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Brief Review |
From the Division of Cardiology and Department of Medicine, 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, 303 E Chicago, Tarry 12-717, Chicago, IL 60611. E-mail n-rajamannan{at}northwestern.edu
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 discuss 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.
Calcific aortic stenosis was once thought to be a degenerative process. Experimental models developed in the 21st century are providing evidence that this disease has an active cellular biology. This review will outline these models and discuss the translational clinical implications for calcific aortic stenosis to provide a foundation for future clinical trials in the field of valvular heart disease.
Key Words: valvular heart disease lipids pathophysiology atherosclerosis experimental models
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