Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology · 2007
Role of inflammation in nonrheumatic, regurgitant heart valve disease. A comparative, descriptive study regarding apolipoproteins and inflammatory cells in nonrheumatic heart valve disease.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wallby Lars, Steffensen Thora, Broqvist Mats
Аннотация
BACKGROUND: Nonrheumatic aortic stenosis is the predominant cause of heart valve surgery in the Western world. Aortic and mitral regurgitation account for a lesser amount of the heart valve surgery. During the 1990s, inflammatory cell infiltrates have been demonstrated in nonrheumatic stenotic aortic valves. These findings suggest an inflammatory component in the pathogenesis of nonrheumatic aortic valve stenosis. However, nonrheumatic regurgitant aortic and mitral valves have not been investigated in this respect. The aim of this study was to compare nonrheumatic regurgitant aortic and mitral valves with stenotic aortic valves regarding the presence of T lymphocytes, macrophages, apolipoprotein B, and apolipoprotein A-I.
METHODS: Valve specimens were obtained from 42 patients referred to hospital for surgery because of significant heart valve disease. From these patients, 29 aortic stenotic valves, 9 aortic regurgitant, and 6 mitral regurgitant valves, all nonrheumatic, were obtained for the study. Fourteen valves collected from subjects undergoing clinical/medicolegal autopsy were used as control. In order to identify mononuclear inflammatory cells and apolipoproteins, sections were investigated with immunohistochemical analyses and then categorized semiquantitatively.
RESULTS: Regurgitant and control valves showed a significantly lower degree of inflammatory cell infiltrate and a lower degree of apolipoprotein deposition as compared to stenotic aortic valves.
CONCLUSIONS: The signs of inflammation seen in nonrheumatic aortic stenosis are not prominent features in the nonrheumatic, regurgitant valves. This is consistent with the multi-factorial pathogenesis of these conditions.
METHODS: Valve specimens were obtained from 42 patients referred to hospital for surgery because of significant heart valve disease. From these patients, 29 aortic stenotic valves, 9 aortic regurgitant, and 6 mitral regurgitant valves, all nonrheumatic, were obtained for the study. Fourteen valves collected from subjects undergoing clinical/medicolegal autopsy were used as control. In order to identify mononuclear inflammatory cells and apolipoproteins, sections were investigated with immunohistochemical analyses and then categorized semiquantitatively.
RESULTS: Regurgitant and control valves showed a significantly lower degree of inflammatory cell infiltrate and a lower degree of apolipoprotein deposition as compared to stenotic aortic valves.
CONCLUSIONS: The signs of inflammation seen in nonrheumatic aortic stenosis are not prominent features in the nonrheumatic, regurgitant valves. This is consistent with the multi-factorial pathogenesis of these conditions.