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Eur J Cardiothorac Surg 2007;31:256-260. doi:10.1016/j.ejcts.2006.11.027
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved
a Division of Cardiac Surgery and Anatomic Pathology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Room 62-266B, CHS, Los Angeles, CA 90095-1741, United States
b Department of Statistics and Center for Computational Biology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Room 62-266B, CHS, Los Angeles, CA 90095-1741, United States
Received 7 September 2006; received in revised form 10 November 2006; accepted 16 November 2006.
* Corresponding author. Address: Division of Cardiac Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Room 62-266B, CHS, Los Angeles, CA 90095-1741, United States. Tel.: +1 760 815 4749; fax: +1 310 8257473. (Email: ddelazerda{at}gmail.com).
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Abstract |
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 Top Abstract 1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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Key Words: Aortic valve • Repair • Cardiac surgery
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1. Introduction |
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TopAbstract1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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2. Patients and methods |
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TopAbstract1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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The diagnoses in the acquired group were: dilatation of the annulus 62% (24/43), redundant leaflet 12% (6/43), restrictive/deficient leaflet 21% (8/43), rheumatic heart disease 4.6% (2/43) and endocarditis 7% (3/43). Combined procedures included mitral valve repair in 32% (14 of 43), tricuspid valve repair in 18% (8 of 43), coronary revascularization in 11% (5 of 43), and aortic aneurysm wrap in 18% (8 of 43).
One limitation of our study is the impossibility of performing a multivariate analysis because of the numerous etiologies for the valve dysfunction. These different etiologies may affect the mid-term results of the repair performed.
2.1 Surgical technique
Surgery was performed under general endotracheal anesthesia, with the patient in the supine position. After heparinization, the vessels were cannulated and patient was connected to extracorporeal circulation and the blood was cooled to 24 °C. The aorta was crossclamped and the heart was arrested with cold blood cardioplegia. The ascending aorta was opened obliquely, and the aortic valve was exposed. Pericardial patches were harvested from under the sternum and treated with glutaraldehyde for 9 min. For clinical use, the University of California, Los Angeles Medical Center pharmaceutical technology laboratory locally prepares the glutaraldehyde solution under aseptic conditions by ultrafiltration and tests the solution for sterility by culturing before use. The preparation constitutes sterile glutaraldehyde 0.625% with a phosphate buffer (pH 7.4) and fluorescein 0.02% formulation. To shape the pericardial patches in the appropriate fashion, the width of each of these patches was 15% greater than the diameter of the aorta. The reduction in the pericardial leaflet free edge width from a purse stringing effect with a running polypropylene suture necessitates the 15% additional length. The height of the pericardial leaflet was measured to bring the extensions just below the sinotubular junction where all extended cusps may naturally coapt in the center of the aorta. The attachments were then extended up onto the wall of the aorta, thus creating commissures to provide coaptation of the leaflets approximately 4–5 mm from the edge of the valve commissures. The leaflets were then trimmed and attached at the proximal portion with through-and-through sutures through the aortic wall that were then passed through external pledgets and tied. The valve leaflets were assessed to assure coaptation. The incision was extended down to the annulus in order to slightly enlarge the ascending aorta to prevent narrowing due to the extra valve tissue. After coming off bypass, transesophageal echocardiogram was done to confirm aortic valve competency and evaluate ventricular function. (Fig. 1
). In most cases, the congenitally bicuspid valve was converted to a natural tri-leaflet configuration using autologous pericardial leaflet extensions.
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2.3 Follow-up
Follow-up was conducted over the last 6 months and was obtained in 114 out of 128 patients (89%). For the acquired group, follow-up was obtained in 38 out of 43 patients (88%) and for the congenital group, 76 out of 85 (89%) patients. The follow-up echocardiograms and medical records from referring cardiologists and hospitals were reviewed. The mean follow-up period was 2.3 ± 2.4 years (range, 0–7.8 years postoperatively) for the acquired group, and 3.0 ± 2.3 years (range, 0–7.7 years) for the congenital group. The endpoints of the study were mortality and reoperation rates.
The Institutional Review Board at the University of California, Los Angeles, approved this study.
2.4 Statistical method
We used nonparametric statistics to study the intra- and intergroup variations as the data did not possess normal characteristics. All statistical results were obtained using the Statistics Online Computational Resource (www.SOCR.ucla.edu) [9]. To assess differences in proportion we again used a distribution-free test, the binomial test for proportions, because of the non-normal nature of the data.
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3. Results |
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TopAbstract1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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3.2 Late mortality
The total late mortality for the cohort was 4.9% (6/127). In the acquired group, 3/43 cases (6.9%) and in the congenital group 3/84 (2.6%) patients died. We have little information about the cause of death in these patients. The first case was a patient who died outside of our institute and the cause of death was reported as a cardiac arrest of unexplained etiology. Additional information was not obtained. The other two cases were reported during the follow-up of this study and there is no information about the cause or date of death. All of the late deaths of the acquired group were at home and there was no autopsy or further medical information about the mechanisms of death. There was no statistical difference (p
= 0.69) between the groups.
Neither early nor late proportion of mortality is significantly different between the two groups, according to the nonparametric Binomial test for proportions.
One limitation of our study is the inability to identify all the etiologies of late mortality because UCLA is a referring institution, where after discharge from the hospital, the patient is followed up only by the primary physician.
3.3 Reoperation
There were 13 total reoperations in 11 patients; 2 patients were reoperated twice. Of the congenital group, five patients had replacement and six underwent re-repair. In the acquired group, both cases were re-repairs.
The reoperation rate was as follows: for the acquired group, 4.6% (2/43) and for the congenital group 13% (11/85). The mean interval between original repair and reoperation was 3.6 ± 5 years (range, 0–7 years) for the acquired group and 3.5 ± 2.5 years (range, 0–7 years) for the congenital group (Wilcoxon 2-sample test, p = 0.7).
Total early reoperation rate (<30 days after first surgery) was 11/128 (8.5%). For the congenital group, 9/85 (10.5%) patients and for acquired group 2/43 (4.6%) of patients required reoperation. Early reoperation rate was significantly higher among the congenital group (p = 0.013). The reasons for early reoperation in the congenital group were as follows: one patient with severe aortic stenosis (grade 4) required aortic valve re-repair. This case is a 1-year-old patient, diagnosed with truncus arteriosus. He underwent a second late reoperation because of moderate aortic insufficiency (grades 2 and 3). The second patient also had a primary diagnosis of truncus arteriosus and underwent re-repair because of a moderate aortic valve insufficiency and stenosis. Eight patients had an initial diagnosis of bicuspid valve, and required reoperation due to narrowing of the ascending aorta as the preoperative diagnosis. Of these eight patients, five underwent aortic valve replacement and three underwent re-repair.
In the acquired group, two patients underwent re-repair. In both cases, the preoperative diagnosis was dilatation of the aortic sinuses and sinotubular junction.
There were six nonvalve-related reoperations at a mean of 1.2 ± 2.6 months (range, 0–4.9 months) after the initial surgery. In the acquired group, only one patient required reoperation for respiratory failure and needed a tracheostomy. The interval between first operation and a reoperation was 0.3 months. Five patients of the congenital group returned to the operating room within a mean interval of 9.8 ± 20.6 months (range, 0–46 months). Two patients were reoperated for postoperative bleeding. One patient returned to surgery for wound debridement of sternal infections. Another patient was a 10-day-old neonate with truncus arteriosus undergoing truncal valve repair with leaflet extensions and delayed sternal closure. The other case was a redo sternotomy for a previous aortic and mitral valve surgery (Figs. 2 and 3 ).
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3.4 Valve function
The remaining patients are well at mean follow-up of 33.4 ± 28.1 months (range, 0–93.1). In the acquired group, the mean preoperative aortic regurgitation and stenosis grades by echocardiogram were 1.6 ± 1.1 and 1.6 ± 1.2, respectively, and the mean follow-up aortic regurgitation and stenosis grades were 0.5 ± 0.3 (scale, 0–4) and 0.3 ± 0.1, respectively. In the congenital group, the mean preoperative aortic regurgitation and stenosis grades were 1.7 ± 1.6 and 1.4 ± 0.9, respectively, and the follow-up mean aortic regurgitation and stenosis grades were 0.9 ± 0.8 and 0.5 ± 0.3, respectively. There is no statistical difference in either aortic regurgitation (Wilcoxon 2-sample test, p
= 0.08) or aortic stenosis (Wilcoxon 2-sample test, p
= 0.1) between the two groups.
3.5 Discussion
The ideal surgical technique for repairing the aortic valve depends on the etiology, the valve's morphology, patient's age and general condition, echocardiographic findings, and other factors. Duran et al. [1–4] first described the possibility of repairing the aortic valve using autologous pericardium leaflet extension. This technique consists of intraoperative treatment of autologous pericardium with a glutaraldehyde solution. The pericardium is then used to increase the height of the leaflets and commissures, thus, creating an additional area of coaptation. Glutaraldehyde treatment provides the pericardium with more resistance to retraction and degeneration and maintains the intrinsic tissue pliability. Immunologic responses consistent with host versus graft reaction remain unknown [10]. This technique can delay and sometimes avoid limitations of other surgical techniques like biological constraints of growing children, pregnancy, tissue antigenicity, calcium metabolism, and bleeding and thromboembolic complications caused by synthetic valve substitutes, prosthesis-patient mismatch, calcification [11], degeneration, and complications related to the use of anticoagulation therapy [11–13] that might influence the long-term durability. Another important issue with valve replacement is its high cost, which may limit the applicability of this technique in many countries.
In 2002, Grinda et al. [7], reported an actuarial survival at 5 years of 96%, and 92% were free from reoperation. Their cohort was afflicted with rheumatic disease. After this study Bozbuga et al. [6] reported in 2004, an actuarial survival of 98 ± 2% at 8.6 years, but with a high reoperation rate (20%). They explain this high reoperation rate by the fact that their cohort consisted of patients with a rheumatic disease etiology. Long-term durability of this technique is becoming clearer. In 2005, Halees et al. reported an overall reoperation free survival of 47 ± 6% at 16 years [14]. Odim et al. [8] described the use of autologous pericardial leaflet extension in the congenital group in 2005. This study demonstrated that aortic valve repair with autologous pericardial leaflet extension is a good alternative option for a congenital diseased aortic valve. They showed that the 2-year freedom from valve-related reoperation for patients with congenital heart disease was 92% and for pediatric patients 
18 years of age this freedom from valve-related reoperation was 100% at 2 years.
Our experience showed improvement in both aortic regurgitation and stenosis in the long-term follow-up when using aortic valve repair with autologous pericardial leaflet extension. We had good results when using this technique, with no difference in either early or late mortality between congenital and acquired groups. The mean interval between original repair and reoperation was 5 ± 3.6 years (range, 0.1–7 years) for the acquired group and 3.5 ± 2.5 years (range, 0.1–7 years) for the congenital group with no statistical difference between the groups. Total early reoperation rate was 11/128 (8.5%); for the congenital group 9/85 (10.5%) and for the acquired group 2/43 (4.6%).
In conclusion, aortic valve repair with autologous pericardial leaflet extension has low mortality and morbidity rates, as well as good long-term durability in both the acquired and congenital groups. The use of this technique can delay and sometimes avoid potential complications associated with other techniques; however, more studies comparing repair and replacement of the aortic valve are needed in order to elucidate which groups of patients are more suitable for each type of technique.
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Appendix A |
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TopAbstract1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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Dr S. Hagl (Heidelberg, Germany): You are talking about reoperation as an end point. That is, as we all know, a question of tolerance to valve dysfunction. You may accept valve dysfunction for a long time until you decide to reoperate. So can you say anything about the function during the intermediate follow-up? Do you have a grade 1 insufficiency or do you have stenosis, or whatsoever?
Dr De La Zerda: Most of the patients that were reoperated in the early stage were because of complication of the operation, like bleeding or hemodynamic instability or difficulties in the operation itself that should have had some other repair or replacement or other things, and that probably was the reason that in the neonate it was a little bit difficult and that is why the incidence was higher.
Concerning the late reoperation, we would follow up these patients and usually took them back to the OR for re-repair or replacement when there was—most of them were more regurgitant than stenotic.
Dr Hagl: So I think a functional analysis should be included. You have the echoes over the follow-up time, so you should give us more specific information about that, I would suggest.
Dr De La Zerda: Yes.
Dr P. Bertolini (Verona, Italy): I would like to discuss two points. You refer to the higher percentage of failure in the cohort of the congenital patients. In the meantime, you refer also to have follow-up completed up to 89%. That is not obviously 100%. Did you miss more patients in the subgroup of congenital diseases or in acquired diseases?
Dr De La Zerda: Did I what? Sorry.
Dr Bertolini: The total follow-up is 89%. That means you lack 11% of all your patients. This leak happens in the cohort of the congenital patients or in the acquired disease patients?
Dr De La Zerda: Most of the leak, as you call it, was in the acquired.
Dr Bertolini: In the acquired. And the second question would be, can you find any correlation between the size or diameter of the aortic valve and the rate of failure?
Dr De La Zerda: I am sorry, I can’t give you this answer right now or the correlation between the size. I don’t have the data here right now. But there was no significance, not in the mortality and not in the late reoperation. The only significance was something in relation directly to the short term after the operation.
Dr R. Frater (Bronx, New York): Did I hear you say just now that a reason for late failure was calcification? I am not sure if you said that. Did you say that?
Dr De La Zerda: The reason?
Dr Frater: You mentioned that the late reoperations, the status of the valve, did I hear you use the word calcification as one of the reasons?
Dr De La Zerda: Calcification?
Dr Frater: Yes.
Dr De La Zerda: Yes.
Dr Frater: So what you are saying then is autogenous pericardium, briefly tanned, has actually deteriorated by calcifying?
Dr De La Zerda: Yes.
Dr Frater: That is very interesting.
Dr De La Zerda: This is not a secret, I think.
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Footnotes |
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References |
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TopAbstract1. Introduction2. Patients and methods3. ResultsAppendix AReferences |
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This article has been cited by other articles:
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  D. S. Jeong, K.-H. Kim, and H. Ahn Long-term results of the leaflet extension technique in aortic regurgitation: thirteen years of experience in a single center. Ann. Thorac. Surg., July 1, 2009; 88(1): 83 - 89. [Abstract] [Full Text] [PDF]
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