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T lymphocyte infiltration in non-rheumatic aortic stenosis: a comparative descriptive study between tricuspid and bicuspid aortic valves

Background: The two most common causes of aortic stenosis are primary “degenerative” calcification of tricuspid aortic valves and secondary calcification of congenital bicuspid valves. T lymphocyte infiltration occurs in stenotic tricuspid aortic valves, indicating an inflammatory component, but it...

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Bibliographic Details
Published in:British heart journal 2002-10, Vol.88 (4), p.348-351
Main Authors: Wallby, L, Janerot-Sjöberg, B, Steffensen, T, Broqvist, M
Format: Article
Language:English
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Summary:Background: The two most common causes of aortic stenosis are primary “degenerative” calcification of tricuspid aortic valves and secondary calcification of congenital bicuspid valves. T lymphocyte infiltration occurs in stenotic tricuspid aortic valves, indicating an inflammatory component, but it has not been shown whether it also occurs in stenotic bicuspid valves. Objective: To compare non-rheumatic tricuspid and bicuspid stenotic aortic valves for the presence and distribution of T lymphocytes. Setting: University hospital. Patients and design: Valve specimens were obtained from 29 patients (15 women, 14 men, mean age 69 years (range 52–81 years)), referred to the hospital for aortic valve replacement because of symptomatic aortic valve stenosis. There were 17 tricuspid valves (from 10 women and seven men, mean age 71 years) and 12 bicuspid valves (from five women and seven men, mean age 67 years). To identify mononuclear inflammatory cells, sections were stained with antibodies for CD3 (pan-T cell antigen, Dako 1:400) and then graded histologically according to the degree of T cell infiltrate. Results: T lymphocyte infiltration was present in both tricuspid and bicuspid stenotic aortic valves, without any significant differences in extent or localisation. Conclusions: Stenotic bicuspid aortic valves show the same degree of T lymphocyte infiltration as degenerative tricuspid aortic valves. Inflammation needs to be considered in the pathogenesis of acquired aortic stenosis, irrespective of the primary valve anomaly.
ISSN:1355-6037
0007-0769
1468-201X
1468-201X
DOI:10.1136/heart.88.4.348