Aortic stenosis

Aortic stenosis may be caused by rheumatic disease, a congenital bicuspid valve or calcification of a trileaflet valve. In Europe and North America, the aetiology of aortic stenosis most often is increased leaflet stiffness, without commissural fusion, caused by lipo-calcific deposits on the aortic side of the valve leaflets. This active disease process affects both congenitally bicuspid and normal trileaflet aortic valves and represents the extreme of a spectrum of disease that includes both aortic sclerosis without outflow obstruction and severe valvar aortic stenosis. Aortic valve sclerosis and stenosis are the most common valve diseases in Europe and North America, with sclerosis present in about 25% of all people over age 65 years and stenosis present in 2–7% of this population.1 Significant outflow obstruction tends to occur at a younger age in patients with a bicuspid valve, possibly related to increased mechanical stress on the valve leaflets.

At the tissue level, aortic valve stenosis is characterised by focal areas of displacement of the subendothelial elastic lamina on the aortic side of the leaflet; there is protein and lipoprotein deposition and an inflammatory cell infiltrate with macrophages, T lymphocytes, and production of proteins, such as osteopontin, that are associated with tissue calcification. Ongoing studies of this active disease process will further clarify mechanisms of disease.