Published online before print September 13, 2001, doi: 10.1161/hh2101.098442
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Submitted on June 25, 2001
Revised on August 17, 2001
Accepted on August 29, 2001
Mechanistic Insights Into Very Slow Conduction in Branching Cardiac Tissue. A Model Study
From the Cardiac Bioelectricity Research and Training Center, Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio.
* To whom correspondence should be addressed. E-mail: jpk12{at}po.cwru.edu or kucera@pyl.unibe.ch.
It is known that branching strands of cardiac tissue can form a substrate for very slow conduction. The branches slow conduction by acting as current loads drawing depolarizing current from the main strand ("pull" effect). It has been suggested that, on depolarization of the branches, they become current sources reinjecting current back into the strand, thus enhancing propagation safety ("push" effect). It was the aim of this study to verify this hypothesis and to assess the contribution of the push effect to propagation velocity and safety. Conduction was investigated in strands of Luo-Rudy dynamic model cells that branch from either a single branch point or from multiple successive branch points. In single-branching strands, blocking the push effect by not allowing current to flow retrogradely from the branches into the strand did not significantly increase the branching-induced local propagation delay. However, in multiple branching strands, blocking the push effect resulted in a significant slowing of overall conduction velocity or even in conduction failure. Furthermore, for certain slow velocities, the safety factor for propagation was higher when slow conduction was caused by branching tissue geometry than by reduced excitability without branching. Therefore, these results confirm the proposed "pull and push" mechanism of slow, but nevertheless robust, conduction in branching structures. Slow conduction based on this mechanism could occur in the atrioventricular node, where multiple branching is structurally present. It could also support reentrant excitation in diseased myocardium where the substrate is structurally complex.
Key words: slow conduction • discontinuous conduction • source-to-load mismatch • atrioventricular node • mathematical model
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