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Ann Thorac Surg 2002;73:1346-1354
© 2002 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery and the Heineman Research Laboratory, Carolinas Medical Center, Charlotte, North Carolina, USA
* Address reprint requests to Dr Robicsek, Carolinas Heart Institute, Carolinas Medical Center, 1000 Blythe Blvd, Charlotte, NC 28203 USA
e-mail: tjohn{at}sanger-clinic.com
Risk factors for both atherosclerotic aortic wall disease and degenerative disease of the trileaflet aortic valve are very similar if not identical. This correlation grows even stronger as the person advances in years. Because of this, it is the prevailing view that sclerosis of the trileaflet aortic valve, unless previously affected by septic or rheumatic endocarditis, is a disease similar in origin to sclerosis of the aortic wall, ie, degenerative aortic valve disease is arteriosclerosis of the aortic valve. Our studies challenge these views. The aortic valve is a functional assembly composed of the three cusps, corresponding sinuses, and the sino-tubular junction, characterized not only by morphologic features but also by its functional properties, which together create an environment that is optimal for distribution of diastolic pressure load and assures proper and timely valve opening and closure. Our more recent experiments also demonstrate that loss of aortic wall compliance at the level of the sinuses leads to significant stress-overload on the aortic leaflets and it is likely to start a chain of events, which begins with minor changes in their microstructure, then continues in more evident sclerosis, and finally ends in gross distortion or calcification of the cusps. The loss of the "pull-and-release" process may also play a part in disintegration of bioprosthetic valves and in degeneration of native aortic valves encased in noncompliant prostheses.
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