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Because little information is available regarding the clinical performance of the Hancock porcine bioprosthesis (JohnsonJohnson Cardiovascular, King of Prussia, Pa.) implanted in the tricuspid position, we reviewed the long-term follow-up of patients who had tricuspid valve replacement with this device. From March 1970 to December 1983, 45 patients had tricuspid valve replacement, either isolated (seven patients) or combined with replacement of other valves (38 patients) by means of a standard, glutaraldehyde-preserved Hancock porcine bioprosthesis. Follow-up ranged from 0.2 to 14.7 years (mean, 7.6 +/- 3.6 years) and was complete. The late mortality rate was 6.6% +/- 1.6%/pt-yr and the actuarial survival rate at 14 years was 23% +/- 9%. Reoperation because of structural deterioration of the tricuspid, the mitral, or both bioprostheses was performed in nine patients (3.7% +/- 1.2%/pt-yr) from 40 to 177 months (mean, 112 +/- 43 months) and resulted in no deaths. Actuarial freedom from structural deterioration of a Hancock tricuspid porcine bioprosthesis at 14 years is 68% +/- 13%. Morphologic examination of explanted porcine bioprostheses showed that those implanted in the tricuspid position had lower degrees of calcification and less severe structural changes than those simultaneously explanted from the mitral position. We conclude that the Hancock porcine bioprosthesis has an acceptable long-term durability and satisfactory performance after tricuspid valve replacement, and we continue to favor its use in the tricuspid position even in association with mechanical prostheses in the left side of the heart.

Large dissecting cuspal hematomas (DCHs) were present in six (3%) of 193 porcine bioprostheses (PBs) explanted at reoperation. In four mitral PBs, the DCHs contributed to valve dysfunction; in one aortic PB, DCH was the only determinant of failure, causing stenosis by cusp thickening and rigidity. In another mitral PB, DCHs were occasionally found in the setting of valve incompetence due to commissural tears. While confirming that DCHs are a potential but infrequent cause of PB failure, these observations demonstrate that they may involve PBs implanted both in mitral and aortic position and might be a complication of anticoagulation.

Glutaraldehyde is considered a promoter of calcification by the action of toxic aldehyde group residuals from cross-linking. Post-fixation treatment with homocysteic acid (HA), besides bonding aldehyde groups and neutralizing toxicity, should enhance biocompatibility due to the strongly electronegative sulfonic group. The aim of this investigation was to evaluate HA efficacy on tissue preservation and dystrophic calcification mitigation in glutaraldehyde cross-linked bovine pericardium (BP) using a subcutaneous rat model.Four samples of BP, two with glutaraldehyde-HA and two with glutaraldehyde treatment, were implanted in each of 24 male Sprague-Dawley rats. Three rats were killed at 14 days, eight at 28 days, eight at 56 days and five at 84 days. Unimplanted glutaraldehyde-HA- and glutaraldehyde-treated samples served as controls. All samples were studied by gross examination, mammography, light transmission and scanning electron microscopy, and atomic absorption spectroscopy. The nature of mineralization was investigated by coupling techniques of scanning electron microscopy, electron microprobe analysis and X-ray powder diffraction.No histological and ultrastructural differences were found between glutaraldehyde-HA- and glutaraldehyde-treated BP, whether implanted or unimplanted. In both groups, calcification progressed with time, but significantly less after glutaraldehyde-HA treatment than after glutaraldehyde alone and at all time intervals (14.63 +/- 21.34 versus 43.17 +/- 15.99 at 28 days, p = 0.003; 56.42 +/- 40.20 versus 90.59 +/- 32.90 at 56 days, p = 0.008; 91.68 +/- 67.68 versus 156.23 +/- 17.85 at 84 days, p = 0.01). Differences were evident by mammography and histology (von Kossa stain). Electron microprobe analysis in both groups showed the composition of calcified nuclei to be calcium phosphate, stoichiometrically close to apatite (Ca5(PO4)3(OH)). The occurrence of crystallized apatite was supported by X-ray powder diffraction findings, the amount of crystallized apatite being higher in glutaraldehyde-treated samples.Post-fixation treatment with HA preserves BP structural properties and significantly mitigates mineralization of long-term subcutaneous implants.