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Homograft Heart Valves

A theory is proposed for aortic valve closure, based on flow studies using a model valve placed in a pulsatile water tunnel (Bellhouse & Bellhouse 1968, 1969a). It is shown that strong vortices form in the aortic sinuses, and that the ridge at the distal end of the sinuses is maintained at freestream stagnation pressure during systole. At peak systole, the cusps project slightly into the sinuses and are held in a stable position by the vortices and the aortic flow. Deceleration of the aortic flow in the latter part of systole causes vortex thrust to dominate the thrust from the aortic side of the cusps, and the valve begins to close. Closure is three-quarters accomplished before forward flow ceases, and reversed flow seals the valve, with backflow less than 5% of stroke volume. When the aortic valve is stenosed, a turbulent jet results, which is not intercepted by the sinus ridge, and no sinus vortices are formed. The pressure at the cusp free-margins is greatly reduced (a Venturi effect), and sinus pressure is reduced accordingly. Since the coronary ostia are located within the sinuses, stenosis of the aortic valve is proposed as a cause of angina pectoris associated with effort. When the sinuses are occluded, thereby removing the fluid-mechanic closure mechanism, the valve is closed suddenly and unevenly by reversed flow with backflow exceeding 20% of the stroke volume. Using a model of the left ventricle pulsated sinusoidally (Bellhouse & Bellhouse 1969b), it is shown that a ring vortex is formed in the ventricle as the valve opens, and that the cusps are held in a stable near-cylindrical shape. After peak diastole, flow deceleration and vortex thrust cause a pressure imbalance across the cusps tending to close them. As in the aortic valve, three-quarters of mitral valve closure is shown to be accomplished before the flow through the mitral ring reverses, so backflow is less than 2% of stroke volume. When the ventricle is expanded slowly, so that both the vortex and flow deceleration are absent, and the ventricle is then suddenly contracted, it is shown that backflow increases to 10% of stroke volume.