The Journal of thoracic and cardiovascular surgery · 2011
Structural deterioration of the cryopreserved mitral homograft valve.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Olivito Silvio, Lalande Stéphanie, Nappi Francesco, Hammoudi Nadjib, D'Alessandro Cosimo, Fouret Pierre, Acar Christophe
Аннотация
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.
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.