title: Biological features (inflammation and neoangiogenesis) and atherosclerotic risk factors in carotid plaques and calcified aortic valve stenosis: two different sites of the same disease?
abstract: 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 1 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.
authors.affiliation: CNR Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy.
authors.forename: Annamaria
authors.initials: A
authors.lastname: Mazzone
authors.forename: Maria Carmela
authors.initials: MC
authors.lastname: Epistolato
authors.forename: Jacopo
authors.initials: J
authors.lastname: Gianetti
authors.forename: Marta
authors.initials: M
authors.lastname: Castagnini
authors.forename: Carlo
authors.initials: C
authors.lastname: Sassi
authors.forename: Roberto
authors.initials: R
authors.lastname: Ceravolo
authors.forename: Stefano
authors.initials: S
authors.lastname: Bevilacqua
authors.forename: Mattia
authors.initials: M
authors.lastname: Glauber
authors.forename: Andrea
authors.initials: A
authors.lastname: Biagini
authors.forename: Piero
authors.initials: P
authors.lastname: Tanganelli
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000209:etiology / Q000473:pathology*; D050197:Atherosclerosis / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D002114:Calcinosis / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007249:Inflammation / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009389:Neovascularization, Pathologic / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D012307:Risk Factors
chemical_list: D015815:Cell Adhesion Molecules; D002118:Calcium