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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:476.)
© 2005 American Heart Association, Inc.

Editorials

Aortic Stenosis and Statins

More Evidence of "Pleotropy"?

Jeffrey S. Borer

From the Weill Medical College of Cornell University, New York.

Correspondence to Jeffrey S. Borer, Weill Medical College of Cornell University, 525 East 68th Street, Room F-467, New York, NY 10021. E-mail ero2002@med.cornell.edu

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

Aortic stenosis (AS) is a relatively common cause of cardiac debility and death, increasing in frequency and severity with age; indeed, AS of at least moderate severity may affect almost 8% of people 75 years of age.¹ The natural history of AS is dependent on the myocardial response to the abnormal left ventricular pressure load caused by the stenotic valve, involving cardiomyocyte hypertrophy, hyperproduction of extracellular matrix collagen by cardiac fibroblasts, and other alterations in myocardial biology. When these changes become critically severe, symptoms develop (angina pectoris, syncope, exertional dyspnea, and other manifestations of pulmonary vascular congestion) followed predictably by cardiac death at an annual rate of 25% unless aortic valve replacement surgery is performed.

See page 592

The basis of the lifesaving effect of aortic valve replacement is clear: the ventricular myocardium is unloaded, enabling myocardial remodeling toward normal, generally with recovery of normal myocardial performance.² A more satisfactory solution than surgery would be prevention of the stenotic process itself. To achieve this goal, the pathophysiology of stenosis development must be known, and effective pharmacological or other countermeasures must be developed and validated clinically.

The first step, elucidation of the pathobiology of AS, began more than a century ago (see, for example, Osler and Gibson³) with the observation at necropsy that the heavily calcified aortic valves of patients with acquired AS of the "degenerative" or "senile calcific" form (now quantitatively the most common) manifest gross and histopathologic characteristics similar to those associated with atherosclerosis. The accretion of calcium . . . [Full Text of this Article]

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