| First Author | Bevilacqua LM | Year | 2000 |
| Journal | J Interv Card Electrophysiol | Volume | 4 |
| Issue | 3 | Pages | 459-67 |
| PubMed ID | 11046183 | Mgi Jnum | J:113087 |
| Mgi Id | MGI:3664488 | Doi | 10.1023/a:1009800328836 |
| Citation | Bevilacqua LM, et al. (2000) A targeted disruption in connexin40 leads to distinct atrioventricular conduction defects. J Interv Card Electrophysiol 4(3):459-67 |
| abstractText | INTRODUCTION: Gap junctions consist of connexin (Cx) proteins that enable electrical coupling of adjacent cells and propagation of action potentials. Cx40 is solely expressed in the atrium and His-Purkinje system. The purpose of this study was to evaluate atrioventricular (AV) conduction in mice with a homozygous deletion of Connexin40 (Cx40(-/-)). METHODS: Surface ECGs, intracardiac electrophysiology (EP) studies, and ambulatory telemetry were performed in Cx40(-/-) mutant mice and wild-type (WT) controls. Atrioventricular (AV) conduction parameters and arrhythmia inducibility were evaluated using programmed stimulation. Analysis of heart rate variability was based on results of ambulatory monitoring. RESULTS: Significant findings included prolonged measures of AV refractoriness and conduction in connexin40-deficient mice, including longer PR, AH, and HV intervals, increased AV refractory periods, and increased AV Wenckebach and 2:1 block cycle lengths. Connexin40-deficient mice also had an increased incidence of inducible ventricular tachycardia, decreased basal heart rates, and increased heart rate variability. CONCLUSION: A homozygous disruption of Cx40 results in prolonged AV conduction parameters due to abnormal electrical coupling in the specialized conduction system, which may also predispose to arrhythmia vulnerability. |
