Modeling the role of the coronary vasculature during external field stimulation.

Abstract

The exact mechanisms by which defibrillation shocks excite cardiac tissue far from both the electrodes and heart surfaces require elucidation. Bidomain theory explains this phenomena through the existence of intramural virtual electrodes (VEs), caused by discontinuities in myocardial tissue structure. In this study, we assess the modeling components essential in constructing a finite-element cardiac tissue model including blood vessels from high-resolution magnetic resonance data and investigate the specific role played by coronary vasculature in VE formation, which currently remains largely unknown. We use a novel method for assigning histologically based fiber architecture around intramural structures and include an experimentally derived vessel lumen wall conductance within the model. Shock-tissue interaction in the presence of vessels is assessed through comparison with a simplified model lacking intramural structures. Results indicate that VEs form around blood vessels for shocks > 8 V/cm. The magnitude of induced polarizations is attenuated by realistic representation of fiber negotiation around vessel cavities, as well as the insulating effects of the vessel lumen wall. Furthermore, VEs formed around large subepicardial vessels reduce epicardial polarization levels. In conclusion, we have found that coronary vasculature acts as an important substrate for VE formation, which may help interpretation of optical mapping data.