Aortic stenosis (AS) is the second most common valvular abnormality. Incidence increases with age and it is present in up to 2% of 60 year olds and 10% of 80 year olds. The disease process comprises fibrocalcification of the valve that results in orifice narrowing and LV outflow obstruction and is referred to as calcific aortic valve disease (CAVD). Aortic valve stenosis causes increased LV pressure, compensatory LV hypertrophy and affects cardiac output. Symptoms comprise a “classic triad” of shortness of beath, chest pain or syncope. Previously AS was considered a “degenerative process” that could not be modified however recent histological assessment confirms that AS is an active process of oxidised lipids and infiltrating inflammatory cells, perhaps opening pathways to future preventative therapies.
Untreated symptomatic AS has a two-year mortality of up to 50%. To date no pharmacological treatment has been shown to slow disease progression. Therefore, treatment options for severe AS are limited to valve replacement either surgically or percutaneously with a transcatheter system.
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