Microscopic variations in interstitial and intracellular structure modulate the distribution of conduction delays and block in cardiac tissue with source-load mismatch.
Journal Article (Journal Article)
Aims
Reentrant activity in the heart is often correlated with heterogeneity in both the intracellular structure and the interstitial structure surrounding cells; however, the combined effect of cardiac microstructure and interstitial resistivity in regions of source-load mismatch is largely unknown. The aim of this study was to investigate how microstructural variations in cell arrangement and increased interstitial resistivity influence the spatial distribution of conduction delays and block in poorly coupled regions of tissue.Methods and results
Two-dimensional 0.6 cm × 0.6 cm computer models with idealized and realistic cellular structure were used to represent a monolayer of ventricular myocytes. Gap junction connections were distributed around the periphery of each cell at 10 μm intervals. Regions of source-load mismatch were added to the models by increasing the gap junction and interstitial resistivity in one-half of the tissue. Heterogeneity in cell shape and cell arrangement along the boundary between well-coupled and poorly coupled tissue increased variability in longitudinal conduction delays to as much as 10 ms before the onset of conduction block, resulting in wavefront breakthroughs with pronounced curvature at distinct points along the boundary. Increasing the effective interstitial resistivity reduced source-load mismatch at the transition boundary, which caused a decrease in longitudinal conduction delay and an increase in the number of wavefront breakthroughs.Conclusion
Microstructural variations in cardiac tissue facilitate the formation of isolated sites of wavefront breakthrough that may enable abnormal electrical activity in small regions of diseased tissue to develop into more widespread reentrant activity.Full Text
Duke Authors
Cited Authors
- Hubbard, ML; Henriquez, CS
Published Date
- November 2012
Published In
Volume / Issue
- 14 Suppl 5 /
Start / End Page
- v3 - v9
PubMed ID
- 23104912
Pubmed Central ID
- PMC3482616
Electronic International Standard Serial Number (EISSN)
- 1532-2092
International Standard Serial Number (ISSN)
- 1099-5129
Digital Object Identifier (DOI)
- 10.1093/europace/eus267
Language
- eng