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Published on: October 19, 2015
Structural deterioration of the cryopreserved mitral homograft valve
Silvio Olivito1, Stéphanie Lalande, Francesco Nappi
1Department of Cardiac Surgery, Hôpital Pitié-Salpétrière, Paris, France.
Insights
Cryopreserved mitral homografts showed significant structural valve deterioration over time, leading to mixed stenosis and insufficiency. Further improvements in homograft preservation are needed for better long-term outcomes.
Area of Science:
- Cardiovascular Surgery
- Biomaterials Science
- Transplantation Immunology
Background:
- Cryopreserved homografts are used for mitral valve replacement.
- Long-term structural valve deterioration (SVD) is a concern for homograft longevity.
Purpose of the Study:
- To evaluate the long-term fate of cryopreserved mitral homografts.
- To focus on the incidence and characteristics of structural valve deterioration.
Main Methods:
- 106 patients underwent mitral valve homograft replacement.
- Follow-up included echocardiography and pathological analysis of explanted valves.
- Causes of disease included rheumatic disease (75) and endocarditis (24).
Main Results:
- Mean follow-up was 9.3 years; 5-year, 10-year, and 15-year freedom from SVD was 90%, 76%, and 65%.
- SVD led to increased mitral regurgitation and stenosis, with decreased valve area.
- SVD was more frequent in total homografts, during pregnancy, in patients <40 years, and with smaller ring sizes.
Conclusions:
- Mitral homografting yields early results comparable to valve repair.
- SVD results in mixed stenosis and insufficiency, with incidence similar to bioprostheses.
- Improved preservation methods for valvular homografts are necessary.
Objective:
The aim of this study was to evaluate the long-term fate of the cryopreserved mitral homograft focusing on structural valve deterioration.
Methods:
Homograft replacement of the mitral valve was performed in 106 patients. The causes of mitral disease were rheumatic disease (n=75), endocarditis (n=24), and others (n=7). There were 40 partial homografts and 66 total homografts.
Results:
Mean follow-up was 9.3+4.7 years (up to 17.8 years). There were 5 early (<3 months) and 15 late deaths. There have been 5 early (<3 months) and 30 late reoperations. Five patients had endocarditis, and 5 patients had an ischemic/hemorrhagic event. Compared with baseline, follow-up echography showed progression of mitral regurgitation grade (from 0.4 to 1.3; P<.001) with stenosis (elevated gradient: from 3.9 to 7.0 mm Hg; P<.001) and decreased valve area (from 2.3 to 1.7 cm2, P<.001). Freedom from structural valve deterioration was 90%, 76%, and 65% at 5, 10, and 15 years, respectively. Structural valve deterioration was more frequent in total homografts (P=.018 vs partial homografts) and in case of pregnancy (P=.016 vs no pregnancy). Stenosis related to structural valve deterioration was more pronounced for age less than 40 years (P=.03) and ring size 30 mm or less (P=.002). Pathologic analysis of the explanted homografts almost invariably showed dense fibrosis with calcification and no cellularity.
Conclusions:
Mitral homografting was accomplished with early echographic results similar to those of valve repair. Structural valve deterioration produced mixed stenosis with insufficiency, and its incidence was comparable to that of bioprostheses structural valve deterioration. An improvement in the preservation mode of valvular homografts is warranted.
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Mitral Valve Prolapse I: Introduction
Mitral Stenosis I: Introduction
Mitral Regurgitation I: Introduction
Mitral Stenosis II: Clinical features and Diagnostic Tests
Mitral Regurgitation II: Clinical Features and Diagnostic Tests
Mitral Stenosis III: Medical Management
