Gap junctions in cardiovascular disease

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 consid ered to be arrhythmogenic. Using a simple model of human ventricular myocar dium, we found that quantitative remodeling data extracted from the literat ure gave rise to only small to moderate changes in conduction velocity and the anisotropy ratio. Especially for longitudinal conduction, cytoplasmic r esistivity (and thus cellular geometry) is much more important than commonl y realized. None of the remodeling data gave rise to slow conduction on the order of a few centimeters per second.