Related Experiment Videos
Activation delay in healed myocardial infarction: a comparison between model and experiment
N Maglaveras1, J M De Bakker, F J Van Capelle
1Laboratory of Medical Informatics, Aristotelian University Medical School, Thessaloniki, Macedonia, Greece.
Insights
Conduction delay in myocardial infarction occurs where cardiac bundles merge or split. This study modeled bundle bifurcation, revealing local delays crucial for understanding reentry mechanisms.
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Myocardial Infarction Research
Background:
- Conduction delay in healed myocardial infarction can facilitate reentry arrhythmias.
- This delay is often due to increased path length in surviving myocardial bundles.
- Bundle bifurcations represent critical sites for additional conduction delay.
Purpose of the Study:
- To investigate and characterize conduction delay at sites where cardiac bundles bifurcate.
- To model the electrophysiological behavior of activation spread in a simplified myocardial structure.
Main Methods:
- Development of a two-dimensional computer model simulating activation spread in excitable elements.
- Modeling a structure of merging and diverging bundles, specifically focusing on bifurcation points.
- Comparison of simulated extracellular electrograms with experimental data from a superfused infarcted papillary muscle model.
Main Results:
- Identification of a zone of local conduction delay (crowded isochrones) at bundle bifurcation sites.
- Observation that the positioning of isochrones was dependent on activation time determination methods.
- Demonstration that lines of activation delay were predominantly oriented perpendicular to the fiber direction.
Conclusions:
- The study enhances understanding of extracellular electrograms at critical "pivoting points" in the cardiac tissue.
- Activation sequences at a microscopic level are best reconstructed using Laplacian signals.
- Findings contribute to a better comprehension of arrhythmogenesis in infarcted myocardium.
Abstract:
Conduction delay in healed myocardial infarction, facilitating reentry, is frequently based on an increased path length the activation has to travel in a matrix of merging and diverging bundles that survive in the infarcted area. Additional delay occurs at sites where bundles bifurcate. The purpose of this study was to investigate conduction delay at sites where bundles bifurcate. A computer model was developed to simulate spread of activation in a two-dimensional sheet of excitable elements. A structure consisting of two isolated bundles merging into a single one was modeled. Extracellular electrograms calculated in the model were comparable to electrograms obtained in a superfused infarcted papillary muscle model. A zone of crowded isochrones or local conduction delay was found at the site where an isolated bundle bifurcated. The position of the isochrones in this area depended on the way activation times were determined. Lines of activation delay were mainly perpendicular to the fiber direction. In conclusion, the results have enabled us to better understand extracellular electrograms at pivoting points and show that activation sequences at a microscopic level can best be constructed on the basis of Laplacian signals.