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11:51
Visually Based Characterization of the Incipient Particle Motion in Regular Substrates: From Laminar to Turbulent Conditions
Published on: February 22, 2018
Structural heterogeneity alone is a sufficient substrate for dynamic instability and altered restitution.
Zoar J Engelman1, Mark L Trew, Bruce H Smaill
1Auckland Bioengineering Institute and the Department of Physiology, University of Auckland, Auckland, New Zealand.
Circulation. Arrhythmia and Electrophysiology
|February 6, 2010
Summary
Structural discontinuities in heart disease amplify electrical alternans and promote reentry, increasing arrhythmia risk. This study shows fibrosis can create a substrate for dangerous heart rhythms.
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Medical Simulation
Background:
- Structural heart disease (SHD) is linked to altered ventricular action potential duration (APD) restitution and alternans.
- The precise role of structural heterogeneity versus cellular changes in SHD-induced electrical instability remains unclear.
Purpose of the Study:
- To test the hypothesis that structural heterogeneity in SHD is sufficient to alter dynamic restitution and promote electrical instability.
- To investigate the impact of simulated fibrosis on cardiac electrical activation and arrhythmogenesis.
Main Methods:
- Simulated cardiac activation in a 2D bidomain model with and without a central region of structural discontinuities (fibrosis).
- Utilized a modified LR1 cardiac activation model with isotropic conductivities.
- Applied bipolar stimulation with progressively decreasing coupling intervals to assess rate-dependent effects.
Main Results:
- Structural discontinuities minimally affected activation at low rates but caused significant nonuniformity at high rates.
- Discordant action potential duration alternans occurred at lower rates and with greater extent in the presence of simulated fibrosis.
- Fibrosis-induced tortuous conduction led to diastolic interval fluctuations, regional instability, conduction block, and reentry.
Conclusions:
- Structural discontinuities amplify discordant alternans and create a rate-dependent substrate for reentry.
- This simulation provides mechanistic insights into how cardiac fibrosis contributes to arrhythmogenesis.
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