There are many similarities in the disease processes of calcific aortic stenosis and coronary artery disease. Both increase in prevalence with age, but neither is thought to be a normal consequence of aging. Calcific aortic stenosis is present in 2–3% of adults over age 65 years and irregular aortic valve thickening without obstruction to left ventricular outflow (aortic sclerosis) is present in about 25% of elderly adults.1 ,2 The presence of an abnormal aortic valve on echocardiography is associated with the same clinical factors, at a similar level of risk, as have been associated with coronary artery disease. Specifically, older age, male sex, increased serum low density lipoprotein (LDL) and Lp(a) lipoprotein concentrations, smoking, hypertension, and diabetes are associated with calcific aortic valve disease.1 ,3-5

Calcific aortic valve disease, ranging in severity from sclerosis to stenosis, is characterised by irregular areas of increased thickening on the aortic side of the valve. Grossly, these areas are opaque, yellowish-white, and are firm on palpation. Microscopically these areas contain evidence of chronic inflammation, with infiltration of macrophages and T lymphocytes. Accumulation of plasma lipoproteins, including LDL and Lp(a) lipoprotein, is present6 and a recent study has shown that these lipoproteins are oxidatively modified.7 In addition, microscopic calcification is present in these early lesions with localisation to areas of lipoprotein accumulation.6 These lesions develop not only in the subendothelium, on the aortic side of the leaflet, but also extend into the adjacent fibrosa, the dense central collagenous layer of the aortic valve …