmonary valve; insertion of the native pulmonary
valve (the autograft) into the aortic position; and then insertion of a
biological tissue valve (usually an aortic homograft) into the
pulmonary position. Insertion of the autograft into the aortic
position was most commonly (107 of 131 patients) performed by means of
a two-layer orthotopic subcoronary technique as in the original
description of the operation: the excised pulmonary valve
apparatus is trimmed of muscle and scalloped to fit within
the aortic root in a subcoronary position.1 9 In
1974, a modification was introduced in which the autograft was inserted
as a free-standing aortic root replacement,9 usually with
reimplantation of the coronary arteries, and this was used in
20 patients. The terms "valve" and "root," respectively,
are used to describe these autograft procedures. In 2 patients, the
autograft was mounted on a Dacron stent for implantation.
In the pulmonary position, a variety of valves were used to replace the excised pulmonary valve. One hundred thirteen patients received homografts, most commonly aortic homografts, with 6 pulmonary homografts implanted (after 1969). Details of homograft preparation and storage are incomplete. The available information shows 54 were used "fresh" and 51 were stored frozen before use. The majority were sterilized with antibiotics, but a small number were treated with ethylene oxide (19) or irradiated (12). Eight patients, in 1970 only, received autologous fascia lata valves, autologous pericardial valves were used in 4 patients, and xenografts were used in 2. One surgeon (D.N.R.) performed 102 of the operations. Mean bypass time was 141 minutes (range, 65 to 226 minutes). Twenty-two patients had an additional cardiac procedure at the same time as the autograft operation, most frequently (8) an open mitral valvotomy. At discharge from the hospital, 34 patients had regurgitant early diastolic murmurs. Cardiac catheterization was not routinely performed after operation, and the early part of the series antedates the routine use of echocardiography.
Postoperative Follow-up
The end of the study period was set at April 1994, by which time
subjects had been followed up for 9 to 26 years (mean, 20 years). Of
the 131 patients, 125 (95%) were identified to this date,
representing 2752 patient-years. There was partial
follow-up (an average of 8 years) for the remaining 6 patients (4 of
whom were from abroad), and their data have been included. The outcome
of patients between the original operation and the end of follow-up was
determined from multiple data sources: Royal Brompton/National Heart
Hospital notes, notes of local hospitals, general
practitioner contact, death certificates, postmortems, and
a departmental card-file database that has been kept prospectively.
Autograft valves removed at reoperation at this center were routinely
sent for histological analysis. The policy of
the hospital to destroy case notes of patients not seen for 10 years
explains the absence of some basic data. All surviving patients
identified were seen as outpatients during the 12 months before study
closure (April 1994). Assessment included NYHA functional class,
requirement for drug therapy, ECG, chest radiogram, and
transthoracic M-mode, two-dimensional, and Doppler
echocardiograms. Other investigations, such as 24-hour tape,
transesophageal echocardiography,
cardiac catheterization, and MRI, were only performed
if clinically indicated. For those who found it too far to travel to
the Royal Brompton Hospital, assessment was performed in their local
cardiology outpatient clinic.
Statistical Analysis
The time-related events of interest included death after
hospital discharge, reoperation on the autograft valve, and replacement
of the pulmonary position valve. In all analyses, time
zero was the time of the original autograft operation.
Nonparametric estimates of the non- risk-adjusted
distribution of the time interval to various morbid events were
obtained by the method of Kaplan and Meier.10 A completely
parametric method was used to resolve the number of hazard
phases, identify the form of the equation for each phase, and estimate
the parameters that characterized the distribution of times
until each event.11 The potential risk factors
(variables) were organized for entry into the analyses of
morbid events as shown in the "Appendix." Exploratory
analysis included correlation analysis,
univariate association of event risk to each variable,
and decile risk analysis of ordinal and continuous
variables to identify possible transformations of scale.
Thereafter, a completely parametric
multivariate analysis of each morbid event was
conducted using hazard function methodology (available from
ftp://uabcvsr.cvsr.uab.edu via the Internet).12 In these
analyses, variables were entered simultaneously
into the scaling parameter of each phase of the
mathematical equation characterizing the underlying distribution of
times until each event. A directed technique of stepwise entry of
variables into the risk factor analyses was
used.12 The probability value criterion for retention of
variables in the final analysis was .10 because the data
set was relatively small. Hazard function regression coefficients are
presented as mean±1 SE. Exploration of the influence of risk
factors in the multivariate analysis was
performed by constructing nomograms representing the
solution of the parametric equation for the specific supplied
values of each factor. For these, typical patient values were entered
for all variables except the one of interest.
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Results |
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Mortality
Of the 131 hospital survivors, 53 had died by 1994 (Table 2
). Early deaths (within 1 year of
operation) were caused by severe autograft
regurgitation (1), endocarditis on a homograft in the
pulmonary position (1), and sudden death (1). Twelve deaths
occurred at reoperation, complicating reoperations for autograft
regurgitation in 6 and endocarditis in 4 patients.
Persistent low cardiac output and sepsis with multiorgan failure were
the principal modes of perioperative death. There were
38 late deaths (cardiac related in 29, noncardiac in 4, and of unknown
cause in 5 patients). Late cardiac deaths included chronic heart
failure (13), acute myocardial infarction (6), and sudden death (8).
Autograft regurgitation was an important causative
factor in 14 deaths, through chronic heart failure in 8 patients and as
the primary indication for reoperation in 6 reoperation deaths.
Endocarditis was responsible for 7 deaths, 4 of which occurred at
reoperation. Survival at 10 and 20 years after surgery was 85% and
61%, respectively (Fig 1). Older
patients, patients with coexistent mitral valve disease,
and patients with noncalcific aortic valves or previous aortic valve
replacement had higher mortality rates (Table 3). The survival differences for other
patient, operative, and experience variables were no greater than
could be expected by chance (P>.10). There was no survival
advantage evident from the root autograft procedure.
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Reoperation
Of the 131 study patients, 46 had reoperations. Patients had up to
three reoperations that involved either the aortic position, the
pulmonary position, some other site (usually mitral valve), or
a combination of these. Freedom from any reoperation was 76% and 62%
at 10 and 20 years after surgery, respectively. The primary indications
for first reoperation are summarized in Table 4. Sixty-two reoperations in 46 patients
resulted in 12 deaths within 1 year of the reoperation.
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Reoperation and Fate of the Autograft Valve
Thirty-five patients had reoperations on the autograft valve, 5
early and 30 late. Early reoperations were for severe autograft
regurgitation (2), hemorrhage from the aortic
root (1), and myocardial ischemia (2), the latter possibly the
result of coronary occlusion from malpositioning of the
autograft. Twenty-eight of 30 late reoperations on the autograft were
performed for severe regurgitation; other indications
were aortic root false aneurysm without evidence of infection
(1) and Staphylococcus albus aortic root abscess (1). These
developed 3 and 10 years after surgery, respectively, in the subvalvar
suture line of root autografts. The first reoperations on the autograft
valve were for replacement (24), autograft repair (10), and repair of a
false aneurysm (1). Autograft repair involved resuspension of a
prolapsing cusp or patching of a cusp hole. Outcome from repair was
judged to be good in 5 cases (minimal regurgitation
postoperatively) but poor in 5 (3 early reoperations for continued
severe regurgitation, 1 perioperative
death, and 1 late death from heart failure due to continued
regurgitation). Freedom from autograft valve
replacement was 88% and 75% at 10 and 20 years, respectively (Fig 2). Determination of the time-related
hazard function for autograft replacement revealed distinct early and
late phases of risk, the latter rising slightly across time (Fig 3). Use of a nonhomograft valve in the
pulmonary position and use of a homograft sterilized with
ethylene oxide or by irradiation were risk factors for late autograft
removal (Table 3). In several patients submitted to reoperation for
severe pulmonary position valve dysfunction (more common with
nonhomograft valves), the surgeon elected to simultaneously
replace a moderately dysfunctional autograft because it was assumed the
autograft regurgitation would deteriorate. The
improvement in autograft valve survival resulting from placement of a
homograft in the pulmonary position is illustrated in Fig 4. Older patients showed a trend to
improved survival of the autograft valve during the first year after
surgery (P<.09), but late survival of the autograft was
unrelated to age at implantation (Fig 5).
No other variable showed a relationship to outcome that reached the
P<.10 level of significance (Table 3), and reoperation
rates for valve and root autografts were similar (Fig 6). However, reoperation for
regurgitation was performed for only 2 of 20 root
autografts compared with 27 of 107 valve autografts (P<.05
by 
2 test). This failed to translate into a lower
reoperation rate for root autografts because there was an excess of
reoperation for other indications. There were 2 Dacron-mounted
autograft valves; 1 required early reoperation for severe
regurgitation, and the other was still in place at the
end of follow-up.
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Regurgitation through the autograft was an important
cause of mortality and the most common indication for reoperation. In
the series of 30 patients who received reoperations for autograft
regurgitation, the valvar dysfunction and its
chronological development were determined. In 3 patients, all with
bacterial endocarditis, regurgitation was acutely
severe. In the rest, autograft regurgitation was slowly
progressive, becoming severe during a period of up to 20 years. An
aortic early diastolic murmur, indicating a degree of
autograft regurgitation, was detected in the immediate
postoperative period in 34 of the 131 study patients; 16 of these
patients subsequently required reoperation for autograft
regurgitation, 14 (41%) within 10 years of the
autograft operation. In 97 patients, the autograft was judged competent
immediately after surgery; 14 of these subsequently underwent
reoperation for autograft regurgitation, 7 (7%) within
10 years of the autograft procedure. At reoperation, cusp prolapse,
avulsion, and perforation were the dominant anomalies identified (Table 5). In 2 patients, the appearance of the
autograft was typically rheumatic with cusp thickening and retraction;
in both cases, the original aortic valve pathology had been
rheumatic.
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Fig 7 is a photomicrograph of an
autograft removed 24 years after implantation; it reveals living cells
in a well-preserved tissue architecture. This histology was found in
all but three specimens in which there was evidence of degenerative
change with focal areas of loss of cellularity, collagen necrosis, and
mucoid degeneration (J.S., MD, FRCP, and D.N.R., FRCS, unpublished
data, 1967 to 1996). These three "degenerate" autografts had been
in place for 5 to 15 years, and the changes found were restricted to
one or two of the three autograft cusps. Annular calcification was
found in two specimens explanted 19 and 21 years after operation.
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Reoperation on the Valve in the Pulmonary Position
Outcome varied according to the type of valve used. Reoperations
were performed on 37 of the 113 patients with homografts in the
pulmonary position by 1994, 27 on the autograft valve and 22 on
the homograft itself. Homograft dysfunction was the primary indication
for reoperation in 11 cases. There were 2 early homograft reoperations
for infection and 20 late reoperations for stenosis (15),
regurgitation (4), and operation damage (1).
Stenosis resulted from calcification (11) or suture line
stricture (4), and regurgitation was caused by loss of
a cusp. One patient needed a further replacement of a calcific,
stenosed second homograft. Retention of the original homograft valve at
10 and 20 years was 89% and 80%, respectively. Ethylene oxide-
treated and irradiated homografts performed less well than other
homografts (Table 3 and Fig 8), but there
were too few pulmonary homografts in the series to draw
conclusions. None of the 8 patients with fascia lata valves have
survived without reoperation; 7 had reoperations 1 to 15 years later
(average, 7 years), and 1 died at 3 years. Severe pulmonary
regurgitation was obvious within the first 2 to 3
years, and at reoperation, the valves were shrunken and stenosed, with
disappearance of the "cusp" tissue.
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Reoperations at Other Sites
In nine patients, the reoperation included intervention at other
cardiac sites: mitral valve procedure (seven), ventricular
septal defect repair (one), and vein graft to anterior descending
artery (one). In five patients, mitral valve disease was the primary
indication for reoperation.
Endocarditis, Thromboembolism, and Arrhythmia
During follow-up, there were 12 definite episodes of endocarditis
in 12 patients. Three episodes occurred in the first year (early) after
the autograft procedure on homografts in the pulmonary
position, which presumably were infected at the time of implantation.
Four episodes of endocarditis occurred in the first year after
reoperation; these "early postreoperation" infections were on
(nonautograft) prosthetic valve replacements (aortic [3] and
mitral [1]). The remaining 5 episodes of definite endocarditis
occurred on the homograft in the pulmonary position (1),
prosthetic aortic valve replacement (1), and autograft (3) 2 to
15 years after operation. Definite autograft infections occurred only
in these last 3 cases. Standard organisms were involved, and infections
occurred 3, 10, and 15 years after the autograft procedure and caused
acutely severe regurgitation requiring reoperation. Two
of these patients were alive and well at the end of follow-up, and 1
died of heart failure 4 years later.
Sixteen patients had thromboembolic events, 11 systemic and 5 pulmonary. Major risk factors for thromboembolism, such as atrial fibrillation, bacterial endocarditis, peripheral vascular disease, or cardiac failure, were identifiable in 15 of the 16 patients. Only 1 patient, with amaurosis fugax, had no risk factors other than the autograft valve itself. Patients with autograft valves were not given anticoagulants unless another indication such as atrial fibrillation or venous thrombosis was present.
Thirty patients had a documented arrhythmia late after operation, but no systematic search was made for them. A minority of these began perioperatively and persisted, whereas the majority developed later. Twenty patients developed atrial fibrillation; 10 of these patients had coexistent mitral valve disease. Complete heart block began early in 2 and several years later in 3 patients. There were 2 deaths from witnessed, unexpected ventricular fibrillation; both had atrial fibrillation, mitral valve disease, and impaired left ventricular function. As described previously, a number of patients died suddenly; the role of rhythm disorders in these deaths is unknown.
State of Survivors
At the end of follow-up, 72 patients were alive, 53 had died, and
6 were lost to follow-up. Survivors were 10 to 26 years (mean, 20
years) postoperative and had an average NYHA class of 1.2 (range, 1 to
3). Two patients were NYHA class 3, 1 of whom had reoperation for
autograft regurgitation 2 months later and is now NYHA
class 1. Survivors were taking an average of 0.8
cardiovascular drugs (anticoagulants and
antihypertensive drugs included). Warfarin treatment was for atrial
fibrillation or mechanical valves but not for the autograft itself.
Fifty-eight survivors (81%) retained their autograft valve; these were
root (14), valve (43), and Dacron-mounted (1) autografts in situ for 10
to 25 years (mean, 19 years). Autograft valve function was assessed by
transthoracic echocardiography during
the last year of follow-up; stenosis was not found in any
valve, and the majority (75%) remained free from significant
regurgitation. Fifty-nine survivors (82%) had their
original valve replacement in the pulmonary position: homograft
(57), autologous pericardial (1), and xenograft (1). The function of 40
surviving homografts (in situ for a mean of 19 years) was assessed by
transthoracic echocardiography; 36 were
free from significant regurgitation, but 25 had some
stenosis (gradient of 
20 mm Hg). The function of the
right ventricular outflow tract valve was often difficult
to assess by transthoracic
echocardiography, and in 8 survivors, valve
function could not be determined.
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Discussion |
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No aortic valve replacement can claim to be perfect. Although mechanical prostheses are durable, they require formal anticoagulation, and some show suboptimal hemodynamic performance, which can result in late left ventricular dysfunction.13 Biological valves do not require anticoagulation but show degeneration that accelerates after 7 to 10 years, particularly in the young, active patient.14 Recognizing these difficulties, Ross conceived the pulmonary autograft procedure, hoping to create an aortic valve replacement closer to the ideal.1 Initially, the operation did not find favor with the cardiac surgical community because of concerns regarding technical complexity, the consequences of creating pulmonary valve disease, and the ability of the pulmonary valve to withstand the hemodynamic stress of the aortic position. Several groups have subsequently shown that the pulmonary autograft procedure can be performed safely and with good immediate hemodynamic results. However, these studies have mostly been short-term in small numbers of patients,5 15 16 17 18 and concerns regarding the late outcome continue to be expressed.
This series, the longest reported for any biological valve replacement, shows the pulmonary autograft to function well in the aortic position over a follow-up period of up to 26 years in terms of both freedom from autograft replacement and function of late surviving valves. The remarkable preservation of cellular viability and tissue architecture demonstrated macroscopically and histologically by late explanted autografts and the absence of age as a risk factor for late autograft valve failure are likely to be related. Among homografts, a clear relation has been shown between preservation of cellular viability and valve longevity, which has culminated in the use of homovital homografts.19 20 However, whereas homograft cusp cells may be immunogenic (they are allogeneic), the autograft valve is de facto tissue matched. The additional protection from degeneration conferred by tissue matching awaits direct assessment, but the longevity of the autograft valve suggests an important effect.
The principal autograft valve dysfunction encountered was regurgitation, which, on the basis of the findings at reoperation and the temporal pattern of development, appeared primarily technical in nature, probably resulting from malsuspension of the autograft cusps at implantation. Similar difficulties have been encountered with homograft valves,21 22 23 and Ross, recognizing the problem from an early stage, started using the free-standing root implantation technique in 1974 to achieve better long-term autograft competence; not only are the aortic sinuses thereby preserved, but misalignment of the transplanted valve cusps is also less likely. Although there is some support for this approach from this series (reoperation for autograft regurgitation was less frequent among root autografts), overall there was no difference in valve replacement rates between the root and the valve autograft procedures. This cohort contained only 20 root autografts, and a larger series is needed to address this question. In small numbers of study patients, autograft regurgitation was caused by endocarditis, degeneration, or rheumatic change. The apparent potential for the autograft to be affected by rheumatism, also reported by Al-Halees et al24 from Saudi Arabia, where active rheumatic valvular disease is more common, is likely to be a hazard of maintained viability. It may be that the use of the pulmonary autograft procedure in populations with a high prevalence of rheumatic fever or in young patients with rheumatic aortic valve disease is not ideal unless compliance with penicillin prophylaxis is certain.
The genesis of pulmonary valve disease, in addition to aortic valve disease, has been one of the main objections to the pulmonary autograft operation. In response, protagonists have argued that biological valves sited here would not only be slow to develop dysfunction, but that any dysfunction would be well tolerated owing to the lower pressures on the right side of the heart. In this series, survival of homografts in the pulmonary position was good (20-year freedom from reoperation of 80%), and homograft dysfunction was infrequently implicated in the observed morbidity and mortality of the series. No other valve performed as well in this position, and homografts (aortic or pulmonary) should be the replacement of choice. Many of the homograft valves in this series had been sterilized with ethylene oxide or irradiation, methods now recognized to have deleterious effects on valve performance, and with the use of fresh homograft valves in the future, the results of the pulmonary autograft procedure are likely to be superior to those reported here. Although the concerns regarding the creation of pulmonary valve disease are justified, we consider that this is a problem that must be accepted (but minimized by the use of fresh homografts) and that is outweighed by the advantages of the autograft replacement of the aortic valve.
Comparison between this report and other series of aortic valve replacements is difficult; not only are there differences in patient groups, but also the series originate in different eras that span improvements in cardiothoracic techniques. The effect of patient age is important; youth has been consistently identified as a risk factor for premature failure of both allograft21 25 and xenograft14 26 valves, and this series is notable for the young age of its subjects. The late outcome of the Hancock and Carpentier-Edwards porcine valves in the aortic position has recently been defined in the Edinburgh Heart Valve Trial.26 The 12-year freedom from reoperation among all patients was 77%, but patients were of a mean age of 56 years. In patients younger than 50 years of age (more comparable to this autograft series), the 12-year freedom from reoperation was as low as 40%. The late outcome for aortic homografts in the aortic position has been addressed in a number of studies. Barratt-Boyes et al,21 in a pioneering series starting in 1968, reported freedom from reoperation of 79% at 10 years for aortic homografts stored in 4°C and placed in the aortic position. However, after this time, the rate of valve degeneration increased markedly, and 14-year freedom from reoperation was only 54%. Cryopreserved and homovital homografts are reported to have better long-term performance than allografts stored at 4°C, with a 10-year freedom from reoperation in the aortic position of 72% to 92%,19 20 25 27 but their fate at 15 or 20 years after implantation is undefined. Enhanced survival is claimed to result from preservation of viable cells; however, any viable cells may be immunogenic and contribute to the degeneration that can occur early. Whether tissue-matched homografts will have enhanced longevity awaits assessment.
Mechanical valves appear to offer similar mortality rates to bioprostheses but lower rates of reoperation. In the Edinburgh Heart Valve Trial, mortality at 5 and 12 years was similar for Bjork-Shiley and porcine valves, but the 12-year reoperation rate was only 4.2% for the Bjork-Shiley valve versus 22.6% for porcine valves (aortic position).26 The disadvantage of the mechanical valves is, of course, the need for anticoagulation, which in that study was associated with a 22.5% incidence of major bleeding episodes over 12 years. Anticoagulation is a particular problem for the young, physically active patient; in pregnancy; and in those with concurrent illnesses requiring treatment with steroids or nonsteroidal, anti-inflammatory drugs. The pulmonary autograft would appear optimal for these groups.28 The pulmonary autograft has also been proposed as the ideal valve for children and adolescents, offering the potential for valve growth with the patient through its viability.18 29 The present cohort included only seven patients younger than 18 years of age at the time of operation, and because serial measurements of root dimensions were not available, the issue of autograft growth could not be addressed. However, the absence of premature valve failure in the young does lend further support to the use of this procedure in these patients.
We conclude from this pioneering series that the autograft valve has good long-term hemodynamic performance that compares favorably with the alternative biological aortic valve replacements. Autograft valve cusps contain living cells up to 24 years after implantation and rarely show degeneration, supporting the possibility that the autograft may be a valve replacement for life. The main complications are calcific stenosis of the homograft in the pulmonary position and autograft regurgitation, which is mainly technical in nature. There is no premature valve failure in the young, and we suggest that the pulmonary autograft procedure is ideally suited to young patients, particularly women with childbearing potential.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Variables Examined in the Multivariate Analysis Patient variables Demographic Age Sex Previous cardiovascular surgery Aortic valvotomy Aortic valve replacement Coarctation repair Any cardiovascular surgery Coexisting cardiac conditions Native valve endocarditis Mitral valve disease Aortic valve pathology Calcific aortic valve Rheumatic aortic valve Endocarditis involving aortic valve Floppy aortic valve Degenerated bioprosthesis Incompetent, stenotic, or mixed aortic valve lesion Previous cardiothoracic surgery Coexisting cardiac lesions Aortic valve pathology Procedural variables Autograft valve implantation technique Miniroot replacement Intraluminal valve replacement Details of pulmonary valve replacement Type of pulmonary valve Autologous tissue Allograft Xenograft Method of allograft sterilization Ethylene oxide Irradiation Method of preservation Fresh Frozen Size of allograft Concomitant procedures Repair of mitral valve Left ventricular outflow resection Elapsed time of cardiopulmonary bypass Experience variables Date of operation Surgeon
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Acknowledgments |
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We are greatly indebted to Professor J. Kirklin and Dr E. Blackstone, University of Alabama, Birmingham, who generously gave their time to conduct the detailed statistical analysis of the data and to comment on the manuscript. We are also grateful to the Grown-up Congenital Heart Association, which funded the project.
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Footnotes |
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The current address for J.C. Chambers, J. Somerville, and S. Stone is Royal Brompton Hospital, Sydney St, London SW3 6NP, England. Dr Somerville may also be contacted at National Heart and Lung Institute, Imperial College of Science Technology and Medicine, Dovehouse St, London SW3 6LY, England. The current address for D.N. Ross is 25 Upper Wimpole St, London W1M 7TA, England.
Received January 22, 1997; revision received May 2, 1997; accepted May 5, 1997.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Ross DN. Replacement of the aortic and
mitral valves with a pulmonary autograft.
Lancet. 1967;2:956-958.[Medline]
[Order article via Infotrieve]
-
Elkins RC, Lane MM, McCue C. Pulmonary
autograft reoperation: incidence and management. Ann
Thorac Surg. 1996;62:450-455.
[Abstract/Free Full Text]
-
Elkins RC. Pulmonary autograft: the
optimal substitute for the aortic valve? N Engl
J Med. 1994;330:59-60.
[Free Full Text]
-
Westaby S. Pulmonary autograft
replacement of the aortic valve. Br Heart J. 1995;74:1-3.
[Free Full Text]
-
Kouchoukos NT, Davila-Roman VG, Spray TL, Murphy SF,
Perrillo JB. Replacement of the aortic root with a
pulmonary autograft in children and young adults with aortic
valve disease. N Engl J Med. 1994;330:1-6.
[Abstract/Free Full Text]
-
Somerville J, Ross D, Sachs G, Emanuel R, McDonald
L. Long-term results of the pulmonary autograft
replacement for aortic valve disease. Lancet. 1972;2:730-734.[Medline]
[Order article via Infotrieve]
-
Matsuki O, Okita Y, Almeida RS, McGoldrick JP, Hooper
TL, Robles A, Ross DN. Two decades' experience with aortic
valve replacement with pulmonary autograft.
J Thorac Cardiovasc Surg. 1988;95:705-711.[Abstract]
-
Gula G, Wain WH, Ross DN. Ten years'
experience with pulmonary autograft replacements for aortic
valve disease. Ann Thorac Surg. 1979;28:392-396.[Abstract]
-
Ross DN. Replacement of the aortic valve with a
pulmonary autograft: the "switch' operation.
Ann Thorac Surg. 1991;52:1346-1350.[Abstract]
-
Kaplan EL, Meier P. Nonparametric
estimation from incomplete observations. J Am Stat
Assn. 1958;53:457-481.
-
Blackstone EH, Naftel DC, Turner ME Jr. The
decomposition of time varying hazard into phases, each incorporating a
separate stream of concomitant information. J Am Stat
Assn. 1986;81:615-624.
-
Baskerville JC, Toogood JH. Guided regression
modelling for prediction and exploration of structure with many
explanatory variables. Technometrics. 1982;24:9-17.
-
Jin XY, Gibson DG, Pepper JR. Left
ventricular function after aortic valve
replacement. Ann Card Surg. 1995;125-134.
-
Al-Khaja N, Belboul A, Rashid M, El-Gatit A, Roberts D,
Larsson S, William-Olsson G. The influence of age on the
durability of Carpentier-Edwards biological valves. Eur
J Cardiothorac Surg. 1991;5:635-640.[Abstract]
-
Hokken RB, Bogers AJ, Taams MA, Willems TP,
Cromme-Dijkhuis AH, Witsenburg M, Spitaels SE, Van Herwerden LA, Bos
E. Aortic root replacement with a pulmonary
autograft. Eur J Cardiothorac Surg. 1995;9:378-383.[Abstract]
-
Prat AG, Doisy VC, Savoye C, Moreau DC, Monier EJ,
Stankowiak C. Total aortic root replacement with
pulmonary autografts: short term results in 45 consecutive
patients. J Heart Valve Dis. 1995;4:368-373.[Medline]
[Order article via Infotrieve]
-
Pacificio AD, Kirklin JK, McGiffin DC, Matter GJ, Nanda
NC, Diethelm AG. The Ross operation: early
echocardiographic comparison of different operative
techniques. J Heart Valve Surg. 1994;3:365-370.
-
Elkins RC, Knott-Craig CJ, Randolph JD, Razook JR, Ward
KE, Overholt ED, Lane MM. Medium-term follow-up of
pulmonary autograft replacement of aortic valves in
children. Eur J Cardiothorac Surg. 1994;8:379-383.[Abstract]
-
O'Brien MF, Stafford EG, Gardner MAH, Pohlner PG,
McGiffin DC, Kirklin JW. A comparison of aortic valve
replacement with viable cryopreserved and fresh allograft valves, with
a note on chromosomal studies. J Thorac Cardiovasc
Surg. 1987;94:812-823.[Abstract]
-
Yacoub M, Rasmi NRH, Sundt TM, Lund O, Boyland E,
Radley-Smith R, Khagani A, Mitchell A. Fourteen-year experience
with homovital homografts for aortic valve replacement.
J Thorac Cardiovasc Surg. 1995;110:186-193.
[Abstract/Free Full Text]
-
Barratt-Boyes BG, Roche AHG, Subramanyan R, Pemberton
JR, Whitlock RML. Long-term follow-up of patients with the
antibiotic-sterilized aortic homograft valve inserted freehand into the
aortic position. Circulation. 1987;75:768-777.
[Abstract/Free Full Text]
-
Christie GW, Barratt-Boyes BG. Identification of
a failure mode of the antibiotic sterilized aortic allograft after 10
years: implications for their long-term survival. J
Card Surg. 1991;6:462-467.[Medline]
[Order article via Infotrieve]
-
Willems TP, Van Herwerden LA, Steyerberg EW, Taams MA,
Kleyburg VE, Hokken RB, Roelandt JR, Bos E. Subcoronary
implantation or aortic root replacement for human tissue valves:
sufficient data to prefer either technique? Ann Thorac
Surg. 1995;60:S83-S86.
-
Al-Halees Z, Kumar N, Gallo R, Gometza B, Duran
CM. Pulmonary autograft for aortic valve replacement in
rheumatic disease: a caveat. Ann Thorac Surg. 1995;60:S172-S175.
-
O'Brien MF, McGiffin DC, Stafford EG, Gardner MA,
Pohlner PF, McLachlan GJ, Gall K, Smith S, Murphy E. Allograft
aortic valve replacement: long-term comparative clinical
analysis of the viable cryopreserved and antibiotic 4°C
stored valves. J Card Surg. 1991;6:534-543.[Medline]
[Order article via Infotrieve]
-
Bloomfield P, Wheatley DJ, Prescott RJ, Miller
HC. Twelve year comparison of a Bjork-Shiley mechanical heart
valve with porcine bioprostheses. N Engl J
Med. 1991;324:573-579.[Abstract]
-
Kirklin JK, Smith D, Novick W, Naftel DC, Kirklin JW,
Pacificio AD, Nanda NC, Helmcke FR, Bourge RC. Long-term
function of cryopreserved aortic homografts. J
Thorac Cardiovasc Surg. 1993;106:154-166.[Abstract]
-
Elkins RC, Knott-Craig CJ, Razook JR, Ward KE, Overholt
ED, Lane MM. Pulmonary autograft replacement of the
aortic valve in the potential parent. J Card
Surg. 1994;9:198-203.[Medline]
[Order article via Infotrieve]
-
Elkins RC, Knott-Craig CJ, Ward KE, McCue C, Lane
MM. Pulmonary autograft in children: realized growth
potential. Ann Thorac Surg. 1994;57:1387-1394.[Abstract]
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