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J Thorac Cardiovasc Surg 1998;115:111-115
© 1998 Mosby, Inc.


SURGERY FOR CONGENITAL HEART DISEASE

Evidence for rejection of homograft cardiac valves in infants

Bijal Rajani, MB, BS, Roger B. Mee, MB, ChB, FRCS, Norman B. Ratliff, MD

From the Departments of Anatomic Pathology and Cardiothoracic Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio.

Received for publication Oct. 1, 1996;> revisions requested Nov. 19, 1996; revisions received Jan. 15, 1997; accepted for publication March 10, 1997. Address for reprints: Norman B. Ratliff, MD, Department of Anatomic Pathology, L25, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland OH 44195.

Objective: Concern about the durability of small homograft cardiac valves has been expressed by surgeons, and evidence has been found that homograft valves evoke a recipient immune response. We reviewed our experience with homograft valves for evidence of rejection.
Methods: A search of our files revealed 11 homograft cardiac valves removed at reoperation and one at autopsy. Six valves were from adults, five were from infants, and one was from a 13-year-old child. Immunohistochemical studies with antibodies against smooth muscle actin, CD20, CD43, CD34, and CD68 were performed on the homografts containing inflammatory infiltrates. These valves happened to be the valves from the five infants. These five valves were also stained with Gram and Gomori's methenamine silver stains.
Results: The failed homografts from the adults and 13-year-old child showed leaflet calcification, fibrosis, and degeneration, but no inflammation. The valves from the infants all failed in less than 8 months. The valve leaflets were thickened, and the valve leaflets and aortic sleeves contained a hyperplastic intimal layer with numerous spindle cells positive for smooth muscle actin embedded in a glycosaminoglycan matrix. The homografts contained multiple foci of inflammation consisting of T lymphocytes (in all five infant valves) and B lymphocytes (in three of the five infant valves). Special stains for organisms were negative.
Conclusions: Rapid failure plus lymphocytic infiltration in valve leaflets and aortic sleeves is consistent with rejection. The hyperplastic intima is similar to coronary arteries in transplant-associated vascular disease. Our observations are consistent with other reports of rapid failure of homograft valves in this age group.




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