title: Inflammation is associated with the remodeling of calcific aortic valve disease.
abstract: Calcific aortic valve disease (CAVD) is the most frequent heart valve disorder. Studies indicate that mineralization of the aortic valve may be related to the inflammatory process. However, no clear evidence has been given regarding clinical evolution of aortic stenosis and the inflammatory process within the aortic valve. Aortic valves excised from 285 patients with CAVD undergoing aortic valve replacement were analyzed for the presence of chronic inflammatory infiltrates, and those findings were related to the hemodynamic severity of aortic stenosis. In a subset of 57 patients, in whom additional valvular tissue and the clinical progression rate of aortic stenosis were available, the density of leukocytes was determined as well as the number of TNF-α transcripts. Histological analyses revealed that in 81 (28.4 %) patients, the presence of chronic inflammatory infiltrates was documented within CAVD tissue, which was characterized by the existence of a cluster of cells as well as the presence of neovascularisation and osseous metaplasia. The presence of an inflammatory process within the CAVD tissue was independently related to the remodeling process and the peak transaortic gradient. In addition, the density of leukocytes within CAVD tended to correlate (r = 0.25, p = 0.05) with the progression rate of aortic stenosis. Dense inflammatory infiltrate within CAVD is associated with an active remodeling process, the severity of aortic stenosis, and the hemodynamic progression rate.
authors.affiliation: Laboratoire d'Études Moléculaires des Valvulopathies-LEMV, Groupe de Recherche en Valvulopathies-GRV, Quebec Heart and Lung Institute/Research Center, Department of Surgery, Laval University, Quebec, Canada.
authors.forename: Nancy
authors.initials: N
authors.lastname: Coté
authors.forename: Ablajan
authors.initials: A
authors.lastname: Mahmut
authors.forename: Yohan
authors.initials: Y
authors.lastname: Bosse
authors.forename: Christian
authors.initials: C
authors.lastname: Couture
authors.forename: Sylvain
authors.initials: S
authors.lastname: Pagé
authors.forename: Sylvain
authors.initials: S
authors.lastname: Trahan
authors.forename: Marie-Chloé
authors.initials: MC
authors.lastname: Boulanger
authors.forename: Dominique
authors.initials: D
authors.lastname: Fournier
authors.forename: Philippe
authors.initials: P
authors.lastname: Pibarot
authors.forename: Patrick
authors.initials: P
authors.lastname: Mathieu
mesh_terms: D000368:Aged; D001021:Aortic Valve / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D001024:Aortic Valve Stenosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D002114:Calcinosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology*; D007958:Leukocyte Count; D008055:Lipids / Q000097:blood; D008297:Male; D009389:Neovascularization, Pathologic; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D008055:Lipids; D014409:Tumor Necrosis Factor-alpha