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Published Online
on May 18, 2006

Arteriosclerosis, Thrombosis, and Vascular Biology. 2006
Published online before print May 18, 2006, doi: 10.1161/01.ATV.0000227513.13697.ac
A more recent version of this article appeared on August 1, 2006
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Submitted on October 28, 2005
Accepted on May 8, 2006

Pathogenesis of Calcific Aortic Valve Disease. A Disease Process Comes of Age (and a Good Deal More)

Kevin D. O’Brien *

From the Division of Cardiology, University of Washington, Seattle.

* To whom correspondence should be addressed. E-mail: cardiac{at}u.washington.edu.

Background--Over the past 10 to 15 years, calcific aortic valve disease, which includes aortic sclerosis and aortic stenosis, has come to be recognized as an active process, based on: (1) epidemiologic studies demonstrating associations of specific risk factors with increased prevalence or rate of progression of aortic valve disease; (2) identification, in valve lesions, of histopathologic features of chronic inflammation, lipoprotein deposition, renin-angiotensin system components, and molecular mediators of calcification; and (3) identification of cell-signaling pathways and genetic factors that may participate in valve disease pathogenesis. These studies will be reviewed and organized into a proposed global hypothesis for the pathogenesis of calcific aortic valve disease.




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