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J Thorac Cardiovasc Surg 1999;118:998-1005
© 1999 Mosby, Inc.


SURGERY FOR ACQUIRED CARDIOVASCULAR DISEASE

BEHAVIOR OF VITAL AND KILLED AUTOLOGOUS PERICARDIUM IN THE DESCENDING AORTA OF SHEEP

David T. Cheung, PhD, Suk Jung Choo, MD, Albert C. Grobe, MS, Douglas C. Marchion, MS, Hong He Luo, MD, David C. Pang, MS, Blaise E. Favara, MD, James H. Oury, MD, Carlos M. G. Duran, MD, PhD

From The International Heart Institute of Montana Foundation, St Patrick Hospital, 554 West Broadway, Missoula, Mont.

Address for reprints: Carlos M. G. Duran, MD, PhD, The International Heart Institute of Montana Foundation, St Patrick Hospital, 554 West Broadway, Missoula, MT 59801 (E-mail: duran{at}montana.com ).

Objectives: Cardiovascular implants of fresh autologous pericardium produced mixed results including fibrosis with retraction or thinning and dilatation. The reasons for these differences are unknown but may involve activation of cells intrinsic to the tissue implant. To better understand the behavior of autologous pericardial implants, we studied the outcomes of vital pericardium (fresh) versus ethanol-killed pericardium.
Methods: Fresh and ethanol-killed autologous pericardium was transplanted as a patch, a conduit, or a rectangular flap bisecting the lumen in the descending aorta of sheep. The implants, recovered at 1, 5, 10, 15, and 30 days, were evaluated macroscopically and microscopically and by immunohistologic studies.
Results: Fresh implants showed good preservation with fibrin deposition on day 15. Microscopically, cells positive for {alpha}-actin and von Willebrand–related antigen appeared in the fibrin by day 10. By day 30 the flap was fibrotic and retracted whereas the patch and conduit retained their original appearance on the luminal aspect. An endothelium-like layer expressing von Willebrand–related antigen was present in the patch and conduit but absent in the flap. In contrast, the ethanol-killed implants were free of fibrin by day 10. By day 30, there were no signs of fibrosis or retraction, and a surface layer of cells expressing von Willebrand–related antigen, characteristic of endothelial cells, was present on all implants. All ethanol-killed implants were repopulated by host cells.
Conclusion: The transluminal flap is an interesting model for studying the behavior of intraluminal autologous pericardial cardiovascular implants. Killing of the pericardial implants alleviated the fibrosis and tissue retraction observed with fresh flap implants.




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