Etiology of degenerative disease of the tri-leaflet aortic valve: a simple explanation for a complex problem

Abstract

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 tri-leaflet aortic valve is a disease similar in etiology with sclerosis of the aortic wall. In other words, degenerative aortic valve disease is atherosclerosis 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 sinotubular junction, characterized not only by morphological features but also 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 experiments also demonstrate that loss of aortic wall compliance at the level of the sinuses leads to significant flexion stress in the aortic leaflets and it is likely to start a chain of events, which begins with mechanical damage to the leaflet microstructure then continues to more evident sclerosis, and finally ends in gross distortion and/or calcification of the cusps.The loss of the "pull-andrelease" process may also play a part in disintegration of bioprosthetic valves and in degeneration of native aortic valves encased in noncompliant prostheses.