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Ann Thorac Surg 2004;78:2076-2083
© 2004 The Society of Thoracic Surgeons
a Sunnybrook and Women's College Health Sciences Center, University of Toronto, Toronto, Ontario, Canada
Accepted for publication May 19, 2004.
* Address reprint requests to Dr Christakis, Sunnybrook Health Science Centre, 2075 Bayview Ave, Suite H-406, Toronto, ONM4N 3M5 Canada
george.christakis{at}sw.ca
Presented at the Fortieth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 26–28, 2004.
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Abstract |
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METHODS: Between 1992 and 2000, 200 patients (131 males, 69 females) underwent aortic valve replacement with the Toronto SPV. Mean patient age at implantation was 64.6 ± 10.9 years (range 33 to 82 years). At the time of operation, 32%, 51%, and 17% of patients were in New York Heart Association class I/II, III, and IV, respectively. Aortic stenosis, aortic insufficiency, and combined lesions were present in 64%, 13.5%, and 22.5% of patients preoperatively. Concomitant coronary artery bypass grafting was performed in 34.5% of patients.
RESULTS: Perioperative mortality occurred in 2.5% (5/200) of patients. There were 31 late deaths. Actuarial survival at 5 and 10 years was 89.2% and 68.0%, respectively. There was no significant difference in overall actuarial survival between isolated valve patients and valve plus coronary artery bypass grafting patients, 71% versus 62% respectively, p = 0.85. Actuarial freedom from valve reoperation at 5 and 10 years was 97.6% and 79.9%, respectively. Actuarial freedom from structural valve deterioration was 98.8% at 5 years and declined to 77.9% at 10 years. Freedom from structural valve deterioration was poorer in patients with preoperative aortic insufficiency or bicuspid disease. Actuarial freedom from embolic events and endocarditis at 10 years were 94.6% and 95.9%, respectively.
CONCLUSIONS: Although early clinical results were excellent, a significant increase in hazard for structural valve deterioration occurred in late follow-up.
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Introduction |
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Patients and Methods |
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| Dr Goldman discloses that he has a financial relationship with St. Jude.
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Between March 1992 and July 2000, 201 Toronto SPV aortic prostheses were implanted into 200 patients at the study institution. Eighty-four of these 200 patients were entered into a multicenter Food and Drug Administration (FDA) study [6]. An additional 34 patients were enrolled as part of a randomized clinical trial comparing stented and stentless bioprostheses [2]. In general, patients were selected for Toronto SPV implantation if they had preserved left ventricular function and were typically elective and deemed to be low risk for perioperative morbidity.
Operative Technique
The Toronto SPV was implanted in the subcoronary position. Details of the insertion technique have been previously reported by our group [7].
Clinical Assessment
Clinical assessment of patients was performed using a standardized clinical interview or telephone questionnaire designed to assess mortality, current cardiac medications, recurrent cardiac events, hospital and outpatient visits, repeat valve operation, and New York Heart Association functional status [8]. The study protocol was approved by the institutional Review Ethics Committee and consent was obtained from patients to participate in the study before administration the study questionnaire. In total, four patients (2%) were lost to long-tem follow-up during the closing interval of April to November 2003.
Definitions and Statistical Methods
Fatal and nonfatal valve outcomes are reported according to the revised consensus guidelines adopted from the Ad Hoc Liason Committee of the Society of Thoracic Surgeons(STS) and the American Association of Thoracic Surgeons(AATS) [9]. Valve-related mortality was defined as all deaths caused by structural valve deterioration, nonstructural valve dysfunction, valve thrombosis, embolism, bleeding event, operated valvular endocarditis, or death related to reoperation of an operated valve. Valve-related morbidity was defined as all nonfatal morbidity from thromboembolic events, operated valvular endocarditis, nonstructural valve dysfunction, bleeding events and structural valve deterioration.
Survival and time-related event analysis was performed using nonparametric actuarial methods. Between groups comparison of actuarial analyses was performed using the log rank test.
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Results |
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Among bicuspid valve patients, mean age at time of operation was 59.3 ± 12.7 years, compared with 65.6 ± 10.4 years for patients with tricuspid valves. Preoperative hemodynamic lesions in bicuspid patients included pure stenosis in 67%, pure insufficiency in 18%, and mixed lesions in 15%.
Operative Data
Toronto SPV valves were implanted by 4 surgeons at the study institution. The distribution of prosthesis sizes in presented in Table 2. Mean cardiopulmonary bypass time was 150.5 ± 33.1 minutes and mean cross-clamp time was 125.0 ± 25.6 minutes. Concomitant coronary artery bypass grafting (CABG) was performed in 34.5% (69/200) of patients. Other concomitant procedures included atrial septal defect repair in 1 patient, ascending aortic replacement in 3 patients, and mitral valve repair in 1 patient.
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Survival
Mean follow-up time was 69.5 ± 32.7 months (median 69.4 months, range 0 to 140 months) for a total of 1,158 years of patient follow-up. Five perioperative deaths (2.5%) occurred either during initial hospitalization or less than 30 days after the operation. There were 31 late deaths (15%). Actuarial survival at 5 and 10 years was 89.2% and 68.0%, respectively (Fig 1).
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Late Death
Valve-related mortality occurred in 10 patients in this study at a mean of 61.9 ± 48 months after operation (range 1 to 140 months). Causes of late death are listed in Table 3. Actuarial freedom from valve-related mortality at 5 and 10 years was 97.2% and 89.3%, respectively (data not shown).
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VALVE THROMBOSIS
Valve thrombosis, verified at autopsy, occurred in 1 patient with a 25-mm Toronto SPV at 1 month after implantation. The etiology of this thrombosis was unknown and the patient's initial valve pathology was bicuspid. There was no history of endocarditis.
OPERATED VALVULAR ENDOCARDITIS
Bacterial endocarditis occurred in 5 patients at a mean follow-up time of 46.4 ± 32.1 month (range 7 to 85 months). There were two deaths from bacterial endocarditis before reoperation and three reoperations. Actuarial freedom from bacterial endocarditis was 98.3% and 95.9% at 5 and 10 years, respectively.
LATE NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION
Twenty-three patients experienced NYHA class III or IV symptoms after the operation. Actuarial freedom from NYHA class III or IV symptoms at 5 and 10 years was 96% and 68%, respectively (data not shown). At last follow-up, 8 patients (4%) were alive, had retained their original prosthesis, and were experiencing NYHA class III or IV symptoms.
Valve-Related Morbidity and Mortality
Valve-related morbidity and mortality occurred in 27 patients. Actuarial freedom from valve-related morbidity and mortality was 95.6% and 68.0% at 5 and 10 years, respectively (Fig 7).
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Comment |
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The Toronto SPV stentless valve was developed to take advantage of the physiologic nature of homograft valves with a more standardized method of implantation. The subcoronary placement of this valve is believed to enable adaptation to the patient's own aortic root, thereby reproducing a normal valve–root complex. Clinical studies have shown residual transvalvular gradients similar to native valves and superior to stented valves at early to midterm follow-up [1]. Exercise gradients were also superior with the SPV at midterm follow-up indicating the valve may perform better under physiologic stresses than stented valves [10]. Despite these potential advantages, small, randomized controlled trials have not shown improved survival or left ventricular mass regression at intermediate follow-up [2–4]. The major remaining potential advantage of this valve is long-term durability.
The patient population in this study was predominantly lower risk with a mean age of 64.6 ± 10.9 years and 91.5% freedom from moderate-to-severe left ventricular dysfunction (EF < 0.40) at the time of operation. Patients with enlarged aortic roots at the time of operation were generally excluded from receiving a stentless prosthesis. Similar to previous reports, mean cross-clamp and pump times were longer than usually required for stented aortic valve implantation [2, 11]. Despite the added complexity of the implantation procedure, overall operative mortality in this population was only 2.5%.
The estimated 10-year survival in this cohort of patients was 68% by actuarial analysis. Previous studies during the same time period in patients with similar age at time of operation have reported 10-year survival between 54% and 67% for patients receiving the Carpentier-Edwards pericardial prosthesis and between 61% and 69% for the Hancock II prosthesis [12–15]. Although previous studies have shown concomitant CABG decreases long-term survival after AVR with a stented prosthesis, in this study, survival between groups was similar [8]. The mortality effect of concomitant CABG may become more pronounced with longer-term follow-up as the competing risks of death from coronary disease progression and valve failure increase.
In the current study, the freedom from SVD was 98.8% and 77.9% at 5 and 10 years, respectively. Ten-year follow-up data of the Toronto SPV has not been reported previously. Intermediate follow-up data on 255 Toronto SPV valves showed freedom from SVD was 100% at 5 years [16]. A six-center evaluation of 447 Toronto SPV patients, including 84 patients from this center, reported 5-year freedom from SVD of 96.1% [17]. By comparison, freedom from SVD for the Medtronic Hancock II stented aortic prosthesis has been estimated to be between 97% and 100% at 10 years [14, 15]. Freedom from SVD for the Carpentier-Edwards pericardial prosthesis ranges from to 86% and 91% at 10 years [12, 13].
In the current study, most cases of SVD led to reoperation with valve explant. Overall freedom from reoperation was 79.7% at 10 years. Ten-year estimated freedom from reoperation ranges from 88% to 91% for the Carpentier-Edwards pericardial prosthesis and is reported at 94% for the Hancock II prosthesis [12–15]. In three cases, severely symptomatic patients with SVD were too unstable to tolerate reoperation and died. It appears that while intermediate follow-up of the Toronto SPV was excellent, 10-year freedom from SVD may be inferior to stented prostheses.
It is important to note that SVD was diagnosed only if there was reoperation or mortality due to a malfunctioning prosthesis. The true incidence of SVD is likely even higher than estimated and, currently, 2 additional patients are experiencing NYHA class III or IV symptoms with a stenotic prosthesis in the one case and AI in the second case.
Progressive AI led to SVD requiring reoperation in 8 patients and mortality in an additional 2 patients. Echocardiographic analysis of these valves showed dilatation of the sinotubular junction (STJ) or aortic root causing AI. David and colleagues [18] previously reported similar dilatation of the STJ in patients with at least 1+ AI but not in patients with trivial or no AI. In the current study, the relationship between preoperative AI and postoperative progressive STJ dilatation was also observed. Ten-year freedom from SVD and valve reoperation was only 60.9% and 63.9%, respectively, in patients with at least 1+ AI compared with 91.8% and 92.3% in patients without AI. Six patients had leaflet tears or flail leaflets. Previous authors have suggested that glutaraldehyde fixation of the valve cusps of the Toronto SPV renders them too inelastic to accommodate circumferential strength, causing them to tear away from their porcine aortic wall attachments in the face of sinotubular dilatation [18]. In this series, 3 of 6 patients with leaflet tears did not have significant aortic root or STJ dilatation, but had mild calcification and degenerative changes. Labeled valve sizes in this study were large, with 60% of implanted valves larger than 27 mm. However, previous work from our institution has shown that the label size of the Toronto SPV greatly overestimates true internal diameter in comparison with other stented prostheses [19].
We also analyzed valve performance by preoperative valve pathology. Patients with bicuspid disease were at substantially higher risk for developing progressive root/STJ dilatation with eventual prosthesis failure. Ten-year actuarial freedom from SVD was 68.8% for patients with bicuspid native valves and 79.5% for patients with tricuspid native aortic valves (p = 0.03). This relationship appears biologically plausible given recent evidence that patients with congenitally bicuspid valve have changes to the extracellular matrix including increased smooth muscle cell apoptosis and deficiency of fibrillin-1 [20, 21].
Several methods have been suggested to prevent dilatation of the STJ including implantation of a stentless valve as a full or inclusion root, or prophylactic banding of the STJ with a nondistensible Dacron graft [18, 22]. The Medtronic Freestyle Stentless valve and the St. Jude Toronto SPV root can be implanted as a full root instead of in the subcoronary position. Full-root implantation may maximize the hemodynamic advantages of stentless valves but has been shown to increase perioperative mortality [22]. The results of STJ banding have not yet been reported.
Studies have suggested that degenerative calcification of the Toronto SPV is extremely uncommon in early and mid-term follow-up [23]. However, degenerative changes may be more common than previously reported. To date, a total of 3 patients including one reoperation and two deaths have experienced SVD due to progressive stenosis from degenerative calcification and leaflet restriction. Severe calcification has also occurred in 1 patient with progressive heart failure symptoms who has not yet undergone reoperation. This calcific degeneration may be due, in part, to the fixation methods of the leaflets of this valve. The Toronto SPV is low-pressure fixed in glutaraldehyde. Previous studies on porcine tissue have shown that low-pressure fixation causes significant loss of transverse cuspal ridges and collagen crimp [24]. In addition, the Toronto SPV is not treated with any antimineralization technique, which may also increase the risk of calcific degeneration. In vivo experiments implanting leaflet tissue subcutaneously in rats showed the Toronto SPV had increased calcification compared with other prosthetic valve tissue [25].
This study summarizes a single institutional experience with the Toronto SPV stentless aortic prosthesis. Our data suggest that at 10 years, patients with the Toronto SPV had increased SVD and need for reoperation than previous reports from stented prostheses in similar patients. Small sample sizes and relatively high event rates in the later years of the study may have overestimated the true rate of SVD. Although many cases of SVD occurred due to dilatation of the STJ, particularly in patients with preoperative AI or bicuspid valve pathology, calcific degeneration was not uncommon. In patients without preoperative AI, freedom from SVD and reoperation were similar to stented prostheses.
Because sample sizes were relatively smaller in the later years of the study, comparison between patients with or without AI as an indication for operation should be interpreted with caution. Further hemodynamic follow-up including measurement of exercise gradients is warranted to assess fully whether the Toronto SPV provides functional benefit over the long-term. In the interim, subcoronary implantation of the Toronto SPV in patients with preoperative AI or bicuspid disease should be avoided.
Discussion
DR ELLIS JONES (Atlanta, GA): Since publication of the Framingham Heart Study in 1990 demonstrating the adverse prognostic significance of increased left ventricular mass by echocardiography, failure to reduce ventricular mass has been proffered to explain poorer survival than would be anticipated in patients undergoing aortic valve replacement. In 1988, David proposed the concept of the stentless prosthesis to improve left ventricular hemodynamics and also to reduce leaflet stress and structural valve deterioration to improve long-term valve survival.
Unfortunately, in the haste to answer the question of whether for comparable bioprosthesis size—and I stress "comparable" size—the stentless valve offers superiority in hemodynamic function or improved durability and better patient survival to justify implantation of this valve, previously published series have reached differing conclusions for reasons which are not readily apparent. A homogeneous series of isolated valve replacement free of coronary disease, valve sizes that are representative of patients without genetic diseases of the aortic root and more similar to sizes that we use clinically every day, and also studies with long mean follow-up would do much to clarify some of these questions.
The study presented by Dr Desai and his associates is both interesting and important. I appreciate the opportunity to have had prior access to this article. First, patients selected for this series were excellent: they were of reasonable age, had good left ventricular function, and operation was mostly elective. Unfortunately, like almost all previously reported series on valve evaluation, more than one third of the patients presented today had significant coronary artery disease and only 70% had isolated aortic valve replacement. In a true 10- to 15-year study, a study that would be categorized as long-term, many patients may die of their coronary disease or stroke before structural valve deterioration becomes manifest and the data are skewed.
The work presented today should not be offered as a long-term follow-up to the Toronto stentless valve. The mean follow-up was less than 6 years, and only 9 patients were available for analysis by the tenth year, again, factors that might skew data. However, to the authors' credit, they noted that an incidence of both structural valve deterioration and reoperation in 20% of patients at the end of 10 years is worrisome, as are their findings that preoperative aortic insufficiency and bicuspid aortic valve disease appeared to be predictors of intermediate-term failure.
Although you stressed this in your closing remarks, would you please elaborate on the methods of valve failure such as flail leaflet, endocarditis, sinotubular dilatation, with particular reference to technical factors such as sizing problems—you mentioned the learning curve—or valve fabrication factors, which could have been important in the results.
Also, does the fact that 83% of the patients had insertion of a 25-mm or larger prosthesis reflect some propensity toward future enlargement of the aortic root, thus dooming the operation from its onset? I, among others, had great hopes that the stentless prosthesis, even though having a more lengthy and complex insertion profile, would be the next logical step to a 20-year biological valve. I hope studies already in progress by many centers will offer better results than those presented here today.
I hope that improved manufacturing techniques, which the author has alluded to, such as zero pressure fixation and anticalcification, will enhance stentless valve survival. The authors are to be commended on bringing these important findings to our attention today. Thank you.
DR DESAI: Thank you for your comments Dr Jones. In response to your question regarding the causes of structural valve deterioration, there were 12 instances of structural valve deterioration. Of these, six were due to leaflet tears. These were instances in which the leaflet had either pulled off of the aortic wall at the commissure or were actually torn in the main body of the leaflet itself. In half of these cases of leaflet tears, the tear occurred in the presence of severe dilatation of the aortic root or sinotubular junction. In these situations the leaflet may have pulled off of the commissure due to expansion of the root. Alternatively, the root may have expanded because the leaflets were no longer intact, although we are not yet sure which method is the true cause. In three cases of leaflet tears, mild degenerative calcification was noted without significant root dilatation. There were also three instances of severe valvular calcific stenosis similar to what we see in other bioprosthetic valves. Additionally, there were three instances of pure dilatation of the sinotubular junction in which the leaflets failed to coapt but were not torn.
In reference to our implantation technique, although there was an interest in oversizing these valves initially when we started implanting them, we soon learned that this tactic may not have led to good leaflet coaptation, and we changed our practice early on in our use of this valve.
The large valve sizes that I mentioned, most of which were larger than 25 mm, were in fact the labeled valve sizes as opposed to the measured valve sizes. We presented a paper previously that demonstrated that the labeled valve size of the Toronto SPV is in fact several millimeters larger than the actual measured size of the internal diameter of that valve, making comparison with other prostheses inaccurate.
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References |
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TopAbstractIntroductionPatients and MethodsResultsCommentReferences |
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