Asian Cardiovasc Thorac Ann 2005;13:112-118
© 2005 Asia Publishing EXchange Ltd
Stentless vs. Stented Aortic Valve Replacement: Left Ventricular Mass Regression
Muhammed Tamim, FETCS,
Thierry Bové, MD,
Yves Van Belleghem, MD,
Katrien François, MD,
Yves Taeymans, PhD,
Guido J Van Nooten, PhD
Heart Centre, University Hospital of Ghent, Ghent, Belgium
For reprint information contact: Muhammed Tamim, FETCS Tel: 32 9 240 4700 Fax: 32 9 240 3882 Email: mttamim{at}yahoo.com, Cardiac Surgery Department, University Hospital Ghent, De Pintelaan, 185 5 K12, 9000 Ghent, Belgium.
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ABSTRACT
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The aim of this retrospective study was to evaluate the time-related regression of left ventricular hypertrophy after stentless vs. stented aortic valve replacement. From January 1992 to December 2002, 145 patients had a Toronto stentless porcine valve and 106 had a stented Carpentier-Edwards aortic valve replacement. Over a 10-year follow-up, survival was superior in the Toronto group vs. the Carpentier-Edwards group (84% vs. 74% at 4 years; 78% vs. 68% at 6 years; p < 0.001). A significant and constant reduction of peak and mean transvalvular gradients after valve replacement resulted in substantial regression of left ventricular mass index in both groups, which did not reach statistical significance. However, this phenomenon stopped at 3 years, and left ventricular mass index increased slowly after 5 years. Stentless and stented bioprostheses both showed good early and late clinical and hemodynamic outcomes, with the advantage of better midterm survival for stentless xenografts.
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INTRODUCTION
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Stented porcine valves have been widely used to replace diseased native cardiac valves. Limited durability due to progressive structural degeneration and occasionally imperfect hemodynamic performance have led to the search for different prostheses. The Toronto SPV bioprosthesis (St Jude Medical, Inc., St Paul, MN, USA), a stentless porcine valve, was designed to overcome both major drawbacks of the stent-mounted xenograft.1–2 In patients with aortic stenosis, left ventricular (LV) hypertrophy develops progressively to compensate for the chronic pressure overload. It has been shown that aortic valve replacement with a stentless prosthesis results in regression of LV mass in the early to midterm phase.3–4 This effect was more pronounced than that seen with stented valves in some series.5–6 The aim of this retrospective study was to evaluate early and late hemodynamic performance and LV mass regression after aortic valve replacement (AVR) with the Toronto bioprosthesis compared to the supraannular Carpentier-Edwards (C-E) aortic bioprosthesis (SAV 2650; Baxter, Inc., Irvine, CA, USA) over a 10-year period.
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PATIENTS AND METHODS
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From January 1992 to December 2002, 251 patients underwent AVR with a bioprosthesis at Ghent University Hospital. The Toronto valve was implanted in 145 patients, and the C-E porcine bioprosthesis was used in 106 patients. The mean age was 75.5 years (range, 40 to 88 years) in the Toronto group, and 75.9 years (range, 43 to 94 years) in the C-E group. The most important patient demographics are listed in Table 1
. These data matched in the two groups, except for gender: a larger number of patients in the Toronto group were female ( p = 0.02).
Standard cardiopulmonary bypass, including cold crystalloid cardioplegia and moderate hypothermia (28°C–32°C), was routinely used. Our technique of stentless valve implantation has been described previously.7 The stented C-E prosthesis was inserted in the conventional supraannular position with interrupted sutures. The size distribution of the implanted valves is shown in Figure 1. The mean valve size was 24.5 mm for the Toronto valve and 24.6 mm for the C-E prosthesis, for mean body surface areas of 1.74 ± 0.18 and 1.78 ± 0.2 m2, respectively. The main indications for the choice of a C-E valve, despite a stentless substitute, were a heavily calcified ascending aorta, dilatation of the sinotubular junction, and unfavorable coronary artery anatomy with opposing ostia. Mean cardiopulmonary bypass time was 125 ± 24.3 min (range, 68–205 min) for the Toronto group and 112 ± 26.3 min (range, 58–209 min) for the C-E group ( p = 0.0001). Mean aortic crossclamp time for isolated AVR in the Toronto group was 69.5 ± 14.3 min (range, 45–86 min) vs. 57.6 ± 17.1 min (range, 35–77 min) in the C-E group ( p = 0.001). The C-E valve was used more frequently in redo patients (10 vs. 2 in the Toronto group; p = 0.005). Coronary revascularization was carried out concomitantly in 67 patients (46%) in the Toronto group and in 57 (53%) in the C-E group ( p > 0.05).
Transthoracic echocardiography was performed in all patients periodically prior to hospital discharge, at 1 month, 6 months, and then yearly after AVR. Imaging (VIVID 7; General Electric Ltd., Vingmed, Norway) included two-dimensional and M-mode assessment and pulsed and continuous-wave spectral Doppler. Fractional shortening, LV end-diastolic and end-systolic diameters were measured in the apical 4-chamber view. Interventricular septal and LV posterior wall thicknesses were measured using the parasternal short-axis view. Mean and peak transvalvular gradients were calculated by the simplified Bernoulli equation. Left ventricular mass index (LVMI) to body surface area was calculated using the modified ASE cube method.8 Clinical, operative, and echocardiographic data were recorded in a computerized database. Additional information was obtained by reviewing the medical records and by contacting the patient’s general practitioner or family, as required. Follow-up was 100% complete in the Toronto group and 98% complete in the C-E group.
The data are presented according to the published guidelines for reporting valve-related morbidity and mortality.8 Statistical analysis was performed using SPSS 10.1 software (SPSS, Inc., Chicago, IL, USA). Absolute and relative frequencies were calculated and expressed as mean ± standard deviation. The 2-tailed Student t test and the chi-squared test were used for parametric and nonparametric data. Survival or event-free survival was analyzed using the Kaplan-Meier product-limit estimation. Univariate analysis of survival curves was performed by a log-rank test (Mantel). Multivariate analysis of survival was undertaken with Cox’s regression proportional hazards model. A value of p < 0.05 was considered statistically significant.
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RESULTS
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There were 7 (4.8%) early deaths in the Toronto group and 9 (8%) in the C-E group. In the Toronto group, 4 patients died from multiorgan failure secondary to combined heart failure and sepsis, 2 from respiratory problems, and 1 from massive gastric bleeding. In the C-E group, 4 patients died from sepsis, 2 from perioperative myocardial infarction, 2 from respiratory infection, and 1 from intractable intestinal bleeding. No statistically significant differences were found between the groups in the incidence of early thromboembolism, atrial fibrillation, endocarditis, and wound infections. Hospital stay was also similar (Table 2).
The mean follow-up was 56 months (range, 12 to 122 months; 1519 patient-years) for the Toronto group and 47 months (range, 12 to 136 months; 987 patient-years) for the C-E group yielding overall 2,606 patient-years. All patients, except those with bleeding diathesis or perioperative hemorrhagic complications, received an anticoagulant (acenocoumarol) for 3 months, with a target international normalized ratio of 2.0–3.0. There were 42(29%) late deaths in the Toronto group and 29 (29%) in the C-E group. None of the deaths was valve-related in the Toronto group, but one patient in the C-E group died 5 years after AVR, because of an acute cerebral thromboembolic event. Actuarial survival (Kaplan-Meier) at 4 to 6 years was in favor of the Toronto group ( p < 0.001) with a survival of 84% vs. 74% at 4 years and 78% vs. 68% at 6 years (Figure 2). Using univariate and multivariate analysis, the risk factors for late death were determined to be: presence of atrial fibrillation ( p = 0.0001), preoperative New York Heart Association functional class III-IV ( p = 0.0008), age > 80 years ( p = 0.0009), and the use of a C-E bioprosthesis ( p = 0.0241). Most survivors in both groups were in functional class I or II at the last follow-up. However, despite using antihypertensive treatment, 80 patients (55%) in the Toronto group and 50 (48%) in the C-E group had significant systolic hypertension (> 150 mm Hg) at their last visit.
There were 7 thromboembolic events in the Toronto group vs. 4 in the C-E group. The freedom from thromboembolic events at 2 and 5 years was 96% and 96% in the Toronto group and 94% and 93% in the C-E group ( p = 0.13). Bleeding occurred twice in each group due to excessive anticoagulation, but without major consequences. While prosthetic endocarditis did not arise in the Toronto group, 3 cases were detected in the C-E group: 2 were successfully treated with antibiotics, and one patient with endocarditis due to staphylococcus aureus in the 10th postoperative month required valve replacement. Reoperation was necessary in 3 patients with a Toronto prosthesis. One hypertensive patient had progressive enlargement of the ascending aorta resulting in significant aortic regurgitation 4 years after implantation of a 29-mm valve. At explantation, the valve was morphologically normal; it was replaced with a 27-mm mechanical valve. Two patients developed structural dysfunction 108 and 114 months after the first procedure. Both xenografts developed rupture of the noncoronary cusp with some calcification of the leaflets; the mean calcium content of the explanted cusps was low at 42 µg·mg–1 (range, 9–75 µg·mg–1). There were 3 late reoperations in the C-E group at 12, 84, and 96 months postoperatively: one for infective endocarditis, another for ascending aortic dilatation necessitating a Bentall procedure, and a third for primary prosthetic valve failure due to tissue degeneration.
Serial measurement of fractional shortening, LV end-diastolic and end-systolic diameters revealed equal but nonsignificant time-related improvements of LV function in both groups (Table 3). As expected, peak and mean transvalvular gradient decreased significantly in both groups ( p = 0.001) after valve replacement, but no statistically significant difference was noted between the stentless and stented valves ( p = 0.149, 0.151; Figures 3 and 4). This gradient reduction remained stable in both groups during the follow-up period. Parallel to the decrease in transvalvular gradient, septal and posterior wall thickness regressed rapidly after the operation in both groups, without reaching a statistically significant difference. However, a significant decrease in LVMI was found in both groups (p = 0.001), but without any advantage for either type of prosthesis (Figure 5). This LVMI regression slowed after 3 years, and thereafter tended to increase again, especially in the C-E group. Comparing the LVMI regression between hypertensive and normotensive patients, a similar trend was noticed for both groups (Figure 6). Overall, there was a positive correlation between the progressive rise in LVMI and a history of arterial hypertension, despite a still functioning aortic xenograft. Prosthetic valve regurgitation was mild in 14% and moderate in 8% of the stentless grafts, while in the C-E group, regurgitation was mild in 8% and moderate in 2% of the grafts ( p = 0.152). Particularly in the stentless group, valve incompetence remained stable over time, except for one patient with worsening aortic insufficiency due to aortic root dilation.
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Figure 6. Left ventricle mass index regression: hypertensive (HT) versus normotensive (NT) patients. Preop = preoperative.
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DISCUSSION
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Generally, replacement of a diseased, calcified, and obstructed valve by a functional prosthesis results in significant regression of LV hypertrophy and subsequent improvement of LV function, even when small-sized bioprostheses are used.9–11 However, the presence of a rigid and sometimes cumbersome stent to support the porcine valve can be responsible for higher transvalvular gradients, and thus an inferior hemodynamic result. This can adversely influence the long-term outcome. Based on the concept that the aortic wall itself offers the most suitable stent for the valve, David and colleagues1 introduced the stentless glutaraldehyde-preserved xenograft. Several studies have demonstrated the hemodynamic superiority of the Toronto valve compared to a stented prosthesis, with the additional benefit that often a larger graft size could be implanted.6,12 Moreover, rapid regression of LV hypertrophy early after the operation had a positive impact on survival after AVR with a stentless prosthesis.6,13 This study comprised a mainly elderly patient population over a 10-year time span. The groups were well matched but the Toronto group comprised significantly more women. It is generally known that older female patients are smaller, and consequently have a smaller aortic root. The stentless profile allowed implantation of prostheses with a size distribution comparable to stented valves, although there was no significant difference in body surface area between the patient populations.
Several series have revealed a survival benefit in favor of a stentless aortic valve, over a period of 5 to 8 years.12,14 This experience confirmed better survival after a stentless xenograft, but the survival gain gradually faded around the 10th year after AVR, probably due to the older age of both patient groups. It has been stated that improved survival after stentless AVR is a reflection of the superior hemodynamics, illustrated by rapid and complete LV mass regression, leading to enhanced ventricular function.5,12,15 Relief of LV outflow obstruction by a well-functioning porcine bioprosthesis, whether stentless or stented, inevitably leads to a decrease in LV wall thickness. The significant and immediate reduction of the transvalvular gradient enhanced ventricular remodeling and function, and was most marked during the first 6 months to 1 year, as noted by others.4–6,15 The observed changes tended to favor a stentless graft, although statistical significant was not reached. Recently, Cohen and colleagues16 published a prospective randomized trial comparing the Toronto valve with the Carpentier-Edwards pericardial valve in younger patients; they were unable to find any hemodynamic differences after one year of follow-up.16 On the other hand, Walther and colleagues5 found faster LV mass regression after stentless AVR. In our series, regression of LVMI was independent of the type of prosthesis. However, beyond the 3rd postoperative year, a slow rise of LVMI occurred in both groups. Again, the trend was slightly in favor of the Toronto valve, without reaching statistical significance. This phenomenon appeared to be unrelated to the transvalvular gradient, indicating that these xenografts were both still functional. As suggested by Del Rizzo and colleagues15, the extent of LVMI regression is dependent on various patient-related factors, such as associated vascular disease, systemic arterial hypertension, and the baseline LVMI. Knowing that regression of ventricular hypertrophy was a major determinant of long-term survival, Lund and colleagues17 concluded that up to 10 years after effective AVR, the underlying patient risk profile is probably the most important factor. This supposes a threshold of LV hypertrophy beyond which functional and histological normalization of the left ventricle becomes irreversible. We found a higher preoperative LVMI in patients with aortic stenosis and a history of chronic arterial hypertension, compared to normotensive patients, despite adequate medical treatment of hypertension. Both patient groups showed the same LVMI regression initially, followed by the same trend of an increase after the 3rd year, but the original LVMI difference persisted over time. According to Lund and colleagues,17 this positive correlation between late LV mass increase and arterial hypertension indicates that systemic hypertension on its own impacts on the evolution of LV function, independent of the efficacy of a well-functioning prosthesis.
This study incorporated the limitations of any retrospective analysis, primarily a bias in the patient selection. It reports on concurrent rather than consecutive surgical treatments in a mostly older population. Although the patient demographics are apparently identical for both valve types, case-controlled matching of each patient would probably be a better starting point. The advanced age of the study population might have weakened the long-term clinical results by progressive lowering of the number of patients at risk. In the hemodynamic comparison, the results obscure the differences in functional behavior between stentless and stented prostheses at rest and during exercise. Moreover, the influence of patient-prosthesis mismatching has not been addressed and might add more or less weight to the conclusions of this study. Nevertheless, it was concluded that stentless and stented bioprostheses both showed good early and late clinical and hemodynamic outcomes, with the advantage of a better midterm survival for those with a stentless xenograft. Regression of LV mass appeared to occur early and it was independent of the type of valve. As LVMI tended to increase again after 3 years, further investigation is needed to define the roles of other factors such as arterial hypertension. This study failed to provide evidence of superior function and durability of the stentless xenograft, especially in older patients.
Presented at The Asian Society of Cardiovascular Surgery (ASCVS) 12th Annual Meeting, Istanbul, Turkey, April 19–23, 2004.
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ACKNOWLEDGMENTS
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We would like to thank Dr Frank Caes and Dr Hans Van Overbeke for their surgical contributions.
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REFERENCES
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ABSTRACT
INTRODUCTION
