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J Thorac Cardiovasc Surg 2003;126:99-105
© 2003 The American Association for Thoracic Surgery

Surgery for acquired cardiovascular disease

Hancock II bioprosthesis: A glance at the microscope in mid–long-term explants

^a Department of Cardiovascular Surgery, University of Padua Medical School, Padua, Italy
^b Department of Pathological Anatomy, University of Padua Medical School, Padua, Italy
^c Division of Cardiac Surgery, Ca’ Foncello Hospital, Treviso, Italy

Received for publication August 2, 2002; revisions received November 14, 2002; accepted for publication November 25, 2002.

^* Address for reprints: Marialuisa Valente, MD, Professor, Pathological Anatomy, Department of Pathological Anatomy, University of Padua Medical School, Via A Gabelli, 61 35121, Padova, Italy
marialuisa.valente{at}unipd.it

BACKGROUND AND OBJECTIVES: The Hancock II bioprosthesis is a second-generation porcine valve xenograft treated with the detergent sodium dodecyl sulphate (T6) to retard calcification. The aim of this investigation was to study the gross and microscopic features in Hancock II explants to assess the structural changes occurring with time.

METHODS: Among 1382 Hancock II bioprostheses (701 isolated aortic, 421 isolated mitral, 130 double) implanted from 1983 to 1997 in 1252 patients, 22 (16 mitral, 6 aortic) were removed at reoperation until 1999 and were available for pathological investigation: infective endocarditis occurred in 5 and structural deterioration in 8, whereas in the remaining 9 xenografts reoperation was performed for nonstructural valve deterioration (paravalvular leak in 4 and prophylactic replacement in 5). Morphological investigation consisted of gross examination and x-ray, histologic, immunohistochemistry, electron microscopic, and atomic absorption spectroscopic examination.

RESULTS: The cause of structural valve deterioration was dystrophic calcification in 4 cases (1 aortic, 3 mitral; range of time graft was in place, 101 to 144 months), non-calcium–related tears in 3 cases (all mitral, range 121 to 163 months), and commissural dehiscence in 1 (aortic, range 156 months). Five of the nonstructural valve deterioration explants (range 42 to 122 months) showed only pinpoint mineralization at the commissures. Mean calcium content in nonstructural deterioration explants was 14.70 ± 22.33 versus 99.11 ± 81.52 mg/g in explants with structural valve deterioration. Electron microscopic examination showed early nuclei of mineralization mostly consisting of calcospherulae upon cell debris. Local or diffuse lipid insudation was observed in all but 2 explants and consisted of cholesterol clefts, lipid droplets, and lipid-laden macrophages featuring foam cells. The lipid insudation was the most plausible cause of tearing in 2 explants.

CONCLUSIONS: These pathologic findings support the clinical results of a delayed occurrence of structural failure of Hancock II bioprostheses and a mitigation of mineralization by the anti-calcification treatment. However, other factors such as lipid insudation may come into play in the long term.

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