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The timing of aortic valve surgery is described for patients presenting with two conditions: aortic stenosis and chronic aortic regurgitation.
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.
The initial phase of the disease process leading to aortic stenosis is mild leaflet thickening without obstruction to ventricular outflow, defined as aortic sclerosis. Although these patients do not have cardiac symptoms, they still are at increased risk for adverse cardiovascular outcomes. In the population based Cardiovascular Health Study, subjects with aortic sclerosis on echocardiography and no known cardiovascular disease had an approximately 50% increased …