End-stage calcified aortic valve stenosis exhibits active inflammatory infiltrates, neoangiogenesis, and hsp60 gene expression, indicating an active immunomediated process absent in control valves.
Case-Control (n=40)
Does end-stage calcified aortic valve stenosis exhibit biomolecular hallmarks of an immunomediated inflammatory process compared to control valves?
End-stage calcified aortic valve stenosis is characterized by an active immunomediated inflammatory process involving neoangiogenesis, T-lymphocyte infiltration, and hsp60 expression.
OBJECTIVES: We investigated the main biomolecular features in the evolution of aortic stenosis, focusing on advanced lesions. BACKGROUND: "Degenerative" aortic valve stenosis shares risk factors and inflammatory similarities with atherosclerosis. METHODS: We compared nonrheumatic stenotic aortic valves from 26 patients undergoing surgical valve replacement (group A) and 14 surgical control patients (group B). We performed semiquantitative histological and immunohistochemical analyses on valve leaflets to measure inflammation, sclerosis, calcium, neoangiogenesis, and intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression. We assessed heat shock protein 60 (hsp60) gene expression as an index of cellular stress and C-reactive protein, erythrocyte sedimentation rate, and fibrinogen as systemic inflammatory markers. RESULTS: In group A valves, we found a prevalence of calcium nodules surrounded by activated inflammatory infiltrates, neovessels, and abundant ICAM-1, VCAM-1, and hsp60 gene expression. Specimens from group B were negative for all of these markers, except 2 of 14 positivity for hsp60. The presence of active inflammatory infiltrates correlated with an abundance of thin neovessels (p < 0.01) and hsp60 gene expression (p = 0.01), whereas neoangiogenesis correlated with inflammation (p = 0.04), calcium (p = 0.01), and hsp60 gene expression (p = 0.04). CONCLUSIONS: "Degenerative" aortic valve stenosis appears to be a chronic inflammatory process associated with atherosclerotic risk factors. The coexistence of neoangiogenesis, T-lymphocyte infiltration, adhesion molecules, and hsp60 gene expression indicates an active immunomediated process in the final phases of the disease.
Mazzone et al. (Fri,) conducted a case-control in End-stage calcified aortic valve stenosis (n=40). Nonrheumatic stenotic aortic valves vs. Surgical control patients was evaluated on Biomolecular features including inflammation, neoangiogenesis, adhesion molecules, and hsp60 gene expression. End-stage calcified aortic valve stenosis exhibits active inflammatory infiltrates, neoangiogenesis, and hsp60 gene expression, indicating an active immunomediated process absent in control valves.
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