First, such a model can be used in conjunction with existing imaging techniques to improve diagnostic criteria and to aid in making decisions regarding timing of existing surgical therapies. Second, such a model could be used to quantify the effects of calcification on valve function and to aid in the design of treatments aimed at preventing CAS onset and delaying valve failure once CAS is present. Methods presently used in deciding when to intervene involve examination both of the valve function and the state of the tissue. Valve function is evaluated by using chest imaging to measure various properties of blood flow and various geometric parameters of the valve. Calcification is examined by cardiac catheterization or, more recently, chest imaging. A model that incorporates both valve function and tissue health could aid in predicting the course of disease and in deciding when to intervene. In addition to aiding decision-making regarding existing procedures, a model of calcific disease could be useful in examining and designing emerging methods. Since the loss of valve function is due to tissue dysfunction, treatments to prevent or slow disease progression must target the tissue. Current options for preventing the onset of CAS or valve failure are limited; pharmaceutical approaches such as statins or other drugs may Cyclen ultimately be useful but have not shown consistent benefit in prior studies. A better understanding of the tissue-based nature of CAS progression will enhance our ability to develop new pharmaceutical and surgical treatments. In this paper, we create a model for valve aging which describes theimpactofchanges totissuepropertiesonvalvefunction.Wehave previously described a multiscale simulation of the healthy aortic valve, where we modeled the valve at one point in the patient’s lifetime. In the present paper, we extend the simulation to model ages from 20 to 80. This collection of simulations describes aging in the aortic valve, including calcification, over a patient’s adult life. We have developed a model for the mechanical consequences of aging in the AV, including normal stiffening and thickening as well as progressive calcification. This model predicts the organ-scale valve motion based on changes to the tissue-scale mechanical properties. As such, the simulation method described above has two directions for potential clinical translation. First, by incorporating the tissue-scale nature of calcification,Brivaracetam the model may be able to more accurately predict the degradation of valve function than current methods. Second, the model may be used to evaluate treatments that aim to modify the tissue properties using input parameters consistent with a diminished rate of calcification owing to prevention or therapy. There are limitations to this study and approximations made in this model. First, a number of assumptions are made to construct a model of the valve at any point in time. These assumptions, which we have previously discussed in detail, include simplified representation of the geometry, and assumptions inherent to the material models: a discrete fiber model for the leaflet mechanics, simple Mooney-Rivlin for the sinus wall, and Newtonian fluid for the blood.