Journal
AMERICAN JOURNAL OF CLINICAL PATHOLOGY
Volume 126, Issue 4, Pages 494-502Publisher
OXFORD UNIV PRESS INC
DOI: 10.1309/W75NTE5QBC9DXE03
Keywords
atherosclerotic risk factors; carotid plaque; aortic valve stenosis; neoangiogenesis; inflammation; adhesion molecule
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Neoangiogenesis and inflammation have a pivotal role in atherosclerosis. Observations support the hypothesis that calcified aortic valve stenosis is an inflammatory process, similar to atherosclerosis in tissue features and risk factors. We studied 2 groups of cases: 47 were affected by hemodynamic atherosclerotic carotid plaque (group 1) and 35 by severe calcified aortic valve stenosis (group 2). We compared the groups for atherosclerosis risk factors, morphologic features, and immunohistochemical phenotypes. In both groups, men, smokers, and hypertensive subjects prevailed, and histologic analysis showed an elevated score for T-lymphocyte infiltrates, neoangiogenesis, calcium, and sclerosis. Adhesion molecule expression was present in both lesions. Expression of intercellular adhesion molecule I correlated with inflammatory infiltrates (group 1, P = .0007; group 2, P = .06). Neoangiogenesis also correlated with inflammatory infiltrates (group 1, P = .035; group 2, P = .045). In valves, neoangiogenesis correlated with calcium (P = .048). Carotid plaque and calcified valve stenosis showed common risk factors and biologic hallmarks of a chronic inflammatory process. Inflammation and neoangiogenesis have a crucial role in plaque evolution and in the progression of aortic valve stenosis.
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