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Ann Thorac Surg 1983;36:187-192
© 1983 The Society of Thoracic Surgeons

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Articles

Porcine Bioprosthetic Valve Calcification in Bovine Left Ventricle-Aorta Shunts: Studies of the Deposition of Vitamin K-Dependent Proteins

Departments of Cardiology and Cardiovascular Surgery, Children's Hospital Medical Center, Boston, MA

Accepted for publication October 19, 1982.

^* Address reprint requests to Dr. Levy, Department of Cardiology, Children's Hospital Medical Center, 300 Longwood Ave, Boston, MA 02115

Calcification of glutaraldehyde-preserved bioprosthetic cardiac valves represents a serious clinical problem. Previous work from this laboratory has established the presence in clinical bioprosthetic valve calcifications of vitamin K-dependent calcium-binding proteins, which contain the calcium-binding amino acid -carboxyglutamic acid; no proteins containing -carboxyglutamic acid are present in nonmineralized valves.

The purpose of the present study was to examine a series of bovine circulatory bioprosthetic valve explants for calcification and proteins containing -carboxyglutamic acid. Biochemical analyses of explanted bioprosthetic valves from calves demonstrated proteins with -carboxyglutamic acid accumulating in calcified valves during both the onset and progression of valve calcification; calcium levels in the explanted calf bioprostheses were in the same range as those noted in clinical material. Accumulation of calcium and protein with -carboxyglutamic acid occurred simultaneously and progressively, beginning 2 months after implantation. Small amounts of osteocalcin, the bone-derived protein containing -carboxyglutamic acid, were present in both human and bovine bioprosthetic valve calcifications at comparable levels. No osteocalcin was detectable in non-mineralized valve tissue. Warfarin anticoagulant therapy did not prevent calcification or accumulation of protein with -carboxyglutamic acid. It is concluded that proteins containing -carboxyglutamic acid are involved in both the onset and progression of bioprosthetic valve calcification, and that conventional means of vitamin K antagonism do not alter this association or the course of bioprosthetic valve mineralization.

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