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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
