The Progression of Aortic Sclerosis to Aortic Stenosis

Abstract

Aortic stenosis is the most frequent valvular heart disease in the western world and its incidence continues to rise. Until recently, aortic valve sclerosis (AVS) was considered to be a normal degenerative process associated with aging. For this reason, the common and well recognized soft, basal ejection murmur of aortic sclerosis was generally regarded by physicians to be of little or no clinical significance. In the last decade, AVS has been the focus of both clinical and animal research. AVS has emerged as a biomarker for cardiovascular risk, and ultimately leads to aortic stenosis in 16% of adults (Stewart et al., 1997; Cosmi et al., 2002). Calcific aortic valve disease ranges from aortic sclerosis, defined as focal, irregular thickening of aortic valve leaflets with no hemodynamically significant derangement (i.e., peak velocity of ≤ 2 m/s and no significant aortic regurgitation), to severe calcification (with impaired leaflet motion and an aortic jet velocity of ≥ 2.5 m/s) referred to as aortic stenosis. The paradigm of aortic stenosis has shifted from being considered a degenerative aging process; it is now recognized as a dynamic inflammatory process with features similar to atherosclerotic plaque. These features include endothelial disruption, focal deposition of low density lipoprotein (LDL) cholesterol and lipoprotein A, accumulation of macrophages and T lymphocytes, and calcification (Freeman et al., 2004).