With the decline of acute rheumatic fever, calcific aortic stenosis has become the most common indication for surgical valve replacement in the USA. In the past decade, Stewart and Otto1 2 have described the risk factors for calcific aortic stenosis, including lipids, hypertension, male gender, renal failure, and diabetes. Furthermore, these risk factors are parallel to those described for vascular atherosclerosis. For years this disease process was thought to be due to a degenerative phenomenon by which calcium attaches to the surface of the aortic valve leaflet. Initial models of experimental hypercholesterolaemia have demonstrated that initiating events in aortic valve disease are similar to those of vascular atherosclerosis. Over the past decade, there have been a growing number of studies evaluating human aortic valve specimens defining the cellular pathways important in this disease process. Studies from two independent laboratories, Mohler et al3 and Rajamannan et al,4 have shown that the presence of calcification in the aortic valve is secondary to a bone formation process present in the aortic valve. The clinical importance of calcification was first described by Rosenhek et al,5 who defined a poor prognostic implication for patients who had heavily calcified aortic valves.

The study by Côté et al6 in this issue (see article on page 1175) demonstrates an association between …