© 2000 American Heart Association, Inc.
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Gap Junctions in Cardiovascular Disease
From the Department of Medical Physiology, University Medical Center Utrecht, Utrecht, the Netherlands.
Correspondence to Habo J. Jongsma, Department of Medical Physiology, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, Netherlands. E-mail h.j.jongsma{at}med.uu.nl
Abstract—Connexins, the protein molecules forming gap junction channels, are reduced in number or redistributed from intercalated disks to lateral cell borders in a variety of cardiac diseases. This "gap junction remodeling" is considered to be arrhythmogenic. Using a simple model of human ventricular myocardium, we found that quantitative remodeling data extracted from the literature gave rise to only small to moderate changes in conduction velocity and the anisotropy ratio. Especially for longitudinal conduction, cytoplasmic resistivity (and thus cellular geometry) is much more important than commonly realized. None of the remodeling data gave rise to slow conduction on the order of a few centimeters per second.
Key Words: connexins • conduction velocity • arrhythmia • computer simulation
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