Modeling dynamics in diseased cardiac tissue: Impact of model choice.

Published

Journal Article

Cardiac arrhythmias have been traditionally simulated using continuous models that assume tissue homogeneity and use a relatively large spatial discretization. However, it is believed that the tissue fibrosis and collagen deposition, which occur on a micron-level, are critical factors in arrhythmogenesis in diseased tissues. Consequently, it remains unclear how well continuous models, which use averaged electrical properties, are able to accurately capture complex conduction behaviors such as re-entry in fibrotic tissues. The objective of this study was to compare re-entrant behavior in discrete microstructural models of fibrosis and in two types of equivalent continuous models, a homogenous continuous model and a hybrid continuous model with distinct heterogeneities. In the discrete model, increasing levels of tissue fibrosis lead to a substantial increase in the re-entrant cycle length which is inadequately reflected in the homogenous continuous models. These cycle length increases appear to be primarily due to increases in the 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. Hybrid models are able to accurately capture some aspects of re-entry and, if carefully tuned, may provide a framework for simulating conduction in diseased tissues with both accuracy and efficiency.

Full Text

Duke Authors

Cited Authors

  • Gokhale, TA; Medvescek, E; Henriquez, CS

Published Date

  • September 2017

Published In

Volume / Issue

  • 27 / 9

Start / End Page

  • 093909 -

PubMed ID

  • 28964161

Pubmed Central ID

  • 28964161

Electronic International Standard Serial Number (EISSN)

  • 1089-7682

International Standard Serial Number (ISSN)

  • 1054-1500

Digital Object Identifier (DOI)

  • 10.1063/1.4999605

Language

  • eng