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Circulation. 2004;110:1180-1182
doi: 10.1161/01.CIR.0000140722.85490.EA
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(Circulation. 2004;110:1180-1182.)
© 2004 American Heart Association, Inc.


Editorial

Targeted Therapy to Prevent Progression of Calcific Aortic Stenosis

Nalini M. Rajamannan, MD; Catherine M. Otto, MD

From the Division of Cardiology, Department of Medicine, Northwestern University (N.M.R.), Chicago, Ill, and Division of Cardiology, Department of Medicine, University of Washington (C.M.O.), Seattle, Wash.

Correspondence to Catherine M. Otto, MD, Professor of Medicine, Division of Cardiology, Box 356422, University of Washington, Seattle, WA 98195-6422. E-mail cmotto@u.washington.edu


Key Words: Editorials • stenosis • statins • inhibitors • valves


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

Calcific aortic valve disease is common, affecting 25% of adults over the age of 65 years, with progression to severe valve obstruction resulting in more than 50 000 aortic valve replacements annually in the United States. "Degenerative" calcific aortic valve disease was thought for many years to be a passive accumulation of calcium binding to the aortic surface of the valve leaflet. Now, convincing data indicate aortic stenosis is an active disease process with a distinctive histological appearance, associated clinical factors, and variable disease progression, which suggests this disease may be amenable to medical therapy to prevent or slow disease progression.

See p 1291

Aortic valve disease is an active cellular process ranging from aortic sclerosis (a process similar to early atherosclerosis) to severe calcification with bone formation and valve obstruction.1–3 Ex vivo studies have defined the cellular markers and potential signaling pathways important in the progression of this disease. Early valvular sclerotic lesions demonstrate a chronic inflammatory cell infiltrate (macrophages and T lymphocytes), lipid accumulation (apolipoprotein [apo] B, apo(a), and apoE), and {alpha}-actin-expressing cells in the lesion and adjacent fibrosa. End-stage calcified valves contain mature lamellar bone2 with expression of specific bone markers important in the development of osteoblast bone formation.3 In addition, angiotensin-converting enzyme (ACE) and angiotensin II type 1 (AT1) and type 2 (AT2) receptors are present in stenotic aortic valves, implicating this signaling pathway in the disease process.4

These observations are analogous to the cellular findings in vascular atherosclerosis and corroborate epidemiological studies that showed similar . . . [Full Text of this Article]


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