Abstract:

In order to be used in a clinical context, numerical simulation tools have to strike a balance between accuracy and low computational effort. For re- producing the pumping function of the human heart numerically, the physical domains of cardiac continuum mechanics and fluid dynamics have a significant relevance. In this context, fluid-structure interaction between the heart muscle and the blood flow is particularly important: Myocardial tension development and wall deformation drive the blood flow. However, the degree to which the blood flow has a retrograde effect on the cardiac mechanics in this multi-physics problem remains unclear up to now. To address this question, we implemented a cycle-to-cycle coupling based on a finite element model of a patient-specific whole heart geometry. The deforma- tion of the cardiac wall over one heart cycle was computed using our mechanical simulation framework. A closed loop circulatory system model as part of the simulation delivered the chamber pressures. The displacement of the endo- cardial surfaces and the pressure courses of one cycle were used as boundary conditions for the fluid solver. After solving the Navier-Stokes equations, the relative pressure was extracted for all endocardial wall elements from the three dimensional pressure field. These local pressure deviations were subsequently returned to the next iteration of the continuum mechanical simulation, thus closing the loop of the iterative coupling procedure. Following this sequential coupling approach, we simulated three iterations of mechanic and fluid simulations. To characterize the convergence, we evaluated the time course of the normalized pressure field as well as the euclidean distance between nodes of the mechanic simulation in subsequent iterations. For the left ventricle (LV), the maximal euclidean distance of all endocardial wall nodes was smaller than 2mm between the first and second iteration. The maximal distance between the second and third iteration was 70μm, thus the limit of necessary cycles was already reached after two iterations. In future work, this iterative coupling approach will have to prove its abil- ity to deliver physiologically accurate results also for diseased heart models. Altogether, the sequential coupling approach with its low computational effort delivered promising results for modeling fluid-structure interaction in cardiac simulations.

Abstract:

Mathematical models of the human heart contribute to understand the physiology and to support doctors in medical treatment. Hence, for applications in daily clinical routine, accurate, personalized and time efficient models are required. To make the models as simple as possible while still providing the necessary accuracy, it is important to understand the interactions of the modeling subdomains, in particular fluid dynamics, elastomechanics and electrophysiology. It is likely that data feedback loops are necessary between elastomechanics and fluid dynamics on the one side and elastomechanics and electrophysiology on the other side. Currently, connections of the subdomains are mostly neglected. In this work the fluid-structure interaction is addressed by using the pressure gradient field of an existing fluid dynamics model as an input boundary condition for an elastomechanics simulation. On the one hand, a framework extracting the pressure from the fluid dynamics is established. On the other hand, the current framework of the elastomechanics simulation is extended in order to use the pressure data. Regarding the mechano-electrical feedback, two formulations of the stretch-activated ion channel are compared with respect to the changes of calcium release and resulting action potential duration in the ventricular cell model. The results show that the deformation is influenced by the fluid dynamics feedback. Keep- ing the mean pressure in the left atrium and ventricle the same as in the initial elastome- chanics simulation, the ejection fraction remains unchanged. In the electrophysiological subdomain, the action potential duration in 0D simulations are influenced by the stretch- activated ion channels. Further, the intracellular calcium concentration is increasing.