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J Thorac Cardiovasc Surg 2000;120:450-458
© 2000 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Homograft mitral valve replacement: Five years' results

A. Sampath Kumar, MCha, Shiv Kumar Choudhary, MCha, Alok Mathur, MSa, Anita Saxena, DMb, Ruma Roy, MDc, Prem Chopra, MDc

From the Department of Cardiothoracic and Vascular Surgery,a Department of Cardiology,b and the Department of Pathology,c All India Institute of Medical Sciences, New Delhi, India.

Address for reprints: A. Sampath Kumar, Professor, Department of Cardiothoracic and Vascular Surgery, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110029, India.

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 = 2) mitral valve replacement with a fresh antibiotic-preserved (n = 23) or cryopreserved (n = 14) mitral homograft. The predominant lesion was mitral stenosis (n = 30).
Results: There were 5 early deaths. Operative survivors were followed up for 1 to 60 months (mean, 26.6 ± 12 months). Among these, 21 patients had severe mitral regurgitation during the follow-up period; 3 died and 8 underwent reoperation. The homograft failure rate was not affected by preoperative physiologic lesion (stenosis vs regurgitation, P = .4), type of homograft (antibiotic-preserved vs cryopreserved homograft, P = .9), papillary muscle pretreatment (yes vs no, P = .9), or addition of posterior collar annuloplasty (yes vs no, P = .2). Among the remaining patients, 5 had moderate mitral regurgitation, 4 had either trivial or mild mitral regurgitation, and 2 were lost to follow-up. Study of the explanted mitral homografts (n = 8) revealed that disruption of one of the donor papillary muscles was responsible for early failures (n = 2), 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 immunologic injury to the homografts.
Conclusion: The mitral homograft did not fulfill our expectations as a suitable substitute for the diseased mitral valve.




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