Genesis of complex fractionated atrial electrograms in zones of slow conduction: a computer model of microfibrosis.

Journal Article (Journal Article)


Complex fractionated atrial electrograms are used as potential targets for catheter ablation therapy of atrial fibrillation. Although fibrosis has been associated with the presence of fractionated electrograms, characterizing the substrate through the inspection of electrograms is challenging.


This study sought to determine how progression of microfibrosis and slow conduction affect electrogram morphology.


A microstructure computer model representing a monolayer of cardiac cells was developed. Slow conduction was induced by: (1) sodium channel blockade, (2) uniform reduction in cell-to-cell coupling, and (3) microfibrosis incorporated as a set of collagenous septa disconnecting transverse coupling. The density (0 to 30%) and length (30 to 945 microm) of these collagenous septa were varied. Unipolar and bipolar electrograms were computed during paced rhythm for a set of electrodes with different tip sizes.


The analysis of unipolar electrograms with realistic temporal and spatial filtering showed that increasing the density and length of collagenous septa decreased conduction velocity by up to 75% and increased the amount of fractionation (up to 14 deflections) and asymmetry of the electrograms. In contrast, slow conduction induced by sodium channel blockade or uniformly reduced coupling did not result in electrogram fractionation. When a larger electrode was used, electrogram amplitude was smaller and fractionation increased in a substrate-dependent way.


Microscale obstacles cause significant changes to electrogram waveforms. Conduction velocity and electrogram amplitude and degree of fractionation can be used to discriminate the nature of the substrate and characteristics of fibrosis, giving rise to slow conduction.

Full Text

Duke Authors

Cited Authors

  • Jacquemet, V; Henriquez, CS

Published Date

  • June 2009

Published In

Volume / Issue

  • 6 / 6

Start / End Page

  • 803 - 810

PubMed ID

  • 19467508

Pubmed Central ID

  • PMC3577929

Electronic International Standard Serial Number (EISSN)

  • 1556-3871

International Standard Serial Number (ISSN)

  • 1547-5271

Digital Object Identifier (DOI)

  • 10.1016/j.hrthm.2009.02.026


  • eng