Supraventricular myocardium of the heart of the B6CBAF1 mice strain reveals genetically determined arrhythmogenic properties due to ectopic automaticity and triggered activity

A lot of studies aimed to the investigation the mechanisms of occurrence and ways to prevent of supraventricular arrhythmias - in particular, atrial fibrillation. The origin of the atrial fibrillation in most part of cases is associated with abnormal electrophysiological properties of the pulmonary veins (PV) myocardium. The most important of characteristic of PV myocardium is highly prone to the ectopic automaticity. Moreover, no murine strains with hereditary predisposition to PVs-derived ectopy or arrhythmogenity are known to the present moment. Nevertheless, mice become more frequent objects in the heart electrophysiology studies. Thus, the aim of the present investigation was to characterize, bioelectric properties of the PV and atrial myocardium of the F1 hybrids (B6CBAF1) received by crossing C57Bl/6 and CBA strains. In ex vivo experiments the action potentials were recorded in PV and atrial multicelluar perfused preparations isolated form B6CBAF1 and control BALB/c mice heart using standard sharp microelectrodes technique. In addition, in in vivo experiments standard approach was used to receive and analyze ECG in B6CBAF1 and BALB/c mice. In 80% of experiments the PV myocardium of B6CBAF1 exhibits permanent ectopic automaticity. Spontaneous action potential (SAP) in 55% of experiments were characterized by excessive afterdepolarizations, which caused extreme repolarization delay reached 1-20 s. Besides PV, the atrial working myocardium of B6CBAF1 in 80% of cases demonstrated SAPs. Unlike B6CBAF1, both BALB/c PV and atrial myocardium were unable to generate permanent SAPs or demonstrate repolarization abnormalities in basal conditions. The in vivo ECG recording revealed no arrhythmia episodes of significant changes of ECG parameters in B6CBAF1 mice except increased heart beat frequency. It is possible that that B6CBAF1 hybrids are the first time described mouse strain with the intrinsically or probably hereditary arrhythmogenic supraventricular myocardium demonstrating an ectopic automaticity and triggered activity.

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