Continuous Models Fail to Capture Details of Reentry in Fibrotic Myocardium

Abstract

Cardiac arrhythmias have traditionally been simulated using continuous models that assume tissue homogeneity and use a relatively large spatial discretization. However, it is believed the tissue fibrosis and collagen deposition, which occur on a micron-level scale, are critical factors in arrhythmogenesis, and it remains unclear how well continuous models are able to accurately capture complex conduction behaviors such as reentry in fibrotic tissue. The objective of this study was to compare reentrant behavior in discrete microstructural models of fibrosis and in two types of equivalent continuous models, a homogenous model and a hybrid continuous model with distinct heterogeneities. In the discrete model, increasing levels of tissue fibrosis lead to substantial increases in reentrant cycle length which are inadequately reflected in the homogenous and hybrid continuous models. These cycle length increases appear to be due primarily to increases in tip path length and to altered restitution behavior, and suggest that it is critical to consider the discrete effects of fibrosis on conduction when studying arrhythmogenesis in fibrotic myocardium.