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J Thorac Cardiovasc Surg 2006;132:175-176
© 2006 The American Association for Thoracic Surgery


Brief Communication

Endothelial and smooth muscle cell populations in a decellularized cryopreserved aortic homograft (SynerGraft) 2 years after implantation

Dylan V. Miller, MD a , * , William D. Edwards, MD a , Kenton J. Zehr, MD b

a Division of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota
b Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota

* Corresponding author: Dylan V. Miller, M.D. Mayo Clinic 200 First Street S.W. Rochester, MN 55905 Phone: 507-284-1192 FAX: 507-284-1599. (Email: miller.dylan@mayo.edu).

The first 20% of the full text of this article appears below.

Introduction

While the cryopreserved homograft heart valve is an established option for patients requiring replacement of damaged or diseased aortic valves, there is evidence that valve durability may be negatively impacted by the allogenicity of residual viable cells. 1 Go Decellularization techniques, like the SynerGraft process, reduce the cellular content of homograft valves, in hopes of modifying the host immune response to the graft. Uncertainty remains over the mechanism and extent of "recellularization" occurring in these decellularized grafts after implantation in humans. Characterization of cells populating the implanted decellularized grafts is important in understanding host adaptation and possibly in-vivo longevity of the grafts. This report details the histomorphologic and immunophenotypic features of cells identified in a decellularized (SynerGraft) aortic valve recovered two years after implantation.

Clinical Synopsis

At age 19, a male patient underwent replacement of his congenitally bicuspid aortic valve. At age 52, he underwent insertion of an aortic SynerGraft homograft for prosthetic aortic valve stenosis and an ascending aortic aneurysm. Postoperatively, left ventricular function did not improve significantly, and he underwent cardiac transplantation two years later. The explanted heart showed moderate left ventricular hypertrophy, coronary atherosclerosis, . . . [Full Text of this Article]




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