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The Aortic Stenosis Complex

Traditionally, calcification of the tricuspid aortic valve resulting in aortic stenosis was thought to be secondary to a wear-and-tear effect on the valve due to the aging process. Over the last several years, however, accumulated evidence suggested that inflammation and other risk factors related to the pathogenesis of atherosclerosis are responsible for valvular calcification and for the development of calcific aortic stenosis [1–7]. Dr. Pomerance [8] introduced almost 5 decades ago the possible role of inflammation in valve calcification. In her pioneering work, she described inflammatory changes in areas adjacent to calcification in the mitral annulus. In this study, the incidence of mitral annular calcifications in patients older than 50 years was 8.5%. Importantly, the incidence of aortic valve calcification in male and female patients with mitral annular calcification was 36% and 30%, respectively. In a review paper published in Cardiology, Dr. Rajamannan discussed in detail the similarities and differences between atherosclerosis and aortic stenosis [9]. She nicely described that atherosclerosis over time may differentiate to form “bone” in the heart producing coronary artery and/or left heart valve calcification; this process has been defined as “osteocardiology.” In Dr. Rajamannan’s paper, several pathways leading to calcific aortic stenosis were described along with traditional risk factors. Further, in an attempt to explain differences between coronary artery disease (CAD) and calcific aortic stenosis, fluid dynamics based on the Bernoulli equation were discussed [9].