Background: Experiments and clinical studies have shown that high-frequency (burst) pacing can induce reentry and fibrillation without a strong shock. We hypothesize that a train of weak stimuli induces quatrefoil reentry, and investigate the mechanism and threshold for this mode of reentry induction.
Methods: We apply a train of weak stimuli at different pacing rates to determine the threshold necessary to induce quatrefoil reentry. Numerical calculations are used to simulate cardiac tissue, based on the bidomain model with unequal anisotropy ratios. We consider both anodal and cathodal stimuli.
Results: Quatrefoil reentry is initiated using much smaller currents during burst pacing (0.9 mA) compared to a single premature pulse (8.6 mA). As we varied the pacing rate, we observed reentry at the border between different modes of phase locking, such as between 1:1 and 2:1 responses.
Conclusion: Burst pacing can significantly reduce the threshold for reentry. However, the extreme sensitivity of reentry induction to the exact number of stimuli in the pulse train makes the method difficult to use as a consistent, reproducible way to induce reentry.
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http://dx.doi.org/10.1111/j.1540-8167.2006.00638.x | DOI Listing |
J Cardiovasc Electrophysiol
December 2006
Department of Physics, Oakland University, Rochester, Michigan 48309, USA.
Background: Experiments and clinical studies have shown that high-frequency (burst) pacing can induce reentry and fibrillation without a strong shock. We hypothesize that a train of weak stimuli induces quatrefoil reentry, and investigate the mechanism and threshold for this mode of reentry induction.
Methods: We apply a train of weak stimuli at different pacing rates to determine the threshold necessary to induce quatrefoil reentry.
Prog Biophys Mol Biol
April 2006
Department of Biomedical Engineering, Lindy Boggs Center, Tulane University, Suite 500, Tulane University, New Orleans, LA 70118, USA.
Despite the fact that elucidating the mechanisms of cardiac vulnerability to electric shocks is crucial to understanding why defibrillation shocks fail, important aspects of cardiac vulnerability remain unknown. This research utilizes a novel anatomically based bidomain finite-element model of the rabbit ventricles to investigate the effect of shock polarity reversal on the reentrant activity induced by an external defibrillation-strength shock in the paced ventricles. The specific goal of the study is to examine how differences between left and right ventricular chamber anatomy result in differences in the types of reentrant circuits established by the shock.
View Article and Find Full Text PDFJ Cardiovasc Electrophysiol
June 2005
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Background: Successful prediction of reentrant ventricular tachycardia duration and form from sinus-rhythm electrogram signals in canine hearts is relevant to clinical studies, to potentially improve catheter ablation treatment during EP study.
Methods/results: Following LAD ligation of canine hearts, activation maps were constructed from 312 border zone sites 4-5 days postinfarction. When reentrant ventricular tachycardia was inducible via programmed stimulation, the core of the circuit was defined on the maps as the enclosed area formed by the adjoining lines of slowest conduction and block bounding the protected region of the reentrant circuit.
J Theor Biol
October 2004
Department of Physics, Oakland University, Rochester, Michigan 48309, USA.
This paper reviews Art Winfree's contributions to the bidomain model of cardiac tissue. Specifically, he first predicted quatrefoil reentry, he showed that an S1 refractory gradient is not required for an S2 stimulus to induce reentry, and his work on spiral wave meandering led to studies on how the path of the tip of a spiral wave is influenced by tissue anisotropy.
View Article and Find Full Text PDFJ Cardiovasc Electrophysiol
September 2001
Department of Physics, Oakland University, Rochester, Michigan 48309, USA.
Introduction: An S3 stimulus can exert a protective effect by terminating reentry induced by an S2 stimulus. Our goal was to examine the mechanism by which an S3 pulse terminates reentry and the role that virtual electrodes and break excitation play in this process.
Methods And Results: In our simulation, the bidomain model represents the electrical properties of the tissue and the Beeler-Reuter model represents the membrane kinetics.
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