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Ann Thorac Surg 2000;70:1953-1957
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

Risk factors for late pulmonary homograft stenosis after the Ross procedure

^a Divisions of Cardiovascular Surgery and Cardiology, Toronto General Hospital, University Health Network, Departments of Surgery and Medicine, University of Toronto, Toronto, Ontario, Canada

Address reprint requests to Dr Yau, 13EN-239, Toronto General Hospital, 200 Elizabeth St, Toronto, ON, M5G 2C4, Canada
e-mail: terry.yau{at}utoronto.ca

Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

	Abstract

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
Background. We reviewed our experience with the Ross procedure to identify the prevalence and predictors of late pulmonary homograft stenosis.

Methods. Between June 1992 and December 1997, 109 consecutive patients (age 34.5 ± 8.6 years) underwent the Ross procedure, with reconstruction of the right ventricular outflow tract with a cryopreserved pulmonary homograft (22 to 30 mm diameter). There was one early and one late death. Echocardiographic follow-up was available in 105 of 108 patients (97%), with a follow-up of 39 ± 20 months. Homograft donor and preservation measurements and patient variables were subjected to multivariable analyses to identify independent predictors of late homograft performance.

Results. The major physiopathologic finding was homograft stenosis. Peak systolic gradients across the homograft were 20 mm Hg or more in 30 of 105 patients (28.5%) and 40 mm Hg or more in 4 of 105 patients (3.8%). One patient required two re-replacements of her homograft for severe stenosis. Moderate or severe homograft insufficiency was noted in 10 of 105 patients (9.5%). The independent predictors of late pulmonary homograft stenosis were younger donor age (p = 0.03), shorter duration of cryopreservation (p = 0.01), and smaller homograft size (p = 0.06). Beating heart donor status, short homograft ischemic time, and other factors that have been shown to be associated with increased graft viability were associated with graft stenosis but did not reach statistical significance. However, mean gradients across the homograft were significantly related (p = 0.002) to the number of these risk factors in each patient.

Conclusions. Stenosis of the pulmonary homograft can be a significant problem following the Ross procedure, and was predicted by younger donor age and shorter duration of cryopreservation. These factors may be related to increased cellular viability, which might actually predispose to late homograft stenosis in a subgroup of patients.

	Introduction

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
Cryopreserved homograft valve conduits have been used extensively to reconstruct the right ventricular outflow tract (RVOT) in patients with a wide variety of congenital cardiac defects. Mid- and long-term follow-up studies have shown, however, a significant rate of homograft valve degeneration and calcification [1, 2].

The Ross procedure entails replacing the transplanted pulmonary valve with a valved homograft conduit to reestablish right ventricular–pulmonary artery continuity. Most of these homografts are cryopreserved, a process that results in variable degrees of donor cell viability [3–5]. The clinical significance of this donor cell viability, however, has yet to be established and remains highly controversial.

The long-term function of these cryopreserved homograft conduits may predict late morbidity and the need for reoperation in these patients. Ward and colleagues [6] previously reported that pulmonary homografts implanted into children during a Ross procedure undergo significant annular reduction within 1 year of implantation.

The prevalence and predictors of late pulmonary homograft stenosis after the Ross procedure in adults, however, are still unclear. In particular, the effects of factors that may relate to donor cell viability within the homograft on pulmonary stenosis have not been determined. Factors that have been shown previously to increase homograft cellular viability include younger donor age, a beating heart donor, short warm and cold ischemic times, and avoidance of amphotericin [3, 4, 7–10]. In this study, we reviewed the midterm results of reconstruction of the RVOT with cryopreserved homografts in adults undergoing the Ross procedure. Preservation as well as donor and recipient measurements were collected and multivariable analyses were carried out to identify independent predictors of late homograft performance.

	Patients and methods

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
Patients
Between June 1992 and December 1997, 109 consecutive patients underwent the Ross procedure. The mean age at operation was 35 ± 9 years (range, 17 to 56 years). There were 70 men (64%) and 39 women. Twenty patients (18%) were in New York Heart Association class III or IV, 73 (67%) were in class II, and the rest were in class I. The pathology of the aortic valve was bicuspid aortic valve in most of the patients (71%), with the remainder having other congenital abnormalities (10%), rheumatic disease (3%), incompetence of a tricuspid aortic valve (8%), or dysfunction of a previously placed prosthetic valve (8%).

Operative considerations
The RVOT was reconstructed with a cryopreserved pulmonary valve homograft in all patients. The mean difference between homograft size and the pulmonary annulus, measured directly during the operation, was 2.5 ± 2.1 mm, indicating a tendency to oversize the homograft. Only 2 patients (1.8%) had a homograft sized 2 mm smaller than the pulmonary valve annulus. The mean homograft diameter was 26.9 mm (range, 22 to 30 mm). The mean diameter of the recipient pulmonary annulus was 24.2 mm (range, 19 to 27 mm). The homograft was secured to the pulmonary artery and pulmonary annulus in an end-to-end fashion with a continuous 4-0 polypropylene suture.

Homograft donor and preservation measurements
Fifty-two homografts (48%) were supplied by Cryolife (Cryolife, Marietta, Georgia), and 57 (52%) from the tissue and stem cell laboratory of the Hospital for Sick Children (Toronto, Canada).

Homograft donor and preservation values were collected from the databases of the homograft banks, and are presented in Table 1. Homograft warm ischemic time was defined as the time from asystole to heart procurement. Cold ischemic time was defined as the time from heart procurement to valve dissection and placement in antibiotic solution.

Measurements were performed in the parasternal short axis plane during diastole and included:

1. The quality and mobility of homograft valve leaflets.
   
2. Peak instantaneous Doppler velocity across the RVOT using pulsed and continuous wave Doppler techniques. The peak pressure gradient was calculated using the simplified Bernoulli equation (gradient = 4 x peak velocity [2].
   
3. The location of any obstruction.
   
4. The diameters of the homograft valve annulus, and of the graft 2 cm above the annulus.
   
5. The degree of pulmonary regurgitation.
   

Data analysis
Homograft donor and preservation measurements and patient variables were subjected to univariate and multivariable analyses using SAS statistical analysis software (SAS, Cary, NC) to identify the independent predictors of late homograft performance. Univariate analysis of categorical data was carried out with -square or Fisher’s exact test. Univariate analysis of continuous variables was carried out with analysis of variance or Student’s t test.

	Results

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
Early outcomes
There was one early death, for a hospital mortality of 0.9%. Other perioperative complications included low-output syndrome in 3 patients with documented myocardial infarction in 2 of them, a transient ischemic cerebral attack in 1 patient, and reexploration for bleeding in 3 patients. No wound infection or sepsis developed in any patient.

Homograft stenosis and regurgitation
Peak Doppler gradients across the homograft increased from 5.9 ± 6.7 mm Hg 1 week postoperatively to 14.5 ± 11 mm Hg during follow-up (p < 0.001). Late peak Doppler gradients across the homograft were 20 mm Hg or higher in 30 of 105 patients (29%) and 40 mm Hg or higher in 4 of 105 patients (3.8%) (Fig 1). The obstruction was usually located at all levels of the homograft, and was associated with calcification of the conduit and thickening of the valve leaflets. One patient required 2 re-replacements of her homograft for recurrent severe pulmonary stenosis.

View larger version (28K): [in this window] [in a new window]   Fig 1. Early and late postoperative gradients across the pulmonary homograft in 105 patients undergoing the Ross procedure. No Doppler gradient across the homograft was noted in any patient 1 week postoperatively, but late peak Doppler gradients were 20 mm Hg or more in 30 of 105 patients (29%) and 40 mm Hg or more in 4 of 105 patients (3.8%).

Predictors of late homograft stenosis
The independent predictors of late pulmonary homograft stenosis were younger donor age (p = 0.03), shorter duration of cryopreservation (p = 0.01), and smaller homograft size (p = 0.06) (Table 2). Beating heart donor status was a univariate predictor of late homograft stenosis, but this association was no longer significant in the multivariable analysis (Table 2 and Fig 2). Within the time frame of our study, the duration of echocardiographic follow-up did not emerge as a predictor of late homograft stenosis (p = 0.63), nor did younger recipient age or the difference in size between the homograft and the diameter of the recipient pulmonary annulus.

View larger version (26K): [in this window] [in a new window]   Fig 2. Univariate relationship of risk factors previously associated with increased homograft viability on mean gradients across the pulmonary homograft. Younger donor age (p = 0.002), shorter length of cryopreservation (p = 0.02), and beating heart donor status (p = 0.059) were most significant, but all factors associated with greater viability demonstrated at least a trend toward increased gradients.

View larger version (17K): [in this window] [in a new window]   Fig 3. Effect of risk factors previously associated with increased homograft viability on late pulmonary homograft gradients. These putative risk factors included donor age less than 30 years, ABO mismatch, beating heart donor status, warm ischemic time less than 2 hours, amphotericin usage, and length of cryopreservation less than 20 months. Mean Doppler gradients across the pulmonary homograft increased from 6 ± 4 mm Hg in homografts with none of these risk factors to 26 ± 3 mm Hg in homografts with all six of these risk factors (p = 0.002).

	Comment

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

Although more recent series have not reported the late hemodynamic performance of the homograft, a number of researchers have previously noted significant reduction of annular diameters and the development of gradients across the conduit with time [6, 13]. Significant transvalvular gradients developed within 1 year of operation, and were thought to represent a consequence of an immune-mediated response to the homograft. Our current study has demonstrated a similar tendency to late homograft stenosis in 105 patients, at a mean follow-up period of 39 ± 20 months. Peak Doppler gradients across the homograft were 20 mm Hg or higher in 29% of patients and 40 mm Hg or higher in 4% (Fig 1). In contrast to Ward and colleagues [6], who found the obstruction to occur mainly in the supravalvar region, and Moidl and coworkers [13], who reported the stenosis to be at the level of the valve leaflets, we found that the obstruction was usually located at all levels of the homograft. This homograft stenosis was associated with calcification of the conduit and thickening of the valve leaflets.

Current strategies aimed at maximizing donor cell viability within homografts are based on the presumption that greater cellular viability is the key to improved late homograft performance and durability [14, 15]. It is hypothesized that the surviving donor fibroblasts may maintain homograft integrity by continued synthesis and remodeling of the extracellular matrix [16]. However, the previous belief that homografts are immunologically privileged has now been challenged repeatedly. Valvular endothelial cells have been shown to express major histocompatibility complex class I and II molecules, and may therefore have significant antigenicity [17, 18]. Both Smith and Shaddy and colleagues [19, 20] reported that implanted homografts stimulate a strong donor human leukocyte antigen-specific antibody response in vivo. The clinical significance of this antibody response, however, remains to be clarified.

Several homograft donor and preservation variables have been related to reduced cellular viability, including greater donor age, long periods of warm and cold preimplantation ischemia, a nonbeating heart donor, and the use of amphotericin in the sterilization process [3, 4, 7–10]. We carried out univariate and multivariable analyses on these and other variables, to determine whether these indirect correlates of homograft cellular viability affected late hemodynamic performance. Younger donor age, a shorter duration of cryopreservation, and smaller homograft size independently predicted late homograft stenosis (Table 2). The expected effect of homograft size on late gradients would appear to support the current practice of oversizing the homograft by 2 to 3 mm.

The other homograft variables may have small incremental effects on homograft antigenicity and thereby affect late stenosis, but in a series of 109 patients, these multiple effects are difficult to elucidate (Table 2, Fig 2). We therefore examined the additive effects of six of these homograft donor or preservation variables. The prevalence of these putative risk factors within each patient was a significant predictor of the late transvalvular gradient (p = 0.002). Mean gradients were low in patients with none of these risk factors, but were more than quadrupled in patients with all of these risk factors (Fig 3). In the absence of preimplantation histology, however, this analysis is only indirect evidence of the effect of donor cell viability on homograft stenosis.

Further studies directly correlating homograft cellular viability, in vivo markers of homograft antigenicity, and late hemodynamic performance are required. If, in at least a subset of patients, increased donor cell viability actually results in greater homograft antigenicity and leads to accelerated graft failure, homografts may need to be human leukocyte antigen-matched to their potential recipients. Alternatively, complete decellularization and reseeding with the recipient’s endothelial cells may allow immunologic compatibility [21].

	Acknowledgments

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
We thank Mr Scott B. Capps (Director of Clinical Research, Cryolife Inc) and Mr Robert Romans (Resource Technologist, Tissue and Stem Cell Laboratory, Hospital for Sick Children, Toronto), for providing the homograft preservation data.

	Footnotes

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/section/atsdiscussion/

	Discussion

Top Footnotes Abstract Introduction Patients and methods Results Comment Acknowledgments Discussion References

 
DR JOSEPH E. BAVARIA (Philadelphia, PA): I was wondering what the "freedom from reoperation" was on the right side in your homograft series?

DR RAANANI: So far, only 1 patient has had two re-replacements of her homograft. We still have 4 other patients with high-grade systolic gradients who we are following closely to determine if they will need a reoperation at some point.

DR ENDRE BODNAR: (London, England): With due respect I slightly disagree with you. If there is anything particular about the pulmonary homograft in conjunction with the Ross procedure, it is that, as per definition, the homograft is implanted into normal anatomic conditions to supply a normal vascular bed under normal pressure conditions. In our experience in London, there were no problems with those homografts, though they were not viable. You may be right. You said that obstruction was at all levels of the graft. What do you mean by that? Is it not true that you had obstruction at the anastomosis and from that area and beyond, the pressure was high everywhere in the homograft?

DR RAANANI: I agree that the "nonviable" homografts may perform better at least in the short- to mid-term follow-up. Regarding the location of the gradient, using pulsed-wave Doppler we observed high velocities at all levels of the graft. Moreover, the echocardiogram demonstrated relative narrowing and wall thickening of the entire conduit. We concluded that the stenosis existed not just at the suture line but rather across the entire graft.

DR BODNAR: So what you are saying is that the pressure changed, that it got higher and higher along the conduit lengths?

DR RAANANI: Yes, the pressure was sustained or increased along the length of the conduit.

DR BODNAR: Does Dr David use continuously running sutures for the distal anastomosis?

DR RAANANI: He usually uses two running sutures.

DR BODNAR: Thank you.

DR GUS J. VLAHAKES (Boston, MA): When you begin to see a gradient evolving in a given patient, do your interventional cardiologists ever dilate or stent any of these homografts early to delay the need for further surgery?

DR RAANANI: Yes. Our cardiologists did initially stent the homograft of the patient that eventually had her homograft replaced and by that they postponed her homograft replacement.

DR AMRAM J. COHEN (Holon, Israel): I would like to congratulate you on an excellent presentation. My question is about the patient that had the two homografts replaced: Was there a difference in the age of the two homografts? Knowing that answer may reveal whether the homograft stenosis was patient specific?

DR RAANANI: Yes. Retrospectively we found that the homografts had three and four of those potential risk factors. We believe that the graft failure was homograft specific rather than patient specific.

DR S. BERTRAND LITWIN (Milwaukee, WI): We recently reported our own series of 220 right heart homograft replacements over a period of 15 years. These replacements were in patients with congenital heart disease and most were children. All of our grafts were cyropreserved, and in fact one of the risk factors for freedom from reoperation was long ischemia time of the graft. In addition, in that series I can recall only 1 patient in whom there was stenosis of the distal part of the graft, and I think that stenosis was because of a technical error. These results are in contrast to your findings, and I wonder if you have any explanation for the stenosis that you see along the major part of the grafts?

DR RAANANI: Your report and others consisted of children with congenital heart disease. Ours consisted of adults with a normal pulmonary vascular resistance and pulmonary artery tree. I would not hesitate to compare homograft performance in entirely different groups of patients.

	References

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This Article Abstract Full Text (PDF) Online Discussion 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): Terrence M. Yau Tirone E. David Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Raanani, E. Articles by Omran, A. Search for Related Content PubMed PubMed Citation Articles by Raanani, E. Articles by Omran, A.