Do bioprosthetic aortic valves deteriorate more rapidly in patients with the metabolic syndrome?
Kevin D O'Brien
Correspondence Division of Cardiology, University of Washington, Box 356422, 1959 NE Pacific Street, Seattle, WA 98195-66422, USA
Email cardiac@u.washington.edu
This article has no abstract so we have provided the first paragraph of the full text.
Calcific aortic valve disease is a progressive, prevalent disease characterized by valve leaflet thickening and calcification, including aortic sclerosis and aortic stenosis. The latter is distinguished from the former by the presence of left ventricular outflow obstruction. Accumulating evidence supports the evolving concept that calcific aortic valve disease is an active process, sharing many histopathological features of and clinical risk factors for atherosclerosis.1 Both aortic sclerosis and aortic stenosis are associated with increased risk of cardiovascular events, and aortic stenosis carries an 80% 5-year risk of progression to aortic valve replacement (AVR) or death.2 This high morbidity and mortality stands in stark contrast to the fact that not a single pharmacological therapy has been proven to slow the progression of calcific aortic valve disease.3 Thus, at present, the only nonexperimental therapy for the disease remains surgical AVR, which is performed only in cases of end-stage aortic stenosis. In the US, bioprosthetic valves are used in the majority (approximately 65%) of AVR surgeries.2
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