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Published on: July 29, 2011
Bradycardic onset of spiral wave re-entry: structural substrates
Christian W Zemlin1, Arkady M Pertsov
1Department of Pharmacology, SUNY Upstate Medical University, Syracuse, NY 13210, USA. zemlinc@upstate.edu
Summary
Spontaneous cardiac arrhythmias like re-entrant arrhythmias can initiate at normal heart rates due to structural heterogeneities. This study reveals how bradycardia can trigger re-entry by unmasking pacemakers in poorly coupled cardiac tissue.
Area of Science:
- Cardiac Electrophysiology
- Computational Biology
- Arrhythmia Mechanisms
Background:
- Re-entrant cardiac arrhythmias are a major cause of sudden cardiac death.
- Spontaneous initiation of re-entry at normal heart rates remains poorly understood.
- Existing models often require premature stimuli or rapid pacing for re-entry induction.
Purpose of the Study:
- To propose and investigate a physiological mechanism for spontaneous re-entry onset.
- To explore re-entry induction at normal and slow heart rates.
- To elucidate the role of structural heterogeneities in arrhythmia initiation.
Main Methods:
- Utilized a two-dimensional cardiac tissue model.
- Incorporated Luo-Rudy II ionic kinetics for realistic cell behavior.
- Simulated electrical propagation in the presence of macroscopic coupling heterogeneities.
Main Results:
- Demonstrated that spiral wave re-entry can occur with side-by-side steep and smooth coupling gradients.
- Identified that critical gradient steepness is frequency-dependent.
- Showed that bradycardia can unmask a slow endogenous pacemaker, leading to re-entry.
Conclusions:
- Structural coupling heterogeneities in cardiac tissue can facilitate spontaneous re-entry.
- A single excitation from a less coupled region can initiate re-entrant arrhythmias.
- This mechanism provides a potential explanation for re-entry onset at physiological heart rates.
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