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Presented in part at the Western Section, American Federation for Clinical Research, Carmel, Calif, February 11, 1994.
From the Division of Cardiology (K.D.O'B., J.K., C.M.O.) and Northwest Lipid Research Laboratories (S.M.M.), Departments of Medicine and Pathology (D.D.R., C.E.A.), University of Washington, Seattle. Dr Kuusisto is now with Kuopio (Finland) University.
Correspondence to Kevin D. O'Brien, MD, Division of Cardiology, Box 356422, University of Washington, Seattle, WA 98195-6422.
Abstract Nonrheumatic aortic stenosis of
trileaflet aortic valves has been considered to be a
"degenerative" process, but the early lesion of aortic
stenosis contains the chronic inflammatory cells,
macrophages and T lymphocytes. Because lipoprotein deposition
is prominent in atherosclerosis, another chronic
inflammatory process, this study examined whether lipoproteins
accumulate in aortic valve lesions. Immunohistochemical studies were
performed to detect apolipoprotein (apo) B, apo(a), apoE,
macrophages, and
-actinexpressing cells on 18
trileaflet aortic valves that ranged from normal to stenotic.
All three apolipoproteins were detected in early through end-stage
lesions of aortic stenosis but not in
histologically normal regions. Comparison with oil red
O staining suggested that most of the extracellular neutral lipid in
these valves was associated with either plasma-derived or locally
produced apolipoproteins. Thus, in early through end-stage aortic
valve lesions, apolipoproteins accumulate and are associated with the
majority of extracellular valve lipid. These results are
consistent with the hypothesis that lipoprotein accumulation in
the aortic valve contributes to pathogenesis of aortic
stenosis.
Key Words: lipids macrophages inflammation foam cells
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