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Ann Thorac Surg 1996;62:169-174
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Calcification of Bovine Pericardium: Glutaraldehyde Versus No-React Biomodification

Departments of Cardiothoracic Surgery and Preventive Medicine and Community Health, New Jersey Medical School; and the Department of Applied Chemistry, New Jersey Institute of Technology, Newark, New Jersey

Accepted for publication March 7, 1996.

Background. Calcific degeneration is the most frequent cause of clinical dysfunction of glutaraldehyde (GA)-pretreated bioprosthetic heart valves. The No-React (NR) process has been shown to be a promising anticalcification treatment. In this comparative study, our objective was to delineate the advantages of the NR treatment over GA.

Methods. Bovine pericardial strips pretreated with GA and NR were individually incubated in calcium phosphate solution for 21 days at 37°C. The pretreated bovine pericardium then was implanted subcutaneously in rats and retrieved at 14, 21, and 35 days after-implantation. Mineral and morphologic analyses were performed on each specimen.

Results. The NR-treated pericardium revealed significantly reduced in vitro calcification compared with the GA-treated tissue (mean tissue calcium content 1.3 ± 0.2 versus 5.9 ± 0.7 µg/mg; p < 0.001). Mineral analysis showed progressive calcification of the GA-pretreated pericardium over the period of implantation (calcium content increasing from 49.6 ± 9.6 µg/mg after 2 weeks to 134.3 ± 9.1 µg/mg at 5 weeks after-implantation). The NR-treated implants had calcified significantly less (p < 0.05) at each corresponding interval. Moreover, morphologic examinations demonstrated a protracted inflammatory response in the form of giant cell and mononuclear cell infiltration associated with intrinsic collagen disruption in the GA-treated tissue; the NR-treated pericardium maintained morphologic integrity with a mild inflammatory response.

Conclusions. The NR biochemical process appears not only to attenuate pericardial calcification, but also to abort the host's destructive inflammatory response to the xenograft.

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