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Ann Thorac Surg 2001;72:2070-2076
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

The fate of small-diameter homografts in the pulmonary position

^a Department of Paediatric Cardio-Thoracic Surgery, Deutsches Kinderherzzentrum, Sankt Augustin, Germany

Accepted for publication July 30, 2001.

* Address reprint requests to Dr Urban, Department of Paediatric Cardio-Thoracic Surgery, Deutsches Kinderherzzentrum, Arnold-Janssen-Strasse 29, 53757 Sankt Augustin, Germany
e-mail: andreas.e.urban.md{at}t-online.de

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Limited durability is expected for small homograft valves that are used to correct congenital cardiac disease.

Methods. All 76 homograft valves with an internal annulus diameter ranging from 8 to 13 mm that were implanted from 1987 through 2000 in the pulmonary position were retrospectively analyzed. In each case, homograft size was normalized to the patient’s body surface area: z-value. For 93% (14 of 15) of the 8 to 9 mm grafts, z was less than 2. For 56% (5 of 9) of the 10 mm grafts and 98% (51 of 52) of the 11 to 13 mm allografts, z was greater than 2. Survival and freedom from complications were estimated by the Kaplan-Meier method. Homograft failure was defined as homograft replacement or late death; significant dysfunction, as homograft obstruction with an echo-Doppler gradient greater than 50 mm Hg or grade III or IV valvular insufficiency. The log-rank test was used to compare outcomes.

Results. Seven patients died early after operation; three, late. Survival was 86.5% ± 3.8% at 1 year and remained stable during the succeeding years. Freedom from failure for all homografts was 90.6% ± 3.7%, 71.8% ± 6.9%, and 61.8% ± 9.0% at 1, 5, and 10 years, respectively. Corresponding freedom from significant dysfunction was 87.6% ± 4.1%, 51.2% ± 7.4%, and 10.1% ± 8.3%. The smaller homografts (z less than 2) failed and deteriorated faster (p < 0.0001): only 32.1% ± 13.0% were still functioning at 24 months. The larger grafts (z at least 2) retained function for the first 4 years, and 73.7% ± 10.4% had not yet failed at 10 years.

Conclusions. Smaller (z less than 2) homografts (the great majority of 8 to 9 mm grafts) have to be replaced early, usually within 2 years of implantation. Larger (z at least 2) grafts (nearly all 11 to 13 mm grafts) show remarkable durability and are suitable valved conduits for establishing right ventricle to pulmonary artery continuity in neonates and young infants.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Small-diameter valved conduits used to repair congenital heart disease in neonates and young infants are not expected to have a long life, either because of accelerated degeneration or because of rapid outgrowth. Their failure leads to reoperation in the first years of life, somewhat tempering the benefits of early complete correction of those cardiac lesions. Since 1987, we have been implanting small homografts between the right ventricle and the pulmonary artery or arteries for total repair of various cardiac malformations in early infancy. We reviewed our experience in terms of lesions corrected, survival of patients, and durability and function of these small conduits.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Definitions
Small-diameter homograft valves are those allografts with an internal annulus diameter ranging from 8 to 13 mm. The z-value or z-score of the homograft is given by the following formula: Z = (A - B)/C, where A is the diameter of the implanted homograft, B the normal diameter of the pulmonary valve based on patient body surface area, and C the standard deviation around the normal dimension of the pulmonary valve. B and C refer to normal individuals of the same body surface area as the patient and are obtained using regression analysis and the equation of Rowlatt and associates [1]. Early survivors are patients who were discharged from the hospital and who survived at least 30 days. Homograft failure is defined as homograft replacement or late death; significant homograft dysfunction, as homograft obstruction causing a trans-homograft peak pressure gradient greater than 50 mm Hg on Doppler-echocardiography, or grade III or IV homograft regurgitation.

Patients–diagnoses
Between June 1987 and December 2000, 76 small homografts were implanted in 76 consecutive children who underwent operations involving reconstruction of the right ventricular outflow tract (RVOT). Table 1 shows the different types and sizes of the homografts used, and Table 2 indicates the corresponding homograft z-values. All homografts except four were cryopreserved, and those four were freshly sterilized by antibiotics. Homografts were supplied by 10 different homograft banks, but most (n = 36) came from a single institution; 42 were aortic and 34 were pulmonic grafts. Homograft z-scores ranged from 0 to 5.2, with a mean of 2.9 ± 1.3 and a median of 3.0. For 93% (14 of 15) of the 8 to 9 mm grafts, z was less than 2. For 56% (5 of 9) of the 10 mm and 98% (51 of 52) of the 11 to 13 mm allografts, z was greater than 2.

The cardiac malformations summarized in Table 3 included truncus arteriosus (n = 60), various forms of the tetralogy of Fallot (n = 15), and one case of aortic atresia (Ross procedure).

At operation, once cardioplegic cardiac arrest was established, the homograft was sutured distally to the pulmonary artery or arteries. The proximal anastomosis was performed on the beating heart. In seventy-one patients the implant was attached to the right ventricle by means of (1) a hood made of pericardium (n = 28), (2) a polytetrafluoroethylene (PTFE) patch (n = 17), (3) a mitral leaflet from the aortic homograft donor (n = 10), (4) a homograft patch (n = 4), or (5) a dacron tube extension (n = 12). To facilitate chest re-entry, if reoperation became necessary, we routinely approximated the pericardium and covered the heart with an artificial membrane. In 12 cases, the sternum was closed secondarily. The median duration of postoperative endotracheal intubation for early survivors was 5 days.

Follow-up: evaluation of homograft function
Echo-Doppler studies were used to evaluate heart and homograft function at least every 6 months for the first 2 years and once a year thereafter. The trans-homograft peak pressure gradient was calculated using the simplified Bernoulli equation: gradient = 4V², where V is the peak instantaneous trans-homograft Doppler velocity. Homograft insufficiency was graded by mapping the dimensions of the regurgitation jet with pulsed or color flow Doppler echocardiography, analogous to the semi-quantitative method described by Perry and colleagues for evaluation of aortic insufficiency [3]. If a problem was detected or suspected, cardiac catheterization with angiocardiography was performed. Right ventricular pressure at least 75% of the systemic pressure was considered an indication for conduit replacement regardless of the clinical status of the patient.

Data analysis
Perioperative and early postoperative data were collected retrospectively. The actual follow-up assessments took place from May 2000 to January 2001. Probabilities of survival, or freedom from homograft failure, and of freedom from homograft dysfunction were estimated by the Kaplan-Meier method (see Fig 1). The following three parameters served as end points in our study: time of death, graft replacement, and first diagnosis of significant graft dysfunction. The probabilities are given as percent (%) ± SEM (standard error of the mean). The connecting line is stepwise for the graph depicting homograft failure. It is straight for homograft dysfunction. The log-rank test was used to calculate the statistical difference between two groups. The fate of the allografts was compared according to their z-scores. Other variables studied included age at operation (neonates versus older infants), type of graft (aortic versus pulmonary), and supplier of homograft (the institution that supplied the most homografts versus other homograft banks), and use (or not) of a dacron tube extension. The difference is considered statistically significant with a p value less than or equal to 0.05. Means ± SD and percentages with 95% confidence limits are given.

View larger version (17K): [in this window] [in a new window]   Fig 1. Kaplan-Meier estimates of freedom from homograft failure for all grafts over time. Vertical bars represent standard error of the mean (S.E.M.).

	Results

Top Abstract Introduction Patients and methods Results Comment References

Homograft failure
Fourteen homografts were explanted 2 to 135 months after insertion (median, 24 months; mean, 40 ± 38 months), four of them in other hospitals, with no operative deaths. The 10 patients who underwent reoperation in our unit had had cardiac catheterization 4 months (median) before operation.

Graft failure was due to infection in two patients. In one, Candida albicans caused digestion of the homograft with pseudo-aneurysm formation that required emergency intervention 2 months after truncus arteriosus repair. In the other case infection was subacute to chronic and caused homograft obstruction that led to reoperation 60 months postoperatively. Right ventricular outflow tract obstruction was the indication for homograft replacement in 13 patients. Significant homograft dysfunction had been detected by echocardiography 2 to 105 months (mean: 21 ± 29 months, median: 9 months) before graft replacement in these 13 patients. At the time of reoperation, the somatic growth in all patients was such that the z-scores of the original grafts were negative: median = -2.3, mean = -2.4 ± 1.0 (-0.87 to -4.1). The right ventricular pressures ranged from 75% to 200% of the systemic pressure (mean: 115% ± 36%, median: 104%). At reoperation, the main site of obstruction was at the proximal anastomosis (n = 2), within the homograft itself (n = 5), or at the distal anastomosis to the pulmonary arteries (n = 2). The point of obstruction could not be clearly determined in four cases, suggesting outgrowth as the single etiology for obstruction. Other causative factors of RVOT obstruction were infection as reported above (n = 1), probable graft degeneration (n = 4) (leaflet shrinkage, wall calcification, or sclerosis), unfavorable anatomy with retrosternal compression of the prosthesis (n = 1), and mixed factors (n = 3), with a combination of outgrowth, conduit degeneration, and peripheral stenosis of the right or left pulmonary artery. Freedom from explantation of the homograft and replacement by another conduit at 1, 5, and 10 years was 95.3% ± 2.7%, 75.5% ± 6.9%, and 65.0% ± 9.3%, respectively.

Failure occurred in a total of seventeen grafts (leading to fourteen replacements and three late deaths). Figure 1 shows the freedom from failure over time for all valved conduits, and Table 4 details the freedom from failure according to the homograft z-scores. The freedom from failure for the grafts with 0–0.9 and 1–1.9 z-scores is not significantly different: p = 0.23. It is also statistically similar for those with z-scores ranging from 2 to 5.2: p = 0.30. Figure 2 compares the results of these two groups: z less than 2 versus z at least 2. The smaller normalized valve prostheses failed more rapidly (p < 0.0001): only 32.1% ± 13.0% were still functioning at 24 months. Almost all of the larger grafts retained their function for the first 4 years, and 73.7% ± 10.4% had not failed at 10 years.

View larger version (19K): [in this window] [in a new window]   Fig 2. Probabilities of freedom from failure according to normalized homograft size over time. It is 64.3% ± 12.8%, 32.1% ± 13.0%, 24.1% ± 12.0%, and 24.1% ± 12.0% at 1, 3, 5, and 10 years for the z < 2 grafts, and 98.1% ± 1.9%, 95.5% ± 3.2%, 86.7% ± 6.6%, and 73.7% ± 10.4% for the z 2 grafts at the same time intervals. Vertical bars represent SEM. The difference is highly significant.

Homograft dysfunction
Fifty-two survivors have their original homografts. In sixteen of them, the trans-homograft peak pressure gradient is higher than 50 mm Hg, and four have grade III homograft insufficiency. In three cases the insufficiency is associated with significant obstruction; in the fourth case, the valve had been mechanically dilated 28 months earlier. Two of these four patients are scheduled for conduit replacement. One child with RVOT obstruction collapsed while playing at school 4 days before admission for surgery. He was resuscitated but suffered severe cerebral impairment so that conduit exchange was abandoned. Two children underwent interventional dilatation of the right and left pulmonary artery with stent insertion.

The estimate for freedom from significant dysfunction for all grafts including those that failed is shown in Figure 3; progressive deterioration occurred over years, with 66 months as a median interval. As evidenced in Figure 4, the smaller normalized allografts deteriorated more rapidly (p < 0.0001), with 50% showing significant dysfunction at 16 months. In contrast, 50% of the larger grafts had satisfactory function at 89 months.

View larger version (17K): [in this window] [in a new window]   Fig 3. Probabilities of freedom from homograft dysfunction for all grafts over time. The dashed lines indicate the standard error of the mean (S.E.M.).

View larger version (18K): [in this window] [in a new window]   Fig 4. Probabilities of freedom from homograft dysfunction according to normalized homograft size over time. It is 57.4% ± 13.2%, 32.8% ± 13.1%, 8.2% ± 7.8%, and 0% at 1, 3, 5, and 10 years for the z < 2 grafts, and 96.0% ± 2.8%, 93.8% ± 3.4%, 64.8% ± 8.2%, and 15.7% ± 12.3% for the z 2 grafts at the same time intervals. The dashed lines indicate the standard error of the mean. The difference is highly significant.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

Outcomes taking into consideration homograft z-values have recently been published by Caldarone and associates [8] and Tweddell and coauthors [9], the latter authors being the first to indicate a z-value less than 2 as a risk factor for homograft failure and dysfunction. Their work reports probabilities of freedom from failure (homograft explantation or late death) of 92%, 60%, and 31% at 1, 5, and 10 years, respectively, for grafts with a z-value less than 2, and of 98%, 86%, and 66% for those with a z-value of at least 2 at the same time intervals (estimated from the published graph).

In our study, after normalizing homograft size to the patient’s body surface area, we found that the great majority of the 8 to 9 mm homografts had a z-score less than 2 and that almost all of the 11 to 13 mm grafts had a z-value of at least 2. The 10-mm grafts seem to constitute a transitional group where about 50% scored either above or below 2 (see Table 2). Studies that mix all small conduits may thus give contradictory results.

The discrepancies in the literature may also be explained by differing definitions of valve failure and differing indications for replacement. Some authors (eg [8]) do not include late death as a valve failure, even if a mild conduit dysfunction may have contributed to clinical deterioration. Whereas florid infection of the valve dictates quick reintervention, there are various thresholds for replacement of a progressively dysfunctional prosthesis. We, like others [10, 11], consider that the conduit should be replaced if the right ventricular pressure approaches the systemic pressure, regardless of the clinical status of the patient. Indeed, most of these patients are in functional New York Heart Association class I, despite severe RVOT obstruction. A waiting policy in such circumstances carries the potential for acute right ventricular failure, as experienced in one of our patients. Reoperation is indicated whenever low right ventricular pressure occurs in the presence of deteriorating right ventricular function or significant tricuspid regurgitation. It must also be considered if cardiac rhythm disturbances occur. Interventional dilatation and stenting has emerged as an occasionally effective technique for reopening the conduit, thereby delaying the need for reoperation [12, 13]. Two of our patients benefited from this procedure. It is important to note, however, that most degraded or outgrown small allografts are not suitable for dilatation.

The difference in quality of homografts supplied by tissue banks is an additional factor in varied middle and long-term outcomes. The single institution that provided conduits with a z-value of at least 2 that did not fail until 135 months generally obtains valves from cadavers. Such grafts are unlikely to contain viable cells and therefore would provoke less host immunological response. As noted by Stark and colleagues [6], if homografts are harvested at the time of heart transplantation, and the time between harvest and preservation is very short, it is possible that immunological factors will play a role.

In the present era, freshly antibiotic-sterilized or cryopreserved small homografts constitute, in many centers, the preferred conduits for right ventricle to pulmonary artery application in the neonate. Because of increasing shortage, our "ideal" conduit size (1.5 times the normal expected diameter of the pulmonary artery: z-value 3.1 to 3.8) could be realized in only 20% (15 of 76) of all cases. The largest homograft we implanted had a z-score of 5.2 in a neonate weighing 2.3 kg who had truncus arteriosus and received a 13-mm prosthesis. Although some authors [14] advocate the use of large conduits, their implantation certainly demands a longer right ventriculotomy, which could lead to increased right ventricular dysfunction and, possibly increased morbidity and mortality. In our series, the freedom from failure for the oversized (z at least 2) allografts, ie, the 11 to 13 mm grafts, at 10 years after implantation matches the durability for those 18 mm or larger implanted in older patients reported by Homann and associates [5]. Outgrowth seems to be the only reason for their explantation. In contrast, time to failure is short for conduits with a z-score less than 2 (generally the 8 to 9 mm grafts), corresponding to the limited longevity usually assigned to homografts implanted during infancy [7, 9, 11, 15].

Limitations of this study
This study carries the usual drawbacks of a retrospective study conducted over a long period (13 years). There was some variability with regard to indications for homograft use and homograft replacement. Shortages compelled us to use smaller or bigger homografts than the preferred size and, moreover, to diversify graft suppliers. As a consequence, some variables related to the homografts cannot be analyzed adequately. The echo-Doppler evaluation of dysfunction is not precise enough: pressure gradients are usually overestimated and quantification of valvular regurgitation varies from investigator to investigator. Time at which significant dysfunction was diagnosed depended on the periodicity of the follow-up. We did not obtain histological data for the explanted homografts.

Despite these limitations, there is evidence to support the findings that small homografts scoring a z-value from 2 to 5.2 (practically all of the 11 to 13 mm grafts) enjoy longer durability.

Conclusion
Small homograft valves enable the surgeon to perform early and complete repair of cardiac malformations that require RVOT reconstruction and offer the best chance for survival and improved quality of life. Reoperation is inevitable as the child grows, usually in the first 2 to 3 years for the very small (z-value less than 2) 8 to 9 mm grafts, and much later for the bigger (z-value at least 2) 11 to 13 mm grafts. The 11 to 13 mm homografts, whether aortic or pulmonary, constitute the best valved conduits in the pulmonary position for neonates and young infants.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

1. Rowlatt U.F., Rimoldi H.J.A., Lev M. The quantitative anatomy of the normal child’s heart. Pediatr Clin North Am 1963;10:499-588.
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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Anne Marie Brecher Andreas E. Urban Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sinzobahamvya, N. Articles by Urban, A. E. Search for Related Content PubMed PubMed Citation Articles by Sinzobahamvya, N. Articles by Urban, A. E. Related Collections Congenital - cyanotic Related Article