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J Thorac Cardiovasc Surg 2003;126:939-941
© 2003 The American Association for Thoracic Surgery

Editorial

Is degenerative calcification of the native aortic valve similar to calcification of bioprosthetic heart valves?

^a Department of Surgery, University of Toronto, Toronto, Ontario, Canada

Received for publication April 23, 2003; accepted for publication April 30, 2003.

^* Address for reprints: Tirone E. David, MD, Department of Surgery, University of Toronto, 200 Elizabeth St, 13EN219, Toronto, Ontario M5G 2C4, Canada
tirone.david@uhn.on.ca

The first 20% of the full text of this article appears below.

Recent epidemiologic, histologic, and molecular studies suggest that the pathogenesis of degenerative disease of the native aortic valve resembles that of atherosclerosis.^1-3 The initial aortic valve lesion, valve sclerosis, is related to infiltration and oxidation of lipoproteins similar to that seen in atherosclerosis.^2,3 Calcification, one of the principal features of degenerative disease of the native aortic valve, is also present in atherosclerotic plaques.^2,3 Not surprisingly, retrospective studies showed an association between risk factors for coronary artery disease, such as male sex, cigarette smoking, high blood pressure, diabetes, and hyperlipidemia, and progression of aortic valve stenosis.⁴ However, a recent prospective, population-based epidemiologic study showed no correlation between coronary artery risk factors and the rate of progression of aortic stenosis.⁵

What many studies have shown more consistently is that treatment with 3-hydroxy-3-methyl-glutamyl coenzyme A reductase inhibitors (statins) reduces the rate of progression of aortic valve stenosis.^4-7 In most studies the slower rate of calcification of the aortic cusps produced by statins did not appear directly related to the reduction of serum cholesterol level but rather caused by its pleiotropic effects.^5-7 Statins affect a multitude of cellular functions: they increase production of nitric oxide by endothelial cells, reduce inflammatory reactions, decrease secretion of metalloproteins and osteopontin by macrophages, stabilize atherosclerotic plaques, prevent thrombus formation, and have many other less defined effects, such as reducing the risk of dementia.^8,9

Calcification of the native aortic cusps is a complex and poorly understood process, but it appears to be related to inflammation, infiltration of lipoproteins, and ossification.^2,3,10,11 Statins probably delay calcification of the native aortic cusps by reducing inflammation and decreasing the deposition of lipoproteins and ossification, as they do in coronary arteries.^8,12 However, the notion . . . [Full Text of this Article]