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Circulation. 2006;114:2007-2009
doi: 10.1161/CIRCULATIONAHA.106.657759
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(Circulation. 2006;114:2007-2009.)
© 2006 American Heart Association, Inc.


Editorial

Calcific Aortic Stenosis

A Disease Ready for Prime Time

Nalini M. Rajamannan, MD

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

Correspondence to Nalini M. Rajamannan, MD, Valve Director, Bluhm Cardiovascular Institute, Northwestern University, Feinberg School of Medicine, 300 East Chicago Ave, Tarry 12–717, Chicago, IL 60611. E-mail n-rajamannan@northwestern.edu


Key Words: Editorials • aging • atherosclerosis • cholesterol • pathology • stenosis • valves


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Calcific aortic stenosis is the number 1 cause for surgical valve replacement in the United States and Europe. In 2006, surgical valve replacement still remains the number 1 indication for the treatment of this disease process, as defined by the American College of Cardiology/American Heart Association guidelines for valvular heart disease by Bonow et al.1 This standard of care for patients with severe symptomatic aortic stenosis requiring surgical valve replacement was defined in 1968 by Ross and Braunwald2 as the main therapy for this disease. For years, this disease has been described as a passive process that develops secondary to serum calcium attaching to the valve leaflet surface to cause nodule formation. Therefore, surgical replacement of the valve is the obvious approach toward relieving outflow obstruction in these patients. Until recently, the lack of experimental models in this field has limited our understanding of the disease.

Article p 2065

In the middle of the last century, the field of cardiology was in a similar position with our understanding of coronary vascular atherosclerosis. This was summarized in 1942 by Dr James B. Herrick,3 who wrote a short history of cardiology. In the chapter on coronary atherosclerosis, he predicted the future of therapeutic approaches for vascular atherosclerosis. In this textbook, he wrote of heart disease: "This is the story of a bad disease. ... The outlook for dread angina it thought to be more favorable than it was first thought ... though the cause ... has not been discovered, and vascular disease . . . [Full Text of this Article]




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