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  • Title: Morphologic findings in explanted Hancock II porcine bioprostheses.
    Author: Butany J, Yu W, Silver MD, David TE.
    Journal: J Heart Valve Dis; 1999 Jan; 8(1):4-15. PubMed ID: 10096476.
    Abstract:
    BACKGROUND AND AIM OF THE STUDY: Heart valve substitutes have been in use for over 30 years. Bioprosthetic heart valves have many advantages, but unfortunately suffer tissue degeneration and calcification. Many approaches, such as antimineralization treatment to prevent or delay these changes, have been tried. We present the morphologic findings from a series of Hancock II (antimineralization-treated) porcine bioprostheses. METHODS: Forty-five Hancock II porcine valve bioprostheses (16 mitral, 29 aortic) surgically explanted between March 1991 and December 1995 at the Toronto Hospital were analyzed for morphologic findings and causes of failure. The prostheses were implanted in 36 adults (mean age 55+/-14.7 years, range: 27 to 75 years) and had been in place between one month and 11 years (mean 5.1+/-3.3 years). RESULTS: Structural valve deterioration (SVD) characterized by tissue degeneration, calcification, cusp tears and increased stiffness, was the single most significant finding and cause of failure, affecting 56% of valves. Some degree of calcification was seen in 55% of prostheses, with severe calcification (grade 3 or 4) in 18%. Aortic bioprostheses showed more severe and earlier calcification than mitral ones (p = 0.03). Compared with the standard Hancock valve, the low incidence of significant calcification suggests a beneficial protective effect of antimineralization treatment. Severe pannus (grade 3 or 4) was seen in 60% of these prostheses. The pattern of pannus growth differs between mitral and aortic sites; mitral prostheses showed pannus on the flow and non-flow surfaces, often associated with cusp tears, mitral regurgitation and mitral leaflet preservation. A similar degree of pannus on aortic prostheses was invariably present on the flow surface and extended onto the valve cusps, leading to changes in the orifice which may cause clinical aortic stenosis. Infective endocarditis was seen in 15 prostheses (five mitral, 10 aortic) from 11 patients, and comprised the second most important cause of prosthesis failure. The risk of recurrent endocarditis was particularly high in patients who had infective endocarditis before valve replacement, even at five and six years post implantation. CONCLUSIONS: SVD is the major finding in explanted Hancock II bioprostheses and is associated with cusp tears and calcification. The incidence of tissue calcification appears lower at the mitral site. These findings suggest that the antimineralization treatment had some beneficial effect. Pannus associated with prosthesis dysfunction at the mitral sites is a prominent finding and on the non-flow surface may be related to the native mitral valve-conserving procedure.
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