Abstract:
The aortic heart valve undergoes significant geometric and mechanical changes over time, affecting its overall function. A normal, healthy valve's cusps thicken and become less extensible with age. In the pathological condition of calcific aortic stenosis (CAS), calcified nodules progressively stiffen the cusps, severely impeding valve opening and potentially closing. Given that local mechanical alterations within the cusps, whether due to normal aging or disease processes, directly impact the valve's global biomechanical performance, there is a critical need for predictive tools.
This paper presents a computational biomechanical model designed to connect these local tissue-level changes to the overall, organ-scale function of the aging aortic valve. Building upon a previous model of the healthy valve, this extended simulation incorporates the effects of aging by varying leaflet thickness and extensibility based on experimental data. To model calcification, initial sites of calcification are defined, typically at regions of high flexure, and their growth over time is governed by a simple growth law. This allows for a temporal simulation of valve function, providing the first theoretical tool to describe the progression of aortic valve calcification. The model tracks overall valve function through measures like peak fluid velocity and valve opening area, demonstrating how these biomechanical parameters degrade with both normal aging and calcification. By simulating various ages of calcification onset and growth rates, the model's sensitivity to these parameters in predicting valve failure (defined as AVA reaching < 1.0 cm 2) is analyzed. This biomechanical simulation offers a crucial tool for better understanding and predicting disease progression, which can significantly aid in the design and optimal timing of patient treatments for CAS. The insights gained from this model regarding tissue property changes and their impact on valve hemodynamics are vital for developing new pharmaceutical and surgical interventions that target the underlying tissue dysfunction.
