title: Allograft vascular disease: comparison of heart and other grafted organs.
abstract: A striking resemblance exists between the vasculopathy in several different allografts. The arteriopathy of epicardial coronary arteries is diffuse, involving proximal, distal, and small branch segments in a generally concentric pattern of intimal thickening. Smooth muscle cells in a lipid- and glycosaminoglycan-rich matrix are the predominant components of this expanded intima. Varying amounts of collagen are present, more being present late posttransplant. A superficial and, to a lesser degree, deep, bandlike infiltrate of T cells and macrophages is uniformly present, although it is somewhat more prominent in early lesions as compared to more severely narrowed arteries from longer-term, susceptible grafts. The media is likewise altered by areas of lipid and glycosaminoglycan deposition associated with smooth muscle cell loss and phenotypic modulation. The media is altered in an outside-to-inside direction, with percolation of adventitial leukocytes into the outer media. Virtually all of the coronary features are seen in the medium to large arteries of liver, pancreas, and kidney allografts. Chronic rejection in lung allografts is manifest by obliterative bronchiolitis; vascular changes, although architecturally similar, are somewhat less common and result in less-severe luminal narrowing. The role of allograft vasculopathy in chronic lung rejection is thus less certain. A finding perhaps unique to epicardial coronary arteries of heart allografts is the presence of eccentric lesions more typical of native atherosclerosis. Many of the latter grafts probably have preexistent, undetected donor disease. Sequential evaluation of vascular changes is limited in human biopsy material by their general absence in endomyocardial or core liver needle specimens. Fortunately, vascular changes can be detected in some renal and pancreas core needle biopsies, and these findings may provide an avenue for monitoring the effectiveness of immunosuppressive therapy, antiviral or lipid-altering therapies, or modifications of smooth muscle cell proliferation and glycosaminoglycan deposition yet to be developed.
authors.affiliation: Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, USA.
authors.forename: S
authors.initials: S
authors.lastname: Radio
authors.forename: S
authors.initials: S
authors.lastname: Wood
authors.forename: J
authors.initials: J
authors.lastname: Wilson
authors.forename: H
authors.initials: H
authors.lastname: Lin
authors.forename: G
authors.initials: G
authors.lastname: Winters
authors.forename: B
authors.initials: B
authors.lastname: McManus
mesh_terms: D016027:Heart Transplantation / Q000276:immunology / Q000473:pathology*; D016041:Heart-Lung Transplantation / Q000276:immunology / Q000473:pathology; D006801:Humans; D016030:Kidney Transplantation / Q000276:immunology / Q000473:pathology; D016031:Liver Transplantation / Q000276:immunology / Q000473:pathology; D016040:Lung Transplantation / Q000276:immunology / Q000473:pathology; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D016035:Pancreas Transplantation / Q000276:immunology / Q000473:pathology; D011183:Postoperative Complications; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D014180:Transplantation / Q000473:pathology*; D014184:Transplantation, Homologous / Q000473:pathology; D014652:Vascular Diseases / Q000209:etiology / Q000473:pathology*