Pulmonary Autograft Procedure for Aortic Valve Disease
Long-term Results of the Pioneer Series
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.
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.)
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.
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.
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.
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.
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.
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.
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 χ2 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.
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.
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.
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.
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  and mitral ). 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.
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.
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
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.
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.
- Copyright © 1997 by American Heart Association
Westaby S. Pulmonary autograft replacement of the aortic valve. Br Heart J. 1995;74:1-3.
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.
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.
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.
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.
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.