Inflammation Is Associated with the Remodeling of Calcific Aortic Valve Disease
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Inflammation Is Associated with the Remodeling of Calcific Aortic Valve Disease Nancy Coté,1 Ablajan Mahmut,1 Yohan Bosse,2 Christian Couture,2 Sylvain Pagé,2 Sylvain Trahan,2 Marie-Chloé Boulanger,1 Dominique Fournier,1 Philippe Pibarot,2 and Patrick Mathieu1,2,3
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 (r00.25, p00.05) 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. KEY WORDS: calcific aortic valve disease; aortic stenosis; inflammation; remodelling; osseous metaplasia; neovascularization.
ture of the aortic valve and causes a stenosis [2]. Histological studies have pinpointed that CAVD shares some similarities with vascular atherosclerosis, namely, the presence of oxidized lipoproteins and of an inflammatory infiltrate [3]. It should be outlined that despite having some similarities with atherosclerosis, the aortic valve has some inherent properties that differ from the vascular wall [4]. To this effect, the tissue and cellular organization as well as the hemodynamic stress imposed upon the aortic valve are quite different from the vasculature. Another point, which should not be overlooked, is that statins, although efficient to reduce clinical events in patients with atherosclerosis, are inefficient in CAVD. In this regard, three recent randomized studies have shown conclusively that statins, when given to patients with moderate to severe aortic stenosis, do not prevent the natural course of the disease, which is a constant progression in a matter of
INTRODUCTION Calcific aortic valve disease (CAVD) is a chronic disorder which is characterized by an active remodeling process [1]. One important feature of CAVD is the relentless mineralization which, over
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