Abstract
Abnormal conduction is fundamental to the pathogenesis of both atrial fibrillation and ventricular tachycardia/fibrillation. Normal atrial and ventricular myocytes express different combinations of multiple gap junction channel proteins and are interconnected by gap junctions in markedly different spatial distributions. These observations suggest that the disparate anisotropic conduction properties of atrial and ventricular muscle are determined, in part, by both structural and molecular features of gap junctions. Alterations in gap junctional coupling likely contribute to conduction abnormalities underlying reentrant atrial or ventricular arrhythmias.
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© 1997 Springer Science+Business Media New York
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Saffitz, J.E. (1997). Gap Junctions: Functional Effects of Molecular Structure and Tissue Distribution. In: Sideman, S., Beyar, R. (eds) Analytical and Quantitative Cardiology. Advances in Experimental Medicine and Biology, vol 430. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5959-7_25
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DOI: https://doi.org/10.1007/978-1-4615-5959-7_25
Publisher Name: Springer, Boston, MA
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