Homograft mitral valve replacement: Five years' results

Citation
As. Kumar et al., Homograft mitral valve replacement: Five years' results, J THOR SURG, 120(3), 2000, pp. 450-458
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
ISSN journal
00225223 → ACNP
Volume
120
Issue
3
Year of publication
2000
Pages
450 - 458
Database
ISI
SICI code
0022-5223(200009)120:3<450:HMVRFY>2.0.ZU;2-E
Abstract
Objective: Results of mitral valve replacement with a mitral homograft were evaluated at 5 years to assess the suitability of the procedure. Methods: Thirty-seven patients (25 male subjects) aged 10 to 49 years (mean , 32 +/- 10 years) with rheumatic mitral valve disease underwent total (n = 35) or partial (n = 3) mitral valve replacement with a fresh antibiotic-pr eserved (n = 23) or cryopreserved (n = 14) mitral homograft. The predominan t lesion was mitral stenosis (n = 30). Results: There were 5 early deaths. Operative survivors were followed up fo r 1 to 60 months (mean, 26.6 +/- 12 months). Among these, 21 patients had s evere mitral regurgitation during the follow-up period; 3 died and 8 underw ent reoperation. The homograft failure rate was not affected by preoperativ e physiologic lesion (stenosis vs regurgitation, P = .4), type of homograft (antibiotic-preserved vs cryopreserved homograft, P = .9), papillary muscl e pretreatment (yes vs no, P = .9), or addition of posterior collar annulop lasty (yes vs no, P = .2). Among the remaining patients, 5 had moderate mit ral regurgitation, 4 had either trivial or mild mitral regurgitation, and 2 were lost to Follow-up. Study of the explanted mitral homografts (n = 8) r evealed that disruption of one of the donor papillary muscles was responsib le for early failures (n = 3), whereas cuspal and chordal degeneration was responsible for late failures (n = 6). Microscopically, the explanted valve lacked any viable cellular elements, and there was no evidence of immunolo gic injury to the homografts. Conclusion: The mitral homograft did not fulfill our expectations as a suit able substitute for the diseased mitral valve.