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J Am Coll Cardiol, 2003; 42:593-599, doi:10.1016/S0735-1097(03)00786-1 © 2003 by the American College of Cardiology Foundation |
* Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
Manuscript received May 1, 2003; accepted May 9, 2003.
* Reprint requests and correspondence: Dr. Kwan-Leung Chan, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, Canada, K1Y 4W7.
kchan{at}ottawaheart.ca
Aortic stenosis (AS) is the most common valvular disease requiring valve replacement. Its prevalence increases with age. When the severity of AS is only mild to moderate, it is well tolerated. When it becomes severe, AS confers significant morbidity and mortality. Adverse events can be avoided if it is possible to prevent or retard the progression from mild or moderate AS to severe AS. Progression of AS parallels the progression of sclerotic changes involving the aortic valve, which share histological and immunochemical similarities with the process of atherosclerosis. Far from being just a degenerative process, the development of AS is a complex and highly regulated process with a number of modifiable factors. One of the key factors appears to be lipoproteins, which are intimately involved in several pathways crucial to the development of AS. The importance of lipoproteins is further supported by epidemiological and clinical studies showing a strong association between lipoproteins and AS. The time has come to initiate prospective studies to assess the effect of cholesterol lowering on the progression of AS.
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