With aortic stenosis, there is a decrease in the effective valve orifice area, resulting in progressive obstruction of the left ventricle. The ventricle adapts through concentric hypertrophy, which increases diastolic stiffness and impairs the efficacy of diastolic coronary blood flow. Diastolic dysfunction precedes systolic dysfunction. With aortic insufficiency, gradual ventricular dilatation occurs, causing an increase in wall stress. This, in conjunction with the decrease in diastolic pressure, reduces diastolic coronary blood flow. With continued dilatation, fibrosis occurs, increasing ventricular stiffness and impairing diastolic relaxation. Eventually, the preload reserve of the ventricle is reached and further dilatation and fibrosis result in a decline in systolic function that may not be recoverable after aortic valve replacement.