Session S74.3

Multi-Scale Modeling of Hypertension

AI Veress*, GM Raymond, GT Gullberg, JB Bassingthwaighte

University of Washington
Seattle, WA, USA

Finite element (FE) based computational models of the heart have been developed to gain a greater understanding of the regional deformation and function in both the normal and pathological heart. The primary limitation of these models is that they are not connected to a model of a circulatory system, so they cannot simulate and respond to changes in the cardiovascular system. The presented work represents a first step toward a coupled system and demonstrates the linking of a circulatory model run under the JSim analysis package to an left ventricle (LV) model developed for and analyzed using the non-linear, large deformation finite element package NIKE3D. The JSim model of the human systemic circulation was composed of a varying elastance LV and LA and of a systemic arterial, capillary and venous system in a closed loop. Two models were developed, a normal LV under normotensive loading (120/81 mmHg) and a mild hypertension (160/109 mmHg) model loading. Identical heart rates (75 bpm) were used for these models. In both cases, coupled analysis was utilized so that at four time points during systole, the values for the LV volumes and pressures were determined from the steady-state JSim solution. These values were stored in an interface program between JSim's 1-D circulatory model and NIKE3D. This program supplied these pressures and volumes to the FE model program. At each of the time points, the volume output of the FE model was optimized by adjusting the active contractile stress until pressures and volumes matched those provided by JSim's circulatory model. The average first principal stress for the LV was determined for each case as a measure of systolic workload using the end-systolic time step. The optimization for the four systolic time points required four NIKE iterations for each step with relatively quick convergence for both the normal and mild hypertension cases. The normotensive model had an average first principal stress of 39.1KPa while the hypertensive case showed an increase value of 51.8KPa. This 32.3% increase in end-systolic stress suggests that even a relatively mild increase in the afterload results in a pronounced increase in workload to maintain the same systemic flow.

(Abstract Control Number: 114)