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Cardiovascular Research 2002 56(3):381-392; doi:10.1016/S0008-6363(02)00598-9
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Modulation of triggered activity by uncoupling in the ischemic border

A model study with phase 1b-like conditions

Andrew E Pollarda,*, Wayne E Casciob,c, Vladimir G Fasta and Stephen B Knisleyc

aDepartment of Biomedical Engineering, Cardiac Rhythm Management Laboratory, University of Alabama at Bermingham, Volker Hall B140 1670 University Blvd., Birmingham, AL 35294, USA
bDepartment of Medicine, Division of Cardiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
cDepartment of Biomedical Engineering, University of Chapel Hill at North Carolina, Chapel Hill, NC, USA

pollard{at}crml.uab.edu

* Corresponding author. Tel.: +1-205-975-4710; fax: +1-205-975-4720.

Objective: Triggered beats during regional ischemia may depend upon the electrical source and sink charge interactions between adjacent regions of normal and ischemic cardiac tissue that are partly controlled by electrical coupling. Methods: To study these relationships, we modified parameters in the Luo–Rudy dynamic membrane equations to reflect physiologic conditions associated with phase 1b arrhythmias. Superthreshold delayed afterdepolarizations (DADs) formed after pacing. Coupling contributions were then examined using: (i) a single phase 1b myocyte connected via a variable resistance to a single normal myocyte, and (ii) a multicellular fiber with a 1-cm segment of phase 1b myocytes connected to a 1-cm normal segment having resistance changes that were confined to the ischemic segment. Integration of ionic, capacitive and coupling currents during DAD initiation allowed charge quantification. Results: In cell pairs, phase 1b myocyte DADs were suppressed at resistances where normal myocyte pacing resulted in phase 1b myocyte excitation. Coupling charge requirements limited capacitive charging in the phase 1b myocyte, which occurred in combination with diastolic hyperpolarization that shifted transmembrane potential from threshold. In multicellular fiber simulations, DADs were suppressed with strong coupling in the phase 1b segment. Moderate uncoupling of that segment allowed superthreshold DAD formation away from the border that initiated action potential propagation in the normal segment. With severe uncoupling, propagation failed at the border. Conclusions: These findings support the clinical and experimental observation that intermediate uncoupling is an important contributor to phase 1b arrhythmogenesis.

KEYWORDS Acidosis; Arrhythmia (mechanisms); Cell communication; Computer modelling; Gap junctions; Hypoxia/anoxia; Impulse formation; Ischemia


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