Localization and not extent of fibrofatty infiltratio is the primary factor determining conduction disturbance in a computational model of arrhythmogenic cardiomyopathy

Our objective was to investigate the influence of patient heart geometry and location of fibrofatty diseased tissue in arrhythmogenic cardiomyopathy on conduction properties in an organ-level model of human electrophysiology. Models including fibrofatty regions were generated from different manifestations of disease progression (via electroanatomic mapping). Non-viable tissue was represented by a passive membrane, and the disturbance in intercellular junctions associated with arrhythmogenic cardiomyopathy by decreased conductivities. At rapid pacing, a shorter action potential in arrhythmogenic cardiomyopathy results in propagation depending on fibrofatty pattern and activation sites, while activation is blocked in the control case. In the model, global conduction velocity through tissue with fibrofatty infiltration is faster than for control during rapid pacing. Increasing differences in conduction velocity between fibrofatty patterns start to develop at rapid pacing prior to early activation associated with fibrofatty infiltration.