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on November 20, 2008

Arteriosclerosis, Thrombosis, and Vascular Biology. 2008
Published online before print November 20, 2008, doi: 10.1161/ATVBAHA.107.156752
A more recent version of this article appeared on February 1, 2009
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Submitted on April 11, 2007
Accepted on October 27, 2008

Calcific Aortic Stenosis. Lessons Learned From Experimental and Clinical Studies

Nalini M. Rajamannan *

From the Division of Cardiology and Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Ill.

* To whom correspondence should be addressed. E-mail: n-rajamannan{at}northwestern.edu.

Abstract—Calcific aortic stenosis is the most common indication for surgical valve replacement in the United States. For years this disease has been described as a passive degenerative process during which serum calcium attaches to the valve surface and binds to the leaflet to form nodules. Therefore, surgical treatment of this disease has been the approach toward relieving outflow obstruction in these patients. Recent studies demonstrate an association between atherosclerosis and its risk factors for aortic valve disease. In 2008, there are increasing number of epidemiology and experimental studies to provide evidence that this disease process is not a passive phenomena. There is an active cellular process that develops within the valve leaflet and causes a regulated bone formation to develop. If the atherosclerotic hypothesis is important in the initiation of aortic stenosis, then treatments used in slowing the progression of atherosclerosis may be effective in patients with aortic valve disease. This review will review the pathogenesis and the potential for medical therapy in the management of patients with calcific aortic stenosis by examining the lessons provided from the experimental research.


Key words: valvular heart disease • lipids • pathophysiology atherosclerosis • experimental models




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