[Structural changes of Hancock bioprostheses in children (author's transl)]

Conservative management is the treatment of choice for either congenital or acquired valvular disease in children. However, prosthetic valve replacement may sometimes be required and in this situation the surgeon is faced with the problem of which valvular substitute is the best for this particular patient. The glutaraldehyde-preserved Hancock porcine xenograft has been considered the safest one to use in the pediatric age group since the risks of thromboembolism as well as the mortality and morbidity related to anticoagulant treatment are reduced with this device. However durability of porcine bioprostheses at this time is still unknown, and it remains one of its major concerns. Recent reports have highlighted that porcine heterografts implanted in children undergo early and severe fibrocalcific degeneration. After having reviewed our pathological collection of explanted Hancock valves we have summarized our experience with pathology of porcine bioprostheses in young patients in the present report. Five Hancock heterografts were available for gross and histologic examination. They came from 3 children, 2 females and 1 male, who died or were reoperated upon because of prosthetic dysfunction. Both girls, aged 8 and 10 years, had undergone total correction of complete a-v canal which required mitral valve replacement in the first and mitrotricuspid valve replacement in the second. The first one was reoperated 2.10 years after surgery because of severe prosthetic stenosis and died in the 1st postoperative day of low output syndrome. The second, who developed the signs of mitral stenosis 3.4 years later, was successfully reoperated, but died in severe heart failure 2.9 years following mitral prosthetic re-replacement. The third patient, a 11-year-old boy, underwent mitral valve replacement because of mitral incompetence due to bacterial endocarditis; 5.4 years after surgery he necessitated reoperation because of mitral prosthetic stenosis. He is currently asymptomatic. Pathologic examination of the 5 explants (4 mitral, 1 tricuspid) which had been in place from 34 to 72 months (average 49 mos), showed a severe stenosis with impairment of the effective prosthetic orifice in all. The stenosis was due to coarse calcific deposits of the cusps and commissures and was worsened in 3 cases by fibrous tissue overgrowth on the inflow aspect of the leaflets. In 2 cases an atrial thrombosis was observed, as a consequence of prosthetic stenosis. Histologic examination together with microradiographic investigation showed in all cases the presence of diffuse calcifications of commissures and leaflets. Our pathological experience confirms that the Hancock bioprostheses, when implanted in children, undergoes structural changes early and severe enough so as to discourage their employment in this group of patients.