Intramural activation and repolarization sequences in canine ventricles. Experimental and simulation studies
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Published on: April 21, 2014
Bruno Taccardi1, Bonnie B Punske, Frank Sachse
1CVRTI Institute, University of Utah, Salt Lake City, 84112 Utah, USA.
Insights
This study mapped 3-D ventricular repolarization, revealing spatial dispersion in recovery times that can promote cardiac arrhythmias. Findings highlight the importance of understanding these sequences for preventing heart rhythm disorders.
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Medical Imaging
Background:
- Limited data exists on 3-D ventricular repolarization sequences and potential fields.
- Spatial dispersion in recovery times and action potential durations is linked to cardiac arrhythmias.
Purpose of the Study:
- To measure and simulate 3-D excitation and recovery sequences in the ventricles.
- To analyze activation-recovery intervals (ARIs) and action potential durations (APDs).
- To investigate the relationship between repolarization patterns and potential arrhythmias.
Main Methods:
- Recorded unipolar electrograms from canine ventricular walls.
- Used specialized software for 2-D and 3-D mapping of excitation, recovery, and ARIs.
- Simulated repolarization sequences using anisotropic monodomain/bidomain models.
Main Results:
- Simulations showed repolarization sequences mirrored excitation but with ~14 ms APD dispersion.
- Electrical measurements revealed recovery pathways varied with pacing rate, with longer ARIs in mid-myocardial regions.
- Transmural dispersion of measured ARIs was 20-25 ms.
Conclusions:
- 3-D mapping provides insights into ventricular repolarization patterns.
- Spatial dispersion in ARIs and APDs may predispose to arrhythmias.
- Anisotropy impacts excitation potentials more than recovery potentials.
Background:
There are no published data showing the three-dimensional sequence of repolarization and the associated potential fields in the ventricles. Knowledge of the sequence of repolarization has medical relevance because high spatial dispersion of recovery times and action potential durations favors cardiac arrhythmias. In this study we describe measured and simulated 3-D excitation and recovery sequences and activation-recovery intervals (ARIs) (measured) or action potential durations (APDs) (simulated) in the ventricular walls.
Methods:
We recorded from 600 to 1400 unipolar electrograms from canine ventricular walls during atrial and ventricular pacing at 350-450 ms cycle length. Measured excitation and recovery times and ARIs were displayed as 2-D maps in transmural planes or 3-D maps in the volume explored, using specially developed software. Excitation and recovery sequences and APD distributions were also simulated in parallelepipedal slabs using anisotropic monodomain or bidomain models based on the Lou-Rudy version 1 model with homogeneous membrane properties.
Results:
Simulations showed that in the presence of homogeneous membrane properties, the sequence of repolarization was similar but not identical to the excitation sequence. In a transmural plane perpendicular to epicardial fiber direction, both activation and recovery pathways starting from an epicardial pacing site returned toward the epicardium at a few cm distance from the pacing site. However, APDs were not constant, but had a dispersion of approximately 14 ms in the simulated domain. The maximum APD value was near the pacing site and two minima appeared along a line perpendicular to fiber directions, passing through the pacing site. Electrical measurements in dog ventricles showed that, for short cycle lengths, both excitation and recovery pathways, starting from an epicardial pacing site, returned toward the epicardium. For slower pacing rates, pathways of recovery departed from the pathway of excitation. Highest ARI values were observed near the pacing site in part of the experiments. In addition, maps of activation-recovery intervals showed mid-myocardial clusters with activation-recovery intervals that were slightly longer than ARIs closer to the epi- or endocardium, suggesting the presence of M cells in those areas. Transmural dispersion of measured ARIs was on the order of 20-25 ms. Potential distributions during recovery were less affected by myocardial anisotropy than were excitation potentials.
