Abstract
OBJECTIVES
The study aimed to assess the long-term follow-up of patients with an autologous pericardial aortic valve (APAV) replacement and to analyse in vivo histopathological changes in implanted APAVs.
METHODS
From 1996 to 1997, 15 patients (mean age, 34 years) underwent aortic valve replacement with the glutaraldehyde-treated autologous pericardium. All patients were followed up after discharge. The excised APAVs were processed for haematoxylin–eosin, Victoria blue-van Gieson and immunohistochemical staining.
RESULTS
The mean clinical follow-up was 11.43 ± 4.50 years. APAV-related in-hospital and late mortalities were both 0%. Five (33%) patients required reoperation because of a prolapse of the right coronary cusp (n = 1), infective endocarditis (n = 1) or fibrocalcific degeneration (n = 3). Freedom from endocarditis, fibrocalcific degeneration and reoperation at the end of follow-up was 93, 80 and 67%, respectively. The remaining 10 patients were alive and well with a mean New York Heart Association class of 1.10 ± 0.32 and normally functioning aortic valves (peak pressure gradient: 7.70 ± 3.41 mmHg; mean pressure gradient: 1.79 ± 0.64 mmHg). Histopathology revealed that (i) a thin factor VIII-positive layer (endothelialization) was found on all non-endocarditis APAVs; (ii) pericardial cells in all APAVs were positive for α-smooth muscle actin (myofibroblast phenotype) and some cells in the fibrocalcific APAVs were positive for alkaline phosphatase (osteoblast phenotype) and (iii) an elastic band was found in 3 cases (in vivo >9 years).
CONCLUSIONS
APAV replacement is a procedure with a low mortality. APAVs adapt to new environmental demands by producing an elastic band and by endothelialization, whereas myofibroblast/osteoblast transdifferentiation seems to be responsible for the fibrocalcification of APAVs.
Keywords: Autologous pericardial aortic valve, Fibrosis, Calcification, Endothelialization, Transdifferentiation
INTRODUCTION
The replacement of diseased valves with mechanical or bioprosthetic valves is the most common treatment for end-stage valvular heart diseases. However, anticoagulant-related complications of the mechanical prosthesis have been a major problem in long-term patient outcomes [1, 2]. Bioprosthesis achieves a superior initial haemodynamic result at the expense of accelerated degeneration in young patients due to fibrosis and/or calcification [3]. The precise mechanism(s) remains to be elucidated, but an immune reaction between the host and implanted bioprosthesis has been shown to be a potent stimulator of valvular degeneration [4, 5]. Therefore, it is necessary to look for autologous substitutes for these valvular prostheses.
The autologous pericardial aortic valve (APAV), moulded with the autologous pericardium and treated briefly with glutaraldehyde, was introduced in 1988 by Duran et al. [6]. Theoretically, this autologous tissue should experience reduced degeneration because of a lack of antigenicity. Furthermore, animal studies [7–9] and short-term follow-up analyses of several clinical studies [6, 10] have demonstrated the efficacy and safety of the procedure. However, there are few data regarding the long-term follow-up in patients who underwent APAV replacement. Furthermore, few data are available about the long-term histopathological changes in the implanted APAV in vivo. This report summarizes our experience with this technique in 15 patients. We prospectively evaluated the clinical outcome and analysed the potential mechanism of fibrocalcific degeneration by evaluating the histological characteristics of the excised APAVs.
MATERIALS AND METHODS
Patients
To avoid permanent anticoagulation and to reduce the potential risk of immune response-related early tissue deterioration, 15 patients with aortic valve disease underwent APAV replacement from 1996 to 1997. The study was approved by our hospital's ethics committee for human research, and full informed consent was obtained from each patient. The medical records of the 15 patients were reviewed, including clinical history, perioperative echocardiograms, operative notes and preoperative and postoperative transthoracic echocardiographic (TTE) reports.
The preoperative demographics of these patients are listed in Table 1. This study included eight men and seven women with a mean age of 34 ± 12 (range 19–59) years. The aetiologies of valvular disease were infective in 6 (40%) cases, rheumatic in 5 (33%), congenital in 3 (20%) and degenerative in 1 (7%). According to the New York Heart Association (NYHA) functional classification, 9 patients were in Class I/II and 6 in Class III/IV. Coronary angiography was performed only in men older than 45 years, unless otherwise indicated by the clinical data. No patient in this series had coronary disease.
Table 1:
Patient demographic data
| Characteristic | n (%) or mean ± SD |
|---|---|
| Patients | 15 |
| Age (years) | 34 ± 12 |
| Gender (female/male) | 7:8 |
| Underlying heart diseases | |
| Infective endocarditis | 6 (40%) |
| Rheumatic valve disease | 5 (33%) |
| Congenital disease | 3 (20%) |
| Aortic valve degeneration | 1 (7%) |
| NYHA functional Class III/IV | 6 (6/15) |
| Electrocardiogram | |
| Sinus rhythm | 10 (67%) |
| Right bundle branch block | 2 (13%) |
| Myocardial ischaemia | 5 (33%) |
| Atrial fibrillation | 1 (7%) |
| Echocardiography | |
| Aortic annulus diameter (mm) | 25.1 ± 4.2 |
| Left ventricular ejection fraction (%) | 60.11 ± 7.01 |
Surgery
The operative details are summarized in Table 2. The surgical methods used were the same as previously described [6]. Briefly, after opening the chest, a rectangular strip of the pericardium was excised with a total length of approximately 3.5 times the aortic annulus diameter measured by intraoperative transoesophageal echocardiography (TEE) and a width of 2.5 times annulus diameter. After clearing of the overlying fatty tissue, the pericardium was sandwiched between the suitable moulds to reproduce the three-valve leaflets with measures corresponding to the different aortic valve diameters, fixed in 0.2% glutaraldehyde solution for 10 min and then taken out and rinsed five times with normal saline. On standard cardiopulmonary bypass, the diseased aortic valve was excised, leaving a 1.5-mm edge. The aortic annulus diameter was measured again, and the moulded pericardium was trimmed into the required size and a trifoliate shape. Subsequently, the prepared APAV was sutured directly to the aortic valve remnant with 4-0 polypropylene running sutures following a technique described in detail elsewhere. Aortic valvular competency was examined by injecting saline into the left ventricle through the valve with a bulb syringe and by TEE.
Table 2:
Operative data
| Characteristic | n (%) or mean ± SD |
|---|---|
| Aortic valve replacement | 15 (100%) |
| Concomitant procedures | |
| Ventricular septal defect occlusion | 3 (20%) |
| Mitral valve repair | 1 (7%) |
| Tricuspid valve repair | 1 (7%) |
| Aortic clamping time | 88.20 ± 18.79 |
| Cardiopulmonary bypass time | 115.33 ± 12.65 |
| ICU stay (days) | 3.00 ± 1.77 |
| Hospital stay (days) | 17.27 ± 5.65 |
Additional procedures included the repair of a ventricular septal defect in 3 (20%) patients, mitral valve repair in 1 (7%) and tricuspid valve repair in 1 (7%).
Follow-up
All patients were followed up prospectively with serial echocardiography, which was performed preoperatively, 6 months and 1 year after operation and annually thereafter. The patients were also interviewed by telephone every 6 months and asked to answer the questions designed to evaluate their quality of life and heart function.
Histology
The diseased APAV was excised and embedded in paraffin. Five normal pericardial specimens free of pericarditis were obtained during cardiac surgery as controls. Paraffin-embedded sections (5 µm) were stained with haematoxylin–eosin (HE) and Victoria blue-van Gieson (VG) using standard procedures.
Immunohistochemical staining was performed using the labelled streptavidin–biotin method (DAKO LASB-2 Kit, Peroxidase, DAKO), according to the manufacturer's instruction. Primary antibodies included anti-α-smooth muscle actin (α-SMA, DAKO), anti-factor VIII (DAKO) and anti-alkaline phosphatase (ALP, Abcam).
Statistical analysis
Data are expressed as mean ± standard deviation (SD) for continuous variables and as percentages for categorical variables. Student's paired t-test was used to compare the values before and after operation.
RESULTS
Surgical outcome
Valve replacement was performed uneventfully in all patients. The mean aortic annulus diameter was 25.1 ± 4.2 (range 20.1–34.9) mm. Cardiopulmonary bypass time was 115.33 ± 12.65 (range 100–129) min, and aortic cross-clamp time was 88.20 ± 18.79 (range 57–128 min; Table 2). Intraoperative TEE showed a very mild degree of aortic valve regurgitation in 15 patients. The mean length of hospital stay was 17.27 ± 5.65 (range 11–28) days, and the mean intensive care unit (ICU) stay was 3.00 ± 1.77 (range 1–6) days.
Valve function and NYHA functional class
The peak and mean pressure gradients were reduced from preoperative 26.34 ± 20.88 to 9.44 ± 4.18 mmHg (P <0.05) and from preoperative 14.98 ± 12.47 to 4.77 ± 1.45 mmHg (P <0.05) within 10 days, respectively. After 6 months, 14 (93%) patients reported a significant improvement in symptoms, and NYHA class improved from preoperative 2.43 ± 0.51–1.43 ± 0.62 at 6 months and 1.43 ± 0.51 at 1 year (all P <0.05), respectively.
Reoperations, mortality and long-term outcome
The follow-up was performed between the operation dates of the patients (1996–97) to the end of December 2010, and the mean follow-up time was 11.43 ± 4.50 (range 0.42–14.08) years. There were five (33%) reoperations (Table 3). As shown in Table 4, the causes of reoperation were the prolapse of the right coronary cusp in 1 patient (Patient 1, 7%) at 5 months, endocarditis in 1 patient (Patient 2, 7%) at 2 years and fibrocalcific degeneration of APAVs in 3 patients (20%) at 9 (Patient 3), 13 (Patient 4) and 14 years (Patient 5). All of these patients underwent mechanical prosthesis replacement at our institution. Freedom from endocarditis, fibrocalcific degeneration and reoperation at the end of follow-up was 93, 80 and 67%, respectively.
Table 3:
Results of aortic valve replacement with the autologous pericardium
| Event | n (%) |
|---|---|
| Deaths | |
| In hospital | 0 (0%) |
| Non-APAV-related late death | 1 (7%) |
| APAV-related late death | 0 (0%) |
| Anticoagulation | 0 (0%) |
| Embolism | 0 (0%) |
| Reoperation | 5 (33%) |
| Autologous pericardium | |
| Dilatation | 0 (0%) |
| Infective endocarditis | 1 (7%) |
| Fibrocalcific degeneration | 3 (20%) |
| Aortic valve prolapse | 1 (7%) |
APAV: autologous pericardial aortic valve.
Table 4:
List of patients
| Patient no. | Age (years) | Gender | Primary diagnosis | Cause of valve re-replacement |
|---|---|---|---|---|
| 1 | 41 | Female | AI, VSD | AI |
| 2 | 44 | Male | AI, TI | Endocarditis |
| 3 | 36 | Male | AI, AS | AI, AS |
| 4 | 29 | Male | Endocarditis, AI | AS |
| 5 | 24 | Male | AI | AS |
| 6 | 29 | Female | AI | None |
| 7 | 59 | Male | AI, AS | None |
| 8 | 37 | Female | AI | None |
| 9 | 46 | Female | Endocarditis, AI | None |
| 10 | 19 | Male | Endocarditis, AI | None |
| 11 | 19 | Male | Endocarditis, AI, VSD | None |
| 12 | 24 | Female | Endocarditis, AI, VSD | None |
| 13 | 31 | Female | Endocarditis, AI, MI | None |
| 14 | 52 | Male | AI, AS | None |
| 15 | 27 | Male | AS | None |
AI: aortic valve insufficiency; AS: aortic valve stenosis; MI: mitral valve insufficiency; TI: tricuspid valve insufficiency; VSD: ventricular septal defect; None: without reoperation.
The remaining 10 patients (patients undergoing reoperations were excluded) had survived well at the end of the follow-up period. All of these patients were in NYHA Class I or II, with a mean of 1.10 ± 0.32. In these 10 patients, the aortic valves functioned normally, with a peak pressure gradient of 7.70 ± 3.41 mmHg and a mean pressure gradient of 1.79 ± 0.64 mmHg; no regurgitation was detected by TTE, and no thromboembolic or haemorrhagic event or endocarditis occurred during follow-up.
Overall, no patient died during the first hospital stay. There was 1 patient (Patient 3) who died of severe renal dysfunction 5 days after the second operation. The APAV-related mortality was therefore 0%.
Histology
The excised APAVs (n = 5) were collected for histological analysis. The APAV in Patient 2 showed features of endocarditis, and some pericardial cells were positive for α-SMA. The remaining four valves were divided into two groups according to the presence of fibrocalcification.
Group 1 (Patient 1)
The APAV was thin, mobile and perfectly healed, showing architectural preservation, extensive cell loss and a few cells present on the surface and in the superficial layers of the valve (Fig. 1). Immunohistochemistry showed that cells on the surface of the valve were factor VIII-positive endothelial cells. Cells located on the superficial layer were positive for vimentin and α-SMA but negative for ALP, suggesting these cells were myofibroblasts.
Figure 1:
Histological analysis of the APAV in Group 1. (a) HE staining showing extensive cell loss and a few cells present on the surface and in the superficial layers of the valve. (b) VG staining showing little elastin in the valve. (c) Immunohistochemical staining showing vimentin-positive cells. (d) Immunohistochemical staining showing cells on the surface of the valve positive for factor VIII. (e) Immunohistochemical staining showing α-SMA-positive cells located in the superficial layers. (f) Immunohistochemical staining showing that there were no ALP-positive cells in the APAV. Representative photographs are shown. Bar = 100 µm. APAV:autologous pericardial aortic valve; HE: haematoxylin—eosin.
Group 2 (Patient 3, 4 and 5)
The three degenerated APAVs displayed similar pathological changes with extensive fibrosis and focal calcification (Fig. 2). Calcification was detected by HE staining as the presence of a calcified matrix with tinctorial characteristics. Increased cellularity was observed in some areas of the APAVs, while acellularity was observed in most other regions. Immunohistochemistry revealed that nearly all of the pericardial cells were myofibroblasts (α-SMA positive), and some were osteoblasts (ALP positive). Approximately 22, 26 and 89% of the surface of the APAVs in Patients 3, 4 and 5, respectively, were covered with factor VIII-positive cells, suggesting partial endothelialization of the APAVs. Similarly, native aortic valve, VG staining revealed a band of elastic tissue in the APAVs of Group 2, which was not observed in the APAV of Patient 1 and in the native pericardium (Figs 2c and 3).
Figure 2:
Histological analysis of the APAVs in Group 2. (a) HE staining showing calcification (black arrow). (b) HE staining showing fibrosis with extracellular matrix accumulation. (c) VG staining showing an elastic band (black arrow). (d) Immunohistochemical staining showing factor VIII-positive cells located on the surface of the APAVs. (e) Immunohistochemical staining showing that nearly all of the pericardial cells were positive for α-SMA. (f) Immunohistochemical staining showing some ALP-positive cells. Representative photographs are shown. Bar = 100 µm (a, c and d through f) and 250 µm (b). APAV:autologous pericardial aortic valve; HE: haematoxylin-eosin.
Figure 3:
VG staining of the native pericardium and the native aortic valve. VG staining showing an elastic band (black arrow) in the native aortic valve but not in the native pericardium. Bar = 100 µm. VG: Victoria blue-van Gieson.
DISCUSSION
This study demonstrated that APAVs have a favourable functional profile as represented by their excellent haemodynamic performance. Ventricular function improved significantly soon after APAV replacement and during follow-up. Furthermore, the high success rate of the procedure in this study was encouraging, with an in-hospital mortality of 0%. Initially, taking surgical safety into consideration, the patients we chose for this study were mostly younger (mean age, 34 years). Several groups have also achieved excellent long-term results in young patients (mean age, 32 years) [11], whereas Gross et al. [12] reported disappointing results in a series of 87 patients with a mean age of nearly 70 years. Thus, younger age may be one of the reasons for the positive results in our series.
Endothelialization of an implanted graft is a key factor in the prevention of subsequent infection [13]. Animal studies [14, 15] of explanted grafts have reported that endothelialization begins as early as 4 weeks after implantation and is completed in 24 weeks, whereas this ‘healing response’ to valve replacement in humans has been much less studied. In this study, we found partial endothelialization in all of the non-endocarditis APAVs. Furthermore, endocarditis occurred in 7% of the patients in our series, which is lower than the reported rate of pericardial prosthetic endocarditis [16, 17]. Some researchers [6, 18] have also reported a low rate of infective endocarditis in patients who underwent APAV replacement. It is not clear whether this discrepancy is due to differences in methodology and/or the selection of patients. Our data seem to suggest that the use of APAVs is generally accepted even in patients with aortic valve endocarditis because no patient with endocarditis in our series developed endocarditis again.
It has been demonstrated that the fresh APAVs in the blood stream undergo very fast deterioration, but calcification and fibrotic shrinkage can be achieved by killing pericardial cells [9, 19, 20]. However, fibrocalcification and increased cellularity (living cells) were observed in the glutaraldehyde-treated APAVs in our series. Because of the osmotic effect of glutaraldehyde and the acellular core of the APAVs, we speculated that the primary pericardial cells were dead after in vivo implantation, and host cells may migrate to APAV and differentiate into new pericardial cells. Importantly, pericardial cells in the fibrocalcific APAVs expressed markers associated with myofibroblasts and osteoblasts, suggesting abnormal transdifferentiation of pericardial cells in the bloodstream. Furthermore, pericardial cells within an APAV free of fibrosis also expressed α-SMA, suggesting that myofibroblast transdifferentiation is responsible for the contraction and distortion of the original pericardium. Indeed, we confirmed in our recent study that differentiation of pericardial cells into myofibroblasts and osteoblasts contributed to fibrosis and calcification, respectively [21]. Therefore, pharmacological inhibition of transdifferentiation to myofibroblasts and osteoblasts may represent a promising approach to slow down the fibrocalcific process of APAVs.
An important finding of this study was that an elastic band, which generally exists in the aortic valve and is not observed in fresh pericardial tissue, was found in the APAVs. A similar finding was also reported in a pedicled autologous pericardium 9 years after implantation for an extracardiac conduit in the Fontan pathway [22]. These results suggest that the autologous pericardium transplants may adapt to new environmental demands, in which the pericardium has transformed from its norm into the structure of the natural valve and vascular tissue after it is used for that purpose.
CONCLUSIONS
In conclusion, this study demonstrates that APAV replacement is a procedure with a low mortality, although more cases and longer follow-ups are needed to better determine its efficacy. Furthermore, histopathological data revealed transdifferentiation from pericardial cells to myofibroblasts and/or osteoblasts, which was responsible for the fibrocalcification of the APAVs. Moreover, the presence of an elastic band in 3 cases indicates the long-term environmental adaptation of the APAVs.
FUNDING
The present study was supported by grant from the National Natural Science Foundation of China (grant 81170217).
Conflict of interest: none declared.
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